INTRODUCTION: In the first article in this series on carbohydrates, I explained that Glycemic Index (GI) is a way to rate carbohydrates based how easily they raise the blood sugar of healthy people and that some carbohydrates are better than others when they cause much less of a rise in blood sugar. I wanted to know how would I react to carbohydrate-based foods now that I have been eating low carb for so long (>1 year) and have seen a partial reversal of symptoms of the Type 2 Diabetes that I’ve had for more than 10 years.

I decided to conduct some impromptu ‘experiments’ and the results led to some reading in the literature. The information I discovered is VERY exciting for me and for others with Type 2 Diabetes or Insulin Resistance.

Once people have achieved significant reversal of symptoms following a therapeutic low carb or ketogenic diet, there is a way to begin to re-introduce carb-based foods in a way that does not cause their blood sugar to spike.

As you may recall from the first article in this series on Carbohydrates, the Glycemic Index of a food is determine by having healthy people eat 50 grams of digestible carbohydrate of a given food, and then measure their blood glucose response over a 2 hour period (30 minutes, 60 minutes, 90 minutes, 120 minutes), plotting the curve then measuring the area under the curve (AUC) and comparing it to the AUC of pure glucose, the reference food.

The problem with the Glycemic Index or even the Glycemic Load (based on individual serving sizes) is that this data does not apply to those with Diabetes or Insulin Resistance.

Since I have been Diabetic for a long time, I decided to go about conducting my own sample-set-of-one (n=1) ‘experiment’, and one thing led to another…

The ‘Test Food’

I ate 1/2 cup of chickpeas (cooked from dried) which has 25 g of carbohydrate and measured my blood sugar response with the same meter at 30 minutes, 60 minutes, 90 minutes, 120 minutes, 180 minutes and 210 minutes.

At the time I did this, I hadn’t eaten in 8 hours (considered a fasted state) and my starting blood sugar was 4.8 mmol/L (86 mg.dl). The chickpeas were part of a mixed meal with some chicken (high biological value protein) and a cucumber salad with olive oil.

At the highest point, my blood sugar went up to 5.8 mmol/L (105 mg/dl),  stayed there, then started to drop at 2 hours.

I was amazed.

When I first began changing my lifestyle a year ago, even eating low GI foods such as chickpeas caused my blood sugar to jump dramatically. I recall the first few months when I would eat 1 cup of hummus, which is chickpeas with tahini (ground sesame seeds) and has even more fiber than chickpeas alone and also has only 25 g of carbs, my blood sugar would always go up to ~ 8.6 – 8.9 mmol/L (155- 160 mg/dl).

This was a HUGE improvement after not eating more than 30 g of carbohydrate per day (i.e. a ketogenic diet) for the last 6 months!

The ‘Reference Food’

Two weeks ago, I was at a social occasion where a milk-chocolate covered cracker was served and I decided (in the interest of science, of course!) to read the nutritional label, measure out exactly 25 g of carbohydrate of this food and eat it, measuring my blood sugar at 0 minutes, 60 minutes, 90 minutes, 120 minutes, and 180 minutes.

This ‘reference food’ (high GI) was eaten after a dinner that had a fair amount of high biological value protein (steak) as well as some healthy fats (olive oil on vegetables) and fiber in the vegetables, and my starting blood sugar was 6.7 mmol/L (121 mg/dl).

Just look at the blood sugar spike!

When I ate 25 gm of carbohydrate as the cracker and chocolate, my blood glucose went from 6.7 mmol/L to 9.8 mmol/L (121 mg/dl -177 mg/dl)! That is, I had eaten the SAME amount of carbohydrate (25 g of carbs) as when I ate the cooked chickpeas and had THREE TIMES the blood sugar response!!

Both the meals I ate just before the ‘reference food’ (high GI, highly refined cracker with chocolate) and the ‘test food’ (low GI, intact chickpeas) had a high biological value protein (chicken, steak) which slows the blood sugar response of the body, and both had the same amount of fiber (the exact same salad).

Below is a graph of the two responses (chickpeas in blue, chocolate covered cracker, orange) over 3+ hours.

