When to Eat and Not Eat, How Many Meals and Intermittent Fasting

The whole matter of ‘when we eat’ meals and ‘when we don’t eat’ was historically a non-issue; we ate when it was daylight and we had food available, and we didn’t eat when it was dark or had no food. With the creation of indoor lighting and electricity, “day” lasted as long as we keep the lights on and for most of us, food is available in our fridges around the clock. Before elaborating on the current science surrounding when to eat meals and to not eat, let’s look at a short history of the origins of eating 3 meals per day, and when the idea of ‘snacks’ became prominent.

Timing of Meals

According to food historian Ivan Day[1], during the Middle Ages, availability of daylight shaped meal times, as there was no electricity. People got up and began to work in the fields at first daylight and by mid-day they were hungry after working for 6 hours or so and lunch was the first and main meal of the day. As there was no artificial lighting, cooking large meals in the evening simply wasn’t possible, so dinner was really a smaller meal, such as bread and cheese.

Breakfast became popular during the mid-19th century when labourers needed an early meal to sustain them at work. It became widely popularized in the early 20th century when John Harvey Kellogg invented the first breakfast cereal. Dinner became the main meal of the day with the creation of artificial (gas) lighting, and by the early 1900s, people were eating 3 meals per day, with the last meal occurring after work. Gas lighting was expensive to run, so after dinner was eaten and cleaned up from, bedtime was shortly after.

Snacks

“Snacks” were frowned upon by the middle class during Victorian era because they did not require use of “proper” utensils (cutlery, plates), were seen as unhygienic and were associated with the lower class [2].

Snacks as we know them took root in the 1950s due to the manufacturing industry’s drive to sell new products in a growing economy after the end of WWII, along with an ability to create inexpensive disposable packaging and unique labelling to market these products. Sale of snack foods escalated in the late 1970s [2], and between 1977 and 2006, Americans were eating approximately 570 calories more per day, much of it as snacks rather than during meals [3].

Historic Dietary Treatment of Diabetes

Before the discovery of insulin, successful management of diabetes involved restricting carbohydrates eaten at meals.

In his text book titled “The Principles and Practice of Medicine” (1892), Dr. William Osler recommended a diet of 65% fat, 32% protein, and 3% carbohydrate, as well as abstaining from ”all fruits and garden stuff.” [4] — not dissimilar to some of the high-fat “keto” diets available today. 

In the early 1900s, Bernard Naunyn encouraged a strict carbohydrate-free diet [5], with energy being provided as fat and protein.

In 1914, Dr. Frederick M. Allen treated people for several days with a period of fasting to clear the excess blood sugar via the urine, and then followed that with a diet that was mostly fat and protein, with a small amount of carbohydrates, mostly as vegetables ⁠[6].

Dr. Elliot P. Joslin was the first doctor in the United States to specialize in treating diabetes, and in 1916 adopted the same low-carbohydrate approach as Fredrick Allen [7].

Medications as Treatment in Diabetes

Type 1 Diabetes

The discovery of insulin by Dr. Fredrick Banting and Dr. Charles Best in 1921 provided life-saving therapy for those with type 1 diabetes (which results from failure of the insulin-producing  β-cells of the pancreas). The insulin was initially isolated from the pancreases of beef and pigs, but “human insulin” became possible in the 1980s due to recombinant DNA technology which enabled the development of both basal insulin, as well as rapid acting insulin. This was life-changing and life-saving to those with type 1 diabetes.

Type 2 Diabetes

Metformin initially became available as a first-line treatment for type 2 diabetes in the late 1990s, and enabled those with type 2 to better control their blood sugar levels along with dietary changes — but when people were unable, or unwilling to adequately limit carbohydrate intake, insulin was prescribed.

Insulin went from being a life-saving therapy for those with type 1 diabetes to  also being a ‘treatment’ for people with type 2 diabetes who ate what they wanted at meals and snacks and “covered it with insulin“. The problem is that this type of “liberalization” of the diet creates a “vicious cycle” for those with type 2 diabetes, described as follows in a new study published ahead of print in September 2019, and to appear in the December 2019 journal, Diabetes Care[8];

“Dietary intervention is usually accompanied by sequential addition of several anti-hyperglycemic agents, including glucagon-like peptide 1 (GLP-1) analogs and sodium—glucose cotransporter 2 (SGLT2) inhibitors. Despite this medical treatment, many patients require insulin therapy, which is gradually augmented according to the glucose target-driven strategy. However, this progressive increase in insulin dose often leads to weight gain, which may increase insulin resistance, leading to a vicious cycle further increasing insulin doses, continued weight gain, decreased likelihood of achieving glycemic targets, a high risk for diabetes complications and increased insulin dose-dependent cardiovascular risk and mortality. It is, therefore, important to prevent the weight gain when insulin treatment is required.”

Of course, medications such as biguanides, sulfonylureas, SLP-1 analogues and SGLT2 inhibitors are very important tools for doctors to add in helping manage blood sugar levels, but too often they are used instead of / in the absence of carbohydrate reducing dietary changes and this results diabetes becomes “a chronic, progressive disease“. It need not be so if people are willing to reduce their carbohydrate intake and time when they do eat some carbohydrate-containing food, in accordance with when their body handles them best.

Dietary Recommendations – meals and snacks

Since 2009, people with type 2 diabetes have been advised to eat 3 meals per day plus several snacks per day ⁠— with carbohydrates evenly distributed across the meals and snacks, in order to achieve the best weight management and blood sugar control [9-11].  They’ve been told to aim for between 45-60 grams of carbohydrate at each meal, and 15-20 grams of carbohydrate for each of 3 daily snacks (between breakfast and lunch, between lunch and dinner, and before bed). Surprisingly, the new study referred to above that will appear in the December 2019 issue of Diabetes Care states that there were no research studies to support these practices [8].

The 45-60 g of carbs for each of 3 meals per day and 15-20 g per snack distribution is still being recommended as goals to those with type 2 diabetes — resulting in between 190 -240 g of carbohydrate being eaten each day. That is a lot of carbohydrate for people who’s bodies can no longer handle that much. Presumably the snacks are to lower the risk of hypoglycemia (low blood sugar) that can result from the anti-hyperglycemic medications that have become necessary to prescribe because these people do not restrict carbohydrate and as a result have blood sugar levels that are too high.

Most concerning is that recent studies have found that snacks consumed later in the day have been associated with an increased risk of obesity and type 2 diabetes, with higher overall blood sugar and higher glycated hemoglobin (HbA1C) [12-13]. These are some of the “costs” of people being told to eat an afternoon and evening snack in order to avoid low blood sugar that can result from taking medication to lower blood glucose, and in an absence of being willing to reduce carbohydrate intake.

Would it not make far more sense to encourage people with type 2 diabetes to eat less carbs and eat less often — along with doctors de-prescribing anti-hyperglycemic medication, including insulin? That way, no snacks are needed to keep them from having low blood sugar and their average blood sugar levels can fall.

In fact, a soon-to-be-published pilot study [8] found that those with type 2 diabetes who ate the same calories each day as 3-meals per day, rather than as 6 meals per day [i.e. 3 meals and 3 snacks] reduced body weight, blood glucose, and insulin dosesWithout even changing how many carbs they ate or how many calories they ate, in just 12 weeks, the subjects in the 3 meal per day group, lost on average 12 pounds (5.4 kg) more than those in the 6 meal per day group, had 1.2% lower HbA1C than the 6 meal per day group and their total daily insulin dose was reduced by 26 units ± 7 (with no reduction in the 6 meal per day group). On top of this, this study found that “there was a significant decrease in hunger and cravings only in the 3 meal per day group“. This makes sense of course, because they were able to lower their injected insulin, which drives hunger and fat storage, leading to weight gain. The mechanism was thought to be an up-regulation in the clock genes of those that ate 3 meals per day, which contributed to the improved glucose metabolism.

Note: it’s important to keep in mind that it is the eating of carbohydrate-containing food that triggers the release of insulin from our pancreas, so even in healthy people i.e. those who are not diabetic, eating the same amount of food as 3 meals per day with no snacks (versus 3 meals plus 3 snacks) will result in less insulin being released. Less insulin means less hunger and less fat storage — whether it is the natural insulin from our own pancreas or it is injected insulin. If our goal is weight management, eating the same amount of food as 3 meals, rather than as meals and snacks makes sense.

This study verified that when we eat and when we don’t eat matters a great deal because our body has evolved over hundreds of thousands of years to function in response to light and day cycles, called circadian rhythms.

When We Eat – especially which meals to eat carbs

Chronobiology is the study of the effect of time of day on living systems and is emerging as an important player in human health.

We now know that the body’s processes involved in the maintaining of blood sugar control such as β-cell function, glucose uptake by the muscles, and glucose production by the liver, are all under the control of circadian rhythms. The body’s “master clock” which controls these circadian rhythms is found in a part of the hypothalamus of our brain, called the suprachiasmatic nucleus (SCN) and is “set” by exposure to light.

Note: Historically, the only light that set the SCN was sunlight, but our increasing exposure to bright lights emanating from office- and store- lights, TVs, computers and smart phones has disrupted this once tightly regulated system. 

Similar “peripheral clocks” are found in our body’s tissues, including muscle cells, liver cells, β-cells of our pancreas which produce and release insulin, and fat cells (adipose), and these are controlled by the “master clock” in our SCN, and by when we eat [14,15]. 

As it turns out, our circadian rhythms are optimized for us to eat during periods of light (daytime), and to fast and sleep in periods of dark (night time) [16,17] — so fasting after supper and overnight is consistent with our body’s built-in circadian rhythms.

In addition, blood sugar control is not the same at all times of the day, but fluctuates according to our body’s circadian rhythms. It has been shown in both healthy individuals and those with type 2 diabetes that identical foods eaten in the afternoon and evening cause much higher elevations in blood sugar, compared with the same foods eaten in the morning [18-20] . Based on this, it makes the most sense for any major carbohydrate sources (milk, fruit, root vegetables etc.) that are going to be eaten during the day to be consumed at breakfast, rather than evenly distributed across the whole day and evening.

When We Don’t Eat – intermittent fasting

It has been shown for those with type 2 diabetes that fasting until noon time actually results in much higher after-meal blood sugar levels (postprandial hyperglycemia), as well as an impaired insulin response after lunch and dinner [21], so while it is currently popular for people to chose their “eating windows” based on a wide range of popular protocols, it seems to me that choosing them in a way that is consistent with our circadian rhythms makes the most sense — especially if the goal is weight loss, appetite control and blood sugar regulation.

More Info

If you would like more information about having me design a Meal Plan for you that arranges your eating times and non-eating times around your schedule and in accordance with your natural circadian rhythms, please have a look under the Services tab or in the Shop. If you have service-related questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
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Instagram: https://www.instagram.com/lchf_rd
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Copyright ©2019 LCHF-RD (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. BBD News Magazine, Winterman, Denise, Breakfast, lunch and dinner; Have we always eaten them? Nov 15 2012, https://www.bbc.com/news/magazine-20243692
  2. Carroll, Abigail (30 August 2013). “How Snacking Became Respectable”. Wall Street Journal. August 30, 2013, https://www.wsj.com/articles/how-snacking-became-respectable-1377906874
  3. Duffey KJ, Popkin BM, Energy Density, Portion Size, and Eating Occasions: Contributions to Increased Energy Intake in the United States, 1977—2006, June 28, 2011, https://doi.org/10.1371/journal.pmed.100105
  4. Osler W. The Principles and Practice of Medicine. New York, D. Appleton and Company, 1892
  5. Woodyatt RT, Bernhard NaunynDiabetes 1952;1:240241, pmid:1493683
  6. Allen FM, Studies concerning diabetesJAMA 1914;63:93994
  7. Joslin EP, Treatment of Diabetes Mellitus2nd ed. PhiladelphiaLea & Febiger1917, p. 409
  8. Jakubowicz D, Landau Z, Tsameret S et al, 
  9. Seagle HM, Strain GW, Makris A, Reeves RS; American Dietetic Association. Position of the American Dietetic Association: weight management. J Am Diet Assoc 2009;109:330—346
  10. Beyond the Basics: Meal Planning for Healthy Eating, Diabetes Prevention and Management. Canadian Diabetes Association, 2014.
  11. Arnold L,MannJI, Ball MJ. Metabolic effects of alterations in meal frequency in type 2 diabetes. Diabetes Care 1997;20:1651—1654
  12. Mekary RA, Giovannucci E, Willett WC, van Dam RM, Hu FB. Eating patterns and type 2 diabetes risk in men: breakfast omission, eating frequency, and snacking. Am J Clin Nutr 2012;95:1182—1189
  13. Gouda M, Matsukawa M, Iijima H. Associations between eating habits and glycemic control and obesity in Japanese workers with type 2 diabetes mellitus. Diabetes Metab Syndr Obes 2018;11:647—658
  14. Dyar KA, Ciciliot S, Wright LE, et al. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock. Mol Metab 2013;3:29—41
  15. Sadacca LA, Lamia KA, deLemos AS, Blum B, Weitz CJ. An intrinsic circadian clock of the pancreas is required for normal insulin release and glucose homeostasis in mice. Diabetologia 2011;54:120—124
  16. Poggiogalle E, Jamshed H, Peterson CM. Circadian regulation of glucose, lipid, and energy metabolisminhumans. Metabolism2018;84:11—27
  17. Saad A, Dalla Man C, Nandy DK, et al. Diurnal pattern to insulin secretion and insulin action in healthy individuals. Diabetes 2012;61:2691—2700
  18. Bo S, Fadda M, Castiglione A, et al. Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic
    pattern? A randomized cross-over study. Int J Obes 2015;39:1689—1695
  19. Jakubowicz D, BarneaM, Wainstein J, Froy O. High caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women. Obesity (Silver Spring) 2013; 21:2504—2512
  20. Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr 2012;108:1286—1291
  21. Jakubowicz D, Wainstein J, Ahren B, Landau Z, Bar-Dayan Y, Froy O. Fasting until noon triggers increased postprandial hyperglycemia and impaired
    insulin response after lunch and dinner in  individuals with type 2 diabetes: a randomized clinical trial. Diabetes Care 2015;38:1820—1826

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Is it Possible to be a Vegetarian and Eat Low Carb or Keto?

Many people think that eating a low carb or ketogenic diet necessitates eating meat — in the same way that many assume that one needs to eat lots of added fat, but neither are true. In a previous article, I addressed the misconception that eating a low carb or keto diet is all about eating lots of extra fat and in this article, I will address the false belief that one has to be a meat-eater to follow a low-carb or ketogenic diet.

Before launching into the article, it’s important to define some terms.

Vegetarian versus Vegan

There is a significant difference between vegetarians and vegans and these two terms seem to get mixed up frequently. Vegans eat no animal products, while vegetarians don’t eat the meat of animals but will eat products that come from animals, such as dairy and eggs.

There are different categories of vegetarians, including ovo-lacto (those who eat eggs and milk-based products), as well as those that only eat one or the other (ovo or lacto). Some classify pescatarians who eat wild fish and seafood as a form of vegetarianism because they don’t eat farmed animals for food but for the purpose of this article I will use the term “vegetarian” to mean ovo-lacto vegetarian, as this is the most common form.

Different Motivations, Same Needs

Religious or cultural vegetarians

People are vegetarian for different reasons; some for religious reasons, including some Hindus, Buddhists, Jains, Sikhs and Seventh Day Adventists. Some people don’t eat meat for cultural reasons.  For example, some people from India may not be religious themselves but don’t eat meat because they were not raised eating it or because others in their social circle don’t eat meat. I refer to these type as being culturally vegetarian. Finally, some don’t eat meat for ethical reasons — believing it is morally wrong to kill an animal to eat it. 

From my perspective as a Dietitian, it is important that people who want to eat a low carb or ketogenic diet for health reasons are able to do even if they are vegetarian.

While type 2 diabetes is on the rise in those of various ethnic backgrounds, people of South Asian descent (those who have their roots in India, Pakistan, Sri Lanka, Bangladesh and Nepal) are thought to be at higher risk, and many people from these regions eat a vegetarian diet for religious or cultural reasons. Given what we now know about the association between a diet high in carbohydrate and both hyperinsulemia and type 2 diabetes (documented in many previous posts), offering people the option of eating a low carb or ketogenic vegetarian diet, enables them to obtain the same health benefit as those that choose to eat meat. And why not?

While many omnivores consider vegetarianism an ‘inferior diet’ it need not be so. A well-designed vegetarian or omnivore diet enables people to access all the essential macronutrients (essential fats and amino acids) from real, whole foods. This article will explains ‘how’, below.

Ethical VEGETARIANS

Oftentimes I find that people that choose vegetarianism for ethical reasons don’t realize that one can purchase ethically-raised meat and poultry. There are butchers in my area that raise their animals out back, where they are humanely treated their entire lives and killed humanely. These are a far cry from the industrial feed-lots that often motivate ethical vegetarians, and for understandable reasons. One place that I shop at has the motto “know your farmer, know your meat“. As well, some of the most ethical meat-eaters I know are hunters that train at the range to make sure that the animal they harvest doesn’t suffer, and they use the whole animal for food; from snout to tail. In fact, one local hunting group I’ve heard of is run in association with a local First Nations band that teach hunters that already have their Federal hunting licence to select animals in accordance with centuries-old First Nations principals for animal stewardship. One does not have to become a vegetarian for ethical reasons, as there are other options.

Defining a Low Carb or Keto Diet

Whether one is a vegetarian or a meat-eater, defining what “low carb” or “keto” is necessary in order to determine how one can eat this way.

As mentioned in a prior article, what makes a diet ”low carb” or ”ketogenic” is how much carbohydrate it has, not how much fat it contains. In the same way, what makes a diet low carb or ketogenic has nothing to do with how much meat one eats, or whether one eats meat at all.

Feinman et al [2] defined three categories of reduced-carbohydrate diets as follows;

(a) very low carbohydrate ketogenic*: carbs limited to 20—50 g per day or < 10% of total energy intake.

(b) low carbohydrate: carbs limited to < 130 g per day or < 26% of total energy intake.

(c) moderate carbohydrate: carbs limited to 130—225 g per day or 26—45% of total energy intake.

In my clinical practice and in other articles on this web page, I define ”low carb” and ”ketogenic” in the same way — with a low carb diet being one that is < 130 g carbohydrate per day, and a ketogenic diet as one that is 20—50 g of carbohydrate per day. What makes a keto diet ketogenic is that carbohydrate intake is low enough to put an individual into a state of ketosis, which is a normal physiological state that people go into after an overnight fast when they have used up their glycogen stores. When the body is in ketosis, it is burning stored fat for energy and releasing ketones which can be used by the brain and other tissues. In general, men can achieve ketosis eating ⩽ 50 g of carbs per day, but women often need to eat ⩽ 35 g of carbohydrate per day.

Essential Macronutrients

As covered in detail in this previous article, from a dietary perspective only protein and fat are essential in the diet. For a nutrient to be ”essential”, it is required to be eaten because the body can’t manufacture it.

There are 2 essential fats; linoleic acid, an omega 6 fat and alpha-linolenic acid, an omega 3 fat, and there are 9 essential amino acids. Amino acids are  are the building blocks from which proteins are made.

For omnivores, getting all the essential nutrients is fairly straight forward and simply requires eating a wide range of meat and animal products, along with nuts and seeds, but for those who are ovo-lacto vegetarians, one needs to be  more intentional to ensure getting all the essential nutrients. 

The 2 essential fatty acids (linoleic and alpha-linolenic acid) can be easily obtained from eggs, nuts and seeds, but ensuring adequate intake of all 9 of the essential amino acids (histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine from low carb, vegetarian sources can be achieves as follows [3];

  • Vegetarians following a low carb or ketogenic diet can obtain histidine from dairy foods such as milk and cheese, as well as from nuts, seeds and eggs.
  • Isoleucine can be obtained from eggs and cheese, as well as from seaweed and soy protein, if people wish.
  • Rich sources of leucine include milk, cheese and egg, as well as from pumpkin or squash seeds. It can also be obtained from tofu and legumes eaten in daily maximum 1/2 cup quantities (as they are a significant source of carbohydrates).
  • Lysine can be found in some cheeses such as Parmesan, eggs and spirulina as well as from tofu, and if needed can be supplemented with whey protein isolate and isolated soy protein.
  • Foods high in methionine include dairy of different types, cheese, eggs, and nuts, as well as soy and legumes.
  • High phenylalanine foods include cheese, nuts and seeds, eggs and dairy, as well as from soybeans and legumes.
  • Foods rich in threonine include cheese, nuts and seeds, and if desired, in soy, and in legumes and lentils (in maximum daily 1/2 cup servings as they are significant sources of carbs)
  • Good sources of tryptophan include egg, milk products such as yogurt, nuts and seeds and soy products, if eaten.
  • High valine foods include nuts and seeds, mushrooms, and soybeans if eaten, as well as legumes.

Note (Nov 8, 2019 @ 10 am): shortly after publishing this article, the topic of whether vegetarians can obtain sufficient vitamin B12 and the long chain fatty acids, DHA and EPA was raised on social media. While this article is about a vegetarian diet providing all the essential macronutrients, I will add the following information for those who are interested:

Re: vitamin B12: 2 cups of yogurt per day provides 100% DV of B12 and so do 4 eggs (which many low carb omnivores eat in a day). Add to that 3 oz of Swiss cheese which provides 100% DV, or a cup of tofu (which provides more than 100%), getting enough vitamin B12 is not an issue, provided vegetarians are not restrained by a “low fat” paradigm.

Re: the long chain fatty acids DHA and EPA: There is no Dietary Reference Intake (DRI) for EPA or DHA, only for alpha-linolenic acid. In healthy young men, approximately 8% of dietary alpha linolenic acid is converted to EPA and ≤4% alpha-linolenic acid is converted to docosahexaenoic acid (DHA). [Burdge GC, Jones AE, Wootton SA. Eicosapentaenoic and docosapentaenoic acids are the principal products of α-linolenic acid metabolism in young men. Br J Nutr. 2002;88(4):355-364].

In healthy young women, approximately 21% of dietary alpha-linolenic acid is converted to EPA and 9% is converted to DHA. [Burdge GC, Wootton SA. Conversion of α-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002;88(4):411-420. ].

The better elongation in young women is related to the effects of estrogen. [Burdge G. α-Linolenic acid metabolism in men and women: nutritional and biological implications. Curr Opin Clin Nutr Metab Care. 2004;7(2):137-144, Giltay EJ, Gooren LJ, Toorians AW, Katan MB, Zock PL. Docosahexaenoic acid concentrations are higher in women than in men because of estrogenic effects. Am J Clin Nutr. 2004;80(5):1167-1174.]

For vegetarians, eating seaweed including nori, spirulina and other types of edible seaweed provides a good source of pre-formed DHA & EPA in the diet. These also form the basis for vegetarian-sourced DHA and EPA supplements that can be purchased. 

Low Carb and Ketogenic Diets are Truly Not “One-Sized-Fits-All”

There really isn’t a “one-sized-fits-all” low carb or ketogenic diet!

There are the high fat / moderate protein varieties popularized by Dr. Jason Fung and that are often associated with high consumption of bacon, heavy whipping cream, and fatty meat, and offset by periods of intermittent fasting.

There is the higher protein lower fat approach during weight loss, followed by a moderate protein higher fat diet during weight maintenance of Dr. Stephen Phinney MD, PhD and Dr. Jeff Volek RD, PhD.

You can read more about the above two approaches in this article.

There are the higher lean protein type, with more grams of protein than grams of fat (popularized most recently by Dr. Ted Naiman in his P:E Diet and referred to in the previous article). More than likely, there are different macronutrient combinations than the ones listed here that are popular with others.

I don’t believe that any of the above can serve as a “one-sized-fits-all” approach because everybody’s nutritional needs and health conditions are different.  

Those who are omnivore can choose a meal pattern that includes meat, and for those that are vegetarian (for whatever reason) can still reap the health benefits from eating a well-designed low carbohydrate diet that does not include meat.

Final thoughts…

It is my observation that many people who follow a low carb or ketogenic lifestyle tend to be overly loyal to their particular dietary style, which inadvertently makes people who need to or choose to eat differently feel that the health and metabolic benefits of following a low carb diet is not available to them.

People that don’t eat meat for religious, cultural or ethical reasons need to know there are options available for them to have a well-designed meal plan that includes the animal derived products they do eat, rather than to be told how ‘inadequate’ their diet is compared to those who eat meat. 

More Info

If you would like more information about the services that I provide and how I can help design a Meal Plan based on your needs, please have a look under the Services tab, or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 LCHF-RD (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only. The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything you have read or heard in our content.

Resources

  1. Gujral UP, Pradeepa R, Weber MB, Narayan KM, Mohan V. Type 2 diabetes in South Asians: similarities and differences with white Caucasian and other populations. Ann N Y Acad Sci. 2013;1281(1):51—63. doi:10.1111/j.1749-6632.2012.06838.x
  2. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13.
  3. USDA Food Composition Databases, https://fdc.nal.usda.gov/

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Which Protein Foods Are Best for Weight Loss on a Low Carb / Keto Diet?

This article is about which protein foods are best for weight loss on a low carb or ketogenic diet, and builds on the previous article, where I outlined that what makes a diet ”low carb” or ”ketogenic” is how much carbohydrate it has, not how much fat it contains.


