For the umpteenth time in as many weeks, I had a client tell me that they were told that “low carb eating is not sustainable” – and this was in the same breath as the decision to increase the second of two medications they are prescribed for Type 2 Diabetes.
What frustrates me is that their physician did not even want this person to try a lower carbohydrate approach.
The client was reminded soberly that “Diabetes is a chronic progressive disease” and that it is “expected” that over time the dosage of both of those medications will increase until they can’t be any more, and that they will eventually be insulin-dependent. I think that for many, this becomes a self-fulfilling statement and believing it to be ‘inevitable’, people are resigned that there is ‘nothing they can do’.
But is this true? Does it have to be a chronic, progressive disease?
Medical professionals across Canada, the United States, Australia and Europe have clinical experience demonstrating that the symptoms of Type 2 Diabetes can be put into remission and that most are able to the majority of their patients off many, if not all of their medications by following a low carbohydrate diet.
What about the claim that “low carb eating is not sustainable“?
Certainly, people who adopt a low carb lifestyle eat differently than they did before – but so do people who choose to be vegetarians. How often are those who choose not to eat meat for ethical or moral reasons told that “a vegetarian diet is not sustainable“? I don’t know of any.
Following a low carb lifestyle is no more or less sustainable than choosing not to eat meat.
For heaven’s sake, for the last 40 years people have been advised to eat a low-fat diet and I don’t recall anyone being told that “a low fat diet is not sustainable“.
I like to think of adopting a low carb lifestyle in terms of someone who has been diagnosed with a food allergy or food intolerance. Someone who’s been diagnosed as Celiac is intolerant to gluten and they make the choice to avoid gluten for health reasons. People with nut allergies also face food restrictions that guide their choices. Do we ever hear Celiacs being told that “eating a gluten restricted diet is not sustainable” or that “eating a nut-free diet is not sustainable“?
No.
People are advised by their doctors, or who have consulted with their doctors to follow these dietary restrictions for health reasons should not view this style of eating as any more or less restrictive or limiting than any other dietary restriction made for heath reasons.
Many people who adopt a low carb lifestyle do so to reduce the risks associated with health conditions such as Type 2 Diabetes, high blood pressure and high triglycerides / cholesterol. People who have seen friends or family members live through or die from complications from these conditions are likely to be highly motivated to make dietary changes and to stick with them. As with any other dietary restriction, a low carb lifestyle is a dietary choice and the willingness to continue with it is tied to the strength of the motivation to make that dietary change in the first place.
Note: The American Diabetes Association gives Type 2 Diabetics the option of following either a moderate low carb diet (130g carbohydrate) or a low calorie calorie restricted diet for up to a year, for weight loss. At the present time, Diabetes Canada does not yet approve this approach.
Once people start eating lower carb, how much better they feel provides the self-motivating to continue! They report that they are no longer driven by food cravings, that they sleep better, have more energy and mental clarity and focus. Many people with joint stiffness and pain find it improves considerably and of course, they lose weight naturally and almost effortlessly, without being hungry.
There is such a sharp contrast between how they feel after adopting a low carb lifestyle to how they felt before, that this serves to reinforce their initial reason for adopting this change. Why would they want to go back to feeling overstuffed, lethargic, hungry and tired? So they continue in their lower carb lifestyle.
What if when a person is faced with the preconceived conclusion that “low carb eating is not sustainable” they responded by suggesting adopting it for 3 months and re-running the blood work, alongwith the commitment to monitor their own blood glucose levels and blood pressure daily, and returning immediately if there are any issues? People could get “buy in” from their doctors in order to improve their own health using dietary changes – in much the same manner as dietary changes are used to manage other conditions. This is what I ask my clients to do before they begin a low carb diet; to discuss the approach with their doctors beforehand and have them follow them over time.
Maybe to change the ‘status quo’ is simply a matter of each of us advocating for change in managing our own “chronic, progressive diseases” – especially those that need not be either chronic, nor progressive.
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.
In two recent A Dietitian’s Journey posts, I wrote about the positive impact certain foods, such as apple cider vinegar, ginger and turmeric root have had on my blood sugar levels and more recently, about kombucha and kimchi. In this article I touch on the science to support the use of these foods to lower blood glucose levels.
Apple Cider Vinegar
Apple cider vinegar has long been popular as a folk remedy for high blood sugar and a 1988 study demonstrated that vinegar lowered both blood glucose levels and insulin following the eating of complex carbohydrates (starch) and simple carbohydrates (sucrose). It is now known that vinegar acts by a similar mechanism as the Diabetes medication Metformin® and increases fat burning, increases glucose movement into cells and increases insulin sensitivity. This may account for the effectiveness of vinegar in lowering blood glucose that has been know historically and has now been demonstrated in human clinical trials.
2004 study
A 2004 study, looked at the effectiveness of apple cider vinegar in reducing blood glucose levels after a meal (postprandial) as well as insulin levels in subjects with varying degrees of insulin resistance. The small study included both non-Diabetic subjects and those with Type 2 Diabetes. The non-Diabetic subjects were either insulin sensitive (n=8) or insulin resistant (n = 11) and there were 10 subjects with Type 2 Diabetes.
Fasting subjects were randomly assigned to either drink (1) 20 g apple cider vinegar with 40 g water and 1 tsp saccharine to sweeten it or (2) a placebo (water) drink. After a week of testing, subjects switched groups, so if they previously drank the placebo, they now took the apple cider vinegar.
After a 2-minute delay, subjects ate a white bagel, butter and orange juice (87 g total carbohydrates) and blood samples measuring blood glucose and insulin levels were taken 30 minutes and 60 minutes after eating the test meal.
As would be anticipated, fasting blood glucose was higher in ∼55% of subjects with Type 2 Diabetes compared with the non-Diabetic insulin sensitive and non-Diabeticinsulin resistant groups and fasting insulin was 95—115% higher in both the subjects with Type 2 Diabetes and the non-Diabeticinsulin resistant group
Compared with the placebo, the insulin resistant subjects that drank the apple cider vinegar had 34% higher whole-body insulin sensitivity 60 minutes after the high carbohydrate test meal and the subjects with Type 2 Diabetes had 19% higher whole-body insulin sensitivity.
This study demonstrated that apple cider vinegar taken before a meal containing carbohydrate can significantly improve insulin sensitivity in insulin-resistant subjects – both those with Type 2 Diabetes and those with ‘pre-Diabetes’ (i.e. insulin resistant, non-Diabetic).
2015 study
A 2015 study looked at the effect of vinegar on glucose metabolism in muscle, as it is considered the most important tissue for insulin-stimulated glucose disposal.
Subjects with Type 2 Diabetes drank either (1) 30″‰mL vinegar (6% acetic acid) and 20″‰mL water or (2) a placebo drink (water) before a mixed meal of bread, cheese, turkey ham, orange juice, butter and a cereal bar (with a total of 75″‰g carbohydrates, 26″‰g protein and 17″‰g fat).
Blood glucose, and insulin levels were measured in the subject’s forearm at 30 minutes and 60 minutes before the meal and 300″‰min after the meal was eaten and compared to placebo, vinegar increased forearm glucose uptake and decreased plasma glucose and decreased plasma insulin.
Researchers concluded that vinegar’s effect on carbohydrate metabolism may be partly accounted for by an increase in glucose uptake, demonstrating an improvement in insulin action in skeletal muscle.
NOTE: The amount of apple cider vinegar taken before meals in these two studies were 1.5 Tbsp. (20 mL) or 2 Tbsp. (30 mL).
Mechanism of Action
When taken with or just before meals, it is believed that vinegar slows gastric emptying, delays the uptake of glucose and slows the rise in blood sugar following a meal (2 hours postprandial).
Vinegar also stimulates an enzyme called AMP-activated protein kinase (AMPK) that increases fat oxidation, improves glucose uptake and insulin sensitivity and lowers glucose production (gluconeogenesis) in the liver. This is similar to how the diabetic medication Metformin works (see Zhou et al, 2001).
NOTE: This article is not proposing that foods such as vinegar are substitutes for medication prescribed by a doctor.
Activation of AMPK by vinegar has been demonstrated in the liver of vinegar fed rats and in human endothelial cells in vitro (see Kondo et al 2009, Sakakibara et al 2006, 2010, Li et al 2013) and this may account for the effectiveness of vinegar in lowering blood glucose that has been demonstrated in the human clinical trials, above.
Taking vinegar at meals has also been reported to significantly lower the glucose response after a meal (postprandial) – presumably by slowing the absorption of starch or polysaccharides (see Johnson 2009, 2010, Ostman et al 2005).
Ginger
Ginger was shown to have blood glucose lowering activity in a 2004 study that found that pre-meal treatment with ginger lowered induced high blood glucose levels (hyperglycemia).
A 2015 study evaluated the effects of a ginger powder supplement on fasting blood glucose levels and hemoglobin A1c (HbA1c) in Type 2 Diabetics. To be included, subjects needed to have been diagnosed as T2D for at least 2 years, have a HbA1c level of 6-8%, as well as taking no antioxidant supplements for at least 3 months prior to the study, and no smoking and drinking. Subjects that took insulin before or during the study were excluded, as were those that had a change in the type or dose of medication, changes in diet or any illnesses during the study.
The fifty subjects of both genders were divided randomly into and experimental and control group, with 25 subjects in each and received either a ginger-containing capsule or a placebo capsule twice a day for 12 weeks. All subjects took their usual medications for T2D and were stable on their dose.
Of 50 patients that began the study, 41 subjects completed the study (22 in the ginger group and 19 in the control group).
Fasting blood glucose levels after the intervention study were 19.4% lower in the ginger supplemented group than in the placebo group and HbA1C was .77% lower in the ginger supplemented group than in the placebo group. It was concluded that a study with more subjects and a longer study period were needed for a better observation of the effects of ginger in improving blood glucose in those with Type 2 Diabetes.
Turmeric Root
Turmeric root (Curcuma longa) is a rhizome of the ginger family that gives curry powder (which is a mixture of several spices) its characteristic yellow colour. Turmeric has been used in both Ayurvedic and traditional Chinese medicine to lower blood sugar levels. The active component of turmeric, is curcumin.
An extensive literature review of studies on curcumin was conducted and published in 2013 with more than 200 publications retrieved using the search term ”curcumin and diabetes” from the MEDLINE database, with the earliest being a case study from 1972 and curcumin has since been extensively studied in animal models of Diabetes and in a few clinical trials with subjects with Type 2 Diabetes. The conclusion of the literature review was that there is ample evidence in the scientific literature regarding the use of curcumin as a potential treatment for Diabetes as well as its associated complications.
Note: when using turmeric, be sure to add a few grinds of black pepper as it increases the bioavailability of the curcumin by ~2000 times.
Fermented Foods – Kombucha, Kimchi and Jun
Kimchi
Fermented foods, such as kombucha and kimchi are popular as probiotics for enhancing the microbiota of our intestine. Research in the field has focused on what role this complex bacterial community plays in health and disease in people, and how we can alter the microbiota through the foods and beverages we consume. The benefit of eating foods and drinking beverages with these probiotics has been demonstrated in studies and include improvement of constipation, diarrhea, irritable bowel syndrome (IBS), intestinal inflammatory conditions such as Crohn’s and colitis, as well as an improvement in immune function.
Lactic acid bacteria are the most widely used strains used to ferment foods; from sauerkraut, kosher dill pickles to kimchi, a staple of the Korean diet. For lactic acid bacteria to benefit the microbiota of the human intestines however, they first must be able to survive the hostile environment of digestion, which include extreme acidity, and digestive enzymes, and bile acids – not to mention low oxygen availability, and regulated temperature. It has been demonstrated in studies that they do.
2014 meta-analysis
A meta-analysis published in 2014 examined the effect of probiotics on glucose metabolism in patients with Type 2 Diabetes Mellitus of randomised-controlled studies where fasting blood glucose, glycosylated hemoglobin (HbA1c), insulin concentration or homeostasis model assessment of insulin resistance (HOMA-IR) changes were reported for the intervention and control groups.
Seven trials met the search criteria and results indicated that probiotic consumption significantly changed fasting plasma glucose by -0.9 mmol/L (-15.92 mg/dL). The duration of intervention for ≥8 weeks resulted in a significant reduction in fasting blood glucose of 1.2 mmol/dL (-20.34 mg/dl). HbA1C was significantly reduced by -0.54% compared with control groups. The results also showed that probiotic therapy significantly decreased homeostasis model assessment of insulin resistance (HOMA-IR) by -1.08 and insulin concentration by -1.35 mIU/L.
This meta-analysis suggests that eating or drinking foods containing probiotics may improve glucose metabolism with a potentially greater effect when the duration of intervention is ≥8 weeks, or multiple species of probiotics are consumed.
2016 meta-analysis
A meta-analysis published in 2016 examined the effect of probiotics on glucose and glycemic factors in Type 2 Diabetes of randomised-controlled studies published in English between January 2000 to June 2015. The main outcomes of interest were mean changes in glucose, HbA1c, insulin and homoeostasis model assessment-estimated insulin resistance (HOMA-IR).
A total of 11 studies with 614 subjects were included. It was found that there was a statistically significant difference between the probiotic consuming groups and the placebo-controlled groups on the reduction of blood glucose of -0.52 mmol/L (10 mg/dl).
Analysis identified that probiotics significantly reduced fasting blood glucose, HbA1c, insulin and HOMA-IR in participants with Type 2 Dabetes.
Kombucha and Jun
Kombucha is a beverage made by fermenting black tea and sugar with some “starter” from a previous batch, called the ‘mother’ or ‘SCOBY’ (symbiotic culture of bacteria and yeast). This is sometimes referred to as the ‘tea mushroom’ or ‘tea fungus’.
After ~ a week or 10 days, a second fermentation takes place with approximately 1 part fruit to about 10 parts fermented tea. This remains in sealed containers where it yields a lightly carbonated, mildly acidic and fruity flavoured beverage, which is the final product. In the photo to the left, this is my first batch.
Green tea and honey can also be used to make a fermented product using a very similar process, but using a different kind of SCOBY (one that is adapted to metabolize these substrates) and the resulting product is called Jun.
The taste of jun is considerably different than kombucha, as is the alcohol content. Kombucha is typically ~1.50% alcohol whereas Jun ranges from 3-7% alcohol.
With some investigation, I was able to determine that kombucha is essentially a symbiotic growth of acetic acid bacteria and osmophilic (water-loving) yeasts in a cellulose mat that the culture makes.
The main bacteria are (1) Acetobacter –acetic acid bacteria that are able to convert the ethanol (alcohol) that is initially produced in the fermentation process to acetic acid, in the presence of oxygen and (2) Gluconobacter – acetic acid bacteria that prefer sugar-rich environments.
This is the same species that converts the ethanol (alcohol) in apple cider, to apple cider vinegar. Hence, it seems reasonable to surmise that it is the acetic acid content of kombucha and jun, which give it its characteristic tart taste, that also provide the same glucose lowering effect as apple cider vinegar.
Some final thoughts…
Given that there is scientific evidence that apple cider vinegar, ginger root, turmeric root, kimchi, kombucha & jun play a role in lowering blood glucose and other markers, these foods should be considered – along with a low carbohydrate diet and intermittent fasting (extending the time between meals) when addressing the problem of high blood glucose levels resulting from insulin resistance.
Food, and the temporary absence of it, as medicine.
NOTE: These foods should not be consumed without first consulting with your doctor, especially if you are on medication for Type 2 Diabetes as they can have a potent blood effect on blood sugar levels.
If you would like to read well-researched, credible ”Science Made Simple” articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please click here.
Akhani SP, Vishwakarma SL, Goyal RK. Anti-diabetic activity of Zingiber officinale in Streptozotocin-induced type I diabetic rats. J. Pharm. Pharmacol. 2004;6:101—105.
Ebihara K, Nakajima A: Effect of acetic acid and vinegar on blood glucose and insulin responses to orally administered sucrose and starch. Agric Biol Chem 52:1311—1312, 1988
Jayabalan R, MalbaÅ¡a R, LonÄar ES, et al: A Review on Kombucha Tea—Microbiology, Composition, Fermentation, Beneficial Effects, Toxicity, and Tea Fungus. Comprehensive Reviews in Food Science and Food Safety 13(4): 1541-4337
Johnston CS, Kim C, Buller AJ, Vinegar Improves Insulin Sensitivity to a High-Carbohydrate Meal in Subjects With Insulin Resistance or Type 2 Diabetes, Diabetes Care 2004 Jan; 27(1): 281-282.
Johnston CS, White AM, Kent SM. Preliminary evidence that regular vinegar ingestion favorably influences hemoglobin A1c values in individuals with type 2 diabetes mellitus. Diabetes Res Clin Pract. 2009 May; 84(2):e15-7
Johnston CS, Steplewska I, Long CA, Harris LN, Ryals RH. Examination of the antiglycemic properties of vinegar in healthy adults. Ann Nutr Metab. 2010; 56(1):74-9.
Khandouzi N, Shidfar F, Rajab A, Rahideh T, Hosseini P, Mir Taheri M. The Effects of Ginger on Fasting Blood Sugar, Hemoglobin A1c, Apolipoprotein B, Apolipoprotein A-I and Malondialdehyde in Type 2 Diabetic Patients. Iranian Journal of Pharmaceutical Research”¯: IJPR. 2015;14(1):131-140.
Kondo T, Kishi M, Fushimi T, Kaga T (2009b) Acetic acid upregulates the expression of genes for fatty acid oxidation enzymes in liver to suppress body fat accumulation. J Agric Food Chem 57(13):5982—5986
Kim NH, et al. (2008). Lipid profile lowering effect of Soypro fermented with lactic acid bacteria isolated from kimchi in high-fat diet-induced obese rats. BioFactors 33(1):49-60. PMID 19276536
Li X, Chen H, Guan Y, Li X, Lei L, Liu J, Yin L, Liu G, Wang Z. Acetic acid activates the AMP-activated protein kinase signaling pathway to regulate lipid metabolism in bovine hepatocytes.
PLoS One. 2013; 8(7):e67880.
Mitrou P, Petsiou E, Papakonstantinou E, et al. Vinegar Consumption Increases Insulin-Stimulated Glucose Uptake by the Forearm Muscle in Humans with Type 2 Diabetes. Journal of Diabetes Research. 2015;2015:175204. doi:10.1155/2015/175204.
Ostman E, Granfeldt Y, Persson L, Bjí¶rck I. Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. Eur J Clin Nutr. 2005 Sep; 59(9):983-8.
Sakakibara S, Yamauchi T, Oshima Y, Tsukamoto Y, Kadowaki T, Acetic acid activates hepatic AMPK and reduces hyperglycemia in diabetic KK-A(y) mice. Biochem Biophys Res Commun. 2006 Jun 2; 344(2):597-604.
Shang Q, Wu Y, Fei X, Effect of probiotics on glucose metabolism in patients with Type 2 Diabetes Mellitus: A meta-analysis of randomized
controlled trials. Medicina 52 (2016) 28-34. doi:10.1016/j.medici.2015.11.008
Sun J, Buys NJ, Glucose- and glycaemic factor-lowering effects of probiotics on diabetes: a meta-analysis of randomised placebo-controlled trials. British Journal of Nutrition, 2016; 115(7):1167-1177
Yusoff et al, Aqueous Extract of Nypa fruticans Wurmb. Vinegar Alleviates Postprandial Hyperglycemia in Normoglycemic Rats, Nutrients 2015, 7(8), 7012-7026
Zhang D, Fu M, Gao S-H, Liu J-L. Curcumin and Diabetes: A Systematic Review. Evidence-based Complementary and Alternative Medicine”¯: eCAM. 2013;2013:636053. doi:10.1155/2013/636053.