It is quite evident that 25 g of carbs as white flour with milk chocolate (refined carbs) is processed VERY differently by my body than 25 g of carbs such as whole, intact chickpeas!!

The area under the curve (AUG) was determined by lowering the cracker and chocolate curve down to sit just above the chickpea curve (grey curve) and then assessing where the respective points were and running the AUG formula relative to baseline.

The AUG of 25 g of carbs as chickpeas was 129.

The AUG of 25 g of carbs as white flour cracker with chocolate was 381.

The difference was 2.95.

The blood sugar response of the cracker with chocolate was THREE TIMES GREATER than the blood sugar response of the chickpeas – and both contained 25 g of carbs!

Some carbs are quite clearly better than others for this Type 2 Diabetic.*

* As I will elaborate on below, people’s blood sugar response to different carbohydrate-based food is quite individual.

Objective Data

Facsimile for Glycemic Index of Cracker with Chocolate

I was able to find for purposes of estimation, that 25 g of carbohydrate as white bread with 5 g of margarine (a pretty good facsimile for 25 g of carbohydrate as white flour cracker covered with milk chocolate made with palm oil) has a GI of 70.1 when compared to the reference which was 25 g glucose in 125 ml water [1].

Studies of Effect of Eating Legumes (Pulses) Alone

A meta-analysis of 10 studies on the effect of pulses (legumes) eaten alone on blood sugar control in people with and without Diabetes [2] provided some helpful information. The pulses in the meta-analysis included chickpeas, black-eyed peas and various other beans (including red and white kidney, black, pinto, fava and white navy).

Seven of the 10 trials that looked at the effect of eating pulses alone had a crossover design (five had a washout period), studied a total of 253 participants, of which only 21 had Type 2 Diabetes, and 232 that had normal blood sugar.

Background diets were largely high-carbohydrate, low-fat diets (carbohydrate 52% of energy, protein 18% of energy, fat 29% of energy).

Due to the length of time I have had Type 2 Diabetes and the very high degree of persistent insulin resistance over the first 6 months of eating low carb but not ketogenic, the last 6 months my diet has been very low in carbohydrate (5-10% of energy), moderate in protein ~23% and 67-77% healthy fats.

It was found that fasting blood glucose following the eating of pulses alone was decreased by 0.82% (95% CI ), but there was no long term effect on HbA1C (3 month average blood sugar) or on HOMA-IR (fasting blood glucose: fasting insulin).

[Of interest, in low GI diets, eating of pulses lowered HbA1C (3 month average blood sugar) by 0.28% but had no change on fasting blood sugar or HOMA-IR. The average GI of the pulse-containing low-GI diets was 67 and as compared to the GI value of bread alone.]

The conclusions of the meta-analysis found that the strongest modifiers of benefit were in Type 2 Diabetes and that the legumes that modified blood sugar the most were black beans, white/navy beans, pinto beans, red and white kidney beans, chickpeas and fava beans.

“Specific to the pulses alone analysis, pulse species including Phaseolus vulgaris (black, white, pinto, red and white kidney beans), Cicer arietinum (chickpeas) and Vicia faba (fava beans) were also identified as significant modifiers.” [2]

Individual Glycemic Response  – role for personalized nutrition

A 2015 study from Israel[3] with 800 people who were monitored with continuous glucose monitors indicates that there isn’t a ‘universal’ blood sugar response to low GI foods or high GI carbs – that glycemic (blood sugar) response is very individual. 

“We continuously monitored week-long glucose levels in an 800-person cohort, measured responses to 46,898 meals, and found high variability in the response to identical meals, suggesting that universal dietary recommendations may have limited utility.

The study also found that an individual’s blood sugar response to different foods was able to be predicted by type and amounts of bacteria in their intestines (the ‘gut biome’ / ‘microbiome’ / ‘microbiota’) . 

Based on the data they collected, the team has since created and validated a machine-learning algorithm that combines blood parameters, dietary habits, anthropometrics (height, weight data), physical activity and gut microbiota  data that they say accurately predicts a person’s individual post meal blood sugar response to actual meals.