I’m not sure where the idea came from that eating a low carb or ketogenic diet for weight loss should include piles of bacon,  bulletproof coffee, fathead pizza and ‘fat bombs’. Perhaps it originated with advocates of eating such a diet which is offset by extended periods of fasting, or by the use of the very term “low carb high fat” / “LCHF“, itself. As explained in the previous article, a low carb diet is higher in fat and protein, because the amount of carbohydrate is reduced — and this is necessary for the the body to be provided with adequate amounts of essential fats and essential amino acids (that make up protein) in order to function properly and make any glucose it needs.

Note: if you haven’t yet read the previous article, I’d highly recommend clicking here and reading it first, as it will help considerably with understanding this one.

As mentioned in the preceding article, some “LCHF” diets that target higher protein may be as high as 50-60% fat — which is considered “high fat” compared to the 30% of calories as fat recommended by previous and current food guides. Other some variations of a low carb diet that target protein may have considerably less fat; depending which protein foods are chosen, and whether fat containing foods that are not rich sources of protein (such as avocado and olives) are also included. In either case, a low carb or ketogenic diet that targets protein will have significantly less than the 75% calories as fat of the high fat versions.  The fat eaten on a low carb or ketogenic diet which targets protein will come from fatty fish such as salmon, tuna, mackerel and sardine, the fat that exists in the lean portions of chicken, pork and steak, in egg and cheese, as well as in nuts and seeds, avocado and olives. What is (pardon the pun) essential is for people to ensure is that they eat foods that contain the two essential fats (linoleic acid, alpha-linolenic acid) and the nine essential amino acids (the building blocks of protein), including histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine that the body can’t manufacture. 

Combined List of Essential Nutrient-Containing Foods

In the previous article, I outlined which foods of animal origin and vegetarian origin are the best sources of each of these essential nutrients and that list should be referred to when selecting specific foods containing these, but combining those into one list, the following taken as a whole are good sources of the essential nutrients for those following a low carb or ketogenic diet:

  • pork
  • beef
  • lamb
  • chicken
  • turkey
  • fish, including tuna
  • shellfish
  • cheese, including Parmesan
  • nuts, including walnuts 
  • pumpkin seeds and flax
  • eggs
  • soy protein
  • whey protein isolate
  • seaweed
  • tofu
  • legumes and lentils
  • spirulina

For those seeking weight loss, it makes good sense to choose foods with the most amount of protein for the least amount of energy (calories). Up until recently, figuring this out would have required lots of calculations, but Dr. Ted Naiman, a board-certified family medicine physician who practices at the Virginia Mason Medical Center in Seattle, Washington has made this easy. Along with William Shewfelt, Dr. Naiman recently published an online book titled The P:E Diet – Leverage Your Biology to Achieve Optimal Health.

Protein to energy (P:E) Ratio

“P:E” is simply the Protein to Energy ratio of a food and Dr. Naiman who is well known on social media for his excellent infographics makes choosing foods with the most amount of protein for the least amount of energy (calories) easy.

from The P:E Diet – Leverage Your Biology to Achieve Optimal Health, available at http://thepediet.com/

Referring to Dr. Naiman’s P:E ratio enables the sorting of the foods available on a low carb or ketogenic diet and which contain the essential nutrients, into those with the highest protein to energy ratio:

  • whey protein isolate
  • egg white
  • fish, including tuna
  • prawns
  • chicken breast
  • other poultry, including chicken legs, turkey, etc.
  • plain non-fat Greek yogurt
  • ground beef
  • pork
  • steak
  • whole eggs
  • soy protein
  • tofu
  • processed meat such as bacon
  • cheese, including Parmesan
  • lentils
  • milk
  • peanuts
  • beans / legumes
  • nuts

Calculations will still need to be done for other meats such as lamb and goat,  and other types of seafood, but this list provides a good means to select foods that have the highest protein to energy ratio.

Low Carb and Ketogenic Diets Include a Range of Fat Intake

In the previous article, I mentioned how a well-designed low carb or ketogenic diet may have in the range of 50-60% calories as fat, but selecting foods with a higher protein to energy ratio (such as egg white and non-fat Greek yogurt) will provide less fat and few calories (energy) than choosing whole egg and Greek yogurt that is 5% fat. Doing this consistently will result in a significantly lower amount of fat yet it is still a low carb or ketogenic diet because of the low amount of carbohydrate it contains.

Use of a higher P:E ratio makes sense for those who are seeking to build muscle mass or to follow a protein-sparing modified fast type of diet. For this, there is Dr. Naiman’s book (link in the References and above). For those seeking simple weight loss, eating whole egg and slightly higher fat yogurt may provide more satiety (feeling of fullness), albeit with higher caloric intake. Since each person’s reasons for wanting to follow a low carb or ketogenic meal pattern is different, which specific protein foods are best to choose in what quantities will vary, person to person. There is no one-sized-fits-all low carb or ketogenic diet.

Final Thoughts…

People following a low carb or ketogenic meal pattern for weight loss and preserving muscle mass should target protein foods with an optimal P:E ratio for their needs, which will likely fall somewhere between the highest P:E ratio (5.0) and those in the 1.0-1.5 range.

Regular inclusion of high fat foods with relatively low protein such as bacon, bulletproof coffee, fathead pizza and fat bombs’ is neither required nor ideal if weight loss is being sought.

More Info

If you would like more information about the services that I provide and how I can help design a Meal Plan based on your needs, please have a look under the Services tab, or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
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Copyright ©2019 LCHF-RD (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Reference

Naiman T, Shewfelt W, The P:E Diet – Leverage Your Biology to Achieve Optimal Health, http://thepediet.com/

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What Makes a Diet Low Carb or Keto is NOT How Much Fat it Contains

Many people assume that a “low carb” or ketogenic (“keto”) diet for weight management and blood sugar reduction requires them to eat a diet high fat — piles of bacon,  bulletproof coffee, fathead pizza and ‘fat bombs’, but this is not true. Not only is eating that way not ideal for many people seeking weight loss — but some actually end up gaining weight doing so.

In fact, what makes a diet “low carb” or “ketogenic” is how much carbohydrate it has, not how much fat it contains.

Defining Low Carb and Keto Diets

Different people define “low carb” or “keto” level of carbohydrates in different ways, but Feinman et al [1] defined three categories of reduced-carbohydrate diets as follows;

(a) very low carbohydrate ketogenic*: carbs limited to 20—50 g per day or < 10% of total energy intake.

Note: What makes a keto diet ketogenic is that that low carbohydrate intake puts people into a state of ketosis, which is a normal physiological state that people go into after an overnight fast. It is where the body burns stored fat for energy, releasing ketones which can be used by the brain and other tissues.

(b) low carbohydrate: carbs limited to < 130 g per day or < 26% of total energy intake.

(c) moderate carbohydrate: carbs limited to 130—225 g per day or 26—45% of total energy intake.

In my clinical practice and on other articles on this web page, I define “low carb” and “ketogenic” as Feinman et al did; with a low carb diet being one that is < 130 g per day and a ketogenic diet as one that is 20—50 g per day.

Protein, Fat and Carbohydrate — are all essential?

Many people assume that people need to eat all three macronutrients; protein fat and carbohydrate but from a dietary point of view, only protein (as specific amino acids) and fat are considered “essential” in the diet. For a nutrient to be “essential”,  it is required to be eaten in food because the body can’t manufacture it.

There are two fats that are considered “essential”; linoleic acid (an omega 6 fat) and alpha-linolenic acid (an omega 3 fat). We need to eat meat and eggs and/or nuts and seeds for the major dietary sources of linoleic acid, as well as nuts such as walnuts and seeds such as flax to get rich sources of alpha-linolenic acid, although many people obtain these from eating chicken, cheese and whole milk [2].

Amino acids are the building blocks of protein, and there are nine amino acids that are considered “essential”; histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

Below are the best low carb foods for obtaining each of these[3]  are listed below.

    • The best sources of histidine include pork, beef, lamb, chicken, turkey, fish, dairy such as milk and cheese, nuts, seeds, eggs.
    • Best sources of isoleucine are eggs, turkey, chicken, lamb, cheese and fish and for vegetarians, soy protein and seaweed.
    • Rich sources of leucine include chicken, beef, pork, tuna, milk, cheese, and egg and for vegetarians tofu, legumes and pumpkin or squash seeds.
    • The best sources of lysine include red meat such as beef and lamb, pork, poultry,  some cheeses such as Parmesan, certain fish such a cod and sardine, egg and whey protein isolate, and for vegetarians there is tofu, isolated soy protein and spirulina.
    • Foods high in methionine include , beef, lamb, cheese, turkey, pork, fish, shellfish, eggs, dairy and nuts, and for vegetarians, soy and legumes.
    • High phenylalanine foods include cheese, nuts and seeds, beef, lamb, chicken, pork, fish, eggs and dairy, and for vegetarians soybeans and legumes.
    • Foods rich in threonine foods include lean cuts of beef, pork, chicken, liver, cheese, shellfish, nuts, seeds, and for vegetarians, soy, legumes and lentils. 
    • While many people associate turkey as being high in tryptophan, there are other foods as well. Tryptophan is required for the body to make the neurotransmitter serotonin, so getting enough tryptophan is…pardon the pun, essential. Good sources of tryptophan include salmon, all kinds of poultry (including turkey), egg, milk, nuts and seeds and for vegetarians, soy products.
    • High valine foods include cheese, beef, lamb, chicken, pork, nuts and seeds, and fish, and for vegetarians, soybeans, legumes and mushrooms.

Carbohydrate is Not Essential in the Diet

The Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids [4] which sets the standard for macronutrient consumption in both the US and Canada states;

The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed. 

The lower limit of dietary carbohydrate

In short, there is no essential need for dietary carbohydrate provided that ”adequate amounts of protein and fat are consumed”The reason carbohydrate is not essential is because the body can make what it needs from dietary protein and fat!

The Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005) goes on to explain the process;

”In the absence of dietary carbohydrate, de novo synthesis of glucose requires amino acids derived from the hydrolysis of endogenous or dietary protein or glycerol derived from fat. Therefore, the marginal amount of carbohydrate required in the diet in an energy-balanced state is conditional and dependent upon the remaining composition of the diet.”

What this means is that the body will synthesize the little bit of glucose needed by the brain and red blood cells, etc from the protein taken in through the diet —provided it is in adequate amounts, or from glycerol which is formed when fat is broken down. 

I encourage people to target protein first, add low carb veggies and fruit (such as lime, lemon, and a few berries), then add a bit of fat to make things taste good and to provide a source of essential fatty acids. Protein and fat both provide satiety (not feeling hungry) but protein has significantly less calories than fat. If one is aiming for weight loss, adding lots of extra dietary fat (in addition to what comes naturally in protein foods) is counter-productive. That doesn’t mean avoid fat, either. Eat the egg with the yolk and marbling in steak is fine and so is using some fat for cooking food or putting on veggies, but for weight loss, it’s best to avoid extra fat that doesn’t come a good source of protein.

Final Thoughts…

What makes a diet low carb or ketogenic is how much carbohydrate it has, not how much fat it contains; with a low carb diet being one that is < 130 g carbohydrate per day and a ketogenic diet as one that is 20—50 g carbohydrate per day. The amount of fat in the diet does not make it low carb or keto!

While a low carb diet is often called a “LCHF diet” i.e. “low carb high fat”, it is really only “high fat” relative to the recommended American or Canadian diet which is supposed to be < 30% fat.  A low carb diet that targets protein may be as high ~50-55% fat or significantly lower if lower fat protein is chosen — but is no where near the 75% fat of a classic ketogenic diet (KD diet) used for those with epilepsy*, or some fat-based variations low carb diets. It is my experience that many people, especially peri-and post menopausal women do much better on the higher protein version. A Low carb or keto diet is not about eating lots of bacon, avocado, heavy whipping cream or ‘fat bombs’ and “bulletproof” coffee. It is about eating less carbs.

*Addendum (Nov 1, 2019 @ 2:35 pm) It was pointed out to me that the Charlie Foundation uses a Low Glycemic Index Treatment Diet for the management of epilepsy that is closer to 60% fat, which allows for less fat than a strict KD diet.

Yes, we need some essential fat in the form of linoleic acid and alpha-linolenic acid which can easily be obtained by eating meat and eggs, and for vegetarians to eat nuts including walnuts and seeds such as flax seed, but for the most part, eating the foods listed above that are rich in the nine essential amino acids will provide all the essential fat we need.

Update (Nov 3, 2019): The following article outlines which protein foods are best for weight loss on a low carb or ketogenic diet.

More Info

If you would like more information about the services that I provide, please have a look under the Services tab, or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 LCHF-RD (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Resources

  1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13.
  2. National Cancer Institute, Food sources of alpha-linolenic acid (PFA 18:3), Epidemiology and Genomics Research Program, Table 6, https://epi.grants.cancer.gov/diet/foodsources/fatty_acids/table6.html
  3. USDA Food Composition Databases, https://fdc.nal.usda.gov/
  4. National Academies of Sciences, Engineering and Medicine, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids, 2005, https://www.nap.edu/catalog/10490/dietary-reference-intakes-for-energy-carbohydrate-fiber-fat-fatty-acids-cholesterol-protein-and-amino-acids

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Low Carb Foods That May Help Protect Against the Flu

INTRO: This article documents the science that supplementing with Vitamin D can help protect us against the flu, recommendations for how much we should be supplementing, as well as excellent low carb dietary sources of this important fat-soluble vitamin. 


The other day I shared an article[1] on social media from a local Canadian news outlet about a 37 year old man from Ontario who decided to forgo his annual flu shot last year and ended up in hospital with pneumonia for two months, after he contracted the flu virus from his daughter. The article indicated that data from Statistics Canada indicates that only 1/3 of Canadians above the age of 12 get the flu shot every year, yet according to deputy chief public health officer for the Public Health Agency of Canada, Dr. Howard Njoo, more than 12,000 Canadians end up hospitalized for flu-related complications each year, and between 3,000-4,000 people die as a result. Dr. Njoo was quoted as saying;

“it makes common sense that you should get your flu shot.”

There was much heated discussion on Facebook whether there is  “proof” that the flu shot prevents people from getting the flu. 

A well-known epidemiologist said that “unlike childhood vaccinations (ie, diphtheria, tetanus, pertussis, polio, measles, mumps, rubella, etc), there is no conclusive proof that flu shots reduce risk of either getting the flu or its complications. There are no large randomized trials, which is the standard for establishing a causal connection. So all we really have are observational studies, which are subject to a lot of confounding“. The epidemiologist noted that there was a meta-analysis of 44 years’ worth of studies that was published in Lancet Infectious Diseases in 2011 which found only “moderate efficacy” of the flu vaccine[2].

In response, a GP referenced a 2012 review of 15 meta-analyses related to the effectiveness of the flu vaccine for adults and the elderly which found they provided what was described as ‘satisfactory immunogenicity’,  but that data on inactivated vaccines for children was scarce[3].

One of the other people that commented about the CTV article brought up studies that I was previously unaware of that indicate that Vitamin D supplementation may reduce the risk of getting the flu  ⁠— especially for those who are low in in this fat-soluble vitamin to begin with. Stats Can data from 2013 indicates that 1/3 of Canadians fall in this category [4]. It was this fact that motivated me to write this article.

Studies Showing that Vitamin D Attenuates the Flu

There are two large-scale meta-analyses — one from 2013 and the other from 2017 that indicate that Vitamin D supplementation can reduce the risk of getting an upper respiratory infection (URI) including influenza (“the flu”).

The first study by Bergman et al [5] analyzed data from 11 placebo controlled trials that involved more than 5,600 subjects and found that those taking a daily dose of Vitamin D had half the risk of developing an upper respiratory infection (URI), including influenza (‘the flu”). This held true even though many of the studies used very low dose of supplementation.

The second of the two large-scale meta-analysis by Martineau et al [6] analyzed the data from 25 randomized controlled trials and involved more than 11,300 subjects. This study found that Vitamin D supplementation reduced the risk of developing an upper respiratory infection (URI), including the flu and those who were the most deficient experienced the most benefit. Even those subjects with very low Vitamin D status had 1/3 the risk when supplementing with Vitamin D, compared to those who did not take any.

Both meta-analysis found that daily dosing with Vitamin D was more effective than taking larger (bolus) doses once a week, or once a month.

There are numerous studies which indicate that people with lower levels of Vitamin D are more likely to get the flu and a 2010 study with healthy adults found that people with lower levels of were twice as likely to get the flu than people with high levels of Vitamin D [7].

Supplementing with Vitamin D to Reduce Risk of Flu

Health Canada’s recommended daily intake (RDAs) for Vitamin D (updated in 2011) are 600 International Units (IUs) for everyone aged one year old to 70 years old and 800 IU for adults over 70 years of age. Health Canada’s safe upper limit (UL) is listed as 4,000 IU per day, however recent scientific publications indicate that there was an error in the calculations used to determine them.

Two researchers from the School of Public Health at the University of Alberta published a paper in October 2014 which indicates that the Institute of Medicine (IOM) that develops the Recommended Dietary Allowances (RDAs) used by both Canadians and Americans made a serious error in their calculations in determining the RDAs for Vitamin D [9] and that rather than 600 IUs being needed to prevent deficiency in 97.5% of individuals, the actual amount is estimated to be 8895 IU of Vitamin D per day — which is above the Health Canada’s tolerable upper intake of 4000 IU per day.

On top of that, researchers from the University of California at San Diego and Creighton University in Omaha, Nebraska published a letter in the same online journal in March 2015 which said that they have confirmed the Institute of Medicine’s miscalculation that was noted by the Canadian investigators [10].

A press release published in Science News on March 17, 201[11] indicated that;

“The recommended intake of vitamin D specified by the IOM is 600 IU/day through age 70 years, and 800 IU/day for older ages. Calculations by us and other researchers have shown that these doses are only about one-tenth those needed to cut incidence of diseases related to vitamin D deficiency.

How much Vitamin D should we supplement?

The Vitamin D Council (a US-based group) recommends adults take 5,000 to 10,000 IU/day, depending on body weight and recommend people have their levels checked to make sure it is > 40 ng/ml (100 nmol/l) and to maintain serum levels at 50 ng/ml (125 nmol/L). Since Vitamin D toxicity manifests as high levels of calcium in the blood and urine, the Vitamin D Council recommends monitoring via blood tests that serum levels don’t exceed 150 ng/ml (374 mmol/L).

Since Health Canada’s current upper limit is 4,000 IUs per day (which may be based on an error in calculation, as noted above), a prudence dosage for supplementation for a healthy adult would not exceed 4,000 IUs per day.

Note: I also recommend people take 100 mcg of Vitamin K2 (menaquinone-4, or menaquinone-7) as Vitamin K2 plays a synergistic role with Vitamin D which regulates blood levels of calcium. Vitamin K prevents calcium from accumulating in soft tissues, such as the blood vessels (contributing to Coronary Artery Calcification)[12].  Put simply, Vitamin K helps ensure that calcium ends up in bone, not arteries.

NOTE: People taking Warfarin (Coumadin) or other anticoagulant medication should not supplement with Vitamin K2 except under the advice of the physician prescribing Warfarin.

If you are a healthy adult under 50 years old with no family risk of cancer* or osteoporosis, 1000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) is probably sufficient. Be sure to choose the D3 form (not D2) as it is more efficient at raising serum levels. For adults under 50 with a family history of cancer or who are at risk for osteoporosis, a dosage of 2000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) may be more appropriate.

*there are many studies indicating that supplementing Vitamin D levels for those in northern latitudes (such as Canada and the northern US) lowers the risk of certain types of cancer, especially breast, colon and prostate cancer.

I usually recommend that healthy adults over the age of 50 double the amounts above ⁠— so 2,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2) and for those with a family history of cancer to take 3,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2).

Remember though that Vitamin D is a fat soluble vitamin, so be sure to have your serum levels checked periodically as your body is able to stores for long periods of time. The best indicator of Vitamin D status is a routine blood test called 25-hydroxy vitamin D.

Best Low Carb Sources of Vitamin D to Help Our Bodies Fight the Flu

Fish and Seafood

Below is a list of foods that are naturally high in Vitamin D and that can be included on a low carb or ketogenic diet. The best source of all comes from the sea in the form of fish and seafood.

Wild-caught salmon

Wild-caught salmon has on average almost 1000 IU of Vitamin D (988 IU) vitamin D per 3.5-ounce (100-gram) serving and some studies have found up to 1,300 IU per serving [13].

Herring

Fresh Atlantic herring provides 1,628 IU Vitamin D per 3.5-ounce (100-gram) serving [14]. That’s huge!

Halibut

Halibut is an exquisitely delicious white-fleshed fish that  provides 600 IU Vitamin D per per 3.5-ounce (100-gram) serving [14].

Mackerel

Mackerel is simply delicious grilled on the BBQ and provides 360 IU Vitamin D per 3.5-ounce (100-gram) serving [14].

OYSTERS

Oysters contains 320 IU of Vitamin D in a 3.5-ounce (100-gram) serving [14].

Sardine

Sardine is an inexpensive and pretty good source of vitamin D — with one serving containing 272 IU of Vitamin D [14].

Canned Tuna

Canned tuna is an easy and inexpensive way to incorporate more Vitamin D into the diet and contains 236 IU of Vitamin D in a 3.5-ounce (100-gram) serving [14].

Non-fish Sources of Vitamin D

Fish and seafood are not the only sources of Vitamin D. Whole egg is a  good source, with most of the Vitamin D found in the yolk.

Egg yolk

The average supermarket egg contains only 18—39 IU of vitamin D, but pastured eggs that roam outside and are exposed to sunlight produce eggs with 3 to 4 times that amount [15]!

Mushrooms

With the exception of fortified foods such as dairy, mushrooms are the only plant source of Vitamin D, however mushrooms only produce Vitamin D2, rather than Vitamin D3 which is not as effective at raising blood levels of Vitamin D. Even then, button mushrooms grown outside under sunlight contain as much as 2,300 IU per 3.5-ounce (100-gram) serving [16].

Final thoughts…

There is good evidence that adding Vitamin D3 supplementation to your daily routine may boost your ability to fight of upper respiratory infections, including the flu.

Supplementing your diet with Vitamin D and/or eating plenty of low carb foods rich in Vitamin D3 can help ensure adequate stores of this important nutrient.

More Info

If you would like more information about my services, please have a look under the Services tab or in the Shop and if you have any questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 LCHF-RD (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. CTV News, Canadian warns against vaccine apathy after flu sends him to hospital for two months, https://www.ctvnews.ca/health/canadian-warns-against-vaccine-apathy-after-flu-sends-him-to-hospital-for-two-months
  2. Osterholm MT, Kelley NS, Sommer A, et al. Efficacy and effectiveness of influenza vaccines: a systematic review and meta-analysis. Lancet Infect Dis 2011 (published online Oct 25)
  3. Manzoli L, Ioannidis JP, Flacco ME, De Vito C, Villari P. Effectiveness and harms of seasonal and pandemic influenza vaccines in children, adults and elderly: a critical review and re-analysis of 15 meta-analyses. Hum Vaccin Immunother. 2012;8(7):851—862. doi:10.4161/hv.19917]
  4. Dairy Nutrition, Vitamin D status of Canadians — Results from the Canadian Health Measures Survey, https://www.dairynutrition.ca/nutrients-in-milk-products/vitamin-d/vitamin-d-status-of-canadians-results-from-the-canadian-health-measures-survey
  5. Vitamin D Council, Dr. John Cannell, MD, Influenza, https://www.vitamindcouncil.org/health-conditions/influenza/
  6. Bergman P, Lindh AU, Bjí¶rkhem-Bergman L et al, Vitamin D and Respiratory Tract Infections: A Systematic Review and Meta-Analysis of Randomized Controlled Trials, PLoS One. 2013 Jun 19;8(6):e65835.
  7. Martineau AR, Jolliffe DA, Hooper RL, Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data,  2017 Feb 15;356:i6583
  8. Sabetta, J.R., DePetrillo, P., Cipriani, R.J., et al., Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS One, 2010. 5(6): p. e11088.
  9. Veugelers PJ, Ekwaru JP. A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients. 2014;6(10):4472—4475. Published 2014 Oct 20. doi:10.3390/nu6104472
  10. Heaney R, Garland C, Baggerly C, French C, Gorham E. Letter to Veugelers, P.J. and Ekwaru, J.P., A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients 2014, 6, 4472-4475; doi:10.3390/nu6104472. Nutrients. 2015;7(3):1688—1690. Published 2015 Mar 10. doi:10.3390/nu7031688
  11. Science News, Recommendation for vitamin D intake was miscalculated, is far too low, experts say, https://www.sciencedaily.com/releases/2015/03/150317122458.htm
  12. Theuwissen E, Smit E, Vermeer C, The role of vitamin K in soft-tissue calcification, Adv Nutr. 2012 Mar 1;3(2):166-73.
  13. Schmid A, Walther B., Natural vitamin D content in animal products, Adv Nutr. 2013 Jul 1;4(4):453-62
  14. USDA, Composition of Foods Raw, Processed, Prepared USDA National Nutrient Database for Standard Reference, Release 27
  15. Kí¼hn J, Schutkowski A, Kluge H.,Free-range farming: a natural alternative to produce vitamin D-enriched eggs, Nutrition. 2014 Apr;30(4):481-4.
  16. Simona RR, Borzelleca JF, DeLuca HF, Safety assessment of the post-harvest treatment of button mushrooms (Agaricus bisporus) using ultraviolet light, Food and Chemical Toxicology, Volume 56, June 2013, Pages 278-289

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New Study in Older Light — lower CVD may be due to lower triglycerides

The new study[1] that I mentioned in an article last week indicates that those with a genetic predisposition to having lower LDL cholesterol and systolic blood pressure have a lower lifetime risk of cardiovascular disease (CVD), but what the study doesn’t mention was that research published last year[2] found that people with the low LDL variant also having a genetic predisposition to lower levels of triglycerides. This begs the question as to whether it is really the lower LDL that lowers the lifetime risk of CVD, or the lower triglycerides or both.