Zhou et al, Role of AMP-activated Protein Kinase in Mechanism of Metformin action. Journal of Clinical Investigation 2001 Oct 15; 108(8): 1167—1174
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.
I often get asked what I recommend people do when it is a special occasion, or a holiday. Are we allowed a “cheat day”. This is how I answer the question.
It may seem like a strange thing for a Dietitian to say, but when it comes to weight loss, or targeting lower blood sugars, or pressure or cholesterol, I don’t believe in “diets”. The way I look at it is, if people go on a diet, then at some point, they go off of it. I prefer to think of what we eat in terms of “everyday foods” and “sometimes foods”.
Eating a low carb high fat (LCHF) diet is a choice, just like becoming a vegetarian. People become vegetarian for different reasons; sometimes it is for religion reasons or ethical reasons and sometimes it is for the perceived health benefits. It’s the same with the reason people start eating LCHF. For some, it is to lower insulin resistance, for others it’s to address high blood sugar or to lose weight. Some decide to eat this way because it was the diet of our ancient ancestors. Since the reasons people start eating LCHF are different, the reasons people might give to eat a high carbohydrate food also differ.
As far as an idea of a “cheat day”, I don’t find the idea of being “allowed” or “not allowed” foods, helpful. It implies that there are rules that we are somehow ‘breaking’ – and this comes with baggage all its own. Restricting calories or restricting food and weighing and measuring every bite that we put in our mouths is not a paradigm that has served most people well – and this type of obsession and attention to “how much” can, in theory, feed a predisposition to disordered eating.
I encourage people to learn to follow a LCHF style of eating and to become adapted to burning fat, rather than just carbohydrate. Then I advise them to eat when they are hungry and stop eating when they are no longer hungry. It sounds simple, but there is some physiology behind it. Without constantly high insulin levels driving food craving, eating a diet rich in healthy fats enables people to stop eating when they are no longer hungry.
Eating or not eating high carbohydrate foods comes with an opportunity cost. The questions I encourage people to ask themselves is “what will the results or conssequences be if I eat the specific food(s) I have in mind, and in what quantities?”
For example, if a person that normally eats ~100g of carbohydrate a day wants to eat a few slices of pizza, the physiological consequences will be different than a woman that normally eats 35g of carbohydrate, or a man that normally eats 50g of carbs per day. If either of them is insulin resistant or Diabetic, it will certainly impact their blood sugars (the symptom), but how long will it have an effect on their insulin levels? That is the more important question.
For people who are in ketosis, eating foods very high in carbohydrates will cause that to cease for a time, and it might take several days of eating LCHF again until they are again in fat-burning mode. Likely there will be a few days of being hungry through the day. Are they okay with this?
I want people to have a healthy relationship with food – and that means that they can eat anything – but how much and how often?
Everyday (i.e. “everyday foods”), I choose to eat LCHF, but sometimes (i.e. “sometimes foods”) I will take a taste of something yummy – and I encourage my clients to feel free to do so too. A bite of an ice cream or cake, in the grand scheme of things, won’t make a huge difference, in fact, I calculate the number of carbs that are in the food I am considering, and decide beforehand, if it is worth it for me.
Tonight I will be having my family over for a special dinner and I have decided in advance that I will have 2 oz of the bread, a spoonful of the noodle pudding and a 2″ x 1″ piece of the honey cake. Sure I can have more, if I wanted, but I’ve come to realize that whether I eat 2 oz of the saffron honey egg bread or 10 oz of it, it will taste exactly the same! Why eat more? I’ve never been a big fan of the noodle dish, so a small taste is fine with me, and the honey cake is only made once a year on this occasion, and it’s my mother’s recipe from 1954, so yes I am going to eat a bigger piece and enjoy every bite. So what am I going to eat?
Chicken! …and some red butter lettuce salad with raspberries on top and drowned in olive oil. Oh! And an apple slice, dipped in honey, for a sweet year.
Eating LCHF is a choice, and a lifestyle and as such, we can choose to eat other things. How much, how often and which things is up to us. If our goal is to lower our insulin levels, we will know (or need to learn) how much of something won’t have a large, lasting impact.
Note: I am a “sample-set of 1” – meaning that how I implement a low carb diet may differ from others who follow a similar lifestyle. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
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.
Several years ago, I began to ask myself how it is that 2/3 of men and ~1/2 of women in Canada are either overweight or obese. In the early 1970s, only ~8% of men and ~12% of women were obese and now almost 22% of men and 19% of women are obese- even though statistics show we are eating much less fat, drinking way less pop and eating more fish than ever before. I wondered if the increase in overweight and obesity might be related to the changes in the Dietary Recommendations that began in 1977 and which encourage us to eat 45-65% of daily calories as carbohydrate and to limit all kinds of fat to 20-35%.
In early 2015, after scouring the scientific literature and reading about the clinical use of a Low Carb High Fat (LCHF) diet, I came to the understanding that those who are insulin resistant or have Type 2 Diabetes or have other indicators that they are not tolerating large amounts of carbohydrate well could improve their symptoms significantly by following a lower carb style of eating, with the oversight of their doctors. Such an adjustment in lifestyle seemed like a small price to pay for the potential of significantly improving – and in some cases reversing symptoms of these conditions, especially when compared with the reality that at best these symptoms will stay the same and very likely will get worse over time.
Many scientific studies as well as physician’s clinical experience indicate that a lower carb style of eating combined with extending the time between meals lowers insulin resistance (which is the underlying cause of high blood sugar). When insulin levels are lowered, blood pressure comes down and triglycerides and some other lipid ratios normalize.
Physicians across Canada, the US, the UK and Australia that prescribe a LCHF Diet to their patients have found that they experience a significant improvement in the symptoms of insulin resistance, Type 2 Diabetes, high blood pressure, high triglycerides and that a natural reversal of many symptoms is possible. Such improvements often enable these doctors to reduce- and sometimes discontinue medications that were previously prescribed to their patients for these conditions. While the American Diabetes Association enables Type 2 Diabetics to choose to follow either a moderate low carb diet (130g carbohydrate) or a low fat calorie restricted diet for up to a year for weight loss, as of yet this approach is not approved by Diabetes Canada.
A low carb diet isn’t new. In fact this was the standard recommendation prior to the discovery of insulin.
It seems to me that a lower carbohydrate intake resulting in improved symptoms and lab results as overseen by one’s own doctor is preferable to living with chronic disease symptoms and taking increasing numbers of medications in an effort to manage symptoms, but each person needs to evaluate the alternative and make their own choice.
For those who want to aim to improve or reverse the symptoms of these chronic diseases, I offer services as the LCHF-Dietitian.
Janssen I, The Public Health Burden of Obesity in Canada, Canadian Journal of Diabetes, 37 (2013), pg. 90-96
from the Public Health Collaborative, Summary Table of Randomized-Controlled Trials Comparing Low Carb to Low-Fat Diets – https://phcuk.org/:
[1] A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on
Body Weight and Cardiovascular Risk Factors in Healthy Women. Brehm et al.
http://press.endocrine.org/doi/full/10.1210/jc.2002-021480
[2] A Randomized Trial of a Low-Carbohydrate Diet for Obesity. Foster et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa022207
[3] A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. Samaha et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa022637
[4] Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.
Sondike et al. http://www.sciencedirect.com/science/article/pii/S0022347602402065
[5] The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein
and Monounsaturated Fat A Randomized Trial. Aude et al. http://archinte.jamanetwork.com/article.aspx?
articleid=217514
[6] A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: A
Randomized, Controlled Trial. Yancy et al. http://annals.org/article.aspx?articleid=717451
[7] Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body
composition in overweight men and women. Volek et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC538279/
[8] Comparison of a Low-Fat Diet to a Low-Carbohydrate Diet on Weight Loss, Body Composition, and Risk
Factors for Diabetes and Cardiovascular Disease in Free-Living, Overweight Men and Women. Meckling et
al. http://press.endocrine.org/doi/full/10.1210/jc.2003-031606
[9] Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a highfat,
low-carbohydrate diet. Hernandez et al. http://ajcn.nutrition.org/content/91/3/578.long
[10] Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women
Consuming a Low-Carbohydrate/High-Protein vs High-Carbohydrate/Low-Fat Diet. Nickols-Richardson et al.
http://www.sciencedirect.com/science/article/pii/S000282230501151X/
[11] Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes—a randomized
controlled trial. Daly et al. http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract
[12] Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Krauss et
al. http://ajcn.nutrition.org/content/83/5/1025.full
[13] Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk
Factors Among Overweight Premenopausal Women The A TO Z Weight Loss Study: A Randomized Trial.
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[14] Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive
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[15] A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic
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[16] The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in
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[18] Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of
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[19] Metabolic Effects of Weight Loss on a Very-Low-Carbohydrate Diet Compared With an Isocaloric HighCarbohydrate
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[20] Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet.
Volek et al. http://link.springer.com/article/10.1007/s11745-008-3274-2
[21] Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet
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[22] Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese
Adolescents. Krebs et al. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892194/
[23] In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves
glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Guldbrand et
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[24] A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohydrate Diet
in Overweight or Obese Individuals with Type 2 Diabetes Mellitus or Prediabetes. Saslow et al.
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[25] Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial. Bazzano et al.
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[26] The Role of Energy Expenditure in the Differential Weight Loss in Obese Women on Low-Fat and Low Carbohydrate
Diets. Brehm et al. http://press.endocrine.org/doi/full/10.1210/jc.2004-1540
[27] Effects of a Low Carbohydrate Weight Loss Diet on Exercise Capacity and Tolerance in Obese Subjects.
Brinkworth et al. http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.134/full
[28] Comparative Study of the Effects of a 1-Year Dietary Intervention of a Low-Carbohydrate Diet Versus a
Low-Fat Diet on Weight and Glycemic Control in Type 2 Diabetes. Davis et al.
http://care.diabetesjournals.org/content/32/7/1147
[29] Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet: A
Randomized Trial. Foster et al. http://annals.org/article.aspx?articleid=745937
[30] Effects of a Low-intensity Intervention That Prescribed a Low-carbohydrate vs. a Low-fat Diet in Obese,
Diabetic Participants. Iqbal et al. http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.460/full
[31] Consuming a hypocaloric high fat low carbohydrate diet for 12″…weeks lowers C-reactive protein, and
raises serum adiponectin and high density lipoprotein-cholesterol in obese subjects. Ruth et al.
http://www.metabolismjournal.com/article/S0026-0495(13)00223-0/abstract
[32] Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated
fat diets on body composition and cardiovascular risk. Noakes et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368980/
[33] Long-term Effects of a Very Low-Carbohydrate Diet and a Low-Fat Diet on Mood and Cognitive
Function. Brinkworth et al. http://archinte.jamanetwork.com/article.aspx?articleid=1108558
[34] The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year
follow-up of a randomized trial. Stern et al. http://www.ncbi.nlm.nih.gov/pubmed/15148064
[35] A Randomized Trial of a Low-Carbohydrate Diet vs Orlistat Plus a Low-Fat Diet for Weight Loss. Yancy
et al. 2010. http://www.ncbi.nlm.nih.gov/pubmed/20101008
[36] A randomized controlled trial of low carbohydrate and low fat/high fiber diets for weight loss. Baron et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1646726/
[37] A very low-carbohydrate, low-saturated fat diet for type 2 diabetes management: a randomized trial. Tay
et al. http://www.ncbi.nlm.nih.gov/pubmed/25071075
[38] Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from
the BBC ”diet trials”. Truby et al. http://www.bmj.com/content/332/7553/1309
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[39] Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for Weight Loss and Heart Disease
Risk Reduction:A Randomized Trial. Dansinger et al. http://jama.jamanetwork.com/article.aspx?
articleid=200094
[40] Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in
Overweight Men. Sharman et al. http://jn.nutrition.org/content/134/4/880.long
[41] Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese
women. McAuley et al. http://link.springer.com/article/10.1007/s00125-004-1603-4/fulltext.html
[42] Diet-Induced Weight Loss Is Associated with Decreases in Plasma Serum Amyloid A and C-Reactive
Protein Independent of Dietary Macronutrient Composition in Obese Subjects. O’Brien et al.
http://press.endocrine.org/doi/10.1210/jc.2004-1011
[43] Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2
diabetes compared with advice to follow a low-fat diet. Jonasson et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025600/
[44] A non-calorie-restricted low-carbohydrate diet is effective as an alternative therapy for patients with type
2 diabetes. Yamada et al. http://www.ncbi.nlm.nih.gov/pubmed/24390522
[45] Low-Fat Versus Low-Carbohydrate Weight Reduction Diets Effects on Weight Loss, Insulin Resistance,
and Cardiovascular Risk: A Randomized Control Trial. Bradley et al.
http://diabetes.diabetesjournals.org/content/58/12/2741.long
[46] Weight loss with high and low carbohydrate 1200 kcal diets in free living women. Lean et al.
http://www.nature.com/ejcn/journal/v51/n4/abs/1600391a.html
[47] Evaluation of weight loss and adipocytokines levels after two hypocaloric diets with different
macronutrient distribution in obese subjects with rs9939609 gene variant. De Luis et al.
http://onlinelibrary.wiley.com/doi/10.1002/dmrr.2323/abstract
[48] Enhanced weight loss with protein-enriched meal replacements in subjects with the metabolic syndrome.
Flechtner-Mors et al. http://onlinelibrary.wiley.com/doi/10.1002/dmrr.1097/abstract
[49] Long-term effects of a low carbohydrate, low fat or high unsaturated fat diet compared to a nointervention
control. Lim et al. http://www.nmcd-journal.com/article/S0939-4753(09)00124-0/abstract
[50] A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on
lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Seshadri et al.
http://www.amjmed.com/article/S0002-9343(04)00344-4/abstract
[51] Comparison of low- and high-carbohydrate diets for type 2 diabetes management: a randomized trial.
Tay et al. http://ajcn.nutrition.org/content/early/2015/07/29/ajcn.115.112581.abstract
[52] Weight loss on low-fat vs. low-carbohydrate diets by insulin resistance status among overweight adults
and adults with obesity: A randomized pilot trial. Gardner et al.
http://onlinelibrary.wiley.com/doi/10.1002/oby.21331/abstract
[53] Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents.
Partsalaki et al. http://www.ncbi.nlm.nih.gov/pubmed/23155696
[54] A randomized controlled trial of 130 g/day low-carbohydrate diet in type 2 diabetes with poor glycemic
control. Sato et al. http://www.clinicalnutritionjournal.com/article/S0261-5614(16)30169-8/pdf
[55] Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss
program versus hypocaloric diet in patients with type 2 diabetes mellitus. Goday et al.
http://www.nature.com/nutd/journal/v6/n9/full/nutd201636a.html
[56] Visceral adiposity and metabolic syndrome after very high—fat and low-fat isocaloric diets: a randomized
controlled trial. Veum et al. http://ajcn.nutrition.org/content/early/2016/11/30/ajcn.115.123463.abstract
[57] An Online Intervention Comparing a Very Low-Carbohydrate Ketogenic Diet and Lifestyle
Recommendations Versus a Plate Method Diet in Overweight Individuals With Type 2 Diabetes: A
Randomized Controlled Trial. Saslow et al. https://www.ncbi.nlm.nih.gov/pubmed/28193599
It bothers me when people make negative comments about a Low Carb High Fat (LCHF) style of eating, without really understanding what it is – and what it isn’t. This article addresses a few of the common misconceptions about a Low Carb lifestyle that were presented in a recent French-language newspaper article.
FALLACY: “The LCHF diet targets a very low carbohydrate and high-fat diet, aimed at rapid weight loss.”
FACT 1: Firstly, there is no single LCHF diet.
The Atkins Diet is one kind of LCHF diet, so is a Paleo Diet, and these are substantially different from each other. There are LCHF diets written by non-healthcare professionals such as the “Bulletproof Diet”, as well as those from Dr. Jason Fung, a Nephrologist (kidney specialist) from Toronto and from Dr. Eric Westman of Duke University. Referring to “the” LCHF diet fails to take this huge range into account.
FACT 2: There is no one “goal” of LCHF diets.
From my experience, most of the well-designed LCHF diets written by healthcare professionals and researchers are aimed at lowering insulin resistance (IR), which underlies the symptom of high blood sugar and Type 2 Diabetes. Weight loss is a natural byproduct of eating in such a way as to lower IR.
FACT 3: LCHF diets that focus on weight management rarely aim for “rapid weight loss”.
LCHF diets designed by healthcare professionals with a weight management goal generally aim for consistent weight loss and/or inches lost, and reducing abdominal obesity. Morbidly obese people or those with a great deal of weight to lose and who begin eating low-carb will lose weight rapidly at first, firstly from water-loss and then from fat loss. That is not the aim, but the result.
FALLACY: “this diet is so restrictive”…
FACT 4: “this diet…”
Which LCHF diet? As mentioned above, there are many different LCHF-style diets and they differ substantially from each other.
Fact 5: The term “restrictive” is not defined, so this statement really has no meaning.
What are all LCHF diets “restrictive” in?
Foods that are not included on an Atkins Diet are very different from what is not included on a Paleo Diet. Dr. Fung’s recommendations differ from Dr. Westman’s. For example, Dr. Fung does not limit any fats, and Dr. Westman does.
Which LCHF-diet is “restrictive” and in what foods or nutrients?
FALLACY: “this diet is so restrictive that the likelihood that the people who adopt it will drop it in the short or medium term is high.”
FACT 6: Which LCHF diet is restrictive and what is it restrictive in? Is there evidence to support that people that stop eating those foods regularly are unable to continue to do so in the short- or medium term?
FALLACY: “There is a difference between processed high-carbohydrate foods such as juice, sweetened beverages, white bread, pastries and sweets, and whole foods high in unprocessed carbohydrates such as brown rice, whole wheat, vegetables, fruits, legumes , which are associated with good health and the prevention of the risk of diabetes, cardiovascular disease and obesity.“.
FACT: 7: all carbohydrates (whether from juice, fruit, pastry, brown rice or whole wheat) are broken down and supply the blood with glucose.
FACT 8: how quickly all carbohydrates are broken down to glucose varies.
FACT 9: how much insulin is released in response to all of these different carbohydrates is what most well-designed LCHF diets endeavor to address.
FALLACY: “Whenever an attempt is made to isolate a nutrient (carbohydrates, proteins or lipids) and make it responsible for all ills, it is wrong. The reality is that we need these three nutrients for the health and enjoyment of eating.”
FACT 10: Well-designed LCHF-diets have all three macronutrients in them; carbohydrates, protein and fat.
The major difference is LCHF diets are low in carbohydrate and high in fat. Which carbohydrates are eaten on different LCHF diets vary. Paleo diets for example eat starchy vegetables that ketogenic-style LCHF diets don’t. In addition, which fats are promoted in the different styles of LCHF diets also differs. Paleo diets are known for promoting lots of red meat, including processed meat such as bacon and sausage and lots of full-fat cream and butter.
LCHF diets, such as the one I teach, include the saturated fat found naturally in foods, such as in steak or in cheese but encourage the “high fat” part of the diet to come from mono-unsaturated fruits such as avocado and olives, from a wide variety of nuts and seeds, as well as from the oils from these foods as well as from omega 3 fats found in fish. It also includes the carbohydrates found in an abundance of non-starchy vegetables, specific fruit, nuts and seeds. A look at just a few of the recipe ideas posted on this web site, certainly do not indicate a “restrictive diet”.
FACT 11: The Dietary Guidelines in Canada (and the US) have “attempted to isolate a nutrient – fat, and make it responsible for all ills”.
In 1977, the Dietary Guidelines in both countries were first changed to restrict fat intake from all sources, especially saturated fat, in the belief that eating fat contributed to heart disease (see previous articles).