Applications in Dietetic Practice for Personalized Nutrition

There is a tremendous opportunity for Dietitians such as myself to help individuals with Type 2 Diabetes or pre-diabetes determine which carbohydrate-based foods cause the lowest, most gradual rise in blood sugar.

This is huge!

This means that after individuals have had significant reversal of Type 2 Diabetes / Insulin Resistance following a therapeutic low carb or ketogenic diet for a period of time, I can help them re-introduce carb-based foods into their diet by selecting ones that have the least impact on their blood sugar!

There are two ways this can be done;

1. USING EXISTING BLOOD GLUCOSE METER – I can help those with Type 2 Diabetes eat a specific amount of a ‘test food’ that contains 50 g of carbohydrate (I will calculate this for them) and have them test their blood sugar every 30 minutes for 2 or 3 hours with the blood glucose meters they already have.  Then, I can take that data, enter it into an Excel sheet just as was done with my data above, and determine their blood sugar response.
2. USING A CONTINUOUS GLUCOSE MONITOR – continuous glucose monitors (CGMs) such as the FreeStyle Libre have become relatively inexpensive and would be ideal for this kind of testing. Test strips for most standard home blood glucose monitors are $1 a piece, so testing every 30 minutes for 3 hours costs $6. The FreeStyle Libre costs $50 for the unit, and while test patches are $90 and last only two weeks, huge varieties of carbohydrate-based foods can be tried and measured in a short time, with no effort.

As a Dietitian I can not only help individuals carry out this kind of individual testing of carbohydrate-based foods, I can help them interpret the results as we begin to re-introduced some foods back into the diet once significant reversal of insulin resistance has been accomplished through the therapeutic use of a low carbohydrate or ketogenic diet.

Have questions how I can help you reverse insulin resistance by following a therapeutic low carb diet? Have you been following a low-carb or ketogenic diet for a while and want to begin determining which carb-based foods don’t spike your blood sugar? I can help.

Please send me a note using the “Contact Me” form on this web page and I will respond shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

1. Aston LM, Gambell JM, Lee DM, Bryant SP, Jebb SA. Determination of the glycaemic index of various staple carbohydrate-rich foods in the UK diet. European journal of clinical nutrition. 2008;62(2):279-285.
2. Sievenpiper, J.L., Kendall, C.W.C., Esfahani, A. et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia (2009) 52: 1479.
3. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

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

In the introduction to this series on Carbohydrates, I explained that Glycemic Index (GI) is a way to rate carbohydrates based how easily they raise blood sugar. If you recall, low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar.

The GI value of a food is determined comparing how healthy people’s blood sugar responds over a two hour period to a food containing 50 grams of digestible carbohydrate from that food compared to 50 grams of glucose (pure sugar). The drawback to this rating scale is that the values are only known for a serving that has 50 grams of carbs in it.  That is, they compare the ability for different foods containing the SAME amount of carbohydrate it (50 g) to raise blood sugar. The problem with the Glycemic Index is that its hard to compare foods because a serving size may have considerably less than 50 g of carbs in it.  For example, the Glycemic Index of watermelon is 76, which is as high as the Glycemic Index of a doughnut, but one serving of watermelon (1/2 a cup) has 11 g of carbohydrate in it, while a medium doughnut (one serving) has 23 g of carbs.

This is where the concept of Glycemic Load (GL) is much more helpful, because it tells us how a healthy person’s body will respond to the carbs in one serving of a food. One usual serving of a food would be considered to have a very high Glycemic Load if it is ≥20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

How to Determine Glycemic Load

To determine Glycemic Load  (GL) of a serving of a food, what needs to be known is:

The Glycemic Index (GI) of that food (found by referring to a table of Glycemic Indexes)

The number of grams of carbohydrate in the quantity of food considered to be one serving.

• GL  = GI x (amount of carbohydrate per serving) / 100

For purposes of comparison,  let’s look at the Glycemic Load of the same foods we looked at the Glycemic Index for in the first article.

One slice of white bread has a Glycemic Load of 10 and so does one slice of whole wheat bread, which is considered low. Both have 15 g of carbs per slice.