*Note: special thanks to George Henderson (@puddleg) from Auckland, New Zealand for bringing this earlier study to my attention.

That is, it could very well be that perceived benefit of having a genetically lower LDL reported in this new study is actually due to the same people also having a genetic predisposition to having lower levels of triglycerides!

In a large-scale study published in 2018 [2], researchers analyzed data from several hundred thousand individuals. First they estimated associations from summary genetic data from more than 670, 000 people from 9 different European databases. Then they analyzed individual-level genetic data from >390 000 people and looked at the associations of naturally occurring genetic variation coding for lipoprotein lipase (LPL) inhibitors with cardiovascular and metabolic health outcomes. Researchers found that a subset of subjects with a genetic variant to lower LDL-cholesterol levels also had a genetic predisposition to lower triglyceride levels and the group that had both had the lowest odds of coronary artery disease [2]. This 2018 study [2] raises the issue as to whether the results of the current study [1] referred to in last week’s article really indicates that genetically lower LDL levels along with lower systolic blood pressure are responsible for lower rates of lower cardiovascular disease, or whether the lower rates of CVD are due to these same people also having genetically lower levels of triglycerides, (or perhaps a combination of both).

The Risk of Higher Triglycerides

A 2016 study published in the Journal of Circulation [3] examined the health risks associated with high levels of triglycerides in those with CVD. Researchers analyzed data from a large-scale study conducted in Israel (Bezafibrate Infarction Prevention (BIP) trial) which followed > 15,300 people with heart disease for a period of 22 years. At the start of the study, participants had their cholesterol and triglyceride levels measured, as well as other health markers. Based on fasting triglyceride levels, subjects were divided into 5 groups, ranging from low triglyceride levels to extremely high triglyceride levels.

Note: Triglycerides below 150 mg/dL (1.70 mmol/L) are considered normal, whereas triglycerides over 200 mg/dL (2.5 mmol/L) are considered high.

After more than two decades of follow-up, researchers found that compared to subjects with low triglycerides, those with the highest triglyceride levels (> 500 mg/dL / 5.6 mmol/L) had almost a 70% greater risk of death over the 22 year period. In fact, even with subjects with triglycerides of 100 to 149 mg/dL (1.13 – 1.68 mmol/L) the elevated risk of death was detected over subjects with lower triglycerides levels (<100 mg/dl / 1.12 mmol/L).

Evidence is emerging that plasma triglycerides represent a causal risk factor for CVD and that genetic variants in a least 6 genes that modulate plasma triglyceride levels have been linked to CVD [4-12].

Using a research method called multivariable Mendelian randomization, researchers are able to group study subjects based on their genetic markers, so they are naturally randomized.  Using this method, researchers are able to separate the effects on CVD associated with triglycerides from those associated with LDL [13]. It has been found that the effect of genetic variations involving triglyceride increases the risk of CVD independently of LDL concentration.

A 2016 review article [14] postulates that the risk factors surrounding increased plasma triglyceride concentration may involve the metabolism of lipoproteins that carry triglycerides in the blood, and that it could lie in a variant gene that encode for the enzyme lipoprotein lipase (which breaks down triglycerides), or for a gene that encodes for regulators of lipoprotein lipase [14].

Final Thoughts

It’s interesting to study whether those with a genetic predisposition to having lower LDL cholesterol have lower lifetime relative risk of cardiovascular events [1], but further study is needed to factor in the subset of subjects that also have a genetic predisposition to lower triglyceride levels, as well as a genetic variant to lower LDL.

More Info?

If you have been diagnosed as having “high cholesterol” and want to know how a low carbohydrate diet may help,  you can learn more about the services I provide under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above.
To your good health!

 

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Ference BA, Bhatt DL, Catapano AL et al, Association of Genetic Variants Related to Combined Exposure to Lower Low-Density Lipoproteins and Lower Systolic Blood Pressure With Lifetime Risk of Cardiovascular Disease, JAMA. 2019 Sep 2. doi: 10.1001/jama.2019.14120. [Epub ahead of print]
  2. Lotta LA, Stewart ID, Sharp SJ, et al, Association of Genetically Enhanced Lipoprotein Lipase—Mediated Lipolysis and Low-Density Lipoprotein
    Cholesterol—Lowering Alleles With Risk of Coronary Disease
    and Type 2 Diabetes, JAMA Cardiology, 2018;3(10):957-966. doi:10.1001/jamacardio.2018.2866
  3. Klempfner R, Erez A, Ben-Zekry S et al, Elevated Triglyceride Level Is Independently Associated With Increased All-Cause Mortality in Patients With Established Coronary Heart Disease, Circulation: Cardiovascular Quality and Outcomes Vol 9(2), 2016, p 100-108, https://doi.org/10.1161/CIRCOUTCOMES.115.002104
  4. Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a Mendelian randomisation study.
    Lancet. 2012;380:572—580. doi: 10.1016/S0140-6736(12)60312-2.
  5. Triglyceride Coronary Disease Genetics Consortium and Emerging
    Risk Factors Collaboration, Sarwar N, Sandhu MS, Ricketts SL, et al.
    Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies. Lancet. 2010;375:1634—1639.
  6.  Jí¸rgensen AB, Frikke-Schmidt R, West AS, Grande P, Nordestgaard
    BG, Tybjí¦rg-Hansen A. Genetically elevated non-fasting triglycerides
    and calculated remnant cholesterol as causal risk factors for myocardial
    infarction. Eur Heart J. 2013;34:1826—1833. doi: 10.1093/eurheartj/
    ehs431.
  7. Do R, Stitziel NO, Won HH, et al; NHLBI Exome Sequencing Project.
    Exome sequencing identifies rare LDLR and APOA5 alleles conferring
    risk for myocardial infarction. Nature. 2015;518:102—106. doi: 10.1038/
    nature13917.
  8. Pollin TI, Damcott CM, Shen H, Ott SH, Shelton J, Horenstein RB,
    Post W, McLenithan JC, Bielak LF, Peyser PA, Mitchell BD, Miller M,
    O’Connell JR, Shuldiner AR. A null mutation in human APOC3 confers
    a favorable plasma lipid profile and apparent cardioprotection. Science.
    2008;322:1702—1705. doi: 10.1126/science.1161524.
  9. TG and HDL Working Group of the Exome Sequencing Project, National
    Heart, Lung, and Blood Institute, Crosby J, Peloso GM, Auer PL, et al Loss-of-function mutations in APOC3, triglycerides, and coronary disease. N Engl J Med. 2014;371:22—31.
  10. Jí¸rgensen AB, Frikke-Schmidt R, Nordestgaard BG, Tybjí¦rg-Hansen A.
    Loss-of-function mutations in APOC3 and risk of ischemic vascular disease. N Engl J Med. 2014;371:32—41. doi: 10.1056/NEJMoa1308027.
  11. Folsom AR, Peacock JM, Demerath E, Boerwinkle E. Variation in
    ANGPTL4 and risk of coronary heart disease: the Atherosclerosis Risk
    in Communities Study. Metabolism. 2008;57:1591—1596. doi: 10.1016/j.
    metabol.2008.06.016.
  12. Varbo A, Benn M, Tybjí¦rg-Hansen A, Jí¸rgensen AB, Frikke-Schmidt R,
    Nordestgaard BG. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol. 2013;61:427—436. doi: 10.1016/j.
    jacc.2012.08.1026
  13. Do R, Willer CJ, Schmidt EM, et al. Common variants associated with
    plasma triglycerides and risk for coronary artery disease. Nat Genet.
    2013;45:1345—1352. doi: 10.1038/ng.2795.
  14. Musunuru K, Kathiresan S, Surprises From Genetic Analyses of Lipid Risk
    Factors for Atherosclerosis, Circulation Research; Compendium on Atherosclerosis, 2016;118:579-585. DOI: 10.1161/CIRCRESAHA.115.306398

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Significance of New Study: Lower LDL Associated with Lower Risk of CVD

A study published September 2, 2019 [1] reported that lower LDL cholesterol levels combined with lower systolic blood pressure are associated with lower lifetime risk of cardiovascular disease (CVD), however there are several factors that need to be kept in mind in considering the results of this study.

First of all, the study looked at data from people that had inherited a genetic marker for having LDL cholesterol that was on average 15 mg/dl (0.39 mmol.L) lower and NOT people that had lower LDL cholesterol due to diet, medication and/or lifestyle interventions. So, even though people with this genetic predisposition of having lower LDL cholesterol had a 26% lower relative risk in of having a serious cardiac event such as a heart attack, need for a stent or death from a heart attack, it says nothing about the amount of benefit that might be achieved by dietary and lifestyle changes or medication.

Secondly, the average triglyceride to HDL ratio of the population studied in the study was 2.5 mg/dl (0.065 mmol/L), which is far from ideal. As outlined in an earlier article about LDL cholesterol and cardiovascular disease, several studies [2,3,4] have found that triglyceride to HDL ratio is a good reflection of LDL particle size; with the small, dense sub-fraction of LDL being atherosclerotic, and the large, fluffy sub-fraction of LDL not being atherosclerotic [5]. In the US, triglyceride to HDL ratio values are expressed in mg/dl and the ratios are interpreted as follows [6];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

In the present study, the triglyceride to HDL ratio was 2.5 mg/dl, which means that they already had a higher than optimal level of small, dense LDL, predisposing them to cardiovascular risk. By comparing people with a genetic predisposition to lower LDL cholesterol to the risk of a population that already has a less than ideal triglyceride to HDL ratio, it makes the benefit of low LDL seem larger.

Significance of this Study

Sure, it is interesting to study whether those with a genetic predisposition to having lower LDL cholesterol have lower lifetime relative risk of cardiovascular events, but it doesn’t tell us anything about any possible benefit to ordinary people (without this genetic marker) lowering their LDL cholesterol.

As well, by comparing the risk of those with a genetic predisposition to lower LDL cholesterol to a population that already had a higher than ideal level of small, dense LDL, it exaggerates the appearance of perceived benefit of lower LDL cholesterol.

Comparing Apples with Apples

The question is, of what predictive benefit is a study that uses a group of people with a genetic variant to lower LDL cholesterol compared with a reference group that already has higher than ideal triglyceride to HDL ratio?

What can we deduce about those that don’t eat a standard American diet, such as those that eat a low carb or ketogenic diet and have lower overall levels of triglycerides and higher levels of HDL?

Nothing.

We can’t deduce anything.

Which raises the common question; does a low-carbohydrate diet increase the risk of cardiovascular disease?

Looking at what we know; a 2017 study by Chui et al [7] demonstrated that in those eating a low carbohydrate diet, HDL cholesterol increased and while LDL cholesterol also increases, it tends to be the large buoyant LDL that increased, with no change in the atherosclerotic small, dense LDL [7].

As well, a 2012 meta-study analysis of 19 randomized control trials (RCTs) by Santos et al [8] reported that in those eating a low carbohydrate diet, triglyceride levels dropped by 29.71 mg/dL (0.34 mmol/L) and a 2014 study by Bazzano [9] reported that a low carbohydrate diet had a greater decrease in 10-year cardiovascular heart disease (CHD) risk score based on the Framingham Risk Score, than those on the low fat diet.

Final Thoughts

When we read headlines that indicate that “low LDL lowers lifetime risk of cardiovascular disease” we need to look closer at who is being studied.

A study about those with a specific genetic variation tell us nothing about the general public without it. It also tells us nothing about whether lowering LDL cholesterol through drugs or diet has any of the same benefits as having this genetic variation.

We also need to ask ourselves about whether the group being used for comparison purposes has optimal markers, or are already sub-optimal and inflates the perceived benefit and what about what they are eating? Is it relevant to those of us that follow a low-carbohydrate lifestyle?

UPDATE (Sept 22, 2019): in a new follow-up article, another study from last year raises a question as to how much of the lower CVD in due to lower LDL and blood pressure or due to this same variant also having lower triglycerides. You can read the new article here.

More Info?

If you have been diagnosed as having “high cholesterol” and want to know how a low carbohydrate diet may help,  you can learn more about the services I provide under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above.
To your good health!

 

Joy

 

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Ference BA, Bhatt DL, Catapano AL et al, Association of Genetic Variants Related to Combined Exposure to Lower Low-Density Lipoproteins and Lower Systolic Blood Pressure With Lifetime Risk of Cardiovascular Disease, JAMA. 2019 Sep 2. doi: 10.1001/jama.2019.14120. [Epub ahead of print]
  2. Hanak V, Munoz J, Teague J, et al, Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B, The American Journal of Cardiology, Volume 94, Issue 2, 2004, Pages 219-222, https://doi.org/10.1016/j.amjcard.2004.03.069
  3. McLaughlin T, Reaven G, Abbasi F, et al. Is there a simple way to
    identify insulin-resistant individuals at increased risk of cardiovascular
    disease? Am J Cardiol. 2005;96(3):399Y404.
  4. Vega GL, Barlow CE, Grundy SM et al, Triglyceride to High Density Lipoprotein Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Melletus in Men, Journal of Investigative Medicine & Volume 62, Number 2, February 2014
  5. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  6. Sigurdsson AF, The Triglyceride/HDL Cholesterol Ratio, updated January 12, 2019, https://www.docsopinion.com/2014/07/17/triglyceride-hdl-ratio/
  7. Chiu S, Williams PT, Krauss RM. Effects of a very high saturated fat diet on LDL particles in adults with atherogenic dyslipidemia: A randomized controlled trial, 2017 Feb 6;12(2):e0170664. doi: 10.1371/journal.pone.0170664
  8. Santos FL, Esteves SS, da Costa Pereira A, Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obes Rev. 2012 Nov;13(11):1048-66. doi: 10.1111/j.1467-789X.2012.01021
  9. Bazzano LA, Hu T, Reynolds K, et al. Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial, Ann Intern Med. 2014;161:309—318. doi: 10.7326/M14-0180

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Two Clinical Reactions: seeing the possibilities or being a pessimist

Yesterday, a client of mine who was on insulin 13 weeks ago and who went off of it with her Endocrinologist’s knowledge and oversight to follow a low carbohydrate diet had her regular two-month follow-up visit, where she saw both the Dietitian and the Endocrinologist. Their respective reactions to her progress really highlights how some clinicians can be transformed by seeing the clinical possibilities of what can be accomplished by someone following a well-designed low carbohydrate diet, whereas others remain pessimistic regardless of the clinical evidence.

This is the 4th article about this young woman’s incredible progress from injecting insulin to following an individually designed low carbohydrate diet. You can read about the first two weeks at the start of her journey here, about her achieving normalized blood glucose in 10 weeks here, and about here achieving target HbA1C in less than 12 weeks here.

NOTE: The different reactions that these clinicians had are in no way reflective of their respective professions; it could have easily been in reverse. It could have been entirely different healthcare professions. There are clinicians in every field who are willing to consider emerging evidence and respond by being open to the clinical possibilities, and there are others who are not.


When this young woman arrived for her appointment, she saw the Dietitian first, which was the same one that she saw the visit before, and who told her that she should be eating ‘60 g of carbohydrate per meal plus snacks’ (see Sept 6 update, here). At yesterday’s visit, the Dietitian only looked at her blood glucose numbers from the last two weeks and not the last 8 weeks since she was last seen. She said her ‘numbers look good’, and asked the name of the Dietitian she was seeing, and my client told her my name.  She responded and said “I hope she told you that you can’t get your numbers under 7 with just Metformin“. My client pointed out that she recently got TWO fasting blood glucose of 4.7 mmol/L, and the Dietitian said she didn’t see that. My client pointed out the two dates where she did, to which the Dietitian said nothing, as she was only considering the numbers from the last two weeks. My client said to me that at this point, she “just shut down” and waited to see the Endocrinologist.

My client then saw her Endocrinologist who had a medical student with him. This is the same Endocrinologist that told her 8 weeks ago that it was unrealistic for her to think that she could lower her HbA1C to below 7 mmol/L following a low carbohydrate diet, and that she should go back on insulin (see more here). The endocrinologist said to her yesterday “these numbers are amazing! What are you doing?”. My client responded by saying she was following a low carbohydrate diet designed by me. He also asked her who her Dietitian was, and my client told her my name.  He said “it would be great if you could get those fasting blood glucose numbers under 7 so keep doing what you’re doing”.  He then added, that should my client get pregnant, that he “might need to talk to her about taking insulin, if she doesn’t continue to eat a low carbohydrate diet”. He added, “you are going down the right path. Keep doing what you’re doing!”.

The contrast between the reactions of these two clinicians is striking. As I said above in the disclaimer, it has nothing to do with their respective professions, but about their willingness as individual clinicians to be open to different clinical possibilities, in light of the evidence. Some are, and some aren’t.

As a Dietitian, I wonder how the advice to someone with type 2 diabetes to “eat 60 g of carbs per meals plus snacksandget fasting blood glucose under 7.0 mmol/L” can be reconciled without prescribing insulin. I don’t see that it can be. It is still expected that “Diabetes is a chronic, progressive disease” and it need not be.

By recognizing a low carbohydrate and very low carbohydrate (keto) diet as two of the options of Medical Nutrition Therapy in the treatment of diabetes (both type 1 and type 2), the American Diabetes Association (ADA) has opened the way for Diabetes to NOT be a chronic, progressive disease! (For more information about the policy changes at the ADA, you can read any one of several articles from April 2019 that are posted under the Science Made Simple tab above, including this one.)

As to the belief that “you can’t get your blood glucose under 7 with just Metformin”, people with type 2 diabetes routinely have fasting blood glucose well under 7.0 mmol/L (126 mg/dl) following a well-designed low carbohydrate diet — both with and without Metformin, and clinicians should be current with the literature to know this. In fact, in the April 2019 Consensus Report on Diabetes and Pre-Diabetes the ADA said;

Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia and may be applied in a variety of eating patterns that meet individual needs and preferences.”

The ADA’s Guidelines do not apply in Canada, but as healthcare professionals, we need to know they exist.

We also need to know that at their annual National Conference, hundreds of Certified Diabetes Educators (CDEs) in the US were recently taught to use a low-carbohydrate diet and a very low carbohydrate (ketogenic) diet as Medical Nutrition Therapy with people with both type 1 and type 2 diabetes, as well as how to manage the many medications prescribed for people with diabetes (you can read about this in this post and this one). As clinicians we need to be aware that a low carbohydrate and a very low carbohydrate (keto) diet are both safe and effective for those with Diabetes, even if it is not public policy in Canada yet.

There are plenty of peer-reviewed studies demonstrating the safety and effectiveness of a well-designed low carb or ketogenic diet for weight loss, as well as for normalizing blood glucose and blood pressure. Many have been reviewed on this site (for more information, please click on the For Physicians & Allied Health Providers tab above).


As I’ve done in previous articles about this client’s progress, I asked her on our weekly call to write in her own words what her visit was like yesterday. This is what she wrote;

“I was excited for my Endocrinologist to see my lowered A1C number and decreasing blood glucose numbers. I went into the appointment knowing that I would see the Dietitian first to review my numbers. She mentioned that the numbers were better, but my fasting glucose was still not ideal. I discussed that they are definitely coming down, although I realize they are not where they should be, and I even got a few under 7 in the past month. This Dietitian was only interested in the past two weeks and mentioned that Joy would not be able to enable me get my fasting glucose under 7 with just Metformin. Seeing the Dietitian really shut me down to discussing anything further with her. I let her gather her information and wanted to move on to my Endo.

Seeing my Endo was a turnaround. He was so amazed with my results, especially with my A1C having come down so much, that he encouraged me to just keep going. I felt so proud and encouraged. He gave me the motivation I was looking for and now I am ready to continue down this path to show him (and that Dietitian!) that it can be done without insulin.”

She has every reason to be proud of her accomplishments! She has been very intentional; about what she eats, about testing her blood sugar and in tweaking the timing of her Meformin.

If you would like more information about my services, please have a look under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

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New Study: Why Eating Less and Exercising More Matters As We Age

There is much “push back” when it comes to the standard advice to “eat less and exercise more” as a means of losing weight, and for good reason. For one, metabolism will slow as a result of caloric restriction — making it that much more difficult to lose weight when deliberately cutting calories. Another reason is that it is exceedingly difficult for an obese person to exercise. For many, just getting around is a chore. It is for this reason that I focus on helping people be less hungry by eating a different mix of protein, fat and carbohydrate — because a natural byproduct of being less hungry, is eating less. Being active is possible once a person is losing weight and not feeling hungry all the time.  Yes, they are still “eating less and moving more” — but as a result, not as the focus.

Addendum (Sept 10 2019) — Weight loss is not only about what we eat.  It’s also about when we don’t eat; whether it’s having times between meals where we don’t eat, or not eating from the end of supper until the first meal of the following day (whenever that is). Thanks Dr. Andy Phung for the reminder!

A new study published yesterday (September 9, 2019) in the journal Nature Medicine[1] has found that “eating less and exercising more” may actually be good advice as we age — because it turns out that we have decreased fat turnover as we age. If we eat the same amount as we always have and don’t increase the amount we exercise,  we will end up gaining approximately 20% over a 10-15 year period [3].

Until recently little was known about fat turnover [2] — which is the storage and removal of fat from adipocytes (fat cells). A 2011 study showed that  during the average ten-year lifespan of human fat cells, the fat in them (triglycerides) turns over six times, in both men and women [2], and that when people are obese, the fat removal rate decreases and the amount of fat as triglyceride stored each year increases [2]. What we didn’t know until now is what happened to fat turnover as we age.  This follow-up study headed by the same lead researcher as the 2011 study explored this issue, as well as differences in fat turnover after people have bariatric surgery which helps explain why some people regain their weight after weight loss, where as others don’t.

Eating Less Matters as We Age

Fat turnover is a difference between the rate of fat uptake into fat cells and the fat removal rate. High fat storage but low fat removal is what results in the accumulation of fat and in obesity. The “bad news” of this new study is that fat accumulation due to decreased fat turnover is what happens as we age, leading to accumulation of fat. That is, even if we don’t eat more or exercise less than previously, we will store more fat — which can result in as much as a 20% increase in body weight over 13 years [3].

“Those who didn’t compensate for that (i.e. decrease fat turnover) by eating less calories gained weight by an average of 20 percent”[3].

Researchers from the University of Uppsala in Sweden and the University of Lyon in France studied the fat cells of 54 men and women over an average 13 year period [3] and regardless of whether the subjects gained weight or lost weight, they had a decreased fat turnover. 

Since fat turnover is decreased as we age, to prevent weight gain we need to take in less calories than we used to, even if we are just as active.

Why We Regain Weight After Weight Loss

The study also looked at fat turnover in 41 women who underwent bariatric surgery. Results showed that only those who had a low lipid turnover rate before the surgery were able to increase their lipid turnover after surgery and maintain their weight loss 4-7 years after surgery [1]. Researchers think that if people had a high lipid turnover rate before surgery, there is less ‘room’ for them to increase their lipid turnover rate after surgery, which is why they regain the weight. This could explain why so many people who lose incredible amounts of weight following any one of a number of “diets” regain it (and then some) afterwards.

Exercise and Lipid Turnover

Previous studies have reported that fat turnover increases as we exercise [2], so based on this new study, the idea of ‘eating less and exercising more’ actually matters as we age. We can either decrease our intake as we age and/or be a little more active and avoid gaining weight — which is easy enough to do for those who are slim, if they know.

But what about those who are already overweight or obese and now find out they are more prone to storing fat now that they’re older, even though they eat the exact same way and haven’t changed their activity level?

I believe the solution is the same regardless of a person’s age focusing on the person eating in such a way as to be less hungry, so that in the end they end up eating less. As they lose weight because they’re not hungry all the time, being more active is easier to implement.  The difference between it being “doable” depends on what we focus on. As covered in a previous article, we understand why a person who eats foods that are a combination of fat and carbs together eat more, but my approach is to gradually adjust the amount of carbohydrate in the diet, so that people can eat more protein and healthy fat, and end up feeling less hungry. When they aren’t being driven by the reward system of their brain (see linked article) to want more and more foods with carbs and fat together, it is much easier for them to eat when they are actually hungry. As they do, their weight drops as a result.

In light of this new study, what is important is that as people age, there is a natural tendency to put on weight even if they eat the same and don’t change their activity level. This means older people need to modify the amount of calories they take in and/or expend more energy, the question is how.