While it is now known that dietary fats do not cause heart disease, and even the Canadian Heart and Stroke Foundation changed their recommendations in this regard, it is my conviction that it was this vilification of fat and the corresponding promotion of diets very high in carbohydrates (45-65% of daily calories as carbs) that contributed to the dual obesity- and Diabetes epidemics that we now have.
Some final thoughts…
A LCHF-style of eating can be done safely, with slow yet consistent weight loss, while being overseen by one’s doctor and monitoring blood glucose and lab work.
It certainly doesn’t have to be restrictive, as one can eat meat, fish, seafood, poultry, cheese and other dairy, vegetables and fruit, nuts and seeds. It can provide a nutritionally adequate diet – certainly no less adequate that the average Canadian eats, following Eating Well with Canada’s Food Guide [see Do Canadian Adults Meet Their Nutrient Requirements Through Food Intake Alone? Health Canada, 2012, Cat.No.: H164-112/3-2012E-PDF].
Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
When people think of getting enough “fiber” they often imagine foods like “bran” and prunes – foods not usually eaten when one is following a LCHF style of eating. But what is fiber and how do we get enough when we don’t generally eat grains or legumes?
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, un-milled brown rice and the outside of oats. It is also found in fruit, legumes (or pulses) such as dried beans, lentils, or peas, some vegetables and in nuts and seeds.
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 insideof certain grains, such as oats, chia seeds or psyillium, as well as the inside of certain kinds of fruit such as apple and pear.
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.
[Reference: Government of Canada, nutrients in food, https://www.canada.ca/en/health-canada/services/nutrients/fibre.html]
Both kinds of fiber are needed and most Canadians eating a conventional diet are getting half of what is recommended.
For those eating a Low Carb High Fat Diet, even though grains and legumes are generally not eaten, getting enough fiber is not that difficult.
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 fruit that I encourage people to use sprinkled on salads, as they 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 a single beet, and eaten with Middle Eastern foods.
Constipation
Even though passing stool is as natural a part of the process as eating is, most feel awkward discussing it. Many don’t know what “normal” is in that regard, or even if there is such a thing. Is once every few days okay, is it detrimental if it is only once a week? Should it be every day and if so, is more than once a day too much? Does texture matter or is it only frequency?
Frequency and Texture
Many physicians consider normal bowel movement (BM) frequency from 3/day to every 3 days whereas I tend to lean towards daily to every two days as preferable. Even if BM frequency is in this range, hard, painful to pass stools are problematic and would be categorized as constipation.
Since the mid-1990s there is a standardized method to classify the texture of stools, called the Bristol Stool Chart based on research which indicated that stool is a useful surrogate measure of how long feces (stool) takes to go through the large intestine (called “colon transit time”).
While Type 3-7 are considered valid for diagnosing diarrhea, Type 1 and Type 2 stool can have normal “transit time”, but be compact and hard due to lack of fluid / water.
The fact is, many, if not most people either have a lack of fiber or a lack of sufficient fluid or both and are constipated to a greater or lesser degree. They eat every day, but they don’t pass stool often and when they do, it is hard and compact. Their bodily waste sits in their colon for several days before finally being eliminated – and when it is, it is hard, dry and compact and often painful to pass.
Constipation is usually due to two factors;
(1) not taking in foods with enough fiber and
(2) not drinking enough water
Sometimes, despite eating the foods mentioned above, people find it isn’t sufficient. This is where what I have dubbed “birdseed” comes in. Of course, I don’t mean actual birdseed!
What I call “birdseed” is a mixture of 1 tbsp. freshly ground whole flax seed (3 gm fiber per tbsp.) to which 1 tbsp. of chia seed is added (5.5 gm fiber per tbsp.).
The chia seeds are ground a little bit with the previously ground flax seed, and then the two ground seeds are placed in a small bowl.
An added portion of psyllium husk (1 tbsp.) is optional.
Drinking “Birdseed”
To drink this mixture, diluted coconut milk can be added, the mixture briefly stirred and then drunk quickly, followed by a good amount of water (I recommend at least 2 cups (500 ml).
Eating “birdseed”
For even more fiber and a delicious taste, 2 tbsp. of tahini (ground sesame paste) can be added and the mixture eaten with a spoon.
Tahini has 0 net carbs, and almost 4 gm of fiber for 2 tbsp.
Note: people often ask if they can make “chia pudding” to which they add ground flax seed, but the idea here is to have the flax and chia seeds do their magic in the intestines, not in a container, beforehand.
Water – how much is sufficient?
Dehydration is another factor that contributes to constipation. Often people simply don’t drink enough water to form a bulky, pliable stool.
The Reference Daily Intake (RDI) for water for men over 18 years is 3.7 liters per day and for women over 18 years, 2.7 liters per day and this is from all water, including that contained in beverages.
Fiber and water together
Drinking one liter of water or club soda / seltzer with each batch of “birdseed” is a good idea, because the last thing we want is to have all this insoluble and soluble fiber this in our intestines, with insufficient water. In the worse case scenario, this can result in an intestinal blockage, so be sure to drink sufficient water when taking “birdseed”.
I usually recommend that people start off with having 1 tbsp of flax seed and 1 tbsp of chia seed once a day – increasing after a few days if needed to twice (or if needed, three times) a day – making sure to drink a liter of water immediately afterwards.
What about carbs in “birdseed”?
While flax seed, chia seed and psyllium are grains, they have very few net carbs.
1 tsp of whole flax seed (3.4 gm) is so high in fiber that it has no net carbs.
1 tsp of whole chia seed has only .3 gm of net carbs.
Even if you add 1 tsp of psyllium husk, that adds only 1 gram of carbs.
“Birdseed” can be drunk as described above, eaten with sesame paste (also very high in fiber and a good source of healthy fat), or sprinkled on salads or omelettes.
…and remember to drink a liter or so of water each time you take “birdseed”, so that passing stools daily, just like eating daily, will be the norm.
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
INTRODUCTION: This recent Canadian study reports that the caffeine contained in 1 1/2 to 3 cups of unsweetened coffee is sufficient to increase plasma levels of ketones, including β-hydroxybuterate, for several hours.
A pilot Canadian study conducted at the Université de Sherbrooke in Sherbrooke, Quebec and published in the Canadian Journal of Physiology and Pharmacology on November 25, 2016 evaluated the effect of caffeine on the production of ketones in healthy adults. Researchers were interested in caffeine as a ketogenic agent based on its ability to increase lypolysis (the breaking down of fat for fuel).
Method of the Study
Two different doses of caffeine were administered to 10 healthy adults who had fasted for 12 hours and who then ate a breakfast that containing 85 gm carbohydrate, 9.5 gm fat and 14 gm of protein.
Subjects were either given;
(1) no caffeine
(2) a cup and a half of regular drip coffee
(3) three cups of regular drip coffee
The subjects plasma caffeine levels were measured over the next 4 hours and it was found that those that drank 1 1/2 cups of coffee had~ 2.5 mg caffeine per kilogram of body weight and those that drank 3 cups of coffee had ~ 5.0 mg caffeine per kilogram of body weight.
Results – the effect of caffeine on ketone production
Subjects that had 1 1/2 cups of coffee (2.5 mg of caffeine per kilogram) had 88% higher ketone production than subjects that had no caffeine.
Subjects that drank 3 cups of coffee (5.0 mg caffeine per kilogram of body weight) had 116% higher ketone production over subjects that had no caffeine.
Expressed as the amount of β-hydroxybuterate in μmol/L, it is evident that this ketone rises significantly in response to caffeine, and rises in a dose-dependent manner. That is, the more caffeine consumed the more β-hydroxybuterate was produced.
Researchers reported that the level of ketones found in the blood after 3 cups of coffee was approximately twice that produced after an overnight fast.
This increase in plasma ketones obtained with these doses of caffeine could, at least in the short term (a few hours) contribute to ~5-6% of brain energy needs.
Mechanism
The increase in free fatty acids as well as β-hydroxybuterate is explained by caffeine blocking phosphodiesterase (PDE), preventing the inactivation of cyclic adenosine monophosphate (cAMP) – with increased caffeine leading to higher levels of cAMP.
Cyclic adenosine monophosphate (cAMP) is a cellular messenger that is involved with transferring hormones such as glucogon, which is the main catabolic hormone of the body and which functions to raise both the concentration of glucose and fat in the bloodstream and has the opposite effect of insulin).
Glucagon needs cAMP in order to pass through the plasma membrane, so as a result cAMP serves to regulate glucose, fats and glycogen.
cAMP activates hormone sensitive lipase, an enzyme which breaks down fat (lypolysis). This increased breaking down of fat, increases free fatty acids (FFAs), which can then be converted in the liver to the ketones acetoacetate and β-hydroxybuterate.
Final Thoughts…
While this is a small study, the data supports that a few cups of regular, unsweetened coffee (without any butter or coconut oil added) increases the amount of ketones produced for several hours.
If you are following a low carb diet and are monitoring your blood or urine ketones, be aware that having coffee can increase the amount of ketones your body is producing.
Vandenberghe C, St-Pierre V, Courchesne-Loye A, et al, Caffeine intake increases plasma ketones: an acute metabolic study in humans, Canadian Journal of Physiology and Pharmacology,2017, Vol. 95, No. 4 : pp. 455-458
Dr. David Perlmutter, MD (www.drperlmutter.com/caffeine-ketosis-friend-or-foe)
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
When people think of “fasting” what comes to mind is an almost-intolerable short period of time without food, and with nothing to drink (except maybe water) and where people usually spend most of the time counting until they can eat again. This is the case when we are used to burning carbs as our fuel source and then just stop eating. Our body slows its metabolism in response to the severe calorie restriction in an effort to spare energy. We feel cold, tired, lethargic and we find it difficult to concentrate because our body is in starvation mode.
When we are fat-adapted, we use the fat in our diet (dietary fat) and our own fat stores (endogenous fat) as our fuel source. When we “fast”, we stop supplying our body with dietary fat, so our body relies solely on our fat stores to supply its energy needs. Most of us who are following a low carb high fat diet have plenty of endogenous fat, so when we aren’t eating, we don’t feel hungry, tired or cold because our body has a plentiful source of energy! Our basal metabolism doesn’t drop. Rather than feeling cold and tired and finding it difficult to think, we are able to think clearly using ketones produced from fat to fuel our body, rather than glucose.
“Intermittent fasting” is simply increasing the amount of time between meals. Fasting is not eating or rather, not eating now. It’s different than “starving” because our basal metabolic rate is being maintained through our fat stores. When we are in starvation mode, our basal metabolism drops significantly in order to spare energy – that’s why we feel cold and tired, because our body is saving calories for our brain and our heart to function. Fasting also doesn’t mean that we can’t consume anything! There are plenty of things we can have during the delay before our next meal. The most natural “intermittent fast” is the one between after supper and breakfast the next morning. Yes, that is why it is called “breakfast”.
Why Fast?
When we eat, insulin is released in response to the presence of carbs in the food we eat and functions to (a) move glucose out of the blood and to (b) store the glucose that is not immediately needed for energy, as fat.
When we are accustomed (as most of us have been) to eating three meals a day plus having a couple of snacks, insulin is released every few hours. If we have been “grazing”, we have been constantly releasing insulin. As a result of this, our cells have become insensitive to insulin – something known as “insulin resistance“, or insulin tolerant. To conceptualize this, think of going into a room with loud music. At first your ears buzz and your auditory system is overwhelmed, but after a bit of time, your body adapts. It’s similar with smell. When you’re exposed to a pungent odor, at first that’s all your can concentrate on, but after time passes, your brain starts to “tune out” the signals from your nose and you become less aware of the smell. It’s not that the odor decreases, but our response to the odor, decreases as we become “tolerant” to that molecule bound to our olfactory receptors.
The difference with “insulin resistance” is that it is more than our body becoming “tolerant” of the circulating insulin, it actually responds less to it.
Think of someone that drinks considerable amounts of alcohol. They can have 3 or 4 drinks and not feel intoxicated, because they have a “high tolerance” to the ethanol in the drink. It takes more and more alcohol for them to respond. When someone is “insulin tolerant” (also called “insulin resistant”), the same amount of insulin has less and less effect, so to adapt, to be able to move the glucose out of the blood and store the excess energy as fat, the body needs to release more and more insulin. From years and years of eating 3 carb-based meals plus a couple of carb-laden snacks each day, our insulin levels simply don’t fall to baseline.
When someone is not insulin resistant, delaying the time before the next meal enables their insulin levels to fall to baseline (10-30 pMol) in approximately 12 hours, so if they don’t eat anything after dinner and their first meal of the day is breakfast the next morning, that time period is usually close to 12 hours. However, for people who are insulin resistant, a longer time period is often needed for their insulin levels to fall to baseline. Just as insulin resistance developed over time, gradually, a new lower baseline can be set over time by increasing the length of time that one intermittently fasts.
Twelve-Hour Fast
A twelve-hour fast is the easiest one for most people to do, because during most of it, they’re asleep!
This is the one I suggest to my clients once they’re fat-adapted (usually after ~4 weeks of eating low carb high fat) as all it entails is not eating anything after supper until breakfast the next morning.
That’s it.
So, say they finish dinner at 6:30 PM, then the next time they eat is breakfast the next morning at 6:30 AM. This simple, short 12-hour “fast” is just enough to enable their insulin to fall to baseline. Doing this often, if not daily is the goal. This is entirely do-able and an important first step in restoring insulin sensitivity and it is certainly not something “radical”. Years ago, people didn’t eat after supper!
People who have Type 2 Diabetes should check with their doctor before beginning doing any form of Intermittent Fasting – and definitely should do so if they are on any kind of medication to manage their blood sugar, blood pressure or cholesterol, without having their doctors oversee it. Medication will often need to be adjusted downward (and sometimes eventually discontinued entirely) as insulin sensitivity returns, so don’t do this without involving your doctor, first!
Eighteen Hour Fast
Once people have become used to not eating from supper until breakfast, they may want to wait to eat their first meal until noon the next day, especially if they don’t feel particularly hungry in the morning. Some people are not “breakfast” people and if they eat well the night before, they may not want to eat in the morning. An eighteen hour “fast” is from after someone has finished dinner (say, at 6:00 PM) until noon the next day.
Many do want their cup of coffee, which is totally fine provided it is unsweetened. I don’t recommend that people use sugar substitutes, especially the sugar alcohols such as sorbitol, mannitol or xylitol which have the same number of carbs per teaspoon as ordinary table sugar.
Cream can certainly be added to drip coffee and there’s no need to give up your morning latte or cappuccino – just a little creativity to replace the milk (which has almost as many carbs per cup as a slice of bread!).
My trick is to foam 1/2 an ounce of cream with an ounce or ounce and a half of cold, filtered water.
This makes fasting until lunch entirely possible!!
Twenty-four Hour Fast
Note: I don’t do these and I don’t recommend that my clients do these unless they are being very closely monitored by their doctor, however I want to describe them, so people know what they are.
A twenty-four hour “fast” is from the end of supper one day, until the start of supper the following day (technically it is a 23-hour fast unless you add the extra hour ). As with the eighteen-hour fast, one can have unsweetened coffee or tea with a drop of cream, club soda (seltzer) with a twist of lime or lemon, or “bone broth”. “Bone broth” can be made from any kind of meat, fish or poultry bones, but for me, when I think of “bone broth”, I think of a wonderful, rich broth made from beef marrow bones, that is gently simmered overnight on the stove, ready to be sipped as desired, on a fast day.
To avoid getting constipated, many people will take psillium fiber with water each morning and which can be added to cups of “bone broth” or dissolved in a little bit of diluted coconut milk.
What’s not to love about sipping this when “fasting”?
The main purpose of delaying the time between meals (“intermittent fasting”) is to restore insulin sensitivity. When we aren’t eating, we aren’t releasing insulin – and as we continue eating low carb high fat and delaying the time between meals, our insulin receptors become sensitive to insulin once again.
Normalized blood sugar levels (both fasting blood glucose and HbA1C) is a natural byproduct, not the goal. The goal is releasing less and less insulin in response to the food we eat and our body’s sensitivity to the insulin that we do release, being restored.
Weight loss is another added benefit!
Have questions about how I can help you? Please send me a note using the “Contact Us” form on the tab above.
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
Changing how and what we eat, as well as managing stress and getting enough restful sleep has been shown in research studies to reduce pain and symptoms in people with chronic inflammatory diseases such as Rheumatoid Arthritis, Fibromyalgia, Hashimoto’s Hypothyroidism, Celiac disease, etc.. As well, there is increasing evidence that cardiovascular disease, including heart attack and stroke are inflammatory in nature and that lowering risk is best managed through dietary and lifestyle changes. For those with a strong family history of heart disease, the Anti-Inflammatory Protocol dove-tails perfectly with a low-carb high healthy fat diet.
Knowing which foods promote inflammation and why and which foods are evidence-based to have anti-inflammatory properties and why is essential for those seeking to reduce pain and symptoms associated with a chronic inflammatory condition. Choosing foods that are nutrient dense, promote gut health, address diet-related disruptions in hormone-regulation and that target immune system regulation are key in the Anti-Inflammatory Protocol.
Nutrient density — Every system in the body, including the immune system requires an array of vitamins, minerals, antioxidants, essential fatty acids, and amino acids to function normally. Micronutrient deficiencies and imbalances are considered key players in the development and progression of autoimmune disease, therefor attention is put on consuming the most nutrient-dense foods available. A nutrient-dense diet provides the building blocks’ that the body needs to heal damaged tissues. The goal is to supply the body with a surplus of micronutrients to correct both deficiencies and imbalances, supporting regulation of the immune system, hormone and neurotransmitter production.
Gut health — It is thought that gut dysbiosis’ (gut microbial imbalance) and leaky gut’ may be key facilitators in the development of autoimmune disease. The foods recommended on the Anti-inflammatory Protocol support the growth of healthy levels and a healthy variety of gut microorganisms. Foods that irritate or damage the lining of the gut are avoided, while foods that help restore gut barrier function and promote healing are encouraged.
Diet-related Disruptions in hormone regulation – What we eat, when we eat, and how much we eat affects a variety of hormones that interact with the immune system. Eating foods with too much sugar or grazing’ throughout the day, rather than eating food at set meals spaced apart deregulate these hormones. As a result, the immune system is typically stimulated. Promoting regulation of these hormones through diet, in turn has a modulating effect on the immune system. As well, dietary hormones that impact the immune system are also profoundly affected by how much sleep we get, how much and what kinds of activity we do, and how well we reduce and manage stress, so looking at diet and lifestyle together, is key.
Immune system regulation — Our intestines are home to millions of bacteria which live in symbiotic relationship with us. We provide food for them and when in balance, they maintain the integrity of the gut wall, which serves as a protective barrier. When our gut ‘flora’ gets out of balance, having an excess of pathogenic bacteria, this protective barrier becomes compromised, resulting in small ‘holes’ that permit exchange between the inside of our gut and the blood stream. This is what is called “leaky gut“. Endotoxins produced by the proliferation of “bad” bacteria can get into the blood stream, stimulating the immune system, and resulting in systemic inflammation. What becomes critical is to limit the factors that contribute to excess of the “bad bacteria” and restore a healthy amount and diversity of ”good” gut microorganisms, so that the gut once again functions as a protective barrier, and immune system regulation is achieved.
What is the Anti-Inflammatory Protocol?
The Anti-Inflammatory Protocol identifies foods that promote inflammation from those that research indicates have anti-inflammatory properties. It isn’t simply a list of “eat this” and “don’t eat that”, but explains what about a particular food promotes inflammation or inhibits it. It explains the role of key inflammatory -producing compounds such as lectins, saponins and protease inhibitors, and which foods they are found in, and how eating those foods contribute to “leaky gut”. Which grains can one eat? Which should be avoided? What about beans and lentils? Are there some better than others?