One 1 cup of cooked white spaghetti has a Glycemic Load of 25 which is considered very high and while 1 cup of whole grain spaghetti only has a Glycemic Load of 14, this is still not low, just lower than white spaghetti.

A cup of boiled white rice has 53 g of carbs in it and has a very high Glycemic Load = 35. A cup of white spaghetti has 44 g of carbs in it and also has a very high Glycemic Load at 25. These foods are high in carbohydrate and will cause a rapid rise in blood sugar in healthy people. To those who are already Diabetic or pre-Diabetic this is a big problem.

One cup of cooked whole grain spaghetti has a Glycemic Load of 14 which is still not low and has 37 g of carbs in it.

A cup of boiled brown rice has a Glycemic Load of 20 which is still considered very high and has 42 g of carbs.  These foods are high in carbohydrate and will cause a fairly rapid rise in blood sugar in healthy people, let alone those who are already having problems.

So what’s the problem?

Eating a high Glycemic Load diet over a period of years and years will result in blood sugar after meals (called post prandial blood glucose) to be high. This puts a huge demand on the body to keep releasing insulin to try to move all that glucose into the body’s cells and get it out of the blood. Over time, a high Glycemic Load diet causes the body’s pancreas β-cells (beta cells) to decrease in function or in many cases, to die, resulting in a diagnosis of Type 2 Diabetes. As can be seen above, even eating the “whole grain” version of favourite foods does not necessarily reduce the insulin demand on our pancreas. Our  β-cells are under continual pressure to release insulin every time we eat – from our breakfast toast or cereal, to our mid-morning muffin, to our pasta lunch. Eating a low carb diet is a very effective way to lower the demand on our pancreas to keep producing and releasing insulin to deal with the constant spikes in our blood sugar from carbohydrate containing foods. But does that mean we need to remain eating a low carb diet forever? More on that in future articles in this series.

Glycemic Load will tell us how much a serving of food will increase our blood sugar but it doesn’t tell us how much insulin our body releases as a result of eating a food – that is, the demand we are putting on our pancreatic β-cells.

For those that have been eating a high carbohydrate diet for years and years or have a family history of Type 2 Diabetes, knowing how much insulin is needed to process the carb -based foods we eat is hugely important, because we need to eating foods that do not put a large demand on our pancreatic β-cells.  For those that already have Type 2 Diabetes, it is especially important to eat in such a way as to preserve whatever β-cell function we have left!  Referring to the Insulin Index enables us to choose between carb-based foods based on the demand they put on our β-cells.

If you have questions as to how I can help you choose foods that result in much less glucose being released and also put much less demand on your  β-cells to keep producing and releasing insulin, please send me a note using the “Contact Me” form located on the tab above.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Reference

Oregon State University, Linus Pauling Institute, Micronutrient Information Centre, Glycemic Index and Glycemic Load http://lpi.oregonstate.edu/mic/food-beverages/glycemic-index-glycemic-load#glycemic-index

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

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

INTRODUCTION: Not all carbs are created equal; some are broken down very quickly into simple sugars and others are broken down very slowly. In the past the terms “simple sugar” and “complex carbohydrate” were used to imply this concept there are newer terms that enable us to know how much eating these foods will raise blood glucose in healthy people. The “in healthy people” is important, as the ability to tolerate carbohydrate in those with insulin resistance (“pre-diabetes”) or Type 2 Diabetes is significantly affected.

This is the first article in a new series on carbohydrate.

Glycemic Index

The Glycemic Index (GI) is a way of rating carbohydrates based on their ability to raise blood sugar.

Low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar. Keep in mind that Glycemic Index only indicates how slowly or quickly foods will increase blood sugar, not how much higher blood sugar will go

Many of the foods people eat lots of in our society, such as bread, rice, pasta and cereal, even vegetables, are high GI foods. As once healthy people continue to eat these foods on a regular basis, they put a high demand on their body to produce and release insulin, which brings all that glucose into their cells. This insulin is released from the beta cells in the pancreas and people eating these high GI foods means that their beta cells have to release insulin over and over all day long and this constant demand on the beta cells, over time, results in the cells throughout their body becoming insulin resistant (no longer responding to insulin’s signal) or burning out their beta cells, resulting in Type 2 Diabetes.