If you would like more information about my services, please have a look under the Services tab or in the Shop and if you have any questions, please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Arner P, Bernard S, Appelsved K-Y et al. (2019). “Adipose lipid turnover and long-term changes in body weight.” Nature Medicine 25(9): 1385-1389.
  2. Arner, P. et al. Dynamics of human adipose lipid turnover in health and metabolic disease. Nature 478, 110—113 (2011).
  3. Karolinska Institutet, New study shows why people gain weight as they get older, Published: 2019-09-09 18:35, https://news.ki.se/new-study-shows-why-people-gain-weight-as-they-get-older

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Achieving the “Impossible”: from injecting insulin to achieving target HbA1C

A few weeks after requesting that her endocrinologist take her off insulin so that she could begin a low carbohydrate diet with his and her GP’s oversight (article here), this young woman was told she needed to get her HbA1C to ≤7.0%, which is the therapeutic target for adults with type 2 diabetes. She was told that it was unrealistic for her to think that she could do so following a low carbohydrate diet, and that she should go back on insulin.  She replied that she wanted to continue to eat a low carbohydrate diet for a total of 12 weeks, and her endocrinologist replied that more than likely he would need to put her back on insulin then, because it was not realistic for her to accomplish those goals using diet, even with Metformin support.

*Metformin doesn’t lower blood sugar, but helps the body become more insulin sensitive and to keep it from manufacturing glucose from stored fat or protein which is what underlies high morning blood sugar.

Well, she achieved the “impossible”!

She had her blood tests yesterday and when she checked her results on-line last night she could not believe it!! Her results were below the 7.0% therapeutic target. . . and this was (1) despite me starting her on a moderate low carbohydrate diet for the first several weeks and only gradually lowering carbohydrate content in order to meet clinical outcomes*, and (2) despite her having two weeks of weddings in mid-July where she ate a little ‘off-track’, which caused her blood sugar levels to rise).

In spite of these, she did it!!

Note: weight loss was only ~5% of her original weight, so would not account for her significant improvement in HbA1C results.

Here are her results:

from injecting insulin to HbA1c within target

*I was asked on social media after the previous update on her progress why I didn’t start this young woman on a very low carbohydrate, ketogenic diet from the outset. This is what I replied; “Diabetes Canada has not (yet?) deemed a LC or very LC diet as safe and effective medical nutrition therapy. I start people at 130 g of carbs, then reduce carbs as necessary to achieve clinical outcomes as a prudent approach. Hence why I conclude the article w/ hope of future policy change.

After this young woman picked up her blood test results last night, she sent me this short email which I have her permission to share here;

“JOY!!!

Such overwhelming feelings right now. We will talk tomorrow but I took my blood test today and have attached the results! Please tell me I am seeing the number I am seeing because it is hard to believe! Also, for the graph this week, I had to change the minimum limit from 5 to 4 to account for my TWO readings of 4.7!! “

As relayed in the second article about her progress (posted here), in 10 weeks this young woman went from a fasting blood glucose of 16.8 mmol/L (303 mg/dl) to 4.7 mmol/L (85 mg/dl). . . and this past week she had her second fasting blood glucose reading of 4.7 mmol/L! Twice in one week, she achieved normal fasting blood glucose numbers; the first time since being diagnosed as having type 2 diabetes in 2017.

As she said in the previous article, she is “invested” in her health and that investment translated to her own determination and hard work to follow her Meal Plan, to speak to her endocrinologist about adding an extra dose of Metformin at bed-time, and to determine when was the best timing to take her before bedtime dose and her early morning dose, in order to prevent her blood sugar from spiking in the morning due to Dawn Phenomena. Yes, I helped but she did the work! 

I asked her to write in her own words what it was like to get her blood test results last night, and this is what she wrote:

“I feel so happy and proud of myself. Patience and consistency has paid off.

Typically, if I were doing this on my own or changing how I was eating, I never stuck with it long enough to see changes.  The number on the scale or one bad meal would take me further back than when I started.  However, keeping track of my blood sugars and being accountable to someone have kept me going, and I feel like nothing can hold me back now.

I am so motivated to keep going and giving myself time to progress. I know I can do this!”

I am so proud of her hard work and accomplishments!

I look forward a day when Diabetes Canada updates its Clinical Practice Guidelines to enable clinicians to recommend a low carb or ketogenic diet as a therapeutic option for those with diabetes ⁠— just like the American Diabetes Association (ADA) did last year.

For more information about the clinical changes at the ADA, you can read any one of several articles from April 2019 that are posted under the Science Made Simple tab above, including this one.

UPDATE (Sept 6, 2019): During our weekly call, this young woman told me that she is meeting her endocrinologist this week and is looking forward to his reaction to her accomplishments, as well as that of his diabetes nurses.  She said during her last visit 8 weeks ago (4 weeks after coming off insulin and beginning a low carbohydrate diet) her doctor told her that she is ‘not eating rice and needs to be eating that’ and reminded her that the ‘insulin will cover that’.  The diabetes nurse also told her ‘she should be eating 60 g of carbohydrate per meal plus snacks’ (which is still the recommendations for those with diabetes in Canada). She assured them that she is carefully monitoring her blood sugar multiple times per day and that they are coming down, and she feels great.

If you would like more information about my services, please have a look under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

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From Injecting Insulin to Normalized Blood Sugar – in 10 weeks

Ten weeks ago, with her endocrinologist’s knowledge, this young woman discontinued insulin to begin a low carb diet. She has been gradually achieving normalized blood sugar, but this morning she had her first totally normal fasting blood sugar level since being diagnosed as type 2 diabetic! How cool is that?

As relayed in the first part of this account (posted here), at this young woman’s insistence her doctor gave her 12 weeks to ‘try a low carb diet’ and then he would put her back on insulin.  Needless to say, he was not optimistic that changing her diet would ‘work’.

When she saw him a few weeks after beginning a low carbohydrate diet, and after lowering her fasting blood blood sugar from 16.8 mmol/L (303 mg/dl) to approximately 7.5 mmol/l, he told her that that the only way she could get her blood sugar below 7.0 mmol/L was to begin injecting insulin again. She responded by saying that she was not even half-way through her 12-week “trial period” and that she wanted to continue. As a result of her on-going “dawn phenomenon” (and upon my recommendation) she asked her endocrinologist to add an extra dose of Metformin* at bed-time to prevent her liver from making so much glucose in the morning (via gluconeogensis) and while he agreed, he said that if her HbA1C was not below 7.0 mmol/L (126 mg/dl) the next time she has it checked, he was putting her back on insulin.

*Metformin does not lower blood sugar, but helps the body become more insulin sensitive and to keep it from manufacturing glucose from stored fat or protein which is what underlies high morning blood sugar.

This coming week she is having her 3 month blood work and she and I both realize that it is unlikely her HbA1C will be below 7.0 mmol/L because there was a two week period this summer where she had several friend’s weddings, and got off-plan a bit. While she was quite disciplined, a few things she ate that were low glycemic index complex carbs still caused her blood sugar to rise above the levels she had been achieving. She got right back on plan after the weddings, and has been doing absolutely amazing! I am so very proud of her!

Here is a graph of her blood work over the past 10 weeks, including the ‘blip’ in the middle from the weddings;

From injecting insulin to normalized blood sugar in 10 weeks

She is not “there” yet, but this week she began having much less variation in blood sugar and the graph continues to be shifted downward. She is doing so well.

She has begun delaying the first meal of the day to noon because she doesn’t feel hungry in the morning, and is making extra effort to try different timing for taking her late-night and early-morning Metformin, so as to maximize the reduction in fasting blood sugar from dawn-phenomena (gluconeogenesis). This morning, while we were on our weekly Skype call, she took her blood glucose. 4.7 mmol/L (85 mg/dl)!  This was her first normal early morning glucose since being diagnosed as being Type 2 diabetic in 2017!! I asked her to hold the meter up to the screen and took a picture of it!

Note: I’ve edited out her name and made the numbers a bit more readable.

In just 10 weeks, this young woman has gone from a 2 hour post-meal glucose reading of 18.7 mmol/L (337 mg/dl) to between 6.5 mmol/L (117 mg/dl) and 7.9 mmol/L (142 mg/dl).

The normal “goal” for 2 hour post-prandial glucose for someone with type 2 diabetes is ≤ 7.8 mmol/L (141 mg/dl) and in just 10 weeks, she is already doing considerably better than that!

As I did in the first post about her progress, I asked her to write in her own words what it has been like and how she feels.  This is what she wrote today;

“I have been working together with Joy for close to 3 months now and I am amazed at the progress being made. Monitoring my blood glucose levels consistently has given me more insight into how and when I should be eating and taking my medication. This is key to the progress that I have made. There have been highs and lows, with life and weddings getting in the way, but getting back on track from any deviation is crucial. Knowing that I was accountable to Joy and my blood glucose monitor motivated me to get back to those lower numbers.

With the guidance of Joy, I have adjusted the timing of my Metformin and made tweaks to my diet which will help lower my numbers and prevent spikes. I found that I was not hungry in the mornings and all I needed was my coffee, so I pushed my first meal to lunch and my second meal has been dinner. My cravings have been close to eliminated and I don’t feel the need to snack between meals.

The biggest issue has been my increased fasting glucose due to the dawn phenomenon. To avoid a nightly prescription of insulin (which I never want to take again), I have been invested in figuring out when the nighttime spike is occurring and how I can adjust the timing of my Metformin to minimize it. For the past couple of nights, I have been checking my blood glucose levels every 1-2 hours, and have narrowed down the time at which the spike occurs. This investigation has lead me to my lowest ever fasting glucose reading today of 4.7!!! This is a number I never thought I would see. I couldn’t believe it. I still can’t believe it. I keep checking to see if I read the number wrong but there it is every time!

This has been a slow and steady road, but being consistent and invested in my health is starting to pay off. It has all been worth it and I cannot wait to see what the next 3 months bring!.”

Note: This is what only one person has been able to achieve following a well-designed low carbohydrate diet the last 10 weeks, but these results are quite consistent with Virta Health‘s 10-week results from their outpatient study with 238 subjects published in October 2017 and outlined in this post.

Post-publication addendum (August 23, 2019): I was asked on social media yesterday why I didn’t start this young woman on a very low carbohydrate, ketogenic diet from the outset. This is what I replied; “Diabetes Canada has not (yet?) deemed a LC or very LC diet as safe and effective medical nutrition therapy. I start people at 130 g of carbs, then reduce carbs as necessary to achieve clinical outcomes as a prudent approach. Hence why I conclude the article w/ hope of future policy change.


I partner with people’s GPs and Endocrinologists to enable them to oversee reduction and de-prescription of injected insulin (or other medications that may result in low blood sugar when following a low carbohydrate diet) while their patients follow a well-designed low carbohydrate diet to effectively manage their blood sugar. It is fantastic to see people such as this very determined young woman replicate what hundreds have done under the care of knowledgeable clinicians and as published in an ever increasing number of peer-reviewed studies.

It was so exciting to recently witness hundreds of CDEs in the United States being taught how to use a low-carbohydrate diet and a very low carbohydrate (ketogenic) diet as medical nutrition therapy with people with both type 1 and type 2 diabetes and how to manage the many medications prescribed for people with diabetes (you can read about these two presentation in this post and this one)!

I long for the day that Diabetes Canada releases an update to Clinical Practice Guidelines similar to what the American Diabetes Association (ADA) did last year, which enables clinicians to recommend a low carb or ketogenic diet as a therapeutic option for those with diabetes.

For more information about the clinical changes at the ADA, you can read any one of several articles from April 2019 that are posted under the Science Made Simple tab above, including this one.

If you would like more information about my services, please have a look under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

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Censorship of Real Food on Social Media as possibly offensive or disturbing

Two days ago I posted a photo on Instagram, Facebook and Twitter of fresh chicken that I had bought and had cut up into pieces for dinner. Real food is perfectly normal for a Dietitian to post about, right…but the photo was blurred out by Instagram because it contained what it deemed was “sensitive content” that some would find offensive or disturbing? Calling it what it is, this is censorship of real, whole food.

The photo I posted is above.

The caption under the photo indicated that this shouldn’t look foreign and that real chicken comes with a head, feet and bones (in contrast to chicken we buy in a supermarket that usually comes boneless or pre-cut, in Styrofoam trays, and covered in plastic wrap).

Presumably, someone found this photo offensive and reported it to Instagram.  I was not notified that the photo had been censored and it looks the same from my end so I wouldn’t have known, but several people that follow me told me that my photo was deemed to contain “sensitive content” and was blurred out.

To anyone viewing the post now, it now looks like this:

This photo contains sensitive content which some people may find offensive or disturbing.

A physician who follows me on Instagram posted the following with regard to the censoring;

I cannot believe a photo of food is blurred as “sensitive content”. It is absolutely mind boggling. But it’s totally fine to be constantly inundated with ads for crap that make us feel bad about ourselves, making us buy junk we don’t need.

This physician is right!

There’s a huge difference between real food and the processed food-like substances (“crap”) that we are encouraged to buy and eat (you can read more about telling the difference between these in this previous article).

The two photos that I posted of chicken before and after being cut up has been censored on Instagram because in contains “sensitive content which some people may find offensive or disturbing“.

Do you know what I consider offensive and disturbing?

I find people having to have toes amputated because of uncontrolled diabetes offensive.

I find obese people trying desperately to lose weight, yet finding themselves unable to curb an insatiable craving for processed food that was deliberately created by its producers, disturbing.

I find the fact that many young children in Canada and the US (and likely in many other countries) think of chicken as something that comes boneless, deep fried in batter and packaged in small individual packages with various flavours of sweetened sauce to dip it in, disturbing.

I find pea protein isolate, industrial seed oil, methyl cellulose and a host of other processed ingredients masquerading in the meat counter, offensive.  But please don’t misunderstand…

I have absolutely no problem with vegetarians and vegans having a wide variety of plant-based food available to eat as alternatives to animal-based foods, but it should not be marketed to consumers as “meat”, but ‘better’.

It may be “better” or “ultra” or “beyond” for those who choose a plant-based lifestyle, but an ultra-processed mixture of pea protein isolate, canola oil, refined coconut oil, cellulose from bamboo, methylcellulose, potato starch, maltodextrin, yeast extract, sunflower oil, vegetable glycerin, dried yeast, gum arabic along with seasoning and flavourings is not ‘better’ or preferable to whole, real food with a single ingredient, “beef”.

These are choices…

…and people have the right to choose what they want to eat, without condemnation and judgement.

There is no one-sized-fits-all-diet and individuals who choose to eat meat, fish or poultry should not be vilified or censored for doing so.

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

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US Assn. of Diabetes Educators Taught Person-Centered Low Carb Plans

This past weekend, thousands of American Certified Diabetes Educators (CDE) gathered at the American Association of Diabetes Educators (AADEs) annual conference in Houston, Texas. Objectives of the conference were for CDEs to learn how to implement novel and innovative ways to advance chronic disease prevention and management, and one of those novel ways was through the use of a Low Carbohydrate Diet.

It is very exciting that CDEs are now learning how to implement the American Diabetes Association’s (ADA) new 2019 Standards of Medical Care in Diabetes that was released this past December and which includes use of a low carbohydrate diet (you can read more about that here).

This conference provided education to enable CDEs to apply the content outlined in the ADA’s April 18, 2019 Consensus Report, which added the use of a very low carbohydrate (ketogenic) diet of 20-50 grams of carbs to the choice of meal patterns to manage both type 1 and type 2 diabetes. You can read more about the Consensus Report here.

As mentioned in the previous post, there were two Educational Sessions this past Saturday, August 11, 2019 about the use of a Low Carbohydrate Diet to manage and treat diabetes. The first session was titled Low Carbohydrate Diets; Fad or Evidence Based Course of Action and was given by Dr. Jim Painter, PhD, RD and Professor Emeritus from Eastern Illinois University, in Charleston, Illinois and this article covers that presentation in detail, including each of the slides and references used.

The second session was titled Person-Centered Implementation of Low Carbohydrate Eating Plans and was given as a joint-session by Dawn Noe, RDN, CDE and Diana Isaacs, PharmaD, CDE, both from Cleveland Clinic Diabetes Center. This second session is the subject of this article.

Copies of the slides and speaking notes for this presentation were sent to me by Dawn Noe, RDN, CDE. Many thanks to her and her colleague Diana Isaacs, PharmaD, CDE for sharing them with us!

The first part of the presentation was given by Registered Dietitian Nutritionist Dawn Noe and is covered in Part A and the second part was given by Doctor of Pharmacy Diana Isaacs and is covered in Part B.

Note: In a few places below, I have added my own clarifications that are clearly marked as *Note (bolded red asterisk *).

Person-Centered Implementation of Low Carbohydrate Eating Plans

Slide 1

The first slide was a disclosure of financial relation / financial conflict of interest, as well as a statement of non-endorsement of products.

Slide 2 – The second slide was a photo of each of the presenters, along with their credentials.

 

Part A: Nutritional Approach – Dawn Noe, RD, CDE

Slide 3 – list of learning objectives.

 

 


Key Points from the American Diabetes Association’s Consensus Report

Slide 4 – Summarized some key points from the American Diabetes Association’s (ADA) Consensus Report

 

(Evert AB et al. Diabetes Care 2019; 43: 731-754.)

Speaking Point Summary
  • There is no ‘ideal percentage of carbs’ shown in the literature, but despite this
    many people with diabetes are told to eat ~60 grams of carbs at each meal, assuming 3 meals per day.
  • These numbers are essentially calculated to be 50% of the calories coming from carbohydrate on a 1500 calorie meal plan.
  • The 130 grams of carb per day recommended for adults without diabetes (which is determined in part by the brain’s requirement for glucose) can be fulfilled by the body’s metabolic processes with include glycogenolysis, gluconeogenesis, and/or ketogensis in the setting of very low dietary carbohydrate intake.

Note: This previous article outlines the ADA’s updated position that the brain’s need for glucose can be fulfilled by the body.


Slide 5 – The Evidence for Low Carb in Type 2 Diabetes and Type 1 Diabetes

Speaking Point Summary
  • Low carb and very low carb eating patterns are among the most studied eating patterns for type 2 diabetes (T2D).
  • Long-term outcomes of Virta Health’s  2-year data published in May 2019 were not included in the new ADA Consensus Report.
  • For those with type 1 diabetes (T1D), no trials met the inclusion criteria for the ADA’s Consensus Report, however one small study limited carbs to 47 grams per day, and another limited carbs to 75 grams per day with positive results relating less glycemic variability, and lower HbA1C respectively.
  • The ADA Consensus Report states that this evidence suggests that a very low carb eating pattern may have potential benefits for adults with type 1 diabetes, but clinical trials of sufficient size and duration are needed to confirm prior findings.
From 2019 Standards of Care
  • Providers should maintain consistent medical oversight and recognize that certain groups are not appropriate for low-carbohydrate eating plans, including pregnant or lactating women, children, people who have renal disease or disordered eating behavior.
  • Low carb and very low carb eating plans should be used with caution for those taking SGLT2 inhibitors due to potential risk of ketoacidosis.
  • There is inadequate research about dietary patterns for type 1 diabetes to support one eating plan over another at this time.

Slide 6 – Different Ways to Define “Low Carb”

Speaking Points Summary

In the ADA’s Consensus Report, Nutrition Therapy for Adults included 2 meta-analysis where “low carb” was defined differently (≤ 45% calories, < 40% of calories) and 1 meta analysis where “ketogenic” was defined as 5-10% calories / ~20-50 grams carbohydrate per day.

In general, the presenters define “low carb” as being ~50 – 130 grams carbs per day, since < 50 grams of carbs could be a ketogenic for some people.

Feinman et al defined three categories of reduced-carbohydrate diets:
(a) very low carbohydrate ketogenic: carbs limited to 20—50 g per day or < 10% of total energy intake.

(b) low carbohydrate: carbs limited to < 130 g per day or < 26% of total energy intake.

(c) moderate carbohydrate: carbs limited to 130—225 g per day or 26—45% of total energy intake.

(Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13.)


Slide 7 – Teaching Low Carb

Speaking Points Summary
  • Food Lists: customize to  each patient / client. Some people prefer to stop buying / eating certain foods which automatically limits their carb choices, e.g. they don’t want to buy bread or keep it in the house
  • Carb Counting: could vary and be personalized depending on the client / patient’s post-prandial (after meal) glucose responses, e.g. up to ___ carbs per day versus set number of carbs at each meal
  • Food Label Reading: focusing on carbs and/or sugars in the ingredient list
  • Track Macros: use of an app such as MyFitnessPal or CarbManager, can be individualized to be gluten free, Mediterranean, etc.

Slide 8 – Teaching Low Carb (cont’d) – shows a handout used in practice to show lower carb options for traditional pasta.


Slide 9– Teaching Low Carb – making it easy

e.g. using leftover vegetables from dinner for breakfast, sample meal plans with carb amounts, resources with recipes and pictures, no—cook put together meal ideas.


Slide 10 – Clinical Pearls for Providing Support

  • real food when possible
  • option when convenience is needed
  • ways to make carb foods less carb-based; e.g. substituting plain yogurt with vanilla for sweetened vanilla yogurt

Slide 11 -Low Carb Empowered Eater

This slide gave an example of a person with diabetes who started eating lower carb on his own by using a Continuous Glucose Monitor (CGM).

i.e. eats the topping off a pizza to minimize glucose spike and is empowered to do so because he can see the results in real-time.


Slide 12 -Virta Health Type 2 Diabetes Trial was not included in the ADA’s Consensus Report because subjects self-selected which group they would be in, i.e. not randomized.

However, the 1-year data showed HbA1C declined 1.3% concurrently with elimination of non-metformin medications in the continuous care intervention group which is notable.

The 2-year data was published in 2019, just prior to the ADA Consensus Report but was not included.


Slide 13 – slide from Virta Health

Data from people who completed 2 years of the Virta Health clinical trial (intervention group versus usual care group)

This slide represents the actual percentage point reduction in prescription (Rx) costs, HbA1C and Body Weight of intervention group compared to the usual care group.


Slide 14 – What people think “keto” is, versus what keto actually is.

The idea here is that people think that all one eats on a ketogenic diet is meat, eggs, butter and lots of bacon, but there is a variety of foods one can eat, including vegetables, nuts, avocado (amongst other things).

 

 

 


Slide 15Well Formulated Ketogenic Meal Plans

A well formulated, ketogenic meal plans can be a great way for people to learn to eat whole, less-processed, and plant foods such as vegetables, nuts and olives and to learn about carbohydrates; a win-win for people with diabetes.


Slide 16 – Ketogenic Meal Plans

  • 20-50 grams carbs per day: 5-10% carbohydrate, 70-85% fat*, 10-25% protein*

[*Note: this is not the only way to define a “ketogenic diet”, but the one the presenters use. Some clinicians use a higher protein/lower fat approach. What makes a diet ketogenic is the number of grams of carbs being ; 50 g per day or less, for men / 35 g of carbs per day or less, for women.]

  • adequate electrolyte supplementation: sodium; 2,000-5,000 mg per day, plus potassium, magnesium
  • can include sample plans, food lists, recipes, pictures, carb counting, tracking macros

Slide 17 – Ketogenic Meal Plans (cont’d)

Keto meal plans can be customized and individualized to the client’s / patient’s food preferences.

(e.g. gluten free, Mediterranean, etc.)


Slide 18 – Ketogenic Meal Plans – keeping it simple.

Many people benefit from basic simple food lists (eg. a “vegetable” list with types of vegetables, a place for them to list their 5 favourite types, along with some pictures).

These food lists can also be used to teach low carb eating.


Slide 19 – Examples of how to include options such as dessert, alcohol, etc. in very low carb eating plans.

 

 


Slide 20 – Recommendations:

  • supplement with multivitamin
  • drink 64 oz / 2 liters water/day, add potassium / magnesium
  • use electrolyte drinks or bone broth to minimize symptoms of “keto flu”
  • the first week: fat / protein to satiety to address hunger
  • after the first week: either eat fat until satisfied and/or limit fat and total calories for weight management*

*Note: Some clinicians encourage people to eat lean protein until satiated, then add some fat for taste. Many clinicians do not limit total calories, but focus on increasing satiety instead, as the end result will be a decrease in overall calories (as a result rather than as an input).


Slide 21 – What is an Individualized Plan (slide credit: Shamera Robinson, RDN)

The following components should all be
considered when assessing, teaching and coaching with any nutrition intervention;

  • energy deficit*
  • dietary preferences
  • health literacy / numeracy
  • resources
  • food availability
  • cooking skills
  • disordered eating
  • sustainability

*Note: Many clinicians do not create an energy deficit (i.e. do not limit total calories) but focus on increasing satiety. Increasing satiety ends up resulting in an energy deficit as a result, which some clinicians prefer over restricting calories as an input.


Slide 22  – Transitioning to a Low Carb (from a Keto) Meal Plan

  • Some people will not want to do very low carb / keto diet forever and/or may benefit from taking planned breaks
  • this requires a period of transitioning from a ketogenic meal plan to other meal plan (e.g. low carb), depending on client / patient’s wishes/needs
  • transition should be customized to the individual
  • can be a mixture of carbohydrate food (e.g. 1/2 baked potato*, 1/2 pita bread*) along with low-carb alternatives (e.g. cauliflower “rice”, zucchini “zoodles”)

* Note: in this type of case, some clinicians would recommend low Glycemic Index / high fiber carbohydrates such as winter squash or peas, instead of potato or bread.