The Anti-Inflammatory Protocol explains which healthy cooking and eating fats won’t contribute to the production of Advanced Glycation End-Products (AGEs) – and how this compound causes oxidative damage to the cells in the body. Knowing this enables people to know whether oils such as grapeseed for example, are a good choice and if not, why – as well as which other oils would be preferable.
I want people to understand in simple terms how omega 6 (ρ‰-6) fats compete for binding sites and elongation enzymes with omega 3 (ρ‰-3) fats, as this enables them to determine whether foods such as nuts and seeds should be included in an anti-inflammatory diet. If they understand the role of hormones such as insulin and what causes it’s release, they can determine for themselves whether products like agave syrup or coconut sugar are preferable to table sugar when following an anti-inflammatory protocol. I find that once people understand the theory as to why they should eat less of certain foods (explained in ways that don’t require an educational background in science!) and they also understand which types of foods they should aim to eat more of, they are empowered to make dietary choices that contribute to reducing inflammation, as well as symptoms, along with risk factors for other inflammation-related conditions.
I consider my primary role is as an educator. I don’t want to tell someone they need to eat this food on this day and this other food on the next day. It is far more rewarding and helpful to them, if I help them know how to make these decisions themselves.
Want to know more? Why not send me a note using the “Contact Us” form above.
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
INTRO: There are a number of tools available for measuring insulin resistance, most of which are more suited to a research setting, including the Quantitative Insulin Sensitivity Check Index (QUICKI) and the Matsuda Index. Others, such as the McAuley -, Belfiore -, Cederholm -, Avignon – and Stumvoll Index are better suited for epidemiological (population) research studies and are often compared to the ”gold standard” for the measurement of insulin sensitivity, the Hyperinsulinemic Euglycemic Clamp (HEC).
The homeostasis model assessment (HOMA-IR) method is suitable for individuals to use with their doctors or Dietitians to assess insulin resistance, and is useful for using over time to measure the impact of dietary and lifestyle changes in lowering insulin resistance.
Visualizing Insulin Resistance
Insulin resistance can be determined by measuring insulin response to a standard glucose load over a 5 hour period and plotting the Insulin Response curves – which is precisely what Dr. Joseph R. Kraft MD, who was Chairman of the Department of Clinical Pathology and Nuclear Medicine, St. Joseph Hospital, Chicago, until his retirement.
Dr. Kraft spent more than a quarter century devoted to the study of glucose metabolism and blood insulin levels – collecting data in almost 15,000 people, aged 3 to 90 years old. Between 1972 and 1998, Dr. Kraft measured the Insulin Response and data from 10,829 of these subjects indicated that 75% of subjects were insulin resistant.
Compiling this data, five distinct Insulin Response Patterns emerged.
Pattern I
The light green curve below, is what a normal insulin response should look like. Insulin levels should rise steadily in the first 45 minutes (in response to the standard glucose load) to no higher than ~60 mIU/L (430.5 pmol/L) and then decrease steadily until baseline by 3 hours.
PATTERN II
People who are in the early stages of insulin resistance (Pattern II, represented by the yellow curve) release considerably more insulin in response to the exact same glucose load. Insulin levels rise to ~ 115 mIU/L (825 pmol/L) in the first hour and then take considerably longer (5 hrs) to drop back down to baseline, than the normal response.
PATTERN III
People who have progressed in insulin resistance to Pattern III have insulin levels that keep rising for the first 2 hours and then drop off more sharply, back down to baseline.
PATTERN IV
Those with Type 2 Diabetes / very high insulin resistance (Pattern IV) release huge amounts of insulin almost immediately, reaching levels of ~ 150 mIU/L (1076 pmol/L) at 1 hour. Then for the next 2 hours, insulin continues to climb, before it begins to decline to baseline. Even at 5 hours, insulin levels never decrease to normal values.
PATTERN V
Is what is seen in Type I Diabetes (T1D), when there is insufficient insulin production.
While a 5 hour glucose tolerance test is not available at most labs, a 2 hour glucose tolerance test (2hrGTT) will indicate whether or not a person is insulin resistant or Type 2 Diabetic.
However, once a person is already diagnosed as Type 2 Diabetic, most medical plans will not cover the cost of having the test re-performed in order to determine if insulin response has changed in response to diet and lifestyle changes.
This is where the the homeostasis model assessment of insulin resistance (HOMA-IR) comes in – a tool easily used by clinicians and relying on standard blood tests.
Homeostasis model assessment of insulin resistance (HOMA1-IR) – Matthew’s Equations (1985)
The homeostasis model assessment was first developed in 1985 by David Matthews et al and is method used which quantifies insulin resistance and β-cell function of the pancreas from fasting blood glucose and either fasting insulin or C-peptide concentrations.
Pancreatic β-cells are responsible for insulin secretion in response to increasing glucose concentrations, so when there is decreased function of the pancreas’ β-cells, there will be a reduced response of β-cell to glucose-stimulated insulin secretion.
In addition, glucose concentrations are regulated by insulin-mediated glucose production in the liver, so insulin resistance is reflected by reduced suppression of hepatic glucose production, stemming from the effect of insulin.
The HOMA-IR model describes this glucose-insulin homeostasis using a simple equation, based on fasting blood glucose and fasting insulin. The equation uses the product of fasting plasma insulin (FPI) x fasting plasma glucose (FPI), divided by a constant of 22.5, providing an index of hepatic insulin resistance:
HOMA1-IR = FPI (mu/I) x FBG (mmol/L) / 22.5
The “Blood Code” book is based on these 1985 equations. The problem with the Matthew’s Equations is that they underestimate Insulin Sensitivity (%S) and overestimate % β-cell function.
Homeostasis model assessment of insulin resistance (HOMA2-IR)
Oxford University, Centre for Diabetes, Endocrinology and Metabolism in the UK, has designed a HOMA2-IR model (2013) that estimates β-cell function (%B) and insulin sensitivity (%S) for an individual from simultaneously measured fasting plasma glucose (FPG) and fasting plasma insulin (FPI) values. It also can be used with fasting specific insulin or C-peptide values, instead of fasting RIA insulin.
It is important to note that HOMA-IR values vary by ethnic group, but looking at humans as one, a normal HOMA-IR value for a healthy person ranges from 0.5-1.4
Less than 1.0 means you are insulin-sensitive which is optimal.
While these tools are primarily used by clinicians, knowing about them is useful in being proactive in managing one’s own health. For example, if you have already started making the dietary and lifestyle changes to lower insulin resistance, having your fasting insulin measured along with your fasting blood glucose, will enable your doctor or myself to calculate your progress, as well as recommend adjustments in your plan.
Have questions?
Why not send me a note using the “Contact Us” form at the top of this web page.
Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
The hormone insulin plays a number of roles, one of which is to help move the glucose that is produced from the digestion of food – from the blood and into the cells for energy. Insulin resistance is where the body isn’t responding to insulin’s signals to take up glucose, so blood glucose remains high, despite normal or high levels of insulin.
Type 2 Diabetes (T2D) is essentially a state of very high insulin resistance.
Insulin normally goes up when we eat foods that contain carbohydrate (breads, pasta, rice, fruit, milk products, etc.) and acts on the liver to help store the incoming food energy – first as glycogen and when liver and muscle glycogen stores are “full”, it acts to store the excess energy as fat (de novo lipogenesis).
When we haven’t eaten for a while or are sleeping, the hormone glucagon acts to break down the glycogen in our muscles and liver (glycogenolysis) in order to supply our brain and cells with glucose. Insulin acts to inhibit glucagon’s action, which signals the body to stop making new glucose from its glycogen stores. When our glycogen stores run out (such as when we are fasting), the body turns to non-carbohydrate sources such as fat to make the glucose it needs for essential functions (gluconeogenesis).
When we are insulin resistant, insulin continues to act on the liver to signal it to store energy. When glycogen stores are “full”, it stores the excess energy as fat. When fat stores are “full”, the body starts storing the excess fat that the liver keeps making, inside the liver itself. There shouldn’t be fat in the liver, but when we are insulin resistant, such as in Type 2 Diabetes excess fat gets stored in the liver in a condition known as “fatty liver disease”.
In insulin resistance, the liver becomes more sensitive to insulin’s signal to make fat (and as a result keeps making more and more fat) yet at the same time, the liver becomes less sensitive to insulin’s inhibition of glucagon – resulting in more and more glucose being produced and released in the blood.
High levels of glucose remain in the blood despite adequate insulin, and it is this high level of blood glucose that is the hallmark symptom of Type 2 Diabetes. For the same quantity of insulin released, the body moves less and less glucose into the cell.
What does the body do to compensate? It makes more insulin!
KEY POINT: Insulin resistance results in the increased production of insulin. Increasing blood sugar CAN a symptom, caused by the insulin resistance, but blood glucose can be normal and one can still be insulin resistant (see Featured Article on Insulin Resistance).
When we are insulin resistant and keep eating a carb-based diet, the body requires more and more insulin in order to move the same amount of glucose into the cell.
The main issue then becomes too much insulin (hyperinsulinemia).
Defining the Problem Defines the Treatment
In Type 2 Diabetes (which is in essence, very high insulin resistance), the symptom is high levels of glucose in the blood. That is not the cause. It is the symptom.
High levels of glucose in the blood resulting from uncontrolled Type 2 Diabetes, results in proteins in the body becoming “glycosylated”. Glucose, is a highly reactive molecule and easily accepts (or “shares”) electrons from other molecules – especially from the amino acid Lysine, which is found in virtually every protein in the body. When Lysine and glucose share an electron, it creates an irreversible chemical bond between the glucose molecule and the protein – and that protein is said to have become glycosylated. It is this glycosylation that lies behind the complications found in Diabetes.
To reduce the glucose in the blood and the glycosylation of the body’s proteins, current treatment for Type 2 Diabetes involves medications that move glucose from the blood into the cells. This doesn’t really remove the excess glucose from the body, it simply moves it to a different location in the body. While these medications can be very helpful in the short term (until people begin to address the underlying dietary causes), over time these medications become less and less effective at removing glucose from the blood. In a sense, we become “medication resistant”, so additional medications are added. Once the various combinations of medications loose their effectiveness, people with Type 2 Diabetes are prescribed insulin as a treatment – because insulin moves excess glucose into the cells. But the cells are already overflowing with too much glucose!
Insulin is added as a treatment when the body is already producing too much insulin. The problem is the cells aren’t responding to the signal from insulin. The body doesn’t need more insulin – it needs the cells that are sensitive to respond to insulin’s signal.
Diabetes as a “chronic, progressive disease”
Type 2 Diabetes is described as a “chronic, progressive disease” because with current medication treatment, people eventually get worse. When they no longer respond to the initial medications prescribed that help move excess glucose from the blood into the cells, they are prescribed insulin which they take by injection – in order to force more glucose into already over-full cells. While people’s blood glucose gets better (i.e. the symptom improves), they gain weight as a result of the insulin injections and develop complications such as heart disease, stroke, kidney disease, blindness etc..
In the end, they don’t get better, but worse, fulfilling the belief that T2D is a chronic, progressive disease.
Redefining the Problem, Redefines the Solution
Rather than looking at the symptom (high blood glucose) as something that needs to be “fixed” with medications and later with insulin (when the medications are no longer effective), when we define insulin resistance and Type 2 Diabetes as a problem of excess insulin, we approach addressing the problem differently.
By changing what we eat, we can lower the amount of glucose in the body, which in turn causes the body to produce less insulin. With less insulin being produced, the cells begin to respond to normal amounts of insulin – reversing insulin resistance and yes, reversing the symptoms of Type 2 Diabetes.
Eating a low carb high fat diet and extending the amount of time between meals (intermittent fasting) lowers the production of insulin, resulting in the cells become more sensitive to its signal. Rather than addressing the symptom (which is high blood glucose) we are addressing the problem of too much insulin.
Have questions? Would like to know how I could help you?
Why not send me a note using the “Contact Us” form on the tab above.
In Part 2, I will explain how insulin resistance is measured and how we can track insulin sensitivity returning, as we continue to eat a low carb diet and increase the time between meals.
The hormone insulin (involved in storing fat) and leptin (involved in burning fat) work very differently in lean people than in overweight people. This is why excess fat such as is found in “bullet proof coffee” or “fat bombs” results in overweight (or obese) people that follow a Low Carb High Fat diet gaining weight—whereas lean people will simply burn it off. This article explains the role of these hormones and how they impact lean people and overweight people very differently.
When we eat, the hormone insulin is released which signals our body to do two things; (1) it tells our cells to uptake energy (in the form of glucose) and (2) to store excess energy as fat. Insulin is the major driver of weight gain. If we are lean, when we eat more than usual and increase our body fat stores, the body responds by increasing secretion of a hormone called leptin. Leptin acts as a negative feedback loop on the hypothalamus area of our brain, reducing our hunger, causing us to eat less and preventing us from gaining too much fat.
The problem occurs when we become insulin resistant.
Insulin Resistance
When we eat a diet that is high in carbs and we eat every few hours(3 meals plus snacks), insulin is released each time we eat (in order to cause our cells to take in energy and store the excess as fat). If we continue to eat this way, over time our body is inundated with insulin, so it sends signals to down-regulate the insulin receptors, making our cells less sensitive to insulin signals. This is called insulin resistance. When we are insulin resistant, our body releases more and more insulin to deal with the same amount of glucose in the blood.
Leptin Resistance
Consistently having high levels of insulin, will also keep stimulating the release of leptin, which normally results in us becoming less hungry and eating less. However, when we are insulin resistant, we keep producing more and more insulin, which results in us producing more and more leptin. Over time, this consistently high leptin level will result in the same type of down-regulation of hormonal receptors that occurred with insulin, resulting in leptin resistance.
Leptin resistance interferes with the negative feed back loop on our hypothalamus which normally reduces our hunger, causing us to eat less. When we are leptin resistance, even when we’ve eaten a great deal of food, we don’t feel satiated — even when our abdomens are straining from feeling full. As a result, we just keep eating, as if there is no “off” switch.
It is this leptin resistance that results in obesity.
Obese people aren’t obese because they lack will-power, but because their body is responding to signals from very powerful hormones produced in response to the types of foods they eat.
Difference between a High Carb Diet and a High Fat Diet
When people consume diets high in carbs it stimulates insulin to be released. In response to all the insulin, energy that is not immediately needed for activity is stored as glycogen in the liver and muscle cells, and the remainder is shipped off to our adipose cells (fat cells), to be stored as fat. When eating a high carb diet, getting excess calories into fat cells is easy, getting the fat out of fat cells, not so much.
When people eat a diet high in fat and low in carbs, the fat is absorbed in the intestines as chylomicrons and is shuttled through the lymphatic system to the thoracic duct, going directly into the blood circulation. From there, the fat is either burned for energy or goes into our fat cells, to be stored. It is important to note that the fat does NOT go to the portal circulation of the liver and as a result, fat needs no help frominsulinto be absorbed.
That’s good, but if excess fat gets stored in fat cells, doesn’t eating fat make one fat?
Not for lean people, because lean people are leptin sensitive and obese people are leptin resistant. When overweight or obese people eat excess fat, it is a different matter.
Lean People versus Obese People
If a lean person eats a diet high in fat and low in carbs, the excess fat will be stored in fat cells, but insulin does not go up. So a lean person does not become insulin resistant, as described above. As their fat mass goes up, leptin also goes up. Since the lean person is sensitive to leptin, the negative feedback loop acts on the brain causing them to stop eating, allowing their body weight to go back down. Even if a lean person deliberately eats more and more fat when they aren’t hungry, what happens is their body’s metabolism goes up, and they burn off the extra calories.
If an overweight or obese person eats a diet high in fat andlow in carbs with moderate amounts of protein, insulin levels don’t go up — which is good of course, however from years of eating high carb low fat diets and from eating a carb rich foods every few hours, overweight and obese people are insulin resistant. This means that their blood glucose levels remain high for long periods after they’ve eaten and as importantly, it also means that they are also leptin resistant. In this case, if they eat too much fat – such as drinking “bullet-proof coffee” or having “fat bombs”, they will respond (as the lean person does) by making more leptin, but the problem is, they are not sensitive to leptin! Their brain doesn’t respond to the signals from leptin, so when an obese or overweight person eats excess fat, beyond that which is naturally found in a low carb high fat foods, their appetite doesn’t drop – nor does their metabolism go up to burn off the excess fat being stored in fat cells. They simply get fatter.
Weight Loss
For those that are overweight or obese and insulin resistant, it is important to keep in mind that with insulin resistance comes leptin resistance. Leptin resistance by definition means that the signals to stop eating don’t work. The “off switch” is defective. As well, the body doesn’t respond to signals from leptin to up-regulate metabolism, so when an overweight or obese person on a low carb diet eats too much fat, they gain weight.
Since increasing carbs is not an option and increasing protein results in glucose being synthesized from the excess (gluconeogenesis), the way to lower insulin resistance (and thus leptin resistance) is by extending the amount of time between meals. This is known as intermittent fasting – a topic that will be covered in a future article.
Have questions?
Want to know how I can help you get started on a low carb high healthy fat diet? Please drop me a note using the “Contact Us” form, located on the tab above.
Ebbeling CB, Swain JF, Feldman HA, et al. Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study. JAMA”¯: The journal of the American Medical Association. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.
Feinman RD, Fine EJ (2003) Thermodynamics and metabolic advantage of weight loss diets. Metabolic Syndrome and Related Disorders, 1:209-219.
Many people who are accustomed to eating a carb-based diet, restrict their salt intake to avoid blood pressure, but when eating low carb high fat, there is the need to add salt to replace sodium right from the beginning. That is how “keto-water” came to be.
When eating low carb and when intermittent fasting (extending the amount of time between meals) insulin levels fall, and with it so does the kidney’s retention of sodium (salt). The kidneys excrete sodium in a process called naturesis so replacing the missing sodium is important. Sodium and potassium (as well as calcium andmagnesium) are used in pairs in a number of systems in the body, so when the kidneys ‘dump’ a lot of sodium, potassium is soon excreted too, in order to balance the two electrolytes. If someone on a low carb diet doesn’t supplement sodium soon enough, their potassium levels could fall too low as a result, which may cause them to have excruciating headaches and/or irregular heart beat (heart palpitations).
It is fairly difficult to meet the Dietary Reference Intake for potassium on a conventional carb-based diet, but on a low-carb diet – even with a very high non-starchy vegetable intake, it is still challenging as many of the good sources of potassium, such as potato and yams are not part of a low carb high fat diet. Mushrooms and avocado are some of the best sources, so include those foods often.
To be sure to get sufficient sodium and potassium, I make what I call ”keto-water”.
NOTE: People with kidney disease (e.g. CKD) must avoid any salt substitutes or half-salts with potassium. Those taking blood pressure medication such as Ramipril have increased potassium retention and should also not use half-salts containing potassium.
”KETO-WATER”
Keto-water is 1 liter of club soda / seltzer to which 1/8 tsp of “half salt” has been added.
“Half salt” is a half-sodium / half-potassium salt that is sold under a number of brand names, including “Nu Salt” and “no Salt”.
I add a tiny twist of lime or lemon to round out the taste and also to add a source of Vitamin C and voila, ”keto-water”!
Unless it is particularly hot out, or one’s needs are increased because they are exercising or have a fever, two liters a day of ”keto-water” is probably sufficient for most people.
Keep in mind that drinking keto-water will result in your body retaining more water along with the sodium, so it may appear as if your ‘weight went up’, but it is only the natural water retention that occurs (and is supposed to occur) when your body has sufficient electrolytes. Remember, weight form most people can fluctuate by as much as 4 – 4 1/2 pounds per day solely from the natural fluctuation in body water, so don’t weigh yourself too much. I recommend a maximum of once a week, on the same day and at the same time. When you are replacing the body’s necessary electrolytes (such as sodium and potassium), it is better to judge fat loss by loss of inches around various parts of your body (mid-arm, mid-thigh, neck, abdomen) than by the scale. Even easier, go by how your clothes feel!