Many people don’t realize that by the time they are diagnosed with Type 2 Diabetes, they already have beta cell dysfunction, beta cell death and/or a decrease in beta cell mass. Once beta cells die, they’re gone. Our once healthy body is no longer healthy.  When we eat foods with significant carbohydrate – especially high GI carbohydrates, our ability to release insulin is significantly impacted and as a result, we can no longer tolerate carbs like we used to.  While the mechanism is different, it’s similar to someone that becomes intolerant to gluten; once they’re celiac, they can no longer tolerate foods that contain gluten without causing damage to their body.  Depending how long someone had Type 2 Diabetes when they were finally diagnosed, or how long they had it before they changed their eating habits will all factor in to how much carbohydrate they can process. For this reason, each person is different.

It’s not that carbs are inherently “bad”. It’s that our bodies are no longer able to process some of them they way we could when we were still healthy – so in those cases the sugar stays in our blood, damaging tissues throughout our body.

Knowing which carbs are high GI is important, because these are the foods that tax our already overtaxed beta cells if we are not Diabetic and limiting these foods significantly, or avoiding may be the best way for healthy people to remain healthy.

The good news is that there are some types of carbohydrates that some people can not only tolerate, but may actually improve their blood sugar control, and that’s the topic of an upcoming article.

How the GI of a Food is Determined

The GI value of a food is determined by feeding a group of healthy people the amount of a food that contains 50 grams of digestible (available) carbohydrate and then measuring the effect on their blood glucose levels over the next two hours. The area under their two-hour blood glucose response (glucose AUC) for this food is then measured.

At another time, the same group of healthy people eat 50 grams of glucose, (which is the reference food) and their two-hour blood glucose response is also measured.

The GI value for the test food is calculated for each person in the group by dividing their glucose AUC for the test food by their glucose AUC.

The final GI value for the test food is the average GI value all the people in the group.

In summary to determine the Glycemic Index of a food healthy (non-diabetic) people;

(a) eat 50 grams of digestible carbohydrate of a particular food

(b) measure their blood glucose response over a 2 hour period

(c) plot the curve and measure the area under the curve (AUC)

(d) compare that AUC of the test food to the AUC of pure glucose (i.e. produced when the same people eat 50 g of glucose, which is the reference food.

Too Much of a ‘Good’ Thing

Many of the foods that people in the West enjoy and eat a lot such as bread, rice and noodles are High GI foods – these are ones that are rated at  ≥ 55 (compared to pure glucose, which is rated at 100).

White bread has a GI of 75 ± 2 and whole wheat bread isn’t much better, at 74 ± 2.

Boiled white rice is high GI at 73 ± 4, and while somewhat better boiled brown rice is still high GI at 68 ± 4.

White spaghetti has a GI of 49 ± 2 and whole grain spaghetti has a GI of 48 ± 5.

Rice noodles, such as those in Pho (Vietnamese Beef Noodle soup) are even higher, at 53 ± 7.

Breakfast cereals, whether boxed or cooked are also high GI.  Here is a table that summarizes some of these [1];

Many people include vegetables such as potato, sweet potato and squash such as pumpkin in their “vegetable quota” for the day, but let’s look at the Glycemic Index for these;

People in our culture eat a lot of bread, rice, pasta, starchy vegetables and cereal but one of the things we know is that eating them with good source of protein slows down how quickly they affect blood sugar. Oftentimes bread and cereal form the basis of breakfast, perhaps with a high GI glass of juice and frequently, people eat pasta with a tomato sauce for supper (or leftovers for lunch), and this kind of meal will spike their blood sugar. We also know that the fiber content of a mixed meal will also slow down the rate at which blood sugar rises from these carbs, so there are ways to ‘tone down’ the response.

Some Final Thoughts…

If you have a family history of Type 2 Diabetes, are overweight or have high blood sugar, it’s important to understand that what you eat matters and to eat in a way that does not put high demand on your beta cells to keep releasing insulin to process all that glucose.