Slide 23  – Clinical Pearls for Providing Support

  • aim for real food when possible
  • convenience options could be protein shakes, pre-portioned cheese or nuts, ready-made mashed cauliflower, ready-made low-carb pizza or low carb wraps
  • emphasize protein, fiber, fat for satiety, electrolyte needs
  • keto dessert ideas
  • how to handle vacations, emotional / stress eating
  • consider incorporating “mindful eating” / “intuitive eating”; rating hunger levels to teach clients to listen to their bodies, eat when they are hungry and stop when full*, etc.

*Note: this approach may not be suitable for those with very high insulin levels that drive food cravings, or addiction to specific foods.


Part B: Pharmacology Approach – Diana Isaacs, PharmaD, CDE

 

Slide 24  – Medication Adjustment for Low Carb Eating

 


Slide 25 – ADA Consensus Report nutrition guidelines

  • adopting a very low carb eating plan can cause increased production of urine (diuresis) and a rapid reduction in blood glucose
  • consultation with a knowledgeable practitioner at the onset is necessary to prevent dehydration, reduce injected insulin and blood sugar lowering medications in order to prevent hypoglycemia (low blood sugar)

(Evert AB et al. Diabetes Care 2019; 43: 731-754.)


Slide 26 – Medication Adjustments for Type 2 Diabetes (T2D)

The first speaking point was to confirm that the patient is truly a type 2 diabetic

i.e. not LADA (Latent Autoimmune Diabetes of Adulthood) which is a form of type 1 diabetes that develops later into adulthood

Medication Adjustments for Type 2 Diabetes (T2D)
  • limit medications that cause hypoglycemia, such as insulin, sulfonylureas, meglitinides (more on that below)
  • other medication likely not needed / not preferred: alpha glucosidase inhibitors (prevent carb digestion), thiazolidinediones (TzD), also known as glitazones (more on that below)

(Clinical Guidelines for Therapeutic Carbohydrate Restriction, August 1, 2019,  Standard of Care Clinical Guidelines, www.lowcarbusa.org/clinical-guidelines)


Slide 27 – Medications to Stop on a Very Low Carbohydrate Diet

  • sulfonylurea, increase insulin release e.g. GlyburideⓇ
  • meglitinide (also called glinides), e.g. PrandinⓇ
  • bolus (meal time) insulin
  • combo insulins: 70/30, convert to basal only
  • alpha glucosidase inhibitors (acarbose), prevent carbohydrate absorption, e.g. GlucobayⓇ

(Clinical Guidelines for Therapeutic Carbohydrate Restriction, August 1, 2019,  Standard of Care Clinical Guidelines, www.lowcarbusa.org/clinical-guidelines), Murdoch C et al, British Journal of General Practice, July 2019)


Slide 28 – Medications to Use Caution on a Very Low Carbohydrate Diet

  • Sodium-glucose co-transporter protein 2 inhibitors SGLT-2 inhibitors (also called gliflozins), e.g. InvokanaⓇ, JardianceⓇ
  • basal insulin (initial 30-50% decrease)
  • insulin U500: cut dose in half
  • thiazolidinediones (TzD), also known as glitazones (risk of weight gain)

(Clinical Guidelines for Therapeutic Carbohydrate Restriction, August 1, 2019,  Standard of Care Clinical Guidelines, www.lowcarbusa.org/clinical-guidelines), Murdoch C et al, British Journal of General Practice, July 2019)


Slide 29 – Medications that are Okay to Use on a Very Low Carbohydrate Diet

  • MetforminⓇ
  • Glucagon-like peptide 1 inhibitors (GLP-1 agonists) e.g. VictozaⓇ, SaxendaⓇ
  • Dipeptidyl peptidase 4 inhibitors (DPP-4 inhibitors) e.g. JanuviaⓇ

(Clinical Guidelines for Therapeutic Carbohydrate Restriction, August 1, 2019,  Standard of Care Clinical Guidelines, www.lowcarbusa.org/clinical-guidelines, Murdoch C et al, British Journal of General Practice, July 2019)


Slide 30 – Medications Adjustments for Type 1 Diabetes on a Low Carbohydrate Diet

  • bolus insulin: may need to intensify carb ratio, ? bolus for protein
  • monitor ketones
  • avoid sodium-glucose co-transporter protein 2 inhibitors (SGLT-2 inhibitors), also called gliflozins, e.g. InvokanaⓇ, JardianceⓇ
  • caution with hybrid closed loop pumps
  • close follow-up required

(Eisworth M et al, Endocrinol Diabetes Metab Case Rep 2018, 2018:18-0002, Krebs JD et al, Asia Pacific Journal of Clinical Nutrt 2016 25:78-84, Nielsen JV et al Upsala Journal of Medical Sciences 2005; 110 267-273)


Slide 31 – Blood Pressure Medications

  • important to keep in mind the initial diuretic effect of a low carb or very low carb diet
  • consider cutting dosage in half or stopping diuretic (e.g. HCTZ or chlorthalidone)
  • monitor blood pressure

(Hussain TA et al, Nutrition 28 (2012) 1016-1021, Evert AB et al. Diabetes Care 2019; 43: 731-754.)


Slide 32 – Other Concerns

  • drink > 2 liters (64 oz /) water/day
  • to avoid muscle cramps, supplement magnesium 200-400 mg/day
  • watch for deficiency in vitamin K, sodium, chloride, vitamin B12, folate, calcium, vitamin D

(Clinical Guidelines for Therapeutic Carbohydrate Restriction, August 1, 2019,  Standard of Care Clinical Guidelines, www.lowcarbusa.org/clinical-guidelines)


Note: Slide 33 and Slide 34 were part of a case study of a 52 year old woman with T2D along with several co-morbid conditions, and on multiple medications who planned to start a ketogenic diet the follow day. The case study reviewed the medications that should be stopped or the dosage changed, and what her new medication regimen would look like. They are not included here.


Many thanks once again to Dawn Noe, RDN, CDE and her colleague Diana Isaacs, PharmaD, CDE for sharing their slides and speaking points with us.

More Info?

If you have been diagnosed with pre-diabetic or as having type 2 diabetes and would like to adopt a low carb diet, I can help.

Please note that I am not a CDE and as a result do not provide clinical services to those with type 1 diabetes, or to those with type 2 diabetes who are currently on insulin or insulin-analogue.

For those with T2D who have only been recently prescribed insulin, I have experience working with people’s endocrinologists and GPs as they seek to transition over to a low carbohydrate / ketogenic diet to manage and treat their diabetes.

You can learn more about my services under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above.
To your good health!

 

Joy

 

You can follow me on:

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Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

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US Association of Diabetes Educators Teaches Evidence for Low Carb Diet

This weekend, thousands of American Certified Diabetes Educators (CDE) gathered at the American Association of Diabetes Educators (AADEs) annual conference in Houston, Texas.

AADE 2019 Learning Objectives – Page 3 of Final Program

One of the Learning Objectives of the conference was for CDEs to learn how to implement novel and innovative ways to advance chronic disease prevention and management, and one of those novel ways was through the use of a Low Carbohydrate Diet.

CDEs are healthcare professionals from a variety of backgrounds who are specialized in diabetes prevention and management and include Registered Dietitians,  Registered Nurses, Pharmacists, Physician Assistants and Nurse Practitioners. 

This is very exciting news indeed!

It means that CDEs are now learning how to implement the American Diabetes Association’s (ADA) new 2019 Standards of Medical Care in Diabetes that was released this past December, and which includes use of a low carbohydrate diet (you can read more about that here).

This conference provided education to enable CDEs to apply the content of the ADA’s April 18, 2019 Consensus Report which added the use of a very low carbohydrate (ketogenic) diet of 20-50 grams of carbs to the choice of meal patterns to manage both type 1 and type 2 diabetes. You can read more about the Consensus Report here.

Two Educational Sessions on Use of a Low Carbohydrate Diet

AADE 2019 Final Program – page 13 – two low carb educational sessions, Saturday August 10 2019

Saturday, August 11, 2019 there were two Educational Sessions at the AADE 2019 Annual Conference related to therapeutic use of a low carbohydrate diet.

The first session was titled Low Carbohydrate Diets; Fad or Evidence Based Course of Action and was given by Dr. Jim Painter, PhD, RD and Professor Emeritus from Eastern Illinois University, in Charleston, Illinois.

The second session was titled Person-Centered Implementation of Low Carbohydrate Eating Plans and was given by Diana Isaacs, PharmaD, CDE and Dawn Noe, RD, CDE both from Cleveland Clinic Diabetes Center. Link to this presentation, including the slides and speaking notes is at the bottom or this article.


This post is a summary of Dr. Jim Painter’s educational session at the AADE’s 2019 Annual Conference titled Low Carbohydrate Diets; Fad or Evidence Based Course of Action.

Note: Photos of the slides were posted on Twitter® on August 10, 2019 by Jake Kushner, MD (@JakeKushnerMD). 

 


Low Carbohydrate Diets: Fad or Evidence Based Course of Action

Slide 1

Dr. Painter’s first slide demonstrates using National Health and Nutrition Examination Survey (NHANES) data (adapted from Ford 2015 Am J Clin Nutr) how carbohydrate content of the US diet increased dramatically after 1980 and continued high, while protein content (and fat content, not visible in this slide) remained stable.

The increase in calories during the obesity epidemic was due largely to carbohydrate intake.

Slide 2

Dr. Painter’s second slide pointed out that not only did carbohydrate consumption increase (dotted graph), the percentage of carbohydrate from fiber decreased (bar graph).

The point Dr. Painter made is that “carbohydrates that lack fiber are high glycemic index” carbs — and these highly refined carbs result in a higher increase in blood sugar than carbohydrates that contain fiber.

Slide 3

Dr. Painter then defined what a “low carbohydrate diet” is according to the American Diabetes Association and the Academy of Nutrition and Dietetics.

What is a low-carbohydrate diet?

The American Diabetes Association defines a low-carbohydrate diet as a diet that contains < 130 grams of carbohydrate per day (including 25-30 grams of fiber)

i.e.  ~100-105 net grams of carbs

Note: Dr. Painter didn’t define a very low carbohydrate diet, which the American Diabetes Association defined in its new Consensus Report as 20-50 g carbs per day. You can read more about that here.

The Academy of Nutrition and Dietetics defined low carbohydrate diets as ≤  35% of energy from carbohydrates.

In the scientific literature, low-carbohydrate diets range from 20 grams of carbohydrate per day up to ~150 grams per day (~20-25% of energy).

Slide 4

Dr. Painter then explained how low carbohydrate diets seek to minimize insulin secretion in the pancreas via their very low glycemic response, and how the reduced insulin affects;

  • weight control
  • type 2 diabetes
  • coronary heart disease (CHD)

Slide 5

Dr. Painter explained how an initial concern with a low carbohydrate diet was with the higher fat aspect, particularly for weight loss, as fat provides 9 kcals / gram and carbs only provides 4 kcals/grams, however;

  1. Fat slow gastric emptying and stimulates the secretion of cholecystokinin (CCK) and Peptide YY (PYY) — which are satiety hormones that result in people feeling full.
  2. Dietary proteins, short chain fatty acids and free fatty acids increase GLP-1 (which is one of the incretin hormones). Glucagon-like Peptide-1 (GLP-1) acts on the brain to decrease appetite, increase satiety (feeling full) and decrease food intake. You can read more about that here.
  3. Branched Chain Amino Acides (BCAA) found in protein reduces appetite.
  4. Ketone bodies (produced in very low carbohydrate diets) such as beta-hydroxybuterate suppress appetite.

Slide 6

Dr. Painter then outlined the findings of a 2014 study titled Effects of low-carbohydrate and low-fat diets: a randomized trial (Baranna LA, Hu T, Reynalds K et al, Ann Intern Med. 2014 Sep 2;161(5):309-18. doi: 10.7326/M14-0180).

Participants in this study had a BMI of between 30-45 kg per meter squared (meaning they were obese to morbidly obese), but did not have any metabolic diseases such as diabetes or cardiovascular disease (CVD).

The low carb group had carbohydrate intake of < 40 grams/day and the low fat group was allowed 55% of energy from carbohydrate (which is with the Recommended Dietary Intake of 45-55%), but restricted calories from fat.

There were 59-60 participants in both the low carb or low fat group…

Slide 7

…and after a year, those in the low carb group had a greater decrease in weight, fat mass, ratio of total-high-density lipoprotein (HDL) cholesterol, triglyceride level, and greater increases in HDL cholesterol level than those on the low-fat diet.

Dr. Painter highlighted that at the end of 12 months; these were the results of the two groups;

Low-carbohydrate diet
  • 5.3 kg weight loss
  • 1.2 kg loss of fat mass
  • 1.3 gain lean body mass
Low-fat diet
  • 1.8 kg weight loss
  • 0.3% gain in fat mass
  • 0.4% loss in lean mass

Slide 8

Dr. Painter then went over the results from a 2006 study by Gannon MC and Nutall FQ, titled Control of Blood Glucose in Type 2 Diabetes Without Weight Loss by Modification of Diet Composition ( (2006 Mar 23;3:16. doi: 10.1186/1743-7075-3-16) which found that even without weight loss, altering the diet composition to a low carb diet (carbs < 20% of energy) can enable people with type 2 diabetes to lower their blood sugar level without weight loss or diabetes medications, and achieve significantly better glycated hemoglobin (HbA1C) levels.

Slide 9

In this slide, Dr. Painter addressed a prevailing concern among many healthcare professionals that a low carbohydrate diet increase cardiovascular disease risk.

Does a Low-Carbohydrate Intake Increase Cardiovascular Disease Risk?

Dr. Painter outlined that a 2017 by Chui demonstrated that HDL cholesterol increases in a low carb diet and that while LDL cholesterol does increase, it tends to be the large buoyant LDL that increase, with no change in the athlersclerotic small, dense LDL.

He also outlined that a 2012 meta-study analysis of 19 randomized control trials (RCTs) by Santos et al reported a global decrease in triglyceride levels of 29.71 mg/dL (0.34 mmol/L) and that a 2014 study by Bazzano reported that a low carbohydrate diet had a greater decrease in 10-year cardiovascular heart disease (CHD) risk score based on the Framingham Risk Score, than those on the low fat diet.

Slide 10

Dr. Painter then elaborated on a study from 2008 by Forsythe CE et al titled Comparison of Low Fat and Low Carbohydrate Diets on Circulating Fatty Acid Composition and Markers of Inflammation that was published in the Journal Lipids ( 2008 Jan;43(1):65-77. Epub 2007 Nov 29).

In this study overweight men and women were put on either a low carb or low fat ~1500 kcal / day diet for 12 weeks. Results indicated that the low carb diet had a 3-fold higher dietary intake of saturated fatty acids (SFA) (36 grams/day versus 12 grams/day) yet the low carb group had a significantly greater reduction in their serum saturated fat levels.

That is, people in the low carb group they ate 3x the amount of saturated fat yet had a significantly greater reduction in their blood levels of saturated fat.

Slide 11

Dr. Painter then reviewed  a 2004 study by Volek JS et al titled Dietary Carbohydrate Restriction Induces a Unique Metabolic State Positively Affecting Atherogenic Dyslipidemia, Fatty Acid Partitioning, and Metabolic Syndrome which indicated how a very low carbohydrate (VLCKD) compared to a low carbohydrate diet (LCD) significantly improved body mass, abdominal fat, triglycerides (TG), ApoB:ApoA1 ratio, small dense LDL, TG:HDL ratio, insulin levels, and HOMA-IR score.

Slide 12

Dr. Painter then looked at the “why” for using a low carbohydrate diet for type 2 Diabetes Mellitus (T2DM).

Dr. Painter outlined the results of a 2015 study titled Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012 by Menke A et al ( 2015 Sep 8;314(10):1021-9. doi: 10.1001/jama.2015.10029) which indicated that;

Recent data indicates 52% of the American population is either diabetic or prediabetic. The cost of diabetes (in the US) is estimated to be over $320 billion annually”.

Slide 13

Dr. Painter then cited a 2013 systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes (Ajala et al) titled Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes, Am J Clin Nutr. 2013 Mar;97(3):505-16. doi: 10.3945/ajcn.112.042457. Epub 2013 Jan 30.).

This paper looked at 20 randomized control trials (RCTs) across 3460 randomly assigned subjects and which found that a low-carbohydrate diet, low-GI diet, Mediterranean diet, and high-protein diet all led to a greater improvement in glycemic control and with the low-carbohydrate diet and Mediterranean diet leading to greater weight loss.

Dr. Painter indicated that each of these dietary philosophies show effectiveness of lower carbohydrate and lower GI diets for treating T2DM.

Slide 14

Dr. Painter then outlined the findings of a 2017 study by Snorgaard O et al titled Systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes (

“Upon subgroup analysis, it was found that carbohydrate of < 26% of energy produces the greatest reduction whereas carbohydrate reduction of 26-45% of total energy produces no additional benefit over low-fat diets.”

Slide 15

In Dr. Painter’s next slide, he summarized the finding of a 2018 systematic review and meta-study paper by Sainsbury E et al with respect to medication use, titled Effect of Dietary Carbohydrate Restriction on Glycemic Control in Adults with Diabetes: A systematic review and meta-analysis ( 2018 May;139:239-252. doi: 10.1016/j.diabres.2018.02.026. Epub 2018 Mar 6).

“There was a greater reduction in medication use for participants on carbohydrate-restricted diets compared with high carbohydrate diets at every time point.”

  • reduced the dosage of oral medication and/or insulin
  • or an elimination of medication

Sainsbury 2018

Slide 16

Dr. Painter then outlined some highlights of a 2015 review paper titled Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base by Feinman RD, et al; namely;

  • The benefits of carbohydrate restriction in diabetes are immediate and well- documented
  • Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss…and leads to the reduction or elimination of medication.

Slide 17

Dr. Painter next slide highlighted Table 2 from the consensus report of October 2018 by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) where they classified a low carbohydrate diet as Medical Nutrition Therapy (covered in this previous article). Table 2 outlines the full range of therapeutic options, including lifestyle management, medication and obesity management and lists a low carbohydrate diet as one of the available therapeutic diets.

Slide 18

Dr. Painter then went over the 2019 American Diabetes Association’s Lifestyle Management; Standards of Medical Care in Diabetes which was released on December 17, 2018 (covered in this previous article) and which outlined key recommendations regardless which of the different types of approved eating patterns people choose, namely;

“As for all individuals in developed countries, both children and adults with diabetes are encouraged to minimize intake of refined carbohydrate and added sugars and instead focus on carbohydrate from vegetables, legumes, fruit, dairy (milk and yogurt) and whole grains. The consumption of sugar-sweetened beverages (including fruit juices) and processed “low fat” or “non-fat” food products with high amounts of refined grains and added sugars is strongly discouraged.”

Slide 19

The next slide was a continuation from the 2019 American Diabetes Association’s Lifestyle Management; Standards of Medical Care in Diabetes, and Dr. Painter highlighted that;

 

“In addition, research indicates that low carbohydrate eating plans may result in improved glycemia and have the potential to reduce anti-hyperglycemic medications for individuals with type 2 diabetes.”

Slide 20

Dr. Painter next highlighted the necessity of medication adjustment soon after initiating a low carbohydrate diet in order to prevent hypoglycemia.

Box 1 from Adapting Diabetes Medication for Low Carbohydrate Management of Type 2 Diabetes: a practical guide by Murdoch C et al (2019), was presented and is as follows;

Summary guidance on adapting diabetes medication for low carbohydrate management of type 2 diabetes

Dr. Painter highlighted the following on his slide;

“Practice expertise suggests a 50% reduction of daily insulin dose at initiation of the low carbohydrate diet (LCD) is appropriate in most cases. In individuals whose HbA1C is markedly elevated, a smaller reduction of perhaps 30% may be appropriate, with further reductions over time…”

Slide 21

Dr. Painter’s next slide simply read;

“Be encouraged! Reversal of Type 2 Diabetes??”

…as if to challenge his listeners to consider that diabetes reversal using a low carbohydrate diet is possible.

Slide 22

Dr. Painter then reviewed the DiRECT randomized control trial by Lean et al, titled Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial (The Lancet, 391 (10120). pp. 541-551. ISSN 0140-6736).

In that study, the 300+ participants from almost 50 primary care sites in the UK were randomly assigned to either a weight management program (which was the intervention group) or to best-practice care by guidelines (which was the control group).

Slide 23

Dr. Painter outlined the results of the DiRECT trial, which found that at 12 months, 24% of the  participants in the intervention group lost 15 kg or more, with no weight loss in the control group.

Diabetes remission varied with weight loss;

  • no remission in those who gained weight
  • 7% achieved remission with under 5 kg of weight loss
  • 34% achieved remission lost between 5—10 kg
  • 57% achieved remission with 10—15 kg loss
  • 86% achieved remission with weight loss of 15 kg or more

“Our findings show that, at 12 months almost half of participants achieved remission to a non-diabetic state and off anti-diabetic drugs. Remission of type 2 diabetes is a practical target for primary care“.

Slide 24

Dr. Painter then proceeded to addressed 3 common misperceptions about low carbohydrate diets, namely;

  1. A low carbohydrate diet puts participants at risk of ketoacidosis…
  2. Low carbohydrate diets ignore the principles of moderation and result in a nutrient-deficient diet…
  3. The majority of weight loss comes from water and lean body mass…

Slide 25 – addressing the misperception that a low carbohydrate diet puts participants at risk of ketoacidosis…

Dr. Painter cited a 2013 study titled Long Term Successful Weight Loss with a Combination Biphasic Ketogenic Mediterranean diet and Mediterranean Diet Maintenance Protocol by Paoli A et al ( 2013 Dec 18;5(12):5205-17. doi: 10.3390/nu5125205).

Using the data from that study, Dr. Painter demonstrated how the glucose range, insulin rang and ketone body range in a ketogenic diet is nothing like the ranges in Diabetic Ketoacidosis.

Normal Diet

Glucose (mg/dl)                       80-100
Insulin (uU/L)                                6-23
Ketone Bodies (mmol/L)         0.1

Ketogenic Diet

Glucose (mg/dl)                        65-80
Insulin (uU/L)                                5.5-9.4
Ketone Bodies (mmol/L)          1-8

Diabetic Ketoacidosis

Glucose (mg/dl)                       >300
Insulin (uU/L)                                ~0
Ketone Bodies (mmol/L)         >25

Slide 26 – addressing the misperception that low carbohydrate diets ignore the principles of moderation and result in a nutrient-deficient diet…

Dr. Painter cited the paper by Zinn C et al, titled Assessing the Nutrient Intake of a Low-Carbohydrate, High-Fat (LCHF) Diet: a hypothetical case study design and highlighted that despite macronutrient proportions not aligning with current national dietary guidelines, that when well-designed a low carbohydrate diet provides all of the essential micronutrients needed by the body.

Even at the lower end of the carbohydrate spectrum, you can still get all of the essential nutrients and energy your body needs by selecting from a broad array of nutrient-dense vegetables and fruit, e.g.:

      • raspberries
      • strawberries
      • blueberries
      • tomatoes
      • olives
      • avocados
      • plain greek yogurt
      • nuts/seeds

“Zinn et all demonstrated that a well-planned Low-Carbohydrate, High-Fat (LCHF) meal plan can be considered micronutrient replete.”

Slide 27 – addressing the misperception that the majority of weight loss comes from water and lean body mass…

Dr. Painter cited the 2014 study by Bazzano LA et al, titled Effects of Low-Carbohydrate and Low-Fat Diets: a randomized trial which found that of the ~60 subjects randomized to either the low-carbohydrate diet (<40 grams/day) or low-fat diet (<30% of daily energy intake from total fat [<7% saturated fat])  which found that at 12 months, participants on the low-carbohydrate diet lost 3.5 kg more weight and lost 1.5% more fat mass, than those in the low-fat diet group.

Slide 28

Dr. Painter concluded his talk by saying that he feels that most low carbohydrate diets are ‘harmful in practice’ because they are low in fiber, but that that can be addressed by;

 

  1. Start with a foundation of 6-8 servings of non-starchy, fiber-rich vegetables (~ 15 grams net carbs per day)
  2. Include additional calories from added fats. Nuts and seeds can provide additional fiber
  3. Depending on weight loss and healthy goals, low glycemic carbohydrates found in whole grains and fruit can be used to provide additional fiber.

For those who want to make sure to meet current fiber consumption recommendations while eating a low carbohydrate diet, please have a look at the article I wrote titled Surprising Ways to Get Adequate Fiber Eating Low Carb High Fat (LCHF), located here.

Final Thoughts…

Just a few years ago, it was viewed as quite ‘radical’ for healthcare professionals to consider a well-designed low carbohydrate or very low carbohydrate (ketogenic) diet as therapeutic, but now organizations in Europe (such as the EASD), the UK and Australia — along with the American Diabetes Association (ADA) consider both meal patterns Medical Nutrition Therapy for management of diabetes and for treating overweight and obesity.

What an exciting time!