Please don’t restrict sodium when eating low-carb for the sake of a number on the scale! Your body needs the sodium and potassium to function properly.
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I have found that people wanting to lose weight simply don’t want to weigh or measure food or count calories – and who can blame them! I design Meal Plans for my clients so they don’t need to. As I will explain in this article, with a Standard Meal Plan (based on a traditional macronutrient distribution), carbohydrate, protein and fat are all laid out, based on the food exchanges. With a Low Carb High Healthy Fat Meal Plan or a Hybrid Meal Plan, carbohydrate percent, protein- and fat percent are also laid out, but for those seeking to lower insulin resistance or lose weight or both, tracking carb intake is important. In this article, I’ll explain tracking carbs.
Firstly, what is a Meal Plan?
A Meal Plan isn’t a “menu” that tells you what foods you have to eat, but indicates how many servings of each category of food you should aim to eat at each meal. I explain more about what a food category is, below.
The first step in designing a person’s Meal Plan after I’ve done their assessment, is to determine their overall caloric needs based on age, gender, activity level, desired weight loss (or gain), as well as any special considerations such as growth, weight loss, pregnancy or lactation, etc.
More about calories in the next article, but suffice to say here, calories are generally not the focus in Low Carb High Healthy Fat eating, carbs are.
The next step is to set the macronutrient distribution (% of calories from carbohydrate, protein and fat) of the Meal Plan according to what would best suit the person’s clinical needs, goals and lifestyle. This is something I discuss with people during the assessment, and which is ultimately up to them. The Standard macronutrient distribution is ~45-65% carbohydrate, ~15-20% protein and ~30% fat. Generally speaking, unless there is a compelling clinical reason for using a Standard Meal Plan, I encourage people to consider the benefits of a low carb high healthy fat eating.
The Low Carb High Healthy Fat macronutrient distribution is ~5-10% carbohydrate, ~20% protein and ~65-70% healthy fat, with the Hybrid macronutrient distribution falling somewhere in between.
In the final step, I design a person’s Meal Plan based on the foods that they’ve told me they like, avoiding those they don’t, and factoring in the time of day they either need to (for scheduling reasons) or prefer to eat. Then we meet for me to go over their Meal Plan with them, and for me to teach them how to easily and accurately estimate their portion sizes, using visual measures. More on visual measures, below.
The only thing left for them to decide is what they want to eat!
Food Categories – Standard Meal Plan
In a Standard Meal Plan or Hybrid, categories include Starchy Vegetables and Grains, Fruit, Non-Starchy Vegetables, Meat, Poultry, Meat and Egg or Cheese, and Legumes (pulses). These categories are based on how many grams of carbs are contained in the foods in make up that category.
Take, for example, the Starchy Vegetable and Grain Category. This group includes all the standard “carbs” such as bread, pasta, rice and cereals as well as “starchy vegetables” such as peas, corn, potatoes, sweet potatoes / yams and winter squash (such as acorn or butternut squash). All foods in this category have 15 gm of carbs per serving (where a serving is 1/2 cup or the equivalent of 1 slice of bread).
So, 1 slice of bread has 15 gms of carb, 1/2 cup of peas has 15 gms of carb, 1/2 cup of rice has 15 gms of carb, 1/2 cup of oatmeal has 15 gms of carb, and 1/2 a hamburger bun has 15 gms of carb.
If a person’s Meal Plan indicates that they can have 2 servings from the Starchy Vegetable and Grain category, that could be 2 pieces of toast, or 1 cup of oatmeal, or 1 cup rice, etc. Their Meal Plan doesn’t tell them what food they have to eat, just how much from each category.
Here is an example of what a Standard Meal Plan looks like;
As you can see, all the calculations have been done.
In this example, this Meal Plan was for an 85 year old man who wanted to gain weight and was based on 45% of his calories coming from carbs, 21% from fat and 34% from fat.
Estimating Portion Sizes
When I’ve taught someone to accurately estimate their serving sizes using visual measures, the amount of macronutrients (carbs, protein, fat and calories) they will take in following their Meal Plan will be what was planned.
What are Visual Measures?
Visual measures are easy and accurate means to estimate serving sizes. For in-person clients, this might be based on the size of their hand or fingers, such as (depending on the size of a person’s hand) a 1/2 a cup (dry measure) may be the amount of something round (like frozen peas) that could be contained in their scooped hand, without rolling out. An ounce (by weight) might be the size of two specific fingers on their hand, or a Tbsp may be the amount of the last digit on their thumb. For Distance Consultation clients, the standard used in teaching visual measures are standard size items, such as the size of a golf ball or four dice stacked up.
Tracking Carbohydrates
Where tracking carbohydrates comes into play is with Low Carb High Healthy Fat Meal Plan or a Hybrid Meal Plan – especially when lowering insulin levels or losing weight is desired. Keeping track of carbohydrates on these kind of Meal Plans is nothing like needing to count calories! It is very easy.
On a Low Carb High Healthy Fat Meal Plans, the macronutrient distribution for carbs is set quite tightly. For men, total carbs would be somewhere between 80-100 grams and for women, it may be set as low as 35 gms carb or as high as 50 gms. It depends on their needs. Naturally, Hybrid Meal Plans will have higher total daily carbs.
Since there are no Starchy Vegetables and Grains and Milk on these Meal Plans (cheese is used, just not milk due to the carb content), the Food Categories on a Low Carb Meal Plan or Hybrid are different than on a Standard (or traditional) Meal Plan).
Food Categories in a Low Carb Meal Plan include Non-Starchy Vegetables, which exclude “Starchy Vegetables” such as peas, corn, potatoes, sweet potatoes / yams and winter squash – with some intake guidelines around root vegetables such as carrots, beets and parsnips. The Fruit category here is specified more narrowly than in a Standard Meal Plan – generally focused on berries and low sugar citrus such as lime and lemon, as well as tomatoes and cucumbers (yes, both are technically ‘fruit’).
Meat, Poultry, Meat and Egg or Cheese is pretty much the same as with a Standard Meal Plan, with an ounce of any of these protein foods being 1 serving and individuals being able to have several servings at each meal (based on their caloric needs, factoring in any weight loss). The fat contained in the Meat, Poultry, Meat and Egg or Cheese is already calculated when the Meal Plan is made, so “Fat” here means added fat. The Fat category includes everything from olive oil, avocado (both the fruit and the oil), coconut oil, butter, olives and nuts and seeds.
Foods in the Meat, Poultry, Meat and Egg or Cheese category have little or no carbs in them and Non-Starchy Vegetables are generally around 5 gm of carb per cup and berries, which are in the Fruit category are roughly 15 gm of carb for 1/2 a cup. A few berries on a salad isn’t usually a problem, but more than that can easily put us over our maximum amount of carbs for the day, which I call the “carb ceiling”.
Where it becomes particularly important to track carbohydrates when one is seeking weight loss is with foods such as nuts and seeds. It is very easy to eat a handful of nuts and end up exceeding one’s daily maximum number of carbs.
“Carb-creep” is when we eat more carbs than we think we are, which results in weight loss slowing, or even stopping. When one reaches a plateau where they haven’t lost any weight for longer than a week or two, then tracking carbs to see if there is carb creep is advised.
A man’s carb limit may be set to 80-100 gms per day and a woman’s may be as low as 35 gms or as high as 50 gms. That is not a lot and it is easy to inadvertently exceed this amount of carbs in the course of a day. A few splashes of milk in several cups of coffee, a handful of peanuts walking by the bowl near the photocopier and an ounce or two of 72% dark chocolate (for heart health, of course!) can quickly put us over our carb ceiling. This is where it’s important to evaluate food choices that may be putting your over your carb ceiling.
Want to know more about having a Meal Plan designed for you?
Please send me a note using the “Contact Us” form above and I will reply to you, usually by the next business day.
A new report released by the Canadian Cancer Society predicts that almost one in two Canadians will be diagnosed with cancer in their lifetime.
“One half” is a very sobering number!
Currently, cancer is the leading cause of death in Canada, accounting for almost 1/3 of all of all deaths (30%).
Heart disease is the second leading cause of death, accounting for 1/5 of all deaths (20%).
In an interview with Peter Goffin of the Toronto Star, Dr. Robert Nuttall, Assistant Director of Health Policy at the Canadian Cancer Society attributed this alarming new statistic that 1/2 will get cancer in their lifetime to the “aging population” – not “lifestyle factors”.
Nutall said;
”The important thing to remember here is that the biggest driver behind this is the aging population. ”Canadians continue to live longer, and cancer is primarily a disease that affects older Canadians.”
Japan has the oldest population in the world, with ~1/3 of people aged over 60.
What do their statistics show?
According to the Institute for Health Metrics and Evaluation, Japan’s leading causes of death (2015) were:
cerebrovascular disease (stroke)
cardiovascular disease (heart disease)
lower respiratory infection
Alzheimer’s disease
Lung cancer was 5th, followed by stomach cancer (6th) and colorectal cancer (7th). In Japan, a country with the oldest population in the world, cancer of any kind wasn’t even in the top four!
Are half of us really going to get cancer because of the “aging population” or is it because of “lifestyle factors”?
Looking at the top 4 Causes of Cancer in Canada:
Lung cancer is the number one form of cancer and the Canadian Cancer Society indicates that more than 85% of lung cancer cases in Canada are related to smoking tobacco.
Colorectal cancer is the second leading cause of cancer and the Canadian Cancer Society indicates that risk factors for colorectal cancer include (a) diet , (b) being overweight, (c) physical inactivity and (d) smoking.
Breast cancer (in both men and women) is the third leading cause of cancer. Apart for personal and family history of breast cancer and other genetic factors, the Canadian Cancer Society list the following known risk factors: (a) exposure to ionizing radiation, (b) use of oral contraceptives (c) alcohol and (d) being obese.
Prostrate cancer which only affects men, is the fourth leading cause of cancer and the only known risk according to the Canadian Cancer Society is family history.
Major Risk Factors for the top 4 Causes of Cancer
Here are the major risk factors for the top four leading causes of cancer in Canada;
smoking
diet
being overweight
physical inactivity
exposure to ionizing radiation (x-rays)
use of oral contraceptives
alcohol
Except for use of x-rays, all of these are lifestyle factors!
Diet, being overweight and being inactive are three things that can be changed easily and sustainably!
A low carb approach can be particularly helpful, as it can not only address being overweight, but new studies have found that a number of cancer cells feed exclusively on glucose. It is thought that a ketogenic lifestyle may play a role in reducing the glucose available for some types of cancer.
We being told that ‘the biggest driver behind the projection that half of us will get cancer in our lifetime is the aging population‘ – when it would seem that the underlying risk factors of these cancers are lifestyle factors.
In fact, the Canadian Cancer Society says themselves that half of the cases are preventable;
“We already know a lot about how to prevent cancer. If we, as a society, put everything we know into practice through healthy lifestyle choices and policies that protect the public, we could prevent about half of all cancers.”
We will all age and this is not preventable, but by addressing lifestyle factors including smoking, diet, overweight and physical inactivity and others, we should be able to prevent almost 1/2 of all cancers.
Have questions on how I can teach you how to eat healthier and work with you to help you tackle being overweight and inactive, then please send me a note using the “Contact Us” form on this web page.
Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/lung/risks/?region=on#ixzz4kZ5AnNz6
Canadian Cancer Society, http://www.cancer.ca/en/about-us/for-media/media-releases/ontario/2011/not-enough-canadians-being-screened-for-colorectal-cancer-leading-to-many-unnecessary-deaths/?region=on#ixzz4kZ5vSGSS
Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/breast/risks/?region=on#ixzz4kZ8RvXbm
Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/prostate/risks/?region=on#ixzz4kZ9J6o64
Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-101/cancer-research/prevention/?region=on#ixzz4kZ9jQJwt
Institute for Health Metrics and Evaluation, http://www.healthdata.org/japan
The Toronto Star, Peter Goffin (Staff Reporter), Tue June 20 2017, https://www.thestar.com/news/gta/2017/06/20/half-of-all-canadians-will-get-cancer-in-their-lifetime.html
As mentioned in the previous article, a new study published Monday, June 12, 2017 in the New England Journal of Medicine analyzed data from 68.5 million adults and children in 195 countries and found that 1/3 of people worldwide are overweight or obese and are at increased risk of chronic disease and death, as a result.
Data from one country, China, stood out among all of them due to record high rates of childhood and adult obesity;
In 2015, China had the highest incidence of obese children in the world (~10%) along with India.
In 2015, China along with the US had the highest incidence of obese adults (>35%).
I wanted to have a look at the Dietary Guidelines for Chinese Residents (Chinese: ä¸å›½å±…民膳食指å—) in the years prior to 2015, to determine how they may have contributed to these high rates of overweight and obesity.
The Food Guide Pagoda
The Chinese Dietary Guidelines, known as the ‘Food Guide Pagoda’ was first published in 1989 and revised in 1997. The 2007 revision was developed in conjunction with a committee from the Chinese Nutrition Society, in association with the Ministry of Health. A new revision came out in 2016.
The 2007 Food Guide Pagoda’ (the one that was in effect at the time the 2015 overweight and obesity statistics came out) was divided into five levels of recommended consumption corresponding to the five Chinese food groups.
Cereals – in the form of rice, corn, bread, noodles, crackers and tubers make up the base of the Pagoda.
Vegetables and Fruits – form the second level of the Pagoda
According to the Chinese Dietary Recommendations, the majority of foods in each meal should be made up of cereals, including rice, corn, bread, noodles, crackers and tubers (such as potatoes), followed by Vegetables and Fruit.
Meat, Poultry, Fish & Seafood and Eggs form the third level, and it is recommended that should be ‘eaten regularly’, but ‘in small quantities’.
Milk & Dairy and Bean & Bean Products – form the fourth level.
Fat, Oil and Salt – form the roof of the Pagoda and are recommended to be eaten in moderation.
Specific Dietary Recommendations (2007-2015)
The main recommendations of the 2007 Chinese Dietary Guidelines were as follows:
Eat a variety of foods, mainly cereals, including appropriate amounts of whole grains.
Consume plenty of vegetables, fruits and tubers (e.g. potato, taro, yam etc.)
Consume milk, beans, or dairy or soybean products every day
Consume appropriate amounts of fish, poultry, eggs and lean meat.
Reduce the amount of cooking oil
Divide the daily food intake among the three meals and choose suitable snacks.
The Results (2005-2015)
1. Leading cause of death
In 2015, heart disease overtook Chronic Obstructive Pulmonary Disease (COPD) as the second leading cause of death, followed by stroke.
In 1990, the leading cause of death in China was Chronic Obstructive Pulmonary Disease (COPD) largely contributed to by smoking, followed by heart disease and diarrhea.
2. Leading cause of premature death
In 2015 as in 2005, stroke was the leading cause of death, followed by heart disease.
3. What caused the most death and disability combined?
In 2015, strokewas leading cause of death in China, followed by heart disease.
Magnitude of the Problem – China compared to the US and Canada
In 2015, for every 100,000 people in China, 2,237 people died from heart disease and 1,672 people died from stroke.
In the US, for every 100,000 people, 457 people died from heart disease and 1,617 died from stroke.
In Canada, for every 100,000 people, 327 people died from heart disease and 1,106 died from stroke.
Rates of stroke in the China and US were quite similar. Both China and the US had the highest number of obese adults (>35%) in the world.
China’s “solution”?
China concluded that “dietary risks drive the most death and disability” – especially stroke and heart disease which were the two leading causes of all forms of death, of premature death and of disability in 2015.
In response to these high rates of stroke and heart disease among Chinese, the Chinese government, with the assistance of the Chinese Nutrition Society produced a revised version of the Chinese Food Pagoda in 2016.
New Dietary Recommendations (2016)
The Chinese have stated that “there have been no significant changes in dietary recommendations” (Wang et al, 2016) when compared with the previous version of the 2007 Food Pagoda and are emphasizing the following recommendations:
Eat a variety of foods, with cereals as the staple – The daily amount of cereals and potatoes consumed for body energy production should be 250—400 g, including 50—150 g of whole grains and mixed beans, and 50—100 g of potatoes. The major characteristic of a balance diet pattern is to eat a variety of foods with cereals as the staple.
Balance eating and exercise to maintain a healthy body weight – this is based on the same “calorie in / calorie out” model that the US and Canadian recommendations have been based on. “Avoiding ingesting excessive food and physical inactivity is the best way to maintain energy balance”.
Consume plenty of vegetables, milk, and soybeans – The daily vegetable intake should be in the range of 300—500 g. Dark vegetables, including spinach, tomato, purple cabbage, pak choy, broccoli, and eggplant, should account for half this amount and should appear in every meal. Fruits should be consumed every day. The daily intake of fresh fruits, excluding fruit juice, should be between 200 and 350 g. A variety of dairy products, equivalent to 300 g of liquid milk, should be consumed per day. Bean products and nuts should be frequently eaten in an appropriate amount for energy and essential oils.
Consume an appropriate amount of fish, poultry, eggs, and lean meat – The consumption of fish, poultry, eggs, and meat should be in moderation. The appropriate weekly intake is set at 280—525 g of fish, 280—525 g of poultry, and 280—350 g of eggs with an accumulated daily intake of 120—200 g on average. Fish and poultry should be chosen preferentially. The yolk should not be discarded when consuming eggs, and less fat and fewer smoked and cured meat products should be eaten.
Final Thoughts…
China now has some of the highest rates of childhood obesity in the world (~10%) and is tied with the US for the highest rate of adult obesity (>35%) yet to address the issue of incredibly high rates of stroke and high rates of heart disease, the 2016 Chinese Dietary Recommendations define a balance diet pattern as a daily adult intake of;
1/2 lb – 1 lb (250-400 gm ) of cereals, grains and potatoes
1/3- 3/4 lb (200 – 350 gm) of fresh fruit
1 1/2 cups of milk
and
1/4 lb – 1/3 lb of fish, poultry or eggs (with meat “in moderation”)
These “new” recommendations seem to be based on the same “calorie in / calorie out” model familiar to us in the West and that fail to take into account how the body compensates on a carbohydrate-based calorie restricted diet diet (see previous blogs).
The Chinese are being told that “the best way to maintain energy balance” (Wang et al, 2016) is to;
exercise more (150 minutes/week plus 6000 steps/day)
eat less fat and animal protein and
consume most of their calories as rice, corn, bread, noodles, crackers and potatoes
Over the last four decades, Americans and Canadians have reduced their fat consumption from ~40% in the 1970’s to ~30%, increased the amount of carbohydrate as whole grains, fruits and vegetables, are consuming low fat milk, eating more fish and drinking less pop and presently, 2/3 of adults considered overweight or obese.
Should we expect different results in China?
If you are looking to achieve a healthy body weight, lower blood sugar, blood pressure and triglycerides, I can help.
I take a low carb high health fat approach and can teach you how to eat well, without weighing or measuring food, or counting “points”.
Want to know more? Send me a note using the “Contact Us” form, on the tab above.
Global Burden of Disease (GBD) 2015 Obesity Collaborators, Health Effects of Overweight and Obesity in 195 Countries over 25 Years, N Engl J Med, DOI: 10.1056/NEJMoa1614362
Global Health Data Exchange (GHDx), http://ghdx.healthdata.org/geography/china
Wang S, Lay S, Yu H, Shen S. Dietary Guidelines for Chinese Residents (2016): comments and comparisons. Journal of Zhejiang University Science B. 2016;17(9):649-656. doi:10.1631/jzus.B1600341.