The time to consider the effect on your body is now – before you get sick by having overtaxed your pancreas’ beta cells and experience beta cell death or mass loss and are diagnosed with Type 2 Diabetes.

Once we’ve crossed that threshold; once our once healthy body is no longer healthy, we need to learn to eat in a way that does not put high demand on our beta cells, that does not require our body to process large amounts of glucose at a time, in order to preserve whatever beta cell mass and function we have left.

Determining which carb-containing foods we can tolerate and in what quantities will enable us to eat in a way that keeps us from getting worse and keeps us from developing the very serious consequences of not doing so, which can include blindness, toe and food amputations and more.

In coming articles, I’ll explain Glycemic Load and the Insulin Index and I’ll also touch on a role for legumes (pulses) such as chickpeas and sources of “resistant starch” in a moderate carb ‘Mediterranean-style’ diet.

If you just found out you are pre-diabetic, now is the time to do something about it. Waiting will not make it better.

If you’ve been recently be diagnosed with Type 2 Diabetes, it’s not too late.  Studies have shown that changing eating habits and lifestyle soon after diagnosis makes it possible for some people to reverse their symptoms and to have their Diabetes go into remission. One thing is known, that doing nothing will bring needless firsthand understanding to the phrase that “Diabetes is a chronic, progressive disease”.  It doesn’t have to be.

If you want to know how I can help you, please send me a note using the “Contact Me” form located on the tab above.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

1. https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods

Also see: Atkinson FS, Foster-Powell K, Brand-Miller JC, “International tables of glycemic index and glycemic load values”, Diabetes Care 31(12); 2281-2283

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

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

Claims are sometimes made that “low carb diets are a fad” and “there needs to be scientific evidence to demonstrate they are both safe and effective“. What is the evidence?

In fact, a low carbohydrate diet is not new and was the standard recommendation for treating Diabetes prior to the discovery of insulin. More than 150 years ago, the first weight-loss diet book (ironically written by William Banting, a distant relative of Sir Frederick Banting, the co-discoverer of insulin) focused on the limiting the intake of carbohydrates, especially those of a starchy or sugary nature. The book was titled Letter on Corpulence — Addressed to the Public (1864) and summarized the advice of the author’s physician, Dr. William Harvey that had enabled Banting to shed his portly stature’.

Recent 10 week results of a nonrandomized, parallel arm, outpatient intervention using a very low carb diet which induced nutritional ketosis  was so effective at improving blood sugar control in Type 2 Diabetes, that at the end of six months >75% of people had HbA1c that was no longer in the Diabetic range (6.5%). Details of the findings from this study titled A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes are available here.

I recently reviewed 2 two-year studies that demonstrated that low carb diets are both safe and effective for weight loss and improving metabolic markers;

1. This long-term study titled Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet clearly demonstrated that a low carb non—calorie-restricted diet was both safe and effective and produced the greatest weight loss, lower FBS and HbA1C, the most significantly lower TG and higher HDL and lower C-reactive protein (when compared with a  low-fat calorie-restricted diet and a Mediterranean calorie-restricted diet).
2. This 2-year, randomized control study of more than 300 participants  titled Low Fat Calorie Restricted Diet versus Low Carbohydrate Diet — a two year study found that both diet groups achieved clinically significant and nearly identical weight loss (11% at 6 months and 7% at 24 months) and that people who ate the low-carbohydrate diet had greater 24-month increases in HDL-cholesterol concentrations than those who ate a low-fat calorie restricted diet. As well, a significant finding of this study was a very favourable lowering of LDL for the first 6 months and lowering of both TG and VLDL for the first year.

These long-term data provide evidence that a low-carbohydrate diet is both a safe and effective option for weight loss and that this style of eating has a prolonged, positive effect on metabolic markers.

But is this all the evidence we have?  By no means!

Below is a list of research studies and meta-analyses (complied by Dr. Sarah Hallberg) that used a low-carb intervention. These span 18 years, 76 publications, involve 6,786 subjects, and include 32 studies of 6 months or longer and 6 studies of 2 years or longer. At the bottom of this post is a downloadable pdf of this list. [Note: text in green represents meta-analyses.]