Here it is, less than a year after the ADA released their 2019 Standards of Medical Care in Diabetes and only 4 months after the ADA released its Consensus Report and this past weekend, thousands of American Certified Diabetes Educators (CDE) gathered at their annual conference znd ~500 learned how to implement a low carbohydrate or ketogenic diet to advance chronic disease prevention and management.

It is my sincere hope that it won’t be much longer before clinicians in Canada are provided with diabetes Standards of Care that support the use of a well-designed low carbohydrate and very low carbohydrate diet as therapeutic options.

More Info?

If you have been diagnosed as being pre-diabetic or as having type 2 diabetes and would like support to put the symptoms into remission by implementing  a low carbohydrate or very low carbohydrate eating pattern, then I can help.
I also don’t believe in a ”one-sized-fits-all” approach and will work with you to design an individual Meal Plan that will meet your needs. You can learn more about my services under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above.

 

To your good health!

 

Joy

 

You can follow me on:

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Fipboard: http://flip.it/ynX-aq


UPDATE
(August 16 2019):
You can find the second presentation from the American Certified Diabetes Educators conference
here. This is where hundreds of CDEs learned about dietary and medication management of lowcarb and ketogenic diets from a Registered Dietitian and Dr. of Pharmacy with CDE certification.

 

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. American Association of Diabetes Educators, Annual Conference, Houston Texas, Friday August 9 – Monday August 12, 2019, https://www.aademeeting.org/
  2. National Certification Board for Diabetes Educators (NCBDE), What is a CDE, https://www.ncbde.org/certification_info/what-is-a-cde/

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Intermittent Fasting Doesn’t Need to be Complicated

Today, a well-known dietary management group asked people on social media to name their favourite fasting protocol and what struck me was that there were as many different styles of intermittent fasting, as people.

Here are some of the answer that were posted;

  • OMAD 20:4
  • eat lunch/dinner Tues/Thurs/Sat/Sun, Fast Mon/Wed/Fri
  • 42 x 3
  • 24 hour fast 1 x week, 48 hour fast 1 x month, 4 day fast 1 x year
  • IF daily : 2 meals, alternate day, OMAD occasionally
  • 36 hrs on Mondays and Thursdays, 18:6 the rest of the days
  • OMAD three days a week. Two meals four days a week. LCHF when eating twice.
  • ADF on MWF, two meals plus snack on the off days
  • Sunday dinner to Tuesday first meal when hungry
  • OMAD with ADF and extended fasts of 72 hours to 7 days throughout the year
  • EF of 5 plus days every 5-6 week
  • 16:8 with an eating window 11 am to 7 pm
  • 42 x 3 times a week plus 18:6 on feasting days

Definition of Terms

OMAD = one meal a day
IF = intermittent fasting
ADF – alternate day fasting
18:6 = fasting 18 hours / day, six-hour eating window
20:4 – fasting for 20 hours / day, 4 hour eating window
EF of 5+ days = extended fasting for 5 or more days

Internal and External Perceptions of Intermittent Fasting

I think to someone reading this who had no experience with these different types of “intermittent fasting”, this would seem terribly complicated. And difficult.  It might even seem like an ‘initiation rite’ of sorts, or perhaps a competition as to who does the most radical type of fasting.

While fasting has therapeutic benefits of enabling insulin levels to fall, those who fashion their diets after books that have been written on fasting often see it as ‘part and parcel’ of a very high fat / moderate protein “keto diet”.

It’s important to understand, as I’ve said many times in different articles such as this one,  there are different types of “low carb” diets and different types of “keto diets”. Not all are super high fat!  Some versions do not have people eating lots of whipping cream and coconut oil and bullet-proof’ing everything and eating ‘fat-head’  bread and pizza, with tons of bacon and avocado. And not all involve “fasting”. In fact, some approaches caution against it, due to the potential of loss of muscle mass.

More than One Type of Low-Carb or “Keto” Diet

Some approaches are high protein with as much fat as people want, whereas other encourage moderate to high level of lean protein with visible fat removed. There is no one “low carb” or “keto diet”, even though when most people think of “keto” they envision the high fat version, which alternates with different types of fasting.

It is understandable though, that if someone is going to eat huge amounts of fat in a day, that it is followed by longer or shorter periods of intermittent fasting, which balance it out. It also balances out the cost of eating that way, as one only has to buy food for 1/2 the amount of time.

My Answer to the Question

I answered the question “what is your favourite fasting protocol” as follows;

My favourite fasting protocol

My favourite ‘fasting protocol’ since my type 2 diabetes is in remission isn’t really “new”.

According to circadian biologists like Dr. Satchidananda Panda of Salk Institute and Dr. Matthew Walker of University of California at Berkeley, this is probably pretty close to how mankind ate for that last few millennia; until the advent of the gas and then electric light and refrigeration.

Until we could artificially extend ‘day’ as long as we wished simply by leaving the lights on — and pushing it even further with our smartphones in bed, people ate well before nightfall and went to sleep when it got dark and didn’t eat until the first meal the following day. According to Panda, the master circadian “clock” in our suprachiasmatic nucleus of our brains are set by these ~24 hour day/night cycles and when we are first exposed to light, and the individual circadian ‘clocks’ in our organs are ‘synced’ by when we sleep and eat.

Literally, for thousands of years, people didn’t eat from after their last meal of the day (which was quite a while before they slept) and then didn’t eat until the first meal the next day (which wasn’t as soon as they opened their eyes, either!). Even after the invention of electric lighting and refrigeration, many people had a long period of time between when they finished dinner and the next morning when they ate breakfast (the meal that broke the “fast”). It would seem that our species did pretty well eating that way, and didn’t seem to suffer the metabolic diseases of overabundance we are now inflicted with.

Given our body’s circadian clocks are literally tied to these approximate 24/hour cycles, and ‘synced’ by when we eat / don’t eat and sleep, eating in accordance with these natural circadian rhythms (when it functioned best for thousands of years) just seems to make “sense”.

In light of this, my general “philosophy” for healthy individuals about when to eat and when to “fast” is simple;

  1. eat real, whole food when genuinely hungry, as part of a meal
  2. don’t eat between meals (avoids keeping insulin high, allows it to fall between meals)
  3. Don’t eat after an early-ish last meal of the day (~3 hours before bedtime) and not until the first meal the following day (whenever that is). This too allows insulin levels to fall, and enables your body to do all the wonderful “housekeeping tasks” that both Dr. Panda and Dr. Walker write and teach about.
    (Note: For those who are metabolically unwell, done with supervision, slightly longer periods of intermittent fasting up to 24 hours may be beneficial for lowering insulin resistance, without loss of muscle mass.)

More Info?

If you would like more information about the different low carb meal patterns available and which might be best for you as well as implementing times for eating and times not eating, I can help.

You can learn more about my services under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

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References

Panda S, Circadian physiology of metabolism, 2016, Science: 354(6315) 

Krause AJ, Simon EB, Mander BAGreer SMSaletin JM, Goldstein-Piekarski AN, Walker MP. The sleep-deprived human brain. Nature Reviews. Neuroscience. PMID 28515433 DOI: 10.1038/nrn.2017.55

 

Keto Diet Doesn’t Cure Diabetes

Note: this is both a Science Made Simple article and an editorial, where I express my own opinion.

A ketogenic diet and the weight loss that can accompany it is well documented to be both safe and effective as medical nutrition therapy in the treatment of type 2 diabetes. While it can enable individuals to put symptoms of the disease into remission, it is not a ‘cure’.

An article widely circulated on social media earlier this week announced “What If They Cured Diabetes and No One Noticed?”[1] and said;

“So you’d think that if someone figured out a way to reverse this horrible disease, there would be big bold headlines in 72-point type. You’d think the medical community, politicians and popular press would be shouting it from the rooftops.

Guess what? Someone did. Yet it appears no one noticed.

The cure was simple — so simple, in fact, that it involved no medication, no expensive surgery and no weird alternative supplements or treatments.

What was this miracle intervention? Diet. Specifically, the ketogenic diet.”

Of course, the author is entitled to hold this opinion and to express it, however in my opinion, a ketogenic diet does not “reverse diabetes” — it does not “cure” it.  Furthermore, I believe the distinction between “reversing diabetes” and “reversing the symptoms of diabetes” is very important, and more than a matter of semantics.

In an article I posted last year titled The Difference Between Reversal and Remission of Type 2 Diabetes, I wrote that;

“Reversal” of a disease implies that whatever was causing it is now gone and is synonymous with using the term ”cured”.  In the case of someone with Type 2 Diabetes, reversal would mean that the person can now eat a standard diet and still maintain normal blood sugar levels. But does that actually occur? Or are blood sugar levels normal only while eating a diet that is appropriate for someone who is Diabetic, such as a low carbohydrate or ketogenic diet, or while taking medications such as Metformin?

If blood sugar is only normal while eating a therapeutic diet or taking medication then this is not reversal of the disease process, but remission of symptoms.”

Addendum (July 18 2019): Type 2 diabetes is the result of beta cell failure resulting from over-taxing them with a highly refined, carb-laden diet over extended periods of time (you can read more about that here). For something to ‘cure’ type 2 diabetes, there would need to evidence of a restoration of beta-cell function. If someone was indeed ‘cured’ they would have a normal glucose and insulin response on a 3 hour glucose-insulin test (OGTT will added insulin assay at 0 hr, 1 hr and 2 hrs.).  Anything short of that is ‘remission’.

I feel that claiming that a keto diet ‘cures diabetes’ or ‘reverses the disease’ does the public a disservice:

  • Firstly, it implies that there is simple, free ‘cure’ that will work for everybody.  As I outline below; some people are able to achieve partial or complete remission of their symptoms following a keto diet, and others are not.
  • Secondly, it implies that there is a simple, free ‘cure’ available, but that it is being ‘withheld’ for some reason — either because doctors don’t know about or are afraid what colleagues might think, or because the agricultural and pharmaceutical industries have ‘big bucks to lose’ by people limiting their intake of bread, pasta and insulin.

There is no question that physicians (and all clinicians) need to be selective about recommending a keto diet for their patients / clients and to be able to document from the literature that it is safe, effective and best clinical practice for the condition for which it is recommended, and appropriate for the individual.

While falling markets for specific types of food products and drugs certainly have an impact on the economics of both the agricultural industry and pharmaceutic industry, it comes across like a ‘conspiracy theory’ to imply there is a ‘cure’ available out there, but that the public is being ‘denied’ access to it by “big food” and “big pharma”.

  • Finally, it implies that if people are unable to ‘reverse their diabetes’ and get ‘cured’ following a keto diet, that it is their fault; they mustn’t have done it properly.  Even if we substitute the terms and say instead “put their diabetes into remission” or “reverse the symptoms of diabetes”, it is unreasonable and unfair to assume that everyone will be successful in doing so, and if they aren’t, the responsibility falls on them.

Virta Health Data

The on-going study from the Virta Health had over 200 adults ranging in age from 46-62 years of age in the intervention group following a ketogenic diet at the end of two years. At one year, participants in the intervention group lowered their glycated hemoglobin (HbA1c) to 6.3% (from 7.7% at the beginning of the study) —  with 60% of them putting their type 2 diabetes into remission based on HbA1C levels >=6.5% (American Diabetes Association and Diabetes Canada guidelines).  HbA1C rose slightly to 6.7% at two years. The keto group did considerably better than the ‘usual care group’ whose average HbA1C actually rose to 7.6% at one-year (from 7.5% at the beginning of the study), and rose again to 7.9% at two years [3]. 

Fasting blood glucose of the intervention group following a keto diet increased slightly from  127 mg/dl (7.0 mmol/L) at one year to 134 mg/dl (7.4 mmol/l) at two years, which was considerably better than the usual care group, whose fasting blood glucose was 160 mg/dl (8.9 mmol/L) at one-year and 172 mg/dl (9.5 mmol/L) at two years [3].

Data so far from this study demonstrates that a well-designed keto diet can be very effective in reversing the symptoms of type 2 diabetes, and that it is more effective than what was ‘standard care’ (prior to the new ADA guidelines), but it is not a ‘cure’.

Dr. Stephen Phinney and the research team at Virta Health have written on the Virta Health website [3];

“A well-formulated ketogenic diet can not only prevent and slow down progression of type-2 diabetes, it can actually resolve all the signs and symptoms in many patients, in effect reversing the disease as long as the carbohydrate restriction is maintained.” [2]

That is, the Virta researchers say that a well-designed keto diet can resolve the signs and symptoms of the disease in many people, which “in effect” (i.e. ‘is like’) reversing the disease —  as long as the carbohydrate restriction is maintained. They don’t promote the diet as a ‘cure’, but as an effective treatment.

There is no question that Virta’s results are impressive — so much so that their studies have been included in the reference list of the American Diabetes Association’s (ADA) new Consensus Report of April 18, 2019, where the ADA included adopted the use of both a low carb and very low carb (ketogenic) diet (20-50 g of carbs per day) as one of the management methods for both type 1 and type 2 diabetes in adults. You can read more about that here.

In fact, the ADA said in that report that;

Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia*’

* blood sugar

A keto diet is not a ‘cure’ for diabetes. At this present time, there is no cure for diabetes. There are, however three documented ways to put type 2 diabetes into remission;

  1. a low calorie energy deficit diet [4,5,6]
  2. bariatric surgery (especially use of the roux en Y procedure) [7,8]
  3. a ketogenic diet [3]

Final Thoughts…

I believe that based on what has been published to date, it is fair to say that a well-designed ketogenic diet can;

  • prevent progression to type 2 diabetes, when adopted early in pre-diabetes
  • slow down progression of type 2 diabetes
  • resolve the signs and symptoms of the type 2 diabetes
  • serve in effect like reversing the disease, provided carbohydrate restriction is maintained

…but to claim that a keto diet ‘cures’ type 2 diabetes is simply incorrect.

A ketogenic diet is a safe and effective option for those wanting to put the symptoms of type 2 diabetes into remission.

More Info?

If you would like more information about adopting a low carb or ketogenic diet in an effort to put the symptoms of type 2 diabetes into remission or for weight loss, I’d be glad to help.

You can learn more about my services under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Steel, P, “What If They Cured Diabetes and No One Noticed? – if the ketogenic diet can reverse diabetes, why isn’t your doctor recommending it?”, The Startup, July 13 2019, https://medium.com/swlh/what-if-they-cured-diabetes-and-no-one-noticed-keto-diet-ketogenic-virta-study-d49c195bf8f5
  2. Phinney S and the Virta Team, Can a ketogenic diet reverse type 2 diabetes? https://blog.virtahealth.com/ketogenic-diet-reverse-type-2-diabetes/
  3. Athinarayanan SJ, Adams RN, Hallberg SJ et al, Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-year Non-randomized Clinical Trial.  preprint first posted online Nov. 28, 2018;doi: http://dx.doi.org/10.1101/476275.
  4. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
  5. Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:27002059
  6. Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet2018;391:541-51.
  7. Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257—264.
  8. Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2

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Trouble-shooting Chronic Constipation on a Low Carb Diet

Constipation is one of the most common problems that people face, with between 2 and 28% of the population in Western countries reporting having this [1-3]. In 2007 in the United States, 19.4% of people reported problems with chronic constipation[4] and in Canada between 15% and 27% of people reported having sought health care support for chronic constipation in 2001 [5].

Defining Constipation

The term “constipation” means different things to different people. For some it simply means they don’t pass their stools (feces) often enough, and for others it means that when they do, their stools are hard, difficult to pass, may cause lower abdominal discomfort, or feel like they “still have to go” afterwards (incomplete evacuation).

What is considered a ‘normal range’ in the number of bowel movements per week varies considerably; from anywhere from 3 – 21 times per week, provided the stools are soft and easy to pass, but not loose or unformed. For some people, having bowel movements 3 times per week may be normal, as long as their stools aren’t hard, dry or compact and there is no abdominal discomfort. For others, 3 times per day (21 times per week) may also be considered fine, provided the stools aren’t unusually loose.

There are many factors that can contribute to chronic constipation; including some medications that people take, inadequate fiber or the wrong kind of fiber, insufficient hydration (not drinking enough water, especially when its hotter out, or exercising), high levels of estrogen and progesterone when a woman is pregnant, or disorders such as Irritable Bowel Syndrome (IBS) and diverticulosis.

The Causes of Chronic Constipation

People often think (or are told) that if they are constipated, they just need to eat more fiber, but in some cases increasing fiber from certain sources such as grains may make the problem worse. For example, some people are wheat sensitive, but not gluten-intolerant (i.e. not Celiac). That is, they are sensitive to wheat only, but not rye or barley (which also contain gluten).  Others have something called non-celiac gluten sensitivity which resolves when gluten is eliminated from the diet, yet don’t test positive for Celiac disease. These people feel better when they avoid grain-based carbs, and may opt instead for eating nutritiously-dense starchy vegetables, such as winter squash or yam, for instance. Since a low-carb diet is non-grain-based, people who experience chronic constipation due to wheat intolerance or non-celiac gluten sensitivity will start to feel considerably better eating this way. The problem may be that for those with non-celiac gluten sensitivity, other sources of gluten, such as those found in malt vinegar or low carb beer may continue to cause them symptoms.

Many people who try a “low-carb” or “keto” diet on their own often complain of being constipated and this may be for a number of other reasons.  They may be taking a medication that causes constipation as a side-effect, they may not don’t drink enough water, or it may be the result of something else.

Inadequate Hydration

I would estimate that ~80% of the people that I assess in my office have observable signs that they are aren’t drinking enough water, so this is something I would recommend most people to consider as a possible contributor to chronic constipation.

The idea that everybody needs to drink “8 glass of water per day” is a fallacy; everyone’s need for water is different. A good rule of thumb to know if you are dehydrated is just to look in the mirror. If your lips are dry and wrinkled, then you probably should aim to increase your water intake. When your lips are plump and without deep lines, you’ve probably had sufficient amount. Water is best, as coffee and tea act as a mild diuretic. They won’t dehydrate you, but you will pass the water contained in them more rapidly. “Keto water” which is water with a pinch of half-salt for electrolytes (i.e. a source of sodium and potassium) can be helpful, provided you’re not taking medications such as ACE-inhibitors (e.g. Ramipril) for blood pressure, or any other medications where potassium may be limited.

If you don’t really like plain water, a Sodastream® that enables you to make carbonated water at home may be the answer. My clients know that there is always a bottle of it on my desk, as that is how I make sure to drink enough water. A twist of lime or lemon makes a nice treat too!

What about Getting Enough Fiber?

In Canada, dietary recommendations  for dietary fiber intake varies with age and gender. Men under the age of 50 years are recommended to take in 38 gm / day of dietary fiber, and men over 50 years to take in 30 gm / day. Women under 50 years old are recommended to take in 25 gm of fiber per day and over 50 years, 21 gm per day [6].

In the US, fiber intake recommendations from the Institute of Medicine range from 19 grams to 38 grams per day, depending on gender and age [7].

While people generally think of “healthy whole grains” as good sources of fiber, many are not. For example, medium grain brown rice only has 3.4 g of fiber per 100 g, whereas wild rice (which is actually a grass and not a grain) has 6.2 g of fiber per 100 g [8]. Many vegetables and fruit such as avocado and berries are excellent sources of fiber. More on that below.

Two Kinds of Fiber — soluble and insoluble

There are two kinds of fiber; insoluble and soluble.

Insoluble fiber is what most people think about when they think of ”roughage” needed to form stool and prevent constipation. It helps form the bulk of the stool. Insoluble fiber is naturally present in the outside of grains, such as whole grain wheat and the outside of oats and is also found in fruit, legumes (or pulses) such as dried beans, lentils, or peas, some vegetables, and in nuts and seeds. Many of these are eaten on a low carb diet and can provide the recommended amount of fiber (more on that below).

Soluble fiber forms a gel’ in the intestine and binds with fatty acids. It slows stomach emptying and helps to make people feel fuller for longer, as well as slow the rate that blood sugar rises, after eating. Soluble fiber absorbs water in the gut, and helps to form a pliable stool. Soluble fiber is found on the inside of certain grainssuch as oats, chia seeds or psyillium, as well as the inside of certain kinds of fruit, such as apple and pear.

For those eating a low carb diet, getting enough fiber is not that difficult. Here are a few examples of the fiber content of foods that can be eaten;

  • Avocado — Surprisingly, avocado which is an excellent source of vegetable fat, is also high in fiber, having more than 10 gm fiber per cup (250 ml). Avocado grown in Florida which are the bright green, smooth-skinned variety have more insoluble fiber than California avocado, which are the smaller, darker green, dimpled variety.
  • Berries — Berries such as blackberries and raspberries are an excellent source of antioxidants, but also have 8 gm fiber per cup (250 ml).
  • Coconut — Fresh coconut meat has 6 gm of net carbs per 100 grams of coconut, but also packs a whopping 9 gms of fiber and is a very rich source of fat (33 gms per 100 gm coconut). It can be purchased peeled, grated and sold frozen in many ethnic stores or in the ethnic section of regular grocery stores.
  • Artichoke — Artichoke is a low-carbohydrate vegetable that is delicious boiled and it’s leaves dipped in seasoned butter. Surprisingly, one medium artichoke has over 10 gm of fiber.
  • Okra — Okra, or lady fingers’ is a staple vegetable in the South Asian diet and is commonly eaten in the Southern US. Just one cup of okra contains more than 8 gm of fiber.
  • Brussels Sprouts — These low-carb cruciferous vegetables are not just for Thanksgiving and Christmas dinner.  Split and grilled on the BBQ with garlic, they are a sweet, nutty addition to any meal, packing almost 8 gm of fiber per cup.
  • Turnip — Turnip, the small white vegetable with a hint of purple is not to be confused with the pale beige, larger rutabaga. Turnip contains almost 10 gm of fiber per cup. It is delicious pickled with salt and one beet and is commonly eaten with Middle Eastern food.

Irritable Bowel Syndrome (IBS) and Diverticulosis

Unfortunately, in addition to the fact that 20-30% of people in the US and Canada experience chronic constipation, approximately 10-15% of the population have Irritable Bowel Syndrome (IBS) [9].

IBS is a functional disorder of the gastrointestinal (GI) tract  â — which means there is no structural or biological abnormality that can be measured on routine diagnostic tests. These people often experience chronic constipation, sometimes alternating with bouts of diarrhea, as often experience abdominal pain and bloating, as well. You can read more about IBS here. As mentioned in the linked article, many people with IBS feel considerably better when they adopt a low-carb diet because they are no longer eating many of the foods that underlie their symptoms such as grains, milk and fruit, other than berries. Unfortunately, even after adopting a low carb diet about 15- 20% of those diagnosed with IBS still have residual symptoms. In my affiliate practice, I have years of experiencing working with those with IBS and offer a specialized package, as well as a one-hour teaching session that can help.

Another common problem is diverticulosis, which an estimated 50% of those over 50 years of age have. Diverticulosis is where your colon (large intestine) has small ”pockets” in it called diverticula, which can cause a number of symptoms including chronic constipation. Like those with IBS, many people with diverticulosis feel much better when they adopt a low-carb diet because they are no longer eating foods such as wheat, dairy products with lactose or high fructose fruit that used to contribute to their symptoms. The problem is that many of the low carb vegetables that are low in carbs and may be rich in fiber also may be contributing to their symptoms. So many of my clients have recently been diagnosed with diverticulosis, that in my affiliate practice I recently added a one-hour teaching session that can be added to the end of a Complete Assessment Package, or taken as a stand-alone session to help.

Final Thoughts

In trouble-shooting constipation, I recommend that people ensure they are adequately hydrated, and that they remember to drink extra water when it’s hot out or when they’ve been ill.

Eating wide variety of low-carb veggies, including those listed above that are known to be high in fiber is also good. For those on a moderate low-carb diet (not a ketogenic diet), small amounts of yam or winter squash are other ways to get added nutrients and fiber.

Berries are a wonderful source of nutrients and anti-oxidants, can be enjoyed by those on a low-carb diet and are a wonderful source of fiber! Strawberries have 3g of fiber per cup and blackberries and raspberries have a whopping 8 g of fiber per cup, with blueberries paling in comparison with a mere 2.4 g of fiber (and are higher in carbs, too).

Of course, exercise as simple as a daily walk can often help people move their bowels and many people swear by their morning cup of coffee!

For those doing all of the things above and still experiencing chronic constipation, it may be time to rule out other possible causes such as Celiac disease, or non-celiac gluten sensitivity, IBS, or diverticulosis.

I can help.

More Info?

If you would like more information about how I can help in this regard, please visit my affiliate practice, BetterByDesign Nutrition Ltd. where you can find a number of services that I offer related to Food Sensitivities / Food Allergies, Celiac Disease, IBS and Diverticulosis.