In the last few years, we’ve heard the term “obesity epidemic“, but a new study published this past Monday, June 12, 2017 in the New England Journal of Medicine seems to indicate that it is now an “obesity pandemic”.
Researchers analyzed data from 68.5 million adults and children in 195 countries to assess (1) the prevalence of overweight and obesity in 2015 and (2) the trends in the prevalence of overweight and obesity between 1980 and 2015.
The “short story” is that a 1/3 of people worldwide are now overweight or obese — put another way, two billion people globally are overweight or obese and are at increased risk of morbidity (chronic diseases) and morbidity (death), as a result.
The Significance
Epidemiological studies (studies of different populations from around the world) have identified high BMI as a risk factor for cardiovascular disease, type 2 Diabetes, hypertension, chronic kidney disease and many types of cancer.
Furthermore, overweight children are at higher risk for the early onset of diseases such as type 2 Diabetes, hypertension and chronic kidney disease.
Body Mass Index (BMI) is the weight in kilograms divided by the square of the height in meters Obesity is defined as having a Body Mass Index (BMI) > 30 kg/(m)2 Overweight is defined as having a BMI between 25 and 29.9 kg/(m)2
Obesity Findings
Data showed that in 2015, there were 603.7 million obese adults worldwide and107.7 million obese children.
The prevalence of obesity has more than doubled in 70 countries since 1980, and there has been a tripling of obesity in youth and young adults in developing, middle class countries such as China, Brazil, and Indonesia.
Worldwide, the prevalence of obesity is now 5% in children and 12% in adults — findings that mirror global trends in type 2 Diabetes.
Most alarming was that in 2015;
high BMI accounted for four million deaths globally
almost 40% of deaths resulting from high BMI occurred in people who were overweight, but not obese
more than 2/3 of deaths related to high BMI were due to cardiovascular disease
Varying Risk
It is important to note that risk of outcomes related to obesity has not been found to be uniform across populations. For example, it has been reported that at any given level of BMI, Asians have been shown to have a higher absolute risk of Diabetes and hypertension, whereas African Americans have a lower risk of cardiovascular disease than other groups.
Addressing the Problem
To address the problem of overweight and obesity both here and around the world, requires correctly identifying its cause and for the last 40 years, excess dietary fat — especially saturated fat has been blamed as the villain and ostensibly responsible for the “obesity epidemic” and resulting “diabetes epidemic”.
But is it?
When one compares the Dietary Recommendations in both Canada and the United States since 1977 to rates of overweight and obesity in both of these countries, it seems apparent that it has been the promotion of diets high in carbohydrate that lies at the root.
In the next article, I’ll take a look at the Dietary Recommendations of the country with the highest rate of childhood obesity and adult obesity in 2015, as well as some of the highest rates of stroke and heart disease per capita, in the world.
How I can help
If you have eaten a ‘low fat diet’ and counted calories (or points) until you are blue in the face and are tired of doing the same thing over and over again, expecting a different outcome, why not drop me a note using the “Contact Us” form, above. I’d be glad to explain how I can help you achieve a healthy body weight, while normalizing your blood sugar, blood pressure and cholesterol levels.
Global Burden of Disease (GBD) 2015 Obesity Collaborators, Health Effects of Overweight and Obesity in 195 Countries over 25 Years, N Engl J Med, DOI: 10.1056/NEJMoa1614362
Gregg EW, Shaw JE, Global Health Effects of Overweight and Obesity, N Engl J Med, doi: 10.1056/NEJMe1706095
Karter AJ, Schillinger D, Adams AS, et al. Elevated rates of diabetes in Pacific Islanders and Asian subgroups: the Diabetes Study of Northern California (DISTANCE). Diabetes Care 2013; 36:574-9
One of the challenges with trying to lose weight is reaching a plateau – where one’s weight stays the same for an extended period of time. When eating a low-carb or ketogenic diet, some foods such as nuts are a common pitfall. Despite being a rich source of heart healthy monounsaturated fats, somenuts contain high amounts of carbohydrate.
Carbs Per Serving of Nuts
Serving Size
A serving size* of nuts is generally considered one ounce (1 oz.) which is about a handful of an ‘average-sized hand’. The problem with using this kind of measurement is that not all nuts have the same mass per volume, nor does everybody have the same size hand!
Here are the number of nuts per ounce for common varieties:
Cashew 16-18 nuts per ounce
Pistachio 45-47 nuts per ounce
Almond 22-24 nuts per ounce
Pine Nuts ~3 Tbsp. (160 kernels) per ounce
Hazelnut 10-12 nuts per ounce
Walnut 8-10 halves per ounce
Peanut 27-29 nuts per ounce
Macadamia 10-12 nuts per ounce
Pecan 16-18 halves per ounce
Brazil Nuts 6-8 nuts per ounce
* When eating shelled nuts, many people eat a few palm fulls, so I’m going to indicate the carbs for a 1 oz and 3 oz serving.
Carbs are listed as “net-carbs” (i.e. once fiber (which is not digestible) has been subtracted from the total amount of carbohydrate).
Carbohydrates per Ounce
1. Cashews
Cashews contain the most carbs per serving; a whopping 9 g per 1 oz serving, which is about 16-18 nuts.
2. Pistachio
Pistachios contain 6 gms of carbs per 1 oz serving ~ 46 nuts – that’s 18 gm of carbs in an average 3 handful serving (3 oz) – a little more than a slice of bread.
3. Almonds
Almonds contain 6 gms of carbs per 1 oz serving ~ 22-24 nuts.
4. Pine Nuts
Pine nuts (also called pignolias) contain 3 gms of carbs per oz. (which is about 3 Tbsp.)
5. Hazelnut
Hazelnuts (~11 nuts per ounce) contain ~2 1/2 gms of carbs for a 1 oz serving (~11 nuts) / 7 gms of carbs for 3 oz / 3 average handfuls.
6. Walnut
An ounce of walnuts (9 halves per ounce) contain the same amount of carbs as an ounce of hazelnuts (~2 1/2 gms of carbs for a 1 oz serving / 7 gms of carbs for 3 average handfuls or ~ 27 halves.
7. Peanut
An ounce of peanuts (~28 shelled peanuts per ounce) also contain the same amount of carbs as an ounce of hazelnuts or walnuts (~2 1/2 gms of carbs for a 1 oz serving.
Top three low carb high fat / keto-friendly nuts:
Macadamias, Pecans and Brazil nuts are the 3 most low-carb and keto-friendly nuts – having between 4 and 5 gms of carbs for a 3 oz serving! That’s far better than the 27 gm of carbs for 3 oz of cashews and 18 gm of carbs for 3 oz of pistachios!
8. Macadamia
Macadamias have slightly more than 1 1/2 gms of carbs for a 1 oz serving (~11 nuts) / 5 gms of carbs for a 3 oz serving.
9. Pecans
Pecans have 1.3 gms of carbs for an ounce of nuts (~17 halves) / 4 gms of carbs for a 3 oz serving.
10. Brazil nuts
Brazil Nuts also have only 4 gms of carbs for a 1 oz. serving (~ 7 nuts)
A Tough Nut to Crack
Back in the day, eating nuts meant cracking nuts.
It was common to see living room tables with bowls of nuts in their shell, with nutcrackers and nut-picks readily available for use.
Each house had its preference for the style of nutcrackers they insisted were the best. Growing up, we had ones like those above.
Nuts and “Carb Creep”
“Carb creep” is when we think we are eating low carb, but hidden sources of carbs are sneaking into our diet without us being aware of it.
When I was pondering why I had reached my own weight plateau, I knew carb creep had to be the reason – but from where?
After analyzing my diet, it seemed that nuts might be the source and it was.
My biggest single downfall was that I like to crack and eat pistachios on the weekend, while working on my foreign language studies – and it is WAY too easy to crack them and eat copious amounts! In fact, I am somewhat of an expert at shelling them, as my brother and I were placated by our parents with bags of pistachios, on long car trips. To get my “fair share”, I learned to be quite efficient at shelling them and so it seems, I haven’t lost that ‘skill’.
Over the course of several hours I can shell and eat 1/2 to 1 lb of pistachios without really noticing eat, and in the worst case scenario that’s almost 100 gms of hidden carbs!
Add to that a handful or two of almonds a day (another hidden 10 gm of carbs per day) and the source of my “carb creep” became clear.
Portioning
Of course to try to prevent eating too many, nuts can be portioned out in 1 oz or 3 oz ‘servings” and the rest put away for another time, but it is still way too easy for someone who is hungry or tired to mindlessly reach for a handful or two of nuts. It seemed to me that having large containers of shelled nuts that are too easy to reach for, may not be the best solution.
Unshelled Nuts
Replacing shelled nuts with nuts in the shell, like we ate in the “old days”, turns out to be a far more effective solution.
It’s very hard to over eat nuts you have to shell first.
Bingo!
Since pecans are a much lower carb nut than pistachios, they have become my go-to nut from the nut-bowl…and let me assure you, it takes quite a while to shell 17 halves for a mere 1.3 carbs! In fact, I’m pretty sure I expend more energy cracking them, than I take in, eating them.
The Right Tools for the Right Job
Despite having a variety of nutcrackers, I found pecans a “very tough nut to crack” – with them frequently flying out of the standard pinch-style cracker.
I found out that there is a special “pecan cracker” that one can order that apparently does the job very well and looks like this:
…but the little contraption below that I invented in my garage (with a d-clamp and a stick-on felt pad, works great, and I use it for pecans, walnuts and even hazelnuts. Even eating walnuts, which are a higher carb nut – it takes quite a while to shell 9 halves (2 1/2 gms of carbs).
How I can help
For the last 2 years, I have helped my clients lose weight and keep it off using a low-carb approach. More recently, I am ‘practicing what I preach‘ (as you can read about in the blogs titled “A Dietitian’s Journal”). The things I am learning “doing it” adds to what I know academically – which makes me able to coach people much more effectively.
Have questions?
Why not send me a note using the “Contact Us” form on the tab above.
Since 1977, the dietary recommendations in Canada and the US has been for people to consume a diet with limited fat and where ”complex carbohydrates” (starches) comprise the main source of calories.
From 1949 until 1977, the dietary recommendations of Canada’s Food Guide were for people to consume
~20-30% of their daily calories as carbohydrate
~40-50% of daily calories as fat
~20-30% of daily calories as protein
From 1977 onward, Canada’s Food Guide recommended that people consume:
55-60% of daily calories as carbohydrate
<30% of daily calories as fat, with no more than 1/3 from saturated fat
15-20% of daily calories as protein
The US recommendations since 1977 have been similar to those in Canada, with the Dietary Goals for the United States recommending that carbohydrates are 55-60% of daily calories and that calories from fat be no more than 30% of daily calories (of which no more than 1/3 comes from saturated fat).
Eating Well with Canada’s Food Guide which came out in 2015, recommends that people eat even more of their daily calories as carbohydrate;
45-65% of daily calories as carbohydrate
20-35% of daily calories as fat, with no more than 1/3 from saturated fat
Health Canada recommends limiting fat to only 20-35% of calories while eating 45-65% of daily calories as carbohydrates and currently advise adults to eat only 30-45 mL (2 — 3 Tbsp) of unsaturated fat per day (including that used in cooking, salad dressing and spreads such as margarine and mayonnaise).
This is what people have come to call a ”balanced diet”.
But is it?
For the past 40 years, the public has come to believe that eating fat made you fat’ and that eating saturated fat caused heart disease. Evidence-based research does not seem to support that having a diet rich in healthy fats – especially monounsaturated fats like from olive and its oil, and avocados, nut and seeds and omega 3 fats from fish causes heart disease.
Our society has become ”fat phobic”. People guzzle skim or 1% milk with little regard to the fact that just 1 cup (250 ml) has almost the same amount of carbs as a slice of bread. And who drinks only one cup of milk at a time? Most people’s ”juice glasses” are 8 oz and the glasses they drink milk from are 16 oz, which is 2 cups. Who ever stops to think of their glass of milk as having the same amount of carbs as almost 2 slices of bread?
In addition, carbs are hidden in the 7-10 servings of Vegetables and Fruit they are recommended to eat — with no distinction made between starchy- and non-starchy vegetables. Many people eat most of their vegetable servings as carbohydrate-laden starchy vegetables such as peas, corn, potatoes and sweet potatoes and then have a token serving of non-starchy vegetables (like salad greens, asparagus or broccoli) on the ”side” at dinner. Who stops to think that just a 1/2 cup serving of peas or corn has as many carbs as a slice of bread — and often those vegetables are eaten with a cup of potatoes, adding the equivalent number of carbs as another 2 slices of bread?
People drink fruit juice and ”smoothies” with no regard for all of the extra carbs they are consuming (not to mention the effect that all of that fructose has). A ”small juice glass” is 8 oz, so just a glass of orange juice has the equivalent number of carbs as another 2 slices of bread! Many grab a smoothie at lunch or for coffee break without even thinking that the average smoothie has the same number of carbs as 5 slices of bread!
Then there is the toast, bagels and cereal or bars that people eat for breakfast, the sandwiches or wraps they eat for lunch and the pasta or rice they have for supper. These are carbs people know as carbs — which are added to all the carbs they consumed as vegetables, fruit and milk.
What has been the outcome of people following these dietary recommendations to eat a high carb diet since 1977 ?
Obesity Rates
In 1977, obesity rates* were 7.6% for men and 11.7% for women, with the combined rate of < 10 % for both genders.
* Obesity is defined as a Body Mass Index (BMI) ≥30 kg/(m)2
In 1970-72 the obesity rate in Canadian adults was 10% and by 2009-2011, it increased two and a half times, to 26%.
In 1970-72, only 7.6% of men were obese but by 2013, 20.1% of men were categorized as obese. In 1970-72, only 11.7% of women were obese but by 2013, 17.4% of women were obese.
In 1978 in Canada, only 15% of children and adolescents were overweight or obese, yet by 2007 that prevalence almost DOUBLED to 29% of children and adolescents being overweight or obese. By 2011obesity prevalence alone (excluding overweight prevalence) for boys aged 5- to 17 years was 15.1% and for girls was 8.0%.
The emphasis since 1977 on consuming diets high in carbohydrates and low in fat has taken its toll.
Effect on Health
Non-alcoholic liver disease is rampant and not surprisingly, considering 37% of adults and 13% of youth are abdominally (or truncally) obese — that is, they are carrying their excess body fat around and in the internal organs, including the liver.
Since the 1970’s, Diabetes rates have almost doubled.
In the 1970s, the rate of Type 2 Diabetes in women was 2.6% and in men was 3.4 %. In the 1980s that number rose in women to 3.8% and in men to 4.5%. In the 1990s the rate was almost double what it was in 1970; in women it was 4.7% and in men, 7.5%.
If people eating a high carb, low fat diet has corresponded to an increase in obesity, overweight and Diabetes, then what’s the alternative?
That is where a low carb high healthy fat diet comes in , which supplies adequate, but not excess protein. It enables us to use our own fat stores for energy, and to make our own glucose (for our blood and brain) with ketones (that are naturally produced by our bodies when we sleep, for example) to fuel our cells and organs. Since humans are designed to run on carbs (in times of plenty) and in our fat stores (when food is less plentiful), being in mild ketosis is a normal physiological state. By eating a low carb high fat diet when we’re hungry and delaying eating for short periods, we can mimic the conditions that were common to our ancestors. By eating this way over an extended period of time, we can bring down insulin levels and as a result, decrease the insulin resistance of our cells. We can improve our blood sugar, lower our blood pressure and see our LDL cholesterol and triglycerides come down to normal, healthy levels.
Want to know more? Why not send me a note using the Contact Us form located above?
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
A low carbohydrate high fat ketogenic diet supplies adequate, but not excess protein and low levels of carbohydrate that is naturally found in foods such as non-starchy vegetables, nuts and seeds, and certain fruit. A low carb high fat ketogenic diet enables our bodies to burn our own fat stores quite efficiently for energy, while making the glucose needed by our blood and brain, and using ketone (which our body naturally produces as we sleep) for energy for our cells and organs.
Note: Not all low carb diets are ketogenic diets. There are many types of low carb diets, ranging from moderately low carb diets (130 g carbs) to ketogenic diets (5-10% net carbs) and everything in between. As well, not all low carb diets are high fat diets. Some approaches are low carb higher protein diets and are also ketogenic, because carbs are limited. More on those in a later article. This article is only about a low carb high fat ketogenic diet.
Ketogenic Macronutrient Ratio
Generally speaking, in a low carb high fat ketogenic diet, the percentage of calories (kcals) from carbohydrate (carbs), protein and fat in a ketogenic diet (called the macronutrient ratio) is as follows;
65-75% of calories from fat
~20% of calories from protein
5-10% of calories from NET carbs (which is the carbohydrate in food, minus the insoluble fiber found in that food)
While each person’s energy needs and macronutrient needs are different (based on theirage, gender and activity level, as well as any pre-existing medical conditions they may have), most people on ketogenic diets take in 10% or less of their calories from net carbohydrates*, with the amount of fat and protein intake varying from person-to-person within the above range.
* Net carbs are determined by subtracting insoluble fiber contained in food from the carbohydrate content of that food.
By eating low levels of carbohydrate, insulin level falls and glucagon and epinephrine levels in the blood rise.
This causes several things to occur;
Fat stores are burned for energy
The fat stored in fat cells (called adipocytes) are released into the blood as free fatty acids and glycerol. Since fatty acids contain a great deal of energy, they are broken down in cells that have mitochondria in a sequence of reactions known as β-oxidation, and acetyl-CoA is produced. This acetyl-CoA then enters the citric acid cycle where the acetyl group is burned for energy.
Glucose is made for energy
When insulin levels are low (or absent) and glucagon levels in the blood are high, glucose is produced via gluconeogenesis (literally, the “making of glucose”) and then released into the blood and used as an energy source. As elaborated on below, while the brain can use ketones for fuel, it has a need for some glucose.
Ketones are produced for energy
In significant carb restriction over several days, gluconeogenesis is stimulated by the low insulin and high glucagon levels results in acetyl-CoA being used for the formation of ketones (i.e. acetoacetate and beta-hydroxybutyrate and their breakdown product, acetone). These ketones are released by the liver into the blood where they are taken up by cells with mitochondria and reconverted back into acetyl-CoA, which can then be used as fuel for energy, in the citric acid cycle. Ketones can cross the blood-brain barrier, so they are used as fuel for the cells of the central nervous system – acting as a substitute for glucose (which is normally the end result of the body breaking down carbs and sugars found in various foods). After ~ 3 days on a very low carb diet, the brain will get ~ 25% of its energy from ketones and the other 75% from the glucose made via gluconeogenesis. After ~ 4 days the brain will get about 70% of its energy from ketones. While the brain can use ketones for some or even most of its fuel, it still has requirement for some glucose and that is supplied from gluconeogenesis. The heart ordinarily prefers to use fats as fuel but when carbs are restricted, it effectively uses ketones.
Ketosis versus Ketoacidosis
Ketones are naturally produced during periods of low carb intake or in periods of fasting and during periods of prolonged intense exercise. This state is called ketosis. Since the human body is designed to use glucose as a fuel source (in times of plenty) and to use fatty acids and ketones (in times of food shortage), ketosis is a normal, physiological state.
In untreated (or inadequately treated) Type 1 Diabetics (where the beta cells of the pancreas don’t produce insulin), the ketones that are produced are as the first stage of a serious medical state called ketoacidosis.
Ketosis, on the other hand is a normal, naturally occurring state that occurs naturally when we sleep for example or miss a meal, whereas ketoacidosis is a serious medical state associated most commonly associated with Type 1 Diabetes. While often confused, these two conditions are very different.