Hardly a passing fad!

Low carb diets have been well-studied and found to be both safe and effective.

Many thanks to Dr. Sarah Hallberg, a Physician and exercise physiologist from West Lafayette, Indiana (Twitter: @DrSarahHallberg) for compilation of this list.

A complete list of the Low Carb Diet studies to date (compiled by Dr. Sarah Hallberg) is available here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

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

What all low carb diets have in common is that they are low in carbohydrates and high in healthy fats, but they vary with respect to the amount of protein and fat. This is part 1 in a new series titled The Role of Protein in the Diet, and outlines the problem with current carbohydrate intake in terms of the recommended dietary requirements.

This article is based largely on a lecture given by Dr. Donald Layman, PhD – Professor Emeritus from the University of Illinois (Nutrition Forum, June 23, 2013, Vancouver, British Columbia, Canada)

Sometimes, when people debate what is, or isn’t a “high protein diet” they define it in terms of the percentage of calories in the diet but this is really meaningless.

For example, someone may be eating only 56 gm of protein  which was 28% of the 800 calories per day they ate and someone else may be eating 160 gm of protein which is 34% of the 2000 calories they are eating per day.

Both are eating ~30% of calories as protein but there is a big difference between 56 gm of protein and 160 gm of protein.

According to Dr. Donald Layman PhD [1], when we speak of a “high protein diet”, we need to discuss the absolute amount of protein in grams, not as a percentage of calories,  because adequacy in determined on the basis of absolute intake.

The Recommended Daily Allowance (RDA) for Protein

The Recommended Daily Allowance (RDA) for any nutrient is the average  daily dietary intake level that is sufficient to meet the requirements of 97 – 98 % of healthy people. This is not the optimum requirement, but the  absolute minimum. The RDA for Protein, Carbohydrate and Fat are as follows;

Protein: 56 g (224 kcals)
Carbohydrate: 130 g* (520 kcals)
Fat: 30 g (270 kcals)

The RDAs for Carbohydrate[2] is set at 130 g / day, but as established in an earlier article, How Much Carbohydrate is Essential in the Diet, we know that even in the absence of dietary carbohydrate (not recommended!), the minimum amount of glucose needed by the brain of 130 g / day can be made from protein and fat,  provided they are eaten in adequate amounts.

The RDA for Protein is set at 56 gm per day, so whether a person is eating 800 calories a day or 2000 calories per day, their body has an absolute requirement for 56 gm of protein per day.

This range from 56 g to 200 g of protein per day is referred to as the range of safe intake[2].

According to Dr. Layman, a high protein diet doesn’t start “until well above 170 g / day“.

There are low carb diets that are higher in protein than others, and to distinguish between the two, the one that is higher in fat than protein (in grams) is referred to as a low carb high fat (LCHF) diet and the one that is higher in protein (in grams) is referred to as a low carb high protein (LCHP) diet – but it really isn’t “high protein”, but higher protein.

Current Dietary Intakes – the problem with carbs

Protein Intake in the US and in Canada is ~70 g of protein per day in women and in men about 90 g of protein per day (~15-16% of calories). Given the range of safe intake of protein from 56 g to 200 g of protein per day, dietary intake of protein in the US and Canada is very low.

The RDAs of macronutrients, which is the minimum amount required per day is just over 1000 calories per day, as follows;

Protein: 56 g (224 kcals)
Carbohydrate: 130 g (520 kcals)
Fat: 30 g (270 kcals)*
         1017 calories*

Current Intake of macronutrients is as follows;

Protein: 70 g (280 kcals)
Carbohydrate: 300 g (1200 kcals)
Fat: 90 g (820 kcals)
         2300 calories

***That means there are between 1000 calories and 1300 calories per day of ‘discretionary calories’ – calories above and beyond the minimum requirements of 97-98% of healthy individuals.***

How should we eat to make the most of these calories?

What is going to give us the best health?

Currently, we are eating 3 times the RDA for carbohydrate (300 g carbohydrate per day!) and very close to the minimum for protein. Is this the right balance?

What evidence is there for this being the ‘right balance’?