If you have questions please feel free to send me a note there or here using the Contact Me form, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Higgins PDR, Johanson JF, Epidemiology of constipation in North America: a systematic review, The American Journal of Gastroenterology 99(4); 750—759, 2004.
  2. Corazziari E, Definition and epidemiology of functional gastrointestinal disorders, Best Practice and Research: Clinical Gastroenterology, 18 (4); 613—631, 2004. 
  3. Harris LA, Prevalence and ramifications of chronic constipation, Managed Care Interface, 18 (8); 23—30, 2005.
  4. Johanson JF,  Kralstein J, Chronic constipation: a survey of the patient perspective, Alimentary Pharmacology and Therapeutics, 25(5); 599—608, 2007. 
  5. Pare P, Ferrazzi S, Thompson WG et al, An epidemiological survey of constipation in Canada: definitions, rates, demographics, and predictors of health care seeking, The American Journal of Gastroenterology, 96(11); 3130—3137, 2001.
  6. Health Canada, Fiber, https://www.canada.ca/en/health-canada/ services/ nutrients/fibre.html
  7. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Energy, Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National Academies Press; 2005
  8. Source: US Department of Agriculture, Agricultural Research Service. 2014. USDA National Nutrient Database for Standard Reference, Release 27. Nutrient Data Laboratory Home Page, http://www.ars.usda.gov/ba/bhnrc/ndl.
  9. Foundation for Gastrointestinal Disorders (IFFGD),  https://www.aboutibs.org/facts-about-ibs/statistics.html

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What is IBS and Why Do Symptoms Improve on a Low Carb Diet?

Quite a few physicians that I know that recommend a low-carb diet to their patients have mentioned to me that those who had previously been diagnosed with Irritable Bowel Syndrome (IBS) and who suffered for years reported significant improvements within a short time of adopting the dietary changes and have asked me why. That is the topic of this article.

Prior to expanding my Dietetic practice to include this low carb division a little over 4 years ago, my main focus was on helping people who were dealing with food allergies and food sensitivities; including Celiac disease, Mast Cell activation disorder (MCAD) / histamine intolerance, fructose intolerance and Irritable Bowel Syndrome  For many of my clients, it was the gastrointestinal (GI) symptoms that caused them to seek out my help in the first place.

What is IBS?

I have often thought of Irritable Bowel Syndrome (IBS) as the diagnosis that people receive when all the other possible options have been ruled out. For the most part, by the time people are told that they have IBS, they already know for sure that they don’t have Celiac disease or inflammatory Bowel Disease (IBD) such as Ulcerative Colitis or Crohn’s, and they don’t have diverticulosis ⁠—as each of those diagnoses are confirmed after a colonoscopy and/or a biopsy, and are often supported with underlying blood test results.

What makes IBS different is that it is a functional GI disorder ⁠— which means there is no structural or biological abnormality that can be measured on routine diagnostic tests.

Of course a person experiencing  a bout of diarrhea or constipation, or abdominal pain does not mean that person has a GI disorder or disease. Those symptoms could be the result of a virus, bacteria, food-borne illness (“food poisoning”) or food sensitivities. Once these have been ruled out, if the symptoms recur over and over again over time, then investigation as to what else it could be is often begun.

How is IBS Diagnosed?

While many of the symptoms of IBS and Celiac disease can be quite similar, including diarrhea and abdominal pain and bloating, there are very specific indicators that a person may have Celiac disease that clinicians such as myself notice as evidence to request further testing. The first stage in ruling out Celiac disease is an ordinary blood test looking for an antibody to gluten. If that comes back positive, then the person is referred to a Gastroenterologist for an endoscopy. If the blood test is negative, the next step may be for the person to be scheduled for a colonoscopy.

A colonoscopy which is where the inside of the large intestine (colon) is examined using a flexible probe about 1/2″ in diameter that’s fitted with a light and telescopic camera at one end and endoscopy is where a fine, flexible probe fitted with a light and telescopic camera is inserted via the mouth to view the esophagus, stomach and the upper part of the small intestine.

Celiac disease will be ruled out or confirmed using endoscopy, as the upper small intestine is where the damage to the villi (little hair-like projections on the wall that increase the surface area in order to help absorb nutrients from food) will be visible, or not.

A colonoscopy enables the Gastroenterologist to see what the lining of walls of the colon look like and to look for physiological signs of diverticulosis (little bulges or “pouches” in the colon) or signs of inflammation and damage consistent with Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis or Crohn’s and to rule out colon cancer.

If the endoscopy and colonscopy come back normal, the person is often told that their symptoms of diarrhea or constipation (or both alternating), flatulence (“gas”), bloating, abdominal pain or cramping, mucous in the stool is Irritable Bowel Syndrome (IBS).

Prevalence of IBS

According to the International Foundation for Gastrointestinal Disorders (IFFGD), approximately 10-15% of the population have IBS; with 40% having a mild form, 35% having a moderate form, and 25% having severe IBS. While many people think of IBS as being a woman’s health issue, 35% to 40%  of people with IBS are men and 60-65% are women [1]. IBS is so common, that it is estimated that 12% of all visits to primary care providers (family doctors) is related to symptoms of IBS [1].

Once a person receives a diagnosis of IBS the first question that is often asked is “now what?” Physicians will often suggest their patients try following a “low-FODMAP diet” which I teach through my non-low-carb division.

Why Eating a Low-Carbohydrate Diet often Improves IBS Symptoms?

A low-FODMAP diet eliminates sources of very specific carbohydrates that are fermented by the gut bacteria and that result in the increased gas production that underlies the classic IBS symptoms of abdominal pain and bloating, and the water flooding into the intestine in response to these fermented carbohydrates is what causes the very common symptom of diarrhea. The constipation results when the contractions of the colon are impaired, resulting in the stool sitting longer in the colon resulting in more and more of the water being re-absorbed.

When people eat a low-carb diet, they either eliminate or greatly reduce sources of fructose (the sugar found in fruit and many processed foods, especially processed condiments like ketchup) and significantly reduce one of the key sources of fructans (inulin) found in wheat; which is a highly fermentable carbohydrate. Galactans, another fermentable carbohydrate found in beans, lentils and legumes such as soy is also eliminated or greatly reduced which is why people with IBS feel so much better after beginning eating a low-carb diet!

Before I taught a low-carbohydrate approach, I used to have people take the IBS Package before the Complete Assessment Package, so we could find out what foods underlie their unpleasant symptoms and eliminate them before I designed their Meal Plan. Now, if they are planning to adopt a lower carb lifestyle anyway, then I recommend they don’t take the IBS Package, as it may not be necessary.  I recommend focus on them adopting a diet that greatly reduces the sources of the fermentable carbohydrates mentioned above, plus a few more that I tell them about and see how they feel. If their symptoms are gone, then there is no reason for them to take the IBS Package!  If however, they feel quite a bit better but still have residual symptoms, then I may recommend that take the Low-FODMAP hourly consultation through my non-low carb division to learn which low-carb foods they may be best to avoid.

More Info?

If you would like more information about the IBS Package, you can find that under Services tab of my affiliate website, BetterByDesign Nutrition Ltd. and if you’re nterested in the low-FODMAP teaching, you can find that in the Shop on that site.

Of course, if you have questions please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
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Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

Foundation for Gastrointestinal Disorders (IFFGD),  https://www.aboutibs.org/facts-about-ibs/statistics.html

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WHO Draft Guidelines on Saturated Fat Excludes Key Facts and Studies

An analysis was published last week in the British Medical Journal which raised several important concerns about the World Health Organization (WHO)’s draft guidelines on fatty acids; including saturated fat.

The international group of 16 nutrition experts who wrote the paper are concerned as “many governments consider the WHO dietary guidelines to be state of the art evidence, translating them into regional and national dietary guidelines” [1].

In fact, this is exactly the case in Canada. The new Canada Food Guide that was just released on January 22, 2019 relied extensively on the WHO’s 2017 Guidelines for it’s policy regarding decreasing dietary saturated fatty acids (SFA), as indicated by the table below from pg. 5 of Health Canada’s Interim Evidence Update 2018 [2]. 

Pg 5 Health Canada’s Interim Evidence Update 2018 [2]
Regarding the significance of the WHO Guidelines, the authors wrote:

“These guidelines have potential health implications for billions of people, so the consistency of the science behind such recommendations and the validity of the conclusions are crucial”.

The authors state that the WHO, in their draft guidelines released in May 2018 “excluded some important aspects and studies” concerning evidence linking saturated fat intake and cardiovascular (CVD) risk.

“They [WHO] recommend reducing intake of total saturated fatty acids to less than 10% of total energy consumption and replacing with polyunsaturated fat and monounsaturated fat to reduce incidence of cardiovascular disease and related mortality. But this fails to take into account considerable evidence that the health effects vary for different saturated fatty acids and that the composition of the food in which they are found is crucially important.”[1]

The authors point out that the composition of the food in which the fatty acid is found has a substantial effect on lipid digestion, absorption, as well as the amount of emulsified fat that is found in the blood after a meal (postprandial lipemia), which “is an independent risk factor for cardiovascular disease.”[1]

The authors point out that recently there have been several meta-analyses of observational studies and randomized controlled trials (RCTs) that found that total saturated fat is NOT associated with coronary heart disease, cardiovascular disease, and all cause mortality (i.e. deaths). In addition they report that a Cochrane analysis found no significant association between reducing saturated fatty acids and total mortality, cardiovascular disease deaths, fatal and non-fatal myocardial infarction (MIs), stroke, coronary heart disease events, and coronary heart disease deaths.

Continued Reliance on Surrogate Endpoints

The authors note that the WHO draft guidelines continue, as they have in the past, to (1) rely heavily on “surrogate endpoints” of the effect of dietary saturated fat intake on the level of lipid and lipoproteins in the blood — and (2) ignores the food source of the saturated fat.

They raise three key points;

1. Not all saturated fatty acids are equal; the amount and even the direction of the effects (raises or lowers) both surrogate and long term endpoints vary, depending on which fatty acid is involved.

2. Influence of the food source that the fatty acid is found in; the authors note that it has still not been determined whether any changes in blood lipoproteins translates into a lowering of cardiovascular risk and death, regardless of food source.

“Most trials included in the meta-analysis did not investigate whole food sources of saturated fat.”[1]

That is, the studies that WHO considered compared the effect of diets supplemented with fats rich in saturated fatty acids — not the effect of saturated fats in a specific food matrix.

One example of saturated fat in a whole food matrix cited in the paper is one of eggs; where there is “no association with coronary heart disease, and there is a reduced risk of stroke, and that randomized control trial data show that two eggs a day has beneficial effects on cardiovascular disease biomarkers“. (table 1, [1]).

3. Using LDL cholesterol concentration as a marker for cardiovascular disease risk. As I’ve written about in several previous articles, the authors note that the degree to which LDL particles are atherosclerotic is determined by, among other things, their size.

“Small and medium LDL particles show the strongest association with risk of cardiovascular disease, whereas large particles show no association.” [1]

in fact, the authors point out as I did in a recent article about red meat and white meat “raising cholesterol”, that a rise in serum LDL cholesterol concentration from total saturated fat consumption has been linked to a parallel increase in particle size “so it might not translate into an
increased risk of cardiovascular disease.”[1]

Excluding Observational Studies and Prospective Cohort Studies

The authors point out that the WHO draft guidelines exclude two types of studies from consideration; observational studies and prospective cohort studies because they argue that the quality of the evidence is lower than from
analyses of RCTs, and that it was not possible to assess the potential differential effects of replacing saturated fatty acids with different nutrients.

The problem with this is that (1) observational studies enable assessing the association between saturated fat and cardiovascular disease  rather than simply looking at the association between surrogate endpoints” (i.e. saturated fat and LDL-c) and (2) observational studies enable examining of the actual foods that people eat, rather than just individual nutrients, as

“Longstanding evidence indicates that the food matrix is more important than its fatty acid content for predicting the effect of a food on risk of coronary heart disease.”

The authors concluded;

“A recommendation to reduce intake of total saturated fat
without considering specific fatty acids and food sources is not
evidence based
; will distract from other more effective food-
based recommendations; and might cause a reduction in the
intake of nutrient dense foods that decrease the risk of
cardiovascular disease, type 2 diabetes, other serious
non-communicable diseases, malnutrition, and deficiency
diseases and could further increase vulnerability to nutrient
deficiencies in groups already at risk.

Final thoughts

This analysis adds a critical academic “voice” to the concern of limited saturated fat intake which may translate a reduction in the intake of nutrient-dense whole foods.

In fact, this was precisely the concern that I raised in my recent article about the Canada Food Guide “Snapshot” which came out at the end of June and which linked an image of ultra-processed foods with the message “limit foods high in sodium, sugars or saturated fat”.  After all, meat is high in saturated fat and cheese is high in saturated fat and sodium, but are these really the types of whole, real foods that Canadians should be advised to limit?

More Info?

If you would like more information about choosing whole, real food and limiting ultra-processed foods, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Astrup A, Bertram HCS, Bonjour J-P et al, WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019; 366: l4137 doi: 10.1136/bmj.l4137
  2. Health Canada. Food, Nutrients and Health: Interim Evidence Update 2018. Ottawa: Health Canada; 2019.

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Focus on Limiting Ultra Processed Food Not Saturated Fat & Sodium

Note: This article is a combination of a Science Made Simple article, with the references below and an editorial which provides my opinion.

Dietary advice — especially National Dietary Guidelines ought to give clear, consistent messages. It would seem that the new Canada Food Guide ‘snapshot’ outlined in the previous article may inadvertently cause considerable confusion as to which foods are healthy and which are not.

The new Canada Food Guide ‘snapshot’ released last week shows a photo of ultra-processed products as foods to avoid, yet the label beneath the photo reads “limit foods high in sodium, sugars or saturated fat” (see circled part of photo, below).

Canada Food Guide 'Snapshot'
Canada Food Guide ‘Snapshot’

In fact, when the image of these processed foods is clicked on the Health Canada website, it brings the reader to a page listing the “Benefits of Limiting Highly Processed foods” and has paragraphs below for Sodium, Sugars, and Saturated Fat. 

In my opinion, this conflates two issues. 

Advising people to limit ultra-processed food is not the same as advising them to limit saturated fat, sodium and sugar

There are many whole unprocessed foods and minimally processed foods such as meat, eggs, cheese, yogourt, olives and berries that have sustained humans through thousands of years of history that contain these elements and are unlikely to be responsible for our current epidemics of obesity, diabetes, hypertension and cardiovascular disease that we now face.

As mentioned in an earlier article about distinguishing between food and food-like products there is a big difference between the three categories of food as defined by the NOVA food classification system [2,3,4]. Unprocessed Foods such as meat, chicken, fish and eggs are whole, real food in their original state and Minimally Processed Foods such as cheese, yogourt or pickled and cured fish or meat or olives are foods that have been preserved in some fashion by curing, smoking or soaking in brine. Foods such as meat, eggs, cheese and olives may be high in saturated fat or sodium but have been part of the human diet for thousands of years without compelling evidence that these pose a risk to human health.

It may be helpful to recommend that people consume pickled, cured meat and fish in smaller quantities, not because these foods are high in saturated fat or sodium, but because many are now made in less traditional ways that involve the use of chemical additives.

The primary health concern that I see it is that Ultra Processed Foods is making up more than 50% of the Canadian (and American) diet and really isn’t food at all. These are manufactured products made from a combination of refined carbohydrates (including sugar) and seed oils and are convenient, hyper-palatable and cheap — and displace real food from the diet. In fact, some of the most addictive foods available to us are ultra processed foods; including breakfast cerealmuffins, pizza, cheeseburgers, French fries and fried chicken — and desserts such as chocolate, ice cream, cookies and cake, as well as the soda we wash them down with [5]. These ultra processed foods are full of “empty calories” / have little nutritional value, and full of refined fats and refined carbs. It is for this reason ultra processed should be limited — not because it is high in saturated fat and sodium. 

Even though fruit as we now know it has been bred over the last 50-100 years to be hyper-sweet, for metabolically healthy people there is still no comparison between natural whole fruit such as berries or an apple, and sugary pop. One is real, whole unprocessed food and the other is ultra processed.

In my opinion, it makes good sense for Health Canada to show a photo of ultra-processed foods as they had (above)with advice to limit them — but because they are ultra processed, not because they are high in saturated fat or sodium.

 

Shifting the Focus off Saturated Fat Based on the Evidence

As covered in several previous article on this site, while research does indicate that dietary saturated fat raises low density lipoprotein cholesterol (LDL-cholesterol) in the blood, distinction in these studies isn’t made between the small, dense LDL sub-fraction which is atherosclerotic, and the large, fluffy LDL which is not. This recent study makes this distinction; demonstrating that saturated fat from red meat and poultry raises the large, fluffy LDL and cardio-protective HDL, but not the small dense (atherosclerotic) LDL.

Epidemiological studies that do exist provide a very mixed picture of any possible association between saturated fatty acids and cardiovascular disease (heart disease and stroke); with recent studies finding no association [6,7]. Even more compelling, the data from the Prospective Urban and Rural Epidemiological (PURE) Study which was the largest prospective epidemiological study to date involving many different countries found that dietary saturated fat was actually beneficial; with those who ate the largest amounts of saturated fat having significantly reduced death rates and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [8].

In addition, according to the Canadian Heart and Stroke Foundation position statement titled ”Saturated Fat, Heart Disease and Stroke” released in September 2015 [9], different saturated fatty acids (e.g. lauric, stearic, myristic and palmitic acids) have different effects on blood cholesterol, so we can’t simply lump all saturated fats together.

Focus on Where Change is Needed

I believe that national guidelines such as Canada’s Food Guide should focus on eliminating ultra-processed foods from the diet because these form almost half of caloric intake with little nutrients and displace real, whole nourishing food from the diet.

This makes good sense.

In my opinion, the linking of ultra processed foods to saturated fat and sodium as has been done in this most recent Canada Food Guide ‘snapshot’ will end up confusing the public that things like fried chicken and cheese are both equally unhealthy because they are high in saturated fat and salt.

It would be far more helpful to highlight the benefits of whole, unprocessed foods and minimally processed foods while encouraging the public to limit ultra processed foods.

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods (plant-based and animal-based), I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
  2. Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
  3. Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are becoming dominant in the global food system. Obes Rev. 2013
  4. Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
  5. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959
  6. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of dietary, circulating and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Ann Internal Medicine 2014;160:398-406.
  7. Sri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nut 2010;91(3):535-546.
  8. Dehghan M, Mente A, Zhang X et al, The PURE Study — Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  9. Heart and Stroke Foundation of Canada, Position Statement ”Saturated Fat, Heart Disease and Stroke, September 24, 2015, https://www.heartandstroke.ca/-/media/pdf-files/canada/position-statement/saturatedfat-eng-final.ashx

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Canada Food Guide Snapshot: Limit Real Whole Food or Ultra-Processed?

Note: This article is a combination of a Science Made Simple article, with the references below and an editorial which provides my opinion.

This past Monday, Health Canada released the Canada’s Food Guide “snapshot”[1] in 28 languages which is not intended to be a stand-alone resource, but to be used as a tool to guide people to the Canada’s Food Guide website.

Canada’s Food Guide includes Canada’s Dietary Guidelines[2], the healthy eating recommendations[3], and all of the other resources and information on the Canada’s Food Guide website. Links to the guidelines and healthy eating recommendations are available in the References, below.

The “Snapshot”

Canada Food Guide "Snapshot"The main message of the “snapshot” is that “healthy eating is more than the foods you eat” ⁠— which I think is an excellent way of summarizing the guidelines and recommendations and encouraging the public to want to learn more. From that point of view, the snapshot is successful in that it is likely to guide people to the website.

The main points on the Snapshot are;

  1. Be mindful of your eating habits
  2. Cook more often
  3. Enjoy your food
  4. Eat meals with others
  5. Use food labels
  6. Limit foods high in sodium, sugars or saturated fat*
  7. Be aware of food marketing

Each of these points link to the sections of Canada’s Food Guide which address those points and in my opinion are all very helpful, except for one elaborated on below.

For example, under “Be mindful of your eating habits” is and encouragement for Canadians to be aware of;

  • how you eat
  • why you eat
  • what you eat
  • when you eat
  • where you eat
  • how much you eat

Being mindful can help you:

  • make healthier choices more often
  • make positive changes to routine eating behaviours
  • be more conscious of the food you eat and your eating habits
  • create a sense of awareness around your every day eating decisions
  • reconnect to the eating experience by creating an awareness of your:
    • feelings
    • thoughts
    • emotions
    • behaviours

As the Snapshot re-iterates, these are factors that are “more than the food you eat” and helpful for people to keep in mind.

My only issue with the “Snapshot” is the use of the image for “Limit foods high in sodium, sugars or saturated fat“, circled below.

Snapshot with “Limit foods high in sodium, sugars or saturated fat” circled

Here is that image by itself;

What I see when I look at this image is ultra-processed food (what I refer to in a previous article about the NOVA Food Classification System as “food-like products“.

These are not whole, real food, but are creations of the food industry that are intended to displace real, whole food from the diet (you can read more about that by clicking here). These are products that are “branded assertively, packaged attractively, and marketed intensively“.

In fact, this picture shows some of the most addictive foods listed in a 2015 study including chocolate, muffins, pizza, pastry and soda pop[4].

Fifteen Most Addictive Fast Foods

If the intention is for Canadians to “limit foods high in sodium, sugars and saturated fat” (not that I think there is solid, scientific evidence that healthy individuals need do so with all sources of saturated fat and sodium), in my opinion the following photo would be a more accurate reflection of the principle;

Real, whole foods that are high in sodium, sugars or saturated fat

Cheese, eggs and meat are high in saturated fat, and cured meats are high in sodium and saturated fat, and dates are certainly very high in sugar, yet are not ultra-processed foods. Are these really foods that all Canadians should limit?

Is there irrefutable scientific evidence that healthy people should limit eggs, real cheese and whole fresh meats and poultry? Is it “unhealthy” for metabolically well folks to eat dates, which are very high in sugar? Or are we conflating whole, real food with ultra-processed food?

Using the NOVA food classification (outlined in the article linked above) that foods such as cheeses, cured meats and olives or anchovies are minimally processed foods that have been processed to make them ore durable and palatable, but they are not “ultra-processed foods” akin to hot dogs, pizza and pop!

I don’t believe that it is helpful to lump “ultra-processed food” and whole, real food that are high in saturated fat, sodium and sugar, together.

In my opinion, it would far better for the image in the Snapshot to read like this;

It makes good sense to advise Canadians to limit ultra-processed food⁠ because they are high in refined carbohydrates and refined fats, and low in nutrient density ⁠— but when ultra-processed food is labelled with the advice “limit foods high in sodium, sugar or saturated fat”, whole, real foods are conflated with food-like products which displace real, whole food from the diet.

Ultra-processed food is not the same as whole, real foods high in sodium, sugars or saturated fat

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods that are both plant-based and animal-based, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
  2. Health Canada, Canada’s Dietary Guidelines, https://food-guide.canada.ca/en/guidelines/
  3. Health Canada, Healthy Eating Recommendations, https://food-guide.canada.ca/en/healthy-eating-recommendations/
  4. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959

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Only Half of People Have Newer Gene that Controls High Blood Sugar

The maintenance of blood sugar is very tightly regulated; with a healthy person’s blood glucose being kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) between meals, however a new study indicates that it may be newer variant of a gene that determines how well (or not) we are able to maintain these levels.

After eating, the higher levels of blood glucose that comes from the broken-down carbohydrate-based food triggers the release of insulin by the pancreas, which in turn causes the release of a special transporter called GLUT4.  The GLUT4 transporter acts like a taxi to remove excess glucose from the blood, taking it into muscle and fat tissue.

Newer Variant of an Older Gene

Between meals and with the help of a special protein (CHC22) produced by the CLTCL1 gene, the GLUT4 glucose transporter remains inside muscle and fat, so that some blood sugar will continue to circulate.

A newly published study [1] by research specialists in population genetics, evolutionary biology, ancient DNA and cell biology analyzed the human genomes to understand how the gene producing CHC22 has changed over human history [2].

By examining the genomes of 2,504 people from the global 1000 Genomes Project compared to the genomes of ancient humans, researchers found that almost half of the people in various ethnic groups have a variant of CHC22 protein that is produced by a new variant of the CLTCL1 gene that became more common as humans moved away from being hunter-gathers and began farming and raising crops. Researchers postulate that the increased consumption of carbohydrates may have been the selective force driving this genetic adaptation.

Researchers found that the newer CHC22 variant of the gene is less effective at keeping the GLUT4 glucose transporter inside muscle and fat tissue between meals, which means that the transporter can more readily clear glucose out of the blood.*

As a result, people with the newer variant of the gene will have lower blood sugar than those with the older variant of the gene.

“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn’t have such easy access to carbohydrates, and this would have helped us evolve our large brains”[2] — lead author Dr Matteo Fumagalli

*Note: It’s important to keep in mind that only GLUT4 transporters are insulin dependent. There are other glucose transporters that allow glucose into the cell that don’t involve insulin, such as the GLUT1 transporter that works on a concentration gradient. That is, the effect of this gene is not on all glucose regulation, but only glucose regulation in adipose and muscle cells that use GLUT4 transporters.

The higher carbohydrate diets that came as a result of the advent of agricultural meant that this newer variant of the gene could be advantageous, as it moves the excess blood sugar from the blood into the muscle and fat tissue and having the older variant of the gene may make people more likely to develop Diabetes and may also make worse the insulin resistance that underlies the process of developing Diabetes.

“People with the older variant (of the gene) may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology”[2] — co-author Dr. Frances Brodsky 

Along with the 2015 study from Israel[3] that demonstrated substantial differences in blood glucose response between both healthy individuals and those with Diabetes predictable by their gut microbiome, this new research adds to the knowledge that multiple factors are involved with determining whether people can tolerate specific dietary carbohydrate loads.