A Low Carb High Fat Ketogenic Diet
A low carb high fat ketogenic diet may appear at first glance to be like the Atkins diet or other low carb high fat diets but the main difference is that in a keto diet, protein is not unlimited. The reason for this is based on the premise that excess protein will be converted into glycogen and have a similar effect on ketosis as eating too many carbs, disrupting ketosis.
Since having too little protein may cause muscle loss, a keto diet is designed to have adequate, but not excess protein.
But why eat a low carb high fat keto diet?
The last 40 years of burgeoning rates of overweight, obesity and Diabetes, provide the motivation. (Please read the next article titled 1977 Dietary Recommendations — forty years on for a summary of those issues).
A low carb high fat keto diet is one low carb approach that is used for clinical reasons, such as to seek to reverse the symptoms of Diabetes by enabling insulin levels to fall, glucagon and epinephrine levels to rise, resulting in the body:
(1) naturally accessing its own fat stores for fuel
(2) manufacturing its own glucose
and
(3) using ketone bodies for energy.
The human body is designed to use either glucose or fatty acids and ketones as a fuel source. Ketosis is a normal, physiological state where our bodies run almost entirely on fat.
Insulin levels become very low, which has benefit to those who are insulin resistant or Type 2 Diabetic.
As a result, burning of our own body fat stores for energy increases dramatically — which is great for those who want to lose weight, without hunger and a steady supply of energy.
Want to know more?
Feel free to send me a note using the Contact Me form, above.
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status are different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
Long before the ‘hybrid car” there was the human body – a hybrid ‘machine’ perfectly designed to use either carbohydrates or fat for energy. Like a hybrid car, we can run on one fuel source or the other at any one time.
If we are eating a largely carbohydrate based diet, we will be in ‘carbohydrate mode’ by default. Carb-based foods will be broken down by our bodies to simple sugars and the glucose used to maintain our blood sugar levels. Our liver and muscle glycogen will be topped up, then the rest will be shuttled off to the liver where it will be converted into LDL cholesterol and triglycerides and stored in fat cells.
Historically, in times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen and thenswitch fuel sources to be in “fat-burning mode” — accessing our own fat stores, for energy.
The problem is now that we rarely, if ever access our stored fat because we keep eating a carb-based diet. So we keep getting fatter and fatter.
GLUCOSE OR FAT AS FUEL
When we are in “carb burning mode”, the carbs we eat are broken down by different enzymes in our digestive system to their simplest sugar form (monosaccharides) such as glucose, fructose and galactose.
Glucose is the sugar in our blood, so starchy foods such as bread and pasta and potatoes are broken down quickly so they are available to maintain our blood sugar levels.
Monosaccharides are the building blocks of more complex sugars such as disaccharides, including sucrose (table sugar) and lactose (the sugar found in milk), as well as polysaccharides (such as cellulose and starch). When we drink milk for example, the galactose found in it is broken down into lactose and glucose. When we eat something sweetened with ‘sugar’ (sucrose), it is quickly broken down to glucose and fructose.
Any glucose that is needed to maintain our blood sugar level is used immediately for that purpose and the remainder is used to “top up” our glycogen stores in our muscle and liver. There are only ~ 2000 calories of glycogen – enough energy to last most people one day, so when our glycogen stores are full, excess energy from what we eat is converted to fat in the liver and stored in adipocytes (fat cells).
One problem is that most of our diets are high in fructose – naturally found in fruit but also as high fructose corn syrup in many processed foods. Fructose can’t be used “as is”, so it is brought to the liver. If our blood sugar is low, it will be used to make glucose for the blood (via gluconeogenesis) otherwise it will be converted into LDL cholesterol (so-called “bad cholesterol”) and triglycerides and stored as fat.
Feasting and Fasting
When we don’t eat for a while, such as would have occurred when our ancestors were hunter-gatherers, we’d use up our glycogen stores hunting for an animal to eat, or gathering other edible foods and if we weren’t successful at finding food to eat, then our bodies would access our fat stores, for energy. This is known as lipolysis. This process is regulated mainly by a hormone called glucagon, but other hormone such as epinephrine (the “fright and flight” hormone), cortisol (the “stress hormone”) as well as a few others (ACTH, growth hormone, and thyroxine) also play a role.
In times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen, switch into “fat-burning mode” and then rely on our stored fat for energy.
The problem for most of us in North America and Europe is that we have access to food in our homes, in stores and at fast food restaurants 24/7. We can’t go for a walk without passing places selling or serving food and if the weather is bad or we are too tired, food is just a phone call or web-click away. So we just keep storing up our fat for ‘lean times’ that never come.
In addition, irrespective of our cultural background, our eating style is carb based; pasta, pizza, sushi, curry and rice or naan, potato, pita – you name it. Every meal has bread or cereal grains, pasta, rice or potatoes – and even what we consider “healthy foods” such as fruit and milk have the same number of carbs per serving as bread, cereal, pasta, rice and potatoes. That wasn’t always so. Our indigenous cultural foods were very different.
Compounding that, many “low-fat” products have added sugar (sucrose) in order to compensate for changes in taste from reducing naturally occurring fat, which then adds to excess carb intake. Sucrose (ordinary table sugar) is made up of half fructose, so a diet high in sugar adds even more fructose transport to the liver, for conversion to cholesterol and fat.
The vilification of fat
In 1977, both the Canadian and US food guides changed in response to the promoted belief that eating diets high in saturated fat led to heart disease. Multiple studies and reanalysis of the data of older studies indicates that saturated fat is not the problem, but that diets high in carbohydrate combined with chronic inflammation and stress, is.
In 2016, it came to light that the sugar industry funded the research in the 1960’s that downplayed the risks of sugar in the diet as being related to heart diseaseand highlighted the hazards of fat instead – with the results having been published in the New England Journal of Medicine in 1967 with no disclosure of the sugar industry funding*. The publication suggested that cutting fat out of the American diet was the best way to address coronary heart disease, and which resulted in the average American and Canadian as inadvertent subjects in an public health experiment gone terribly wrong. Overweight and obesity has risen exponentially and with that Diabetes, hypertension (high blood pressure) and high cholesterol.
*(Kearns CE, Schmidt LA, Glantz SA. Sugar Industry and Coronary Heart Disease Research A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016;176(11):1680-1685. doi:10.1001/jamainternmed. 2016. 5394).
Over the last 40 years the promotion of “low fat eating” by governments and the food industry has resulted in carbohydrate-intake skyrocketing. Every high-carb meal is followed by another high-carb meal, and if we can’t wait, a snack, too. We eat every 2-3 hours, and eating carb-based foods every 2 or 3 hours all day, every day is quite literally killing us.
How do we get fat out of “storage”?
The “key” to unlocking our fat stores, is decreasing overall intake of carbohydrates by decreasing the amount of carbohydrates we eat, both by eating much less of it and on occasion, by delaying the amount of time between meals.
Decreasing carb intake lowers insulin, the fat-storage hormone. At first our bodies access liver and muscle glycogen for energy, but since that is only about a one day’s supply, our bodies then turn to our own fat stores as a supply of energy.
By eating a diet rich in fat and keeping protein at the level needed by the body but not in excess, dietary protein is not used to synthesize glucose, but fat is.
An added bonus is that since insulin also plays a role in appetite, as insulin falls, appetite decreases.
This is the role of a low carb high healthy fat diet, a topic covered in this article.
Have questions?
Why not send me a note, using the “Contact Me” form above? I’d be happy to answer your questions.
To your health!
Joy
If you would like to read well-researched, credible ”Science Made Simple” articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please click here.
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
People who are eating differently in an effort to lose weight often hop on the scale daily to see how they’re doing. What they fail to consider is that an average adult’s body weight can fluctuate by as much as 4 1/2 pounds per day — solely as a result of changes in the amount of water they are retaining or excreting.
The Limitations of Using a Scale to Determine Fat Loss
An 80 kg person has, on average 48 liters of water in their body. The problem with using body weight as an assessor of fat loss is that the human body does not precisely regulate body water content.
Above 49 liters of water, the kidneys of an 80 kg person will clear the excess water by causing the person to urinate more and below 47 liters of water, the 80 kg person will feel thirsty and increase their fluid intake. People’s “weight” is affected by this change in body water content of ~2 liters per day — which weighs approximately 2 kg or 4.4 pounds! Put another way, each day our “weight” can fluctuate by this amount solely due to the difference in retained or excreted water.
Since there is no way to measure this daily change in water weight in non-clinical settings, the standard scale is a very imprecise way to measure fat loss over the short-term.
Waist Circumference
Many people know that carrying excess weight around the middle increases one’s risk of cardiovascular disease, including heart attack so they measure their waist circumference frequently. Even if waist circumference is measured halfway between the lower rib and the top of the hip bone, with a fully relaxed abdomen, their are limitations to using this as a short term measure of weight loss.
The Limitations of Using a Tape Measure to Determine Fat Loss
Since the average person’s body weight fluctuates by as much as ~4 1/2 pounds per day due only to changes in body water, a tape measure fails to capture decreases in waist circumference stemming from the kidneys excreting water.
That said, waist circumference is helpful as a long-term indicator of weight loss, just not a short-term one.
Body Fat Percent
Some people have bathroom scales that have body fat analyzers built in and think that what it is measuring is the amount of fat they are carrying, however a number of factors can influence this reading.
The Limitations of Using a Body Fat Analyzer to Determine Fat Loss
Body Fat Analyzers use electrical impedance to determine fat percentage, and this measurement is affected by a number of conditions, including environmental (room) temperature, a person’s hydration status, as well as emotional stress. Since hydration status can fluctuate by ~4 pounds per day, a body fat analyzer is no more accurate as a short-term measure than a standard bathroom scale, without it.
How to assess short-term weight loss
How one’s own clothes fit and comparative ‘before’ and ‘after’ photos are a much better short-term assessor of fat loss than a scale, a tape measure and a body fat analyzer. Since body water fluctuates considerably on a low carb high fat diet due to changes in sodium levels, I recommend that people eating a low carb high fat diet weigh themselves once every two weeks on the same day of the week, at the same time of day and measure their waist circumference at the same time. If they have a scale that assesses body fat percent once every two weeks is sufficient for taking these measurements.
None of these will provide much information on actual fat loss over the short term…so why rely on them for that, but they will be helpful measurement over the longer term.
Sodium and Body Water Content
As mentioned in a previous article, by eating only when hungry and only until no longer hungry, insulin levels have the opportunity to fall to baseline – something they do naturally after not eating for 12 hours.
On days where the time until eating is extended by a few hours (i.e. “intermittent fasting”), insulin levels stay low for an even longer period of time. In response, our kidneys excrete sodium in a process called naturesis.
Failing to supplement sodium while eating low-carb high fat can result in intense headaches – and if sodium remains low, potassium will also be excreted to keep the necessary sodium-potassium balance. This drop in potassium often results in irregular heart beats, known as arrhythmia.
Phinney and Volek (The Art and Science of Low Carbohydrate Living) recommend that if one is eating less than 60 gms of carbs per day, that 2-3 grams of sodium should be added to the diet (provided the person is not taking any diuretics or other blood pressure medication).
A half a teaspoon of table salt or sea salt provides 1000 mg or 1 gram of sodium.
Final Thoughts
Since hopping on the scale daily or even several times a week won’t provide any useful information, nor will measuring our waist circumference or using a body fat analyzer too often – why do it? Part of ‘getting healthy’ ought to include having a healthy body self image – something that won’t be nurtured by obsessing about such “numbers”.
Short-term measures of success
Short-term success is best measured visually – with comparative photos taken from the same distance away, from the same relative height and wearing the same clothing.
How one’s clothes are fitting is another way.
A person who is insulin resistant or Type 2 Diabetic should be seeing both their fasting blood glucose and post-prandial (2 hours after a meal) glucose levels gradually coming down. If they aren’t then they should schedule an appointment with their Dietitian to find out why that is.
Medium-term measures of success
Medium-term measures of success in eating low carb high fat can be measured both subjectively and objectively. Subjective measures include weighing oneself and taking one’s own waist circumference once every two weeks. Objective measures include having your Dietitian weigh you on a clinical scale, having her assess your waist circumference and body fat percentage using both a device that measures electrical impedance, as well as using good old-fashioned calipers, that measure subcutaneous (under the skin) fat, in 3 or four specific locations on the body.
A person with high blood pressure should be seeing both systolic (the first number) and diastolic (the second number) blood pressure coming down and Type 2 Diabetics or those with insulin resistance should be continuing to observe lower fasting blood glucose and post-prandial (2 hours after a meal) glucose levels.
Longer-term measures of success
After 6 or 8 months eating low carb high fat, both subjective and objective measures should be continuing to lower in a reasonably linear fashion. Of course there will be times where a ‘plateau’ is reached, but if that lasts more than two or three weeks, then its important to check in with your Dietitian to make sure the amount of carbs you think you are eating is what your Dietitian has been determined as being best for you.
A Type 2 Diabetic should be seeing both their fasting blood glucose and post-prandial (2 hours after a meal) glucose levels approaching more normal levels and both Type 2 Diabetics and those with insulin resistance (“pre-diabetes”) should have their HbA1C assessed at a lab every three months, as this provides insights into one’s 3-month average blood glucose level. Fasting blood glucose provides a ‘snap-shot’ of blood sugar in the morning after not eating, and should be done twice a year by a lab, especially if one is Diabetic. Comparing lab test results to previous lab test results is an objective indicator of the effect that eating low-carb high fat is having on specific markers and provides an opportunity to determine if the amount of carbs being eaten may still be too high.
The most accurate assessor is a 2 hour glucose tolerance test, however few doctors will requisition this after one is diagnosed as Type 2 Diabetic.
Finally, every year or so, it is helpful for those who have been diagnosed as Diabetic to have their fasting insulin, C-Protein and AM Cortisol levels assessed and compared to previous results. For these, your doctor may refer you to an Endocrinologist.
Remember, achieving health is a journey and takes time and like most journeys, it is best not done alone.
Have questions about how I can help or about the services I provide?
Please send me a note using the form on the “Contact Us” tab, above.
To your good health!
Joy
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
Prior to the domestication of animals and the development of agriculture, the human diet centered around the ‘hunt’. They ate when they caught something, and didn’t eat until again until they either caught something else, or were successful in finding edible vegetation, berries or nuts. ”Feasting” and ”fasting” were normal events in the rhythm of life, and our bodies were designed to function using our fat stores for energy, as evidenced by our continued existence.
From hunter-gatherers to farmers
After the Ice Age, those that survived were left with an increasingly unpredictable climate, decreases in big-game species that were hunters’ first-choice prey, and increasing human population in the available habitats for hunting and gathering. To decrease the risk of unpredictable variation in food supply, people broadened their diets to second- and third-choice foods, which included more small game, plus plant foods which required much preparation, such as grinding, leaching and soaking. As I will demonstrate below, these plant foods, including grains were very different in carbohydrate and protein composition than they are today.
The domestication of animals and plant cultivation of ~ 13,000 years ago, forms a significant turning point in the human diet.
Humans began to transport some wild plants, including grains from their natural habitat to more productive selected habitats, and so began intentional cultivation, or farming. With the development of agriculture and the domestication of animals – the plants and animals themselves began to change.
This is important.
The fruit of today bear little resemblance to their ancient predecessors. The grains of today don’t either. For example, wild wheat and wild barley bear their seeds on top of a stalk, and sheds its seed spontaneously — enabling it to germinate where it falls.
Once people began bringing some wild wheat or barley seeds back with them in order to intentionally plant them, some seeds would accidentally spill along the way, germinating in new places. Over time, some seed would cross-pollinate with wild grain, while others would undergo spontaneous mutations, leading to wheat and barley varieties with non-self-shattering heads. Eventually, these non-shattering grains were selected for by humans for cultivating, leading to a very different type of grain than the wild species — and one with very different nutritional content than their wild predecessors.
Similarly, domesticated animals were selected based on traits that were considered desirable to people — chickens were selected to be larger, wild cattle to be smaller, and sheep to lose their bristly outer hairs and not to shed their soft inner wool. Eventually, the land where hunter-gatherers lived was overrun and replaced by people who had become agricultural – and who were ever-expanding the amount of land they required for raising animals, as well as for growing crops.
At Tell Abu Hureyra, in the Euphrates valley of modern Syria are the remains of a civilization that lived between 13,000 and 9,000 years ago, spanning the Epipaleolithic and Neolithic periods. This site is significant because the inhabitants of Abu Hureyra started out as hunter-gatherers, but gradually moved to agriculture, making them the earliest known farmers in the world. Meals consisting of the meat of gazelle, wild goat and game birds were supplemented with wild-growing Einkorn wheat-porridge, as well as berries, nuts or fruit, if in season. Tools such as sickles and mortars for harvesting and grinding grain, as well as pits for storing it have been found at Tell Abu Hureya and remains of harvested Einkorn wheat (which was ground by hand and eaten as porridge) have been found at Tell Aswad, Jericho, Nahal Hemar, Navali Cori and other archeological sites.
The diet of man forever changed at that point.
As previously mentioned, plants underwent change as a result of both natural cross-pollination as both underwent change as a result of intentional manipulation by man. This occurred everywhere that man settled — from the lush valleys of the Middle East*, to Africa and Asia.
[*yes, the Fertile Crescent of the Middle East was lush and green, then.]
The grain we know today as ”wheat” and ”rice” is nothing like their wild ancient predecessors. Likewise with fruit. The fruit of today has been bred to be sweet — not so with the wild cultivar. A brief history of wheat will help illustrate this type of change.
Evolution of Wheat – but one example
The first wild grass that was cultivated was Einkorn wheat. As cultivation techniques improved, Einkorn eventually became an essential component of the diet — reducing the need for hunting and gathering. Einkorn wheat contained only 14 chromosomes.
Shortly after the cultivation of the first Einkorn, the Emmer variety of wheat (Triticum turgidum) appeared in the Middle East; a natural offspring of Einkorn and an unrelated wild grass, calledgoatgrass’ (Aegilops speltoids.
Emmer wheat is what is referred to in the Hebrew Bible (Exodus 9, Exodus 32, Isaiah 28, Isaiah 25) as Kes-emmet (כֻּסֶּמֶת) and both Eikorn wheat (חִטָּה) and ”Emmet” (ֻּסֶּמֶת), translated in English as ‘spelt’, are referred to together as distinct species (e.g. Exodus 9:32). It was the ancient Egyptians that are credited with the addition of wild strains of yeast in order to make bread rise — which gives an added dimension to the story of Passover, where the Jews left slavery in Egypt in ”great haste”, “not having time to let their bread rise”.
Since plants do not combine genes but add (or sum) them which provides evidence of what cross-bred with what. Goatgrass added its genetic code to that of Einkorn , so Emmer wheat had 28 chromosomes.
Emmer wheat then naturally cross-bred with another wild grass called Triticum taushii, giving rise to the original cultivar of Triticum aestivum, the predecessor of modern wheat, which has 42 chromosomes. This was a higher yielding wheat variety which had many desirable baking properties that Eikorn and Emmer lacked. This new strain remained largely unchanged until the mid-eighteenth century when Carolus Linneaus, who invented the Linnean system of categorizing species, counted only 5 species.
Today, Eikorn, Emmer and the original cultivated strains of Triticum aestivum have been replaced by almost 25,000 strains of modern human-bred wheat strains that are hundreds, if not thousands of genes apart from the original Eikorn and Emmer wheat species.
Our food is not the food of our ancestors.
Modern Triticum aestivum is on average 70% carbohydrate by weight and only 10% protein. Emmer wheat, on the other hand was 57% carbohydrate and 28% protein — and was suitable to supplement the protein of a meal.
Paleo Diet compared with the Low Carb High Healthy Fat diet
The premise of Paleo eating to eat like our Paleolithic ancestors did is understandable, however the foods that exist now are nothing like the foods our ancient ancestors ate. Fruit, for example is considered “paleo” -but the carb content of paleo fruit was substantially less than that of today.