Eating Well with Canada’s Food Guide, as with the US Dietary Recommendations emphasizes lots of whole grains and high carb intakes and very low protein intake. For a long time in both countries, we’ve highlighted that the issue is fat. But is this correct?

It was thought that since fat has a high caloric density, reducing fat intake would reduce calorie intake and that’s where the US Food Pyramid and Eating Well with Canada’s Food Guide comes from.

In both cases, the message is ‘stay away from fats‘, ‘stay away from proteins‘, ‘eat lots of cereal grains‘.

So how did that work out for us?

The Food Guide Pyramid first appeared in the US in 1988- exactly when obesity rates exploded.  It tracks back almost to the date…obesity, Diabetes.

This occurred as we started consuming more and more cereal grains and this, according to Dr. Layman “is the origin of the problem”.

Let’s first look at children;

• In 1978, only 15% of children and adolescents were overweight or obese.
• By 2007, that rate had doubled to 29% of children and adolescents being overweight or obese.
• By 2011, obesity prevalence alone for boys was 15.1% and for girls was at 8.0% in 5 to 17 year olds.

What about adults?

• The prevalence of obesity [body mass index (BMI) ≥30 kg/m²] in Canadian adults increased from 10% in 1970-72 to 26% in 2009-11
• Based on waist circumference 37% of adults and 13% of youth are abdominally obese.
• Looking at these numbers slightly differently, as of 2013, there were approximately 7 million obese adults and 600 000 obese school-aged children in Canada.

What exactly changed in the Dietary Guidelines that caused us to  get fat?

For one, Dr. Layman points out, caloric intake was increased by 300 calories per day and according to the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010 these extra 300 calories per day came from these 6 categories:

1. grain based desserts and snacks
2. yeast bread
3. pasta
4. pizza
5. chicken and chicken products
6. soda and sports drinks

These are all grain-derived products in excess of our caloric needs. See the pattern? The fifth category includes breaded chicken products, such as chicken fingers and chicken nuggets and even soda and sports drinks, sweetened with high fructose corn syrup are grain derived.

All of these grain-derived products are in excess of our caloric needs. This is only part of the problem with current dietary intake of carbohydrates.

In the next article in this series, I’m going to take a look at our current high intake of dietary carbohydrates in terms of the history of man’s diet and the length of time that we’ve had to adapt to eating them.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

1 – Layman, Donald, The Evolving Role of Dietary Protein in Adult Health, Nutrition Forum, British Columbia, Canada, June 23, 2013 https://youtu.be/4KlLmxPDTuQ

2 – Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005), pg 275

3 – Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

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

INTRODUCTION: To date, there have been 3 long-term clinical trials (2 years) published over the past 10 years involving “low carb diets”.

The first long-term study that was presented in the previous article (which can be read here) clearly demonstrated that a low carb non—calorie-restricted diet was both safe and effective and produced the greatest weight loss, lower FBS and HbA1C, the most significantly lower TG and higher HDL and lower C-reactive protein (when compared with a low-fat calorie-restricted diet and a Mediterranean calorie-restricted diet).

In this, the second of the three long term studies, researchers looked at the effectiveness of four dietary interventions with different composition of fat, protein and carbohydrate – including one “low carb” diet..

Did this study demonstrate that a “low carb” diet was safe and effective to result in weight loss?

Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates

Participants

This study involved over 800 overweight and obese subjects, of which 40% were men. Subjects were between the ages of 30 and 70 years and had a Body Mass Index (BMI) of 25-40, where BMI is the weight in kilograms divided by the square of the height in meters.

BMI =25.0-29.9 is considered overweight
BMI = 30.0-34.9 is Class I obesity
BMI = 35.0-39.9 is Class II obesity
BMI ≥ 40.0 is Class III obesity

Major criteria for exclusion from this study were the presence of Diabetes or unstable cardiovascular disease, the use of medications that affect body    weight and insufficient motivation as assessed by interview and questionnaire.

Of the 811 subjects that began the study, at the end of two years, 645 subjects remained enrolled. Approximately 80% of the participants were white, 15% black, 4% Hispanic and the remaining 1% Asian.

The Four Diets – high/low fat, high/