Nutritional guidelines for maintaining healthy blood glucose levels are portrayed as universally applicable, however this new study and the 2015 Israeli study demonstrates that blood glucose varies significantly between individuals based on genetics as well as on gut microbiota composition, which necessitates the need for personalized nutrition in managing blood glucose levels.

More Info

If you are interested in a personalized approach aimed at helping you gain control of your blood sugar levels, I can help.

I offer both in-person services in my Coquitlam, British Columbia office as well as remote services via Distance Consultation. You can find more information about my packages under the Services tab or in the Shop and if you would like to learn more about how Distance Consultation services work, you can click here.

Have Questions?

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Matteo Fumagalli, Stephane M Camus, Yoan Diekmann, Alice Burke, Marine D Camus, Paul J Norman, Agnel Joseph, Laurent Abi-Rached, Andrea Benazzo, Rita Rasteiro, Iain Mathieson, Maya Topf, Peter Parham, Mark G Thomas, Frances M Brodsky. Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism. eLife, 2019; 8 DOI: 10.7554/eLife.41517
  2. University College London. “Gene mutation evolved to cope with modern high-sugar diets.” ScienceDaily. ScienceDaily, 4 June 2019, https://www.sciencedaily.com/releases/2019/06/190604084857.htm
  3.  Zeevi D, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163:1079—1094.
  4. Noecker C, Borenstein E. Getting Personal About Nutrition. Trends Mol Med. 2016;22(2):83—85. doi:10.1016/j.molmed.2015.12.010

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Lowering LDL and Saturated Fat to Lower Risk of Cardiovascular Disease

INTRODUCTION: There much debate in the health community about the effect of dietary fat — especially saturated fat on cholesterol levels and whether there is an association between dietary saturated fat intake and cardiovascular disease.

In the first part in this two-part series titled High Cholesterol and the Risk of Cardiovascular Disease, I explained what cholesterol is, the different types of cholesterol (HDL-C, VLDL, LDL-C and triglycerides (which are not actually cholesterol), what their role is, and what “high cholesterol” is.

In this article which is Part 2 in the two-part series, I will explain the association between dietary intake of saturated fat and higher levels of total LDL, and whether reducing total LDL — whether through the use of statin medication or diet lowers the risk of cardiovascular disease.


Dietary Saturated Fat and LDL

When people are told that they have “high cholesterol”, what is meant is that they have high total LDL. They are told they have high “bad” cholesterol, with no regard that there are different sub-fractions of LDL.

It is well known that eating foods high in saturated fat can raise LDL-C (total LDL cholesterol, but as covered in Part 1 of this two-part series, the first question one should ask when told they have “high LDL cholesterol” is “which LDL? The small dense ones or the large fluffy ones?”[1].

More often than not, the clinician that breaking the ‘bad news’ to the patients has absolutely no idea that there are different sub-fractions of LDL and that it is only the small, dense ones that are atherosclerotic [1].

Furthermore, there is almost a knee-jerk reaction on the part of many clinicians to prescribe statin medication in order to lower their LDL, on the assumption that lowering LDL will lower their risk of cardiovascular disease. In fact, aggressive treatment to lower total LDL-C has been at the (pardon the pun) heart of preventative cardiology for decades.

While statin medication (e.g. Lipitor®, Crestor®, etc.) is well-documented to reduce LDL-C levels, these are only surrogate markers (not direct markers) of cardiovascular disease (CVD). The assumption of an association between high LDL levels and CVD goes back as far as Ansel Keys and the Seven Country Study, and that the Diet Heart Hypothesis (covered in several previous articles) is simply an “establish fact”. But it is?

What evidence is there that lowering total LDL with statin medication lowers one’s risk of cardiovascular disease (CVD)?

The brand new guidelines on cholesterol management issued by the American Heart Association (AHA) and American College of Cardiology (ACC) which has just been published online ahead of print[2], places a renewed focus on LDL-C as a means to assess risk. In fact, these guidelines propose that non-fasting lipids be adopted as a screen in the general population, including “non-adults” (children and youth) [2]. As has been the case for decades., this is based on the assumption that total LDL (LDL-C) is an accurate surrogate marker for elevated cardiovascular risk, but does lowering LDL-C really lower CVD?

Of particular interest, the new American Heart Association (AHA) and American College of Cardiology (ACC) guidelines state that the traditional Friedewald equation which is used to calculate total LDL (i.e. LDL-C) as covered in Part 1 of this series of articles has been “prone to inaccuracy …at low-LDL-C and high triglyceride levels — yet decades of statin treatment has been based on the previous “inaccurate” Friedewald equation. The new guidelines promote the use of a new Martin/Hopkins LDL-C calculation method which is said to “perform better in these settings”. The question remains ‘does lowering LDL-C lower the risk of cardiovascular disease?’.

There are 44 randomized controlled trials of drug or dietary interventions to lower total LDL ( LDL-C) published in the literature which show no benefit in lowering rates of death [3] and most did not reduce CVD events [4].

Furthermore, despite a 37% drop in LDL-C and a 130% increase in HDL-C (so-called “good cholesterol”), the ACCELERATE double-blind randomized control  trial showed no significant reduction in CVD or death [3.4].

In addition, there does not appear to be a clear reduction in CVD deaths in Western European countries either as a result of using statins for prevention [5].

This begs the question as to whether using statin medication to aggressively lower LDL-C has any benefit.

A 2018 article published in Expert Review of Clinical Pharmacology concluded;

“For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.” [6]

What about lowering the intake of dietary saturated fat? Does that lower the risk of cardiovascular disease?

A 2014 meta-analysis of data of 72 studies involving more than 600,000 participants from 18 countries published in the journal Annals of Internal Medicine in 2014 [7] concluded that total saturated fat; whether measured in the diet or in the bloodstream showed no association with heart disease [7].

Take away: While eating dietary fat may raise the level of total LDL cholesterol (LDL-C), lowering its intake does not show any benefit in reducing the incidence of heart disease, nor does lowering LDL-C using statin drugs.

Which LDL?

A brand new study published June 4, 2019 in the American Journal of Clinical Nutrition sheds some very helpful light [8].

The study enrolled 113 people and randomized them to either a high saturated fat diet (40% carbs, 24% protein, 35% fat; 14% saturated fat) or a low saturated fat diet (40% carbs, 24% protein, 35% fat; 7% saturated fat replaced by monounsaturated fat).

Each group changed their diet every 4 weeks from (a) a high red meat diet (mostly from beef), (b) a high white meat diet (chicken and turkey) and (c) a non-meat protein diet (legumes, nuts, grain and soy).

Researchers found that LDL cholesterol and Apolipoprotein B (explained in the first part of this article) were higher with red and white meat alike and that the increase “was due primarily to increases in large LDL particles” with no change in the small particles and no significant change in the total cholesterol to HDL ratio.

This is highly significant!

What this means is that yes, eating meat; whether it’s red meat (such as beef, lamb or goat) or white meat (such as chicken or turkey) DOES increase LDL but it’s the large, fluffy LDL particles that are increased; the ones that are not associated with cardiovascular disease[1]!

In fact, in the paper, the researchers acknowledge;

Large LDL particles, measured by several different methodologies, have not been associated with CVD in multiple population cohorts in contrast to the associations observed for concentrations of medium, small, and/or very small LDL… Thus, the estimated impact of red meat, white meat, and dairy-derived saturated fatty acids (SFA) on CVD risk as reflected by their effects on LDL cholesterol and ApoB concentrations may be attenuated by the lack of their effects on smaller LDL particles that are most strongly associated with CVD.

Essentially, there has been on over-reliance on total LDL cholesterol (LDL-C) as a marker of cardiovascular disease, without distinguishing the atherosclerotic small, dense LDL from the non-atherosclerotic large, fluffy LDL.

The authors conclude;

“…the impact of high intakes of red and white meat, as well as saturated fatty acid (SFA) from dairy sources, which selectively raised large LDL sub-fractions may be overestimated by reliance on LDL cholesterol, as is the case in current dietary guidelines.”

This means that eating red meat (such as beef or lamb) or white meat (such as chicken or turkey) or eating saturated fat from full-fat dairy (such as full fat milk, cheese and yogurt) are associated with increased levels of the large, fluffy LDL sub-fraction and based on multiple population studies the large, fluffy LDL subfraction has not been found to be associated with cardiovascular disease.

Simply put, this means that eating foods high in saturated fat does not raise small LDL particles (which are the atherosclerotic sub-fraction) and results in no change to the total cholesterol to HDL ratio, and increases the large, fluffy LDL-subfraction (which are NOT found to be associated with cardiovascular disease)!

While this is a small pilot study, it adds further evidence that eating saturated fat does not increase cardiovascular risk.

Note: high levels of the small, dense LDL sub-fraction is thought to be genetic, but is also associated with intake of trans fatty acids and high intake of refined carbohydrates. More on that in future articles.

More Info?

If you would like to learn more about my services, you can find more information under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  2. Cao J, Devaraj S, Recent AHA/ACC guidelines on cholesterol management expands the role of the clinical laboratory, Clinica Chimica Acta 495 (2019) 82—84, Available online 03 April 2019.
  3. DuBroff R. Cholesterol paradox: a correlate does not a surrogate make. Evid Based Med,2017;22(1):15—9. doi: 10.1136/ebmed-2016-110602
  4. Demasi M, Lustig RH, Malhotra A, The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance, Clinical Pharmacist, 14 July 2017.
  5. Vancheri F, Backlund L, Strender L et al. Time trends in statin utilisation and coronary mortality in Western European countries. BMJ Open 2016; 6(3):e010500. doi: 10.1136/bmjopen-2015-010500
  6. Ravnskov U, de Lorgeril M, Diamond DM, et al, LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature, Expert Review of Clinical Pharmacology, 2008;11:10, 959-970, DOI: 10.1080/17512433.2018.1519391
  7. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary RiskA Systematic Review and Meta-analysis. Ann Intern Med. 2014;160:398—406. doi: 10.7326/M13-1788

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From Injecting Insulin to a Low Carb Diet – the first two weeks

Note: This article is a personal account, and I have written consent from the person whose story this is, to share these details in this article. She hopes it encourages someone. Keep in mind, individual results following a low carb or ketogenic diet vary person-to-person.

At the end of May, a young woman was coming to see me for an assessment appointment, and as I was reviewing her chart in preparation, I noticed that she was taking insulin. It was apparent that she didn’t see the notice on  my web page that I don’t treat Type 1 Diabetics or Type 2 Diabetics on insulin, as I am not a CDE (Certified Diabetes Educator).

Discontinuing Insulin

When she arrived, we discussed some of the options she had, and she decided to go and see her endocrinologist and request that they discontinue her insulin and give her 12 weeks to follow a Meal Plan that I would design for her. She then signed and sent me the Confirmation of Non-Insulin Use Form, indicating that with her doctor’s permission and oversight, that she was no longer taking insulin. To support her in being successful, she decided to book weekly 1/2 hour check ins with me for the following 12 weeks.

Note: If you are taking insulin to manage blood glucose in Type 2 Diabetes or other medications do not attempt to discontinue these on your own, as the results can be very serious. Please read this post titled “Don’t Try This at Home – the need for medical supervision” for more information.

Last Friday was her first follow up appointment and she was very excited to show me her blood sugar results, her first week off insulin.  Here is the graph;

Week 1 - no insulin, low carbAs can be seen, her fasting blood sugar the first morning was 16.8 mmol (303 mg/dl) which went up to 18.7 mmol/L (337 mg/dl) 2 hours after her low carbohydrate breakfast.

The following morning her fasting blood glucose was 12 mmol/L (216 mg/dl) where it stayed more or less for a few days, then dropped to 9.9 mmol/L (178 mg/dl). This was after only one week.

I asked her to speak to her doctor to see if they would be willing to add a dose of Metformin at bedtime, to help control “dawn phenomenon”; the rise in glucose due to gluconeogenesis of the liver.  Her doctor agreed and this week she started that.

This morning was her second follow up appointment and again, she was so excited to show me her blood sugar results.

As can be seen, her fasting blood sugar the first morning of the second week was 10.8 mmol (195 mg/dl) which hardly went up at all to 10.9 mmol/L (196 mg/dl) 2 hours after her low carbohydrate breakfast.

The second morning of the second week, her fasting blood glucose was 9.2 mmol/L (166 mg/dl). The rest of the week, her morning fasting blood sugar ranged from 8.4 mmol/L (151 mg/dl) to 9.6 (173 mg/dl) where it stayed. This was only her second week off insulin.

Moderate Low Carb (not Ketogenic) Diet

Understand, that this young woman (aged 33 years of age) achieved these results eating a moderate low carbohydrate diet of 130 g of carbs per day — which is no where near the level of 25-35 g per day that most women would need to be at in order to be in ketosis, and she has been Type 2 Diabetic since 2017.

2 weeks graph – June 8 – 20, 2019 – moderate low carb diet

Here is the graph of her first two weeks of blood glucose results, tracked at fasting, before a meal, and 2 hours after a meal. The steady, linear drop is quite apparent.

She saw her GP yesterday and he is thrilled with her progress! He agreed to provide her with a requisition to do the fasting insulin that I requested, along with a fasting blood glucose and HbA1C — which we have agreed together to have re-run in 3 months, at the end of the 12 weeks.

For this week, no changes are being made in the number of carbs she is eating, however this may be adjusted in the future in order to achieve clinical outcomes.

These results speak for themselves in terms of the effectiveness of a  moderate-low carbohydrate diet to significantly lower blood sugar, as well as the adjunct treatment with Metformin, largely to control early morning gluconeogenesis.

These results also speak to the incredible benefits of her having the support of a healthcare team; me designing and monitoring her Meal Plan and her GP overseeing her care, along with her Endocrinologist.

In two weeks she will see her Endocrinologist again and she (and I!) are looking forward to hearing their response to her progress at that point in time. Given her results the first two weeks, I am confident that she will have much to be proud of!

When I asked her to send me her written consent to share these details in a blog article, I ask her to say a few words about what it was like for her to go from injecting insulin to control her blood sugar, to eating real, whole food to do it — and achieving these types of results.

This is what she wrote;

“I had done so much research into diet and lifestyle changes for Type 2 diabetes as I did not want to go on insulin. Prior to starting on insulin, I was put on Metformin and given the chance from my endocrinologist to change my diet. There was so much information about a low carb diet and its positive effect on blood sugar, so I gave it a try. It could be that I was overwhelmed, but I followed what I believed to be a low carb diet and did not see any significant changes to my blood sugar levels. They were all over the place with huge spikes, even when I would have zero carbs. Clearly something was not right. It gave me no motivation to continue and really made me feel defeated.

I knew I needed help and the only answer my endocrinologist gave me was a prescription for insulin.

I started insulin and was on it for 2 weeks without seeing any significant changes in my blood sugar levels again. This was not working.

So I decided to look for help on the nutrition side of it. Then I found you, Joy Kiddie. I read a little bit about your journey and it inspired me that you have been in my position and therefore would understand my challenges. Your journey gave me hope that there is still something that can be done. Meeting with you was even more of a motivation because you wanted what I wanted; lower A1C and more importantly, no insulin!

These past two weeks, following your guidance and eating a LCHF diet the right way, has been eye opening. I never thought I would get results like this in such a short time.

I used to hate checking my blood sugar levels and poking my poor fingers just to see a discouraging number. Now, I could check all day long because I see numbers that I never thought I would.

Seeing the levels come down and that linear decline in the graph just encourages me to continue down this path and work with you to create a healthier lifestyle.

I cannot wait to see what next week brings!”

For the last 4 years I have been working with those with Type 2 Diabetes and seen so many significantly improve their blood glucose management, and lose weight. Working with this young woman has inspired me to consider learning about insulin management and writing the CDE (Certified Diabetes Educator) certification exam next year while I will  continue to partner with people’s GPs and Endocrinologists (as is my current practice) to wean them off insulin while using a well-designed low carbohydrate diet to effectively manage their blood sugar. The literature, including the studies from Virta Health demonstrate it can be done safely and effectively and the American Diabetes Association recognize both a low carbohydrate meal pattern, and a very low carbohydrate (ketogenic) meal pattern as Medical Nutrition Therapy in the management of pre-diabetes, as well as Type 1 and Type 2 Diabetes in adults.  For more information on this, please see several articles from April 2019, under the Science Made Simple tab including this one.

My hope is that  in the days ahead, Diabetes Canada will arrive at a similar conclusion as the American Diabetes Association, the EASD, Diabetes Australia and others and recognize a low carbohydrate and ketogenic diet as options for those with Diabetes in Canada. Towards that end, I want to be credentialed as a Certified Diabetes Educator in order to be able to support those using insulin.

If you would like more information about my services, please have a look under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

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High Cholesterol and the Risk of Cardiovascular Disease

INTRODUCTION: There is much debate in the scientific community about the effect of dietary fat — especially saturated fat on cholesterol levels and risk of cardiovascular disease. To best understand this complex topic, I have broken the subject into two articles. In this first part, I explain the different ways cholesterol values are assessed, what they are used for and what they mean. In the next part I will explain whether lowering LDL and dietary saturated fat lowers the risk of cardiovascular Disease.


What is Cholesterol?

Cholesterol is a essential structural component of all the cell membranes in the body and is used in the making of steroid hormones such as cortisol and aldosterone by the adrenal glands, sex hormones such as estrogen, testosterone and progesterone by the gonads, and is also used in the making of bile acid. Approximately 80% of cholesterol made daily by the body occurs in the liver and  intestines, with the remainder being made in the adrenal glands and reproductive organs.

Different Types of Cholesterol

Triglyceride isn’t actually a type of cholesterol, but is measured on lipid panels along with cholesterol.

Triglyceride is made up of three fatty acids (hence “tri-“) attached to a glycerol molecule (also known as glycerine), which is a sugar alcohol. Some triglyceride is taken in through the diet and the rest is manufactured by the body during lipogenesis (literally meaning the ‘making of fat’). Lipogenesis is how the body stores the excess carbohydrate we eat in our diet that isn’t immediately needed for energy.  Yes, excess dietary carbohydrate is stored in the body as glycogen and when glycogen stores are full, it is stored as fat.

As for cholesterol itself, there are several different types found in the blood;

  • high density lipoprotein (HDL)
  • low density lipoprotein (LDL)
  • very low density lipoprotein (VLDL)

Most people think of high density lipoprotein (HDL) as ”good cholesterol” and low density lipoprotein (LDL) as ”bad cholesterol” but there are actually two sub-fractions of LDL; the small, dense LDL sub-fraction which is associated with atherosclerotic plaque, and the large, fluffy LDL sub-fraction which is considered protective against cardiovascular disease[1].

This is important, because when people are told they have “high cholesterol“, this is usually implies that they have high LDL. This is often presented to them as them having a high level of “bad” cholesterol.

High Cholesterol

A couple of things need to be clarified about “high cholesterol”;

Firstly, “high LDL” cholesterol means high total LDL cholesterol. When blood tests are said to indicate “high LDL” a good question to ask is which LDL cholesterol is high; the small dense ones or the large fluffy ones?”. More on this below.

Secondly, it is important to note that lab tests don’t actually measure total LDL but calculate it from the Friedewald formula; which (in mg/dl) is calculated by total cholesterol (TC) – HDL lipoprotein (HDL)-cholesterol – triglycerides (TGs) / 5. 

When people are told that they have “high LDL” results on a blood test, they are often presented with a recommendation to begin statin medication, but does high total LDL provide sufficient information about cardiovascular risk? More on this below. The use of statin medication will be covered in the subsequent article.

Very low density lipoprotein (VLDL) is produced in the liver and the best way to understand its role is to think of it as a “taxi” which the liver makes and then release into the bloodstream to shuttle triglycerides around to the various tissues.  VLDL cholesterol on blood test results isn’t actually measured either, but estimated as a percentage of the triglyceride value. High VLDL is said to be a risk for cardiovascular disease but as elaborated on below, a more accurate measure is the ratio of Apopoprotein B (the lipoprotein in VLDL) compared to the Apoprotein A (the lipoprotein in HDL). 

Where does LDL come from?

Once a large amount of triglyceride has been unloaded in the tissues by the VLDL “taxi”, it becomes a new, smaller lipoprotein called low density lipoprotein, or LDL which contains mostly cholesterol and some protein.

Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

A key point here is that the only source of LDL is VLDL. This is important.

LDL is what is left once the VLDL which is made by the body has offloaded its triglyceride ‘passenger’ to the tissues.

LDL and Heart Disease

Research has often reported that elevated LDL-cholesterol is a risk factor for cardiovascular disease, including heart disease and stroke and it has been assumed that lowering LDL-cholesterol in the blood would decrease cardiovascular deaths and illness. It is this premise that lead to recommendation of treatment of high LDL with statin drugs.

One major problem is that these studies looked at total LDL which doesn’t distinguish between the small, dense sub-fractions of LDL that are atherosclerotic, and the large, fluffy ones that are not [1].

Total LDL (LDL-C) calculates (not measures!) the total content or concentration of cholesterol within all the LDL particles.

LDL particle number (LDL-P) measures the particle concentration.

Since the amount of cholesterol in each particle varies, measuring LDL-C does not necessarily reflect the actual number of particles  — but an increased number of LDL particles occurs in patients with lots of small, dense particles.

Therefore, LDL-particle number (LDL-P) is a more accurate predictor of cardiovascular events than total LDL (LDL-C).

An NMR lipid profile test directly measures the number of LDL particles (as well as HDL particles). For LDL particles, a value of less  than 1.000 in nmol/L is considered ideal, a value of 1000-1299 is considered moderate,  a value of 1300-1599 is considered borderline high, and a value >1600 is considered high.

Apolipoprotein B:Apolipoprotein A1

Apolipoprotein B (apo B) is the main lipoprotein in VLDL, and subsequently in LDL after the VLDL has offloaded its triglyceride to the tissues. Apolipoprotein B is correlated with the actual number of LDL-particles, which makes it a very good assessor of the risk of cardiovascular disease, 

Apolipoprotein A1 (apo A1) is the main lipoprotein in HDL (commonly called “good” cholesterol).

An Apo B / Apo A1 ratio of > 0.9 is considered at risk for CVD.

Measuring Apo B to Apo A1 requires special blood tests, but a proxy can be calculated by dividing triglycerides (TG) by HDL-cholesterol (HDL-C) from a standard lipid panel. Studies have found this to be a very good assessor of cardiovascular risk.

Triglyceride:HDL Ratio

In Canada (as well as Europe), values are expressed as mmol/L and the ratios are interpreted as follows [2];

TG:HDL-C < 0.87 is ideal

TG:HDL-C > 1.74 is too high

TG:HDL-C > 2.62 is much too high

In the US, values are expressed in mg/dl and the ratios are interpreted as follows [2];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

Several studies have found that TG:HDL-C ratio also reflects particle size;

One study from 2004 reported that almost 80% of people with a TG:HDL-C ratio of greater than 3.8 (when values are expressed in mg/dl) had mostly small, dense LDL particles, indicating cardiovascular risk. This same study found that more than 80% with a TG:HDL-C ratio of less than 3.8 (when values are expressed in mg/dl) had mostly large, fluffy LDL particles, indicating lower cardiovascular risk[3].

A 2005 study [4] reported that a TG:HDL-C ratio of 3.5 or greater was highly correlated with atherosclerosis in men, as well as insulin resistance and metabolic syndrome.

A recent 2014 [5] study found that a high TG:HDL-C ratio was a strong independent predictor of cardiovascular disease, coronary heart disease and all-cause mortality both before- and after adjustment for age, smoking, BMI and blood pressure.

Based on this metric, lower cardiovascular risk would be associated with lower triglycerides, raising HDL or both.

But how?

Lowering TG:HDL-C ratio

Losing weight will lower triglycerides, however low-fat diets are not usually helpful in this regard because they are often also high in carbohydrate[2].

Decreasing intake of carbohydrates especially fructose which is found in fruit, as well as processed products made with high fructose corn syrup has been anecdotally reported to decrease hunger, making weight loss easier. Most importantly, clinical studies using well-designed low carbohydrate diets (already covered in several previous articles) are associated with both a lowering of triglycerides and a increase in HDL.

Lowering the risk of cardiovascular disease through weight loss, along with a lowering of triglycerides and an increase in HDL is where I can help.

UPDATE (June 23, 2019): Part 2 of this article titled Lowering LDL and Saturated Fat to Lower the Risk of Cardiovascular Disease is available by clicking here.

More Info?

If you would like to learn more about my services, you can find more information under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  2. Sigurdsson AF, The Triglyceride/HDL Cholesterol Ratio, updated January 12, 2019, https://www.docsopinion.com/2014/07/17/triglyceride-hdl-ratio/
  3. Hanak V, Munoz J, Teague J, et al, Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B, The American Journal of Cardiology, Volume 94, Issue 2, 2004, Pages 219-222, https://doi.org/10.1016/j.amjcard.2004.03.069
  4. McLaughlin T, Reaven G, Abbasi F, et al. Is there a simple way to
    identify insulin-resistant individuals at increased risk of cardiovascular
    disease? Am J Cardiol. 2005;96(3):399Y404.
  5. Vega GL, Barlow CE, Grundy SM et al, Triglyceride to High Density Lipoprotein Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Melletus in Men, Journal of Investigative Medicine & Volume 62, Number 2, February 2014

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