In a low carb high healthy fat way of eating, carbs are not avoided. It is the foods that are high in carbs that are easily broken down to glucose and have little nutrient-density that are limited.
[It is hard to justify eating grain products made from varieties of wheat that were bred for no other reason than they could be grown in nutrient- poor soils in novel parts of the world.]
No justification is needed to eat carbs that come as part of fibre- and nutrient-rich non-starchy vegetables and to eat carbs found in nuts that are a good source of protein and monounsaturated fat.
A diet where 45 – 65% of calories are as carbohydrate is has us eating ”carbs for carb’s sake”, but a low carb high healthy fat diet should not be about “fat for fat’s sake”.
Some people think they should eat large amounts of saturated fat ”just because they can”, and I suppose that’s true. One can certainly eat a pound of bacon, but when compared with a fat marbled grain-fed steak or a Brome Lake- or wild duck, one is more nutrient-dense than the other. The yolks of free-range egg comes as part of a nutrient-dense package, which includes good quality protein, as well as other nutrients. A pound of bacon, does not. That doesn’t mean that eating bacon is ”bad”, but in comparison to grilled salmon with a large serving of non-starchy vegetables bathed in cold-pressed olive- or avocado oil, it doesn’t quite measure up. It is not just about not being hungry, but about being healthy.
A Low-Carb-High-Healthy-Fat Diet is about ”nutrient density” — not just ”fat density”.
Final Thoughts
In a Low-Carb-High-Healthy-Fat Diet, carbs are not ”bad” and fat is not ”good”. Carbs and fat that come in nutrient-dense food and in particular ratios are what we are striving for.
As well, protein quantity is based on physiological need and not unlimited (as excess in a low carb diet will be converted and stored as fat). The source of that protein ought to be considered, as well. For example, it is well documented that fatty fish such as salmon, mackerel and tuna are high in omega-3 fatty acids and are good for our brains and our hearts so for those that enjoy fish, eating it often is ideal.
The good thing about the Low-Carb-High-Healthy-Fat Diet is that it can be adapted to culture- or religious restrictions. Don’t eat pork? No problem. Don’t eat beef? Not an issue. Take fast days? That is easily worked-in.
Want to know more?
Feel free to send me a note using the form on the “Contact Us” tab, above. Remember, Nutrition is BetterByDesign.
To your health!
Joy
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
Binford LF. New Perspectives in Archaeology, 1968; 313—341
David, W. Wheat Belly: Lose the Wheat, Lose the Weight and Find Your Path Back to Health Rodale Books, 2011; 15-32
Diamond J. Evolution, Consequences and Future of Plant and Animal Domestication. Nature, 2002; 418:700-7
Flannery KV. The Domestication of Plants and Animals, 1969;73—100
Hillman GC, Davies, MS. Measured Domestication Rates in Wild Wheats and Barley under Primitive Cultivation, and their Archaeological Implications. J. World Prehistory; 1990; 4:157—222
Raeker RO, Gaines CS, Finney PL, Donelson T. Granule size distribution and chemical composition of starches from 12 soft wheat cultivars. Cereal Chem 1998;75(5):721-8
Shewry PR. Wheat. J Exp Botany 2009;60(6):1537-53
Stiner MC, Munro ND, Surovell TA. The Tortoise and the Hare: small-game use, the broad-spectrum revolution, and Paleolithic demography. Curr. Anthropol. 41, 39—73 (2000).
Zohary D, Hopf M. Domestication of Plants in the Old World 3rd edn (Oxford Univ. Press, Oxford, 2000).
This weekend has been a challenging one, as I received two pieces of news. The first was of one client’s incredible success following the low carb high healthy fat dietand the shocked reaction of his doctor, and the other was of the death of a friend who had Diabetes, high blood pressure and high cholesterol. In this blog, I will share how these two events embody the two options each of us have; (1) living a healthy life to the fullest or (2) living with diet-related disease and dying prematurely of ‘natural causes’.
“JP” – a Picture of Success
Last fall, I had a reasonably fit 35-year-old client contact me wanting to lose 15 pounds. He went to the gym twice a week for an hour, and ran 10 km per week, but had put on some pounds and wanted to lose them.
As I always do, I asked for a copy of recent blood test, assessing his fasting blood glucose, HbA1C (3 month average of blood glucose), cholesterol (lipid panel) and requesting his doctor-assessed blood pressure. (Sometimes people insist that I counsel them without seeing blood work, but I explain that they ran out of crystal balls when I was graduating, so I have no choice but to get labs.) I gave my new client a Lab Test Request form to bring his doctor. The GP scoffed at the Lab Test Request Form asking him to requisition a lipid panel for a young, fit 35 year old whose parents are both living. That changed when the tests came back, and this man’s triglyceride level was higher than I had ever seen anyone’s, ever. His non-HDL cholesterol was very high and his HDL was very low. LDL wasn’t even available because his triglycerides levels were through the roof. His ferritin was astronomically high – not a sign of excess iron, but likely inflammation.
His doctor called him into the office immediately and wanted to put him on statin medication right away and referred him to the Lipid Clinic at a major local hospital.
My client told his doctor he wanted to wait 3 months and first follow my dietary recommendations and see what would happen to his lipids, and was advised against it by his doctor. My client was insistent, so the doctor told him that his recommendations were for him to eat “decrease saturated fat and carbohydrates, increase fruit and vegetables, increase insoluble fiber and fish, make his plate 1/2 vegetables, 1/4 protein, 1/4 starch“.
After seeing me, he agreed to limit fruit to max 1 / day, preferably a few berries on top of 2 or 3 huge salads with plenty of good quality olive oil and to have most of his carbs as vegetables. He learned that “not all vegetables are created equal” and I taught him to differentiate between those he could eat as much as he wanted at each meal and those he should limit or avoid. We talked about milk consumption, and the health benefits of eating plenty of fatty fish, such as salmon, mackerel and fresh sardine. And we talked about carbs. We talked a lot about carbs. Carbs in fruit, carbs in milk, carbs in bread, pasta and rice, and carbs in vegetables.
I designed an Individual Meal Plan for him, making sure he obtained sufficient macronutrients (protein, fat and carbs) as well as micronutrients (especially potassium, magnesium, sodium, vitamin C and calcium, vitamin D and vitamin K) – and factoring in his desired weight loss. I explained that if he followed his Meal Plan, it is perfectly reasonable for his triglyceride levels to be <2.00 mmol/L in 2 more months.
Three weeks later, his doctor ran his labs again. His triglyceride level was almost a third what it was! His non-HDL was down substantially and his HDL was rising nicely. When he was seen at the Lipid Clinic, they were willing to give him 2 more months to get his lipids in the normal range before starting him on medication.
Friday, he wrote me telling me that his triglycerides we down well below 2.00 mmol/L and added;
“this amazed the doctor!”
My client left his doctor’s office without a medication prescription and with only the recommendation to keep eating the way I taught him. My client added that he was already within 2 – 3kg of his goal weight.
It’s not magic.
The doctor should not have been amazed that diet alone can be this effective – even for someone for whom high cholesterol has a genetic component. The literature documents the role of a low carb high fat diet.
But it is easier to write a prescription than educate a patient.
My High School Friend – preventable premature death
Last night I learned that my friend since high school, died from natural causes. She had Type 2 Diabetes, high blood pressure and high cholesterol. She and I were the same age.
Three years ago, when my friend was first diagnosed as having Diabetes, she asked my opinion about having received Diabetes counselling in her province to eat 45 gm of carbohydrates at each meal and at least 15 gm of carbohydrates at each of 3 snacks – that’s 180 gm of carbohydrates per day. A mutual friend of ours from the same province, who had also been recently diagnosed with Diabetes confirmed that she too was advised to eat 45 gm of carbohydrates at each meal and at least 15 gm of carbohydrates at snacks. At that time, I had explained to my friend what I had been learning about the role of excess carbs in Diabetes, hypertension (high blood pressure) and high cholesterol. While I provide distance consultations in my practice (using a combination of phone, email and fax), as Dietitians we are advised specifically not to provide dietary counselling to family members or friends. With my ability to help directly being very limited, I recommended that she find a Dietitian near her who could teach her about managing this triad (called “metabolic syndrome”) using a low carb high fat diet. She followed the standard dietary recommendations to the letter and took her multiple medications as prescribed. Her blood sugar levels came down using medication (but that was effectively treating the symptom of high blood sugar, not the cause which is the underlying insulin resistance). Her blood pressure kept going higher and higherdespite medication, so more medication was added. She then developed high cholesterol.
Today, my friend is dead, in what may have been an entirely preventable, premature death.
So I am left asking myself ‘could following the standard recommendations of eating 180 gm of carbohydrate per day (or more) with Type 2 Diabetes, high blood pressure and high cholesterol — without treating the underlying cause (insulin resistance) have contributed to her death’?
The literature is certainly full of studies documenting the beneficial effects of a low carb high fat diet on metabolic syndrome – but she was never given that as an option. She was prescribed medication for lowering blood sugar and blood pressure, but nothing was done to lower her insulin resistance.
A lifetime of work by the late Dr. Joseph Kraft with almost 300,000 people documents that it is the insulin resistance that underlies cardiovascular disease – not the high blood sugar. Furthermore, 65-75% of people with normal blood sugar levels still have insulin resistance – and the same elevated risk of having a heart attack.
We keep treating the symptoms and people keep dying anyways – and those without any symptoms are walking around with elevated risk of dying from cardiovascular disease, and don’t even know it.
We are told;
“Diabetes is a chronic, progressive disease”
which means that once diagnosed with Diabetes, you’ll have it forever – and that eventually it will get worse, requiring medication, then more medication and finally insulin.
When people have bariatric surgery (“stomach stapling”), their blood sugars come back to normal within weeks and at the end of a year, they no longer have any of the clinical symptoms of Diabetes. Their fasting blood glucose levels are normal and their HbA1C levels are normal. They are essentially as if they don’t have Diabetes. Their Diabetes is in remission.
So is Diabetes REALLY a “chronic, progressive disease”? No, it can be stopped.
If the reason people became Diabetic was because of how they were eating, why is it SO hard to grasp the concept that they could get well, but changing how they are eating?
At the end of the day, we have a choice.
We can do as my client above did and put everything we have into changing how we eat based on good, sound scientific studies and with medical supervision, or we can keep doing what we’ve been doing, expecting different results.
I made my choice a month ago tomorrow, and will write an update in the blog titled “A Dietitian’s Journey” tomorrow, for week four (see Food for Thought tab, above). Here’s a teaser; two days ago my blood sugar levels were several times at normal levels – and were overall much lower than a month ago. Last night (twice) and once this morning, my blood pressure was in the normal range. One month!
I ask myself, what will my labs look like in 3 months or 6 months of addressing the underlying insulin resistance (instead of the symptom of high blood sugar?) What will be life be like, when I have normal blood sugar levels and normal blood pressure and normal cholesterol levels?
Note: Everyone’s results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody’s nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.
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.
Insulin resistance is a condition where your body keeps producing more and more insulin in order to transport glucose out of the blood and store the excess by converting it to fat. When cells have become resistant to insulin, glucose builds up in the blood and results in ”high blood sugar”. The problem is that high blood sugar is a symptom of the problem, it is not the problem itself. Insulin resistance is the underlying cause and is highly significant to those with completely normal blood sugar levels.
Those with high fasting blood glucose may notice symptoms that are associated with Type 2 Diabetes; including excess urination and excess thirst. This is the body’s way of trying to dilute the high levels of glucose in the blood. A very sobering fact is that 75% of people with insulin resistance have normal fasting blood glucose levelsand don’t know that they are insulin resistant.
They have NO symptoms whatsoever.
They don’t know that they are at increased risk for heart attack and stroke.
The Silent Risk of Insulin Resistance
Insulin resistance is a risk factor for atherosclerosis* – also called “hardening of the arteries”. Atherosclerosis is where plaque builds up inside the body’s arteries and if the plaque build-up occurs in the heart, brain or kidney, it can result in in coronary heart disease, angina (chest pain) or chronic kidney disease. These diseases are normally associated with Diabetes, but it is the underlying insulin resistance of Diabetes that creates the increased risk – not the high blood sugar itself. Worthy of note, it is being insulin resistance that increases one’s risk – whether or not one also has high blood blood sugar.
The plaque that builds up in atherosclerosis may partially block or totally block blood flow to the heart or brain and if a piece of the plaque breaks off or if a blood clot (thrombus) appears on the plaque’s surface – thiscan block the artery resulting in a heart attack or a stroke (in the brain).
Three quarters of people with normal fasting blood glucose are at increased risk of atherosclerosis and as a result, to heart attack and stroke due to insulin resistance and they don’t even know it, because their blood sugar is normal!
* a few recent references (there are many more): Pansuria M, Xi H, Li L, Yang X-F, Wang H. Insulin resistance, metabolic stress, and atherosclerosis. Frontiers in Bioscience (Scholar Edition). 2012;4:916-931. Santos, Itamar S. et al., Insulin resistance is associated with carotid intima-media thickness in non-diabetic subjects. A cross-sectional analysis of the ELSA-Brasil cohort baseline, Atherosclerosis 2017 Mar 10;260:34-40
Insulin Resistance with Normal Blood Glucose
Dr. Joseph R. Kraft, MD was Chairman of the Department of Clinical Pathology and Nuclear Medicine at St. Joseph Hospital in Chicago, Illinois for 35 years. He spent a quarter century devoted to the study of glucose metabolism and blood insulin levels.
Between 1972 and 1998, Dr. Kraft measured the Insulin Response to a carbohydrate / glucose load in almost 15,000 people aged 3 to 90 years old using a 5-hour oral glucose tolerance test with insulin assays. Data from 10,829 of these subjects indicated that 75% of subjects were insulin resistant — even though their fasting blood sugar level was normal.
That is, having a normal fasting blood glucose level, and normal HbA1C level does not preclude someone from being insulin resistant and at increased risk for heart attack and stroke.
The American Heart Association states on its web page that;
“exactly how atherosclerosis begins or what causes it isn’t known, but some theories have been proposed. Many scientists believe plaque begins to form because the inner lining of the artery, called the endothelium, becomes damaged. Three possible causes of damage to the arterial wall are (1) elevated levels of cholesterol and triglycerides in the blood (2) high blood pressure and (3) cigarette smoking”.
It is known that high triglycerides in the blood are largely a result of diets high in carbohydrates where excess carbohydrate that isn’t converted to glycogen and stored in muscle and liver is stored as triglyceride (three fatty acids attached to a glycerol molecule).
Insulin resistance in our cells, results in our bodies releasing more and more insulin in order to try to clear the same amount of glucose from our blood to store it in our liver as triglyceride (fat!). As covered in the blog post on the hormonal effect of insulin, it is the insulin which drives increased hunger and specifically increased craving for carbohydrates. A viscous circle is created. Diets that are 45-65% carbohydrate result in more and more insulin to handle the same carb load (that is the very nature of insulin resistance) and this increased insulin leads to even more insulin resistance, increased hunger and craving for….you guessed it: more carbs.
Since insulin’s main role is to store the excess glucose not needed immediately to fat – our bodies produce more and more triglyceride (fat!) the more carbs we eat and the more insulin resistant we are. That is, a high carb diet results in high triglycerides – which the American Heart Association recognizes as playing a role in the development of atherosclerosis. That is because triglycerides are converted to VLDLs to transport fat around the body and when their triglycerides ‘passengers’ are depleted, what is left is LDL, the “bad cholesterol” we have all heard about. The ONLY source of LDL is VLDL, and high triglyceride is largely the result of a diet that is too high in carbohydrate.
Insulin also plays a significant role in the regulation of blood pressure through its effect on sodium transport. As insulin rises, excess sodium is retained by the kidneys, increasing blood pressure. Insulin resistance compounds this problem, causing blood pressure to rise even more. It has long been known that people with Diabetes develop high blood pressure – but it is the underlying insulin resistance that is driving that, not the symptom of high blood sugar.
What is alarming is that based on Kraft’s research with ~11,000 people over 20 years, potentially 75% of people are insulin resistant — even though their fasting blood sugar level is normal. This insulin resistance drives the increased triglycerides and high blood pressure that characterize what the American Heart Associations states is believed what underlies the development for atherosclerosis – and the corresponding risk of heart attack and stroke.
Could insulin resistance be a silent killer?
Kraft’s Patterns of Insulin Response
Kraft plotted the data from ~11,000 subjects and five distinct Insulin Response Patterns emerged.
‘Pattern I: is a normal, healthy insulin response to a standard glucose load. Dr. Kraft called this ‘Euinsulin’.
Pattern II — is a hyperinsulinemic insulin response to a standard glucose. Note that Pattern II is considerably greater than the normal insulin response curve (Pattern I) and this greater insulin response is sustained for 5 hours after the ingestion of the glucose.
Superimposing the hyperinsulinemic insulin response of Pattern II over the normal Pattern I insulin response curve, it is easy to see how much higher the Pattern II (yellow curve) is over the normal Pattern I (green) curve. This is the early stages of insulin resistance.
Pattern III — is a hyperinsulinemic insulin response to a standard glucose load. Compared to the normal insulin response curve (Pattern I), it much greater during for 5 hours after taking in the glucose.
Superimposing Pattern III (hyperinsulinemia) insulin response curve over the normal (Pattern I) insulin response curve, its easy to see how the insulin response is delayed (skewed to the right). This results in blood glucose remaining high, as insulin is not responding as it should. Keep in mind, this is occurring in people with normal fasting blood glucose levels.
The Pattern III curve also goes so much higher than the normal Pattern I insulin response curve — which means that more insulin is released and this higher insulin release is sustained for the 5 hours after taking in the glucose.
This is ”silent” pre-diabetes – delayed insulin response and much higher levels of insulin for a much longer time — but with normal fasting blood glucose!
Pattern IV — Pattern IV is what Dr. Kraft calls “Diabetes in Situ” – literally “Diabetes in Place”. Looking at the Pattern IV insulin response curve compared to Pattern I (the normal insulin response), it is apparent that it is much greater for the entire 5 hours after taking in a standard amount of glucose.
Surprisingly, 40% of people with a Pattern IV Insulin Resistance still had normal fasting blood glucose.
75% of people displaying Pattern II, II or IV insulin responses do not know that they are at greater risk for atherosclerosis and as a result to heart attack and stroke because they have no symptoms. Their blood sugar levels are normal.
Finally, insulin resistance is the most common cause of Type 2 Diabetes.
Normal fasting blood glucose and normal HbA1C results do not reveal whether or not a person is insulin resistant – only a 2 hr glucose tolerance test can do that. Unfortunately, a 2 hour glucose tolerance test is usually only requisitioned when fasting blood glucose and HbA1C results come back abnormal.
Potentially, up to 75% of people are insulin resistance and have NO IDEA!
They are at increased risk for heart attack and stroke and have NO SYMPTOMS.
They don’t have increased thirst or increased urination like Type 2 Diabetics, but are at the same risk.
The Good News
The good news is, we can lower insulin resistance – and as a byproduct of that, shed excess weight in the process. This is accomplished through (1) a low carbohydrate diet with or without the use of (2) stretching the amount of time between meals (sometimes called “intermittent fasting”).
When designed properly, a low carbohydrate diet can provide all of the recommended intake of vitamin and minerals – while lowering insulin resistance.
That is where I come in.
I can assess your physiological needs for energy and nutrients and design an Individual Meal Plan that will enable you to lose weight, without being hungry all the time – and that will help lower your insulin resistance and the associated risk of cardiovascular disease related to insulin resistance.
Want to know more? Click on the “Contact Me” tab above and send me a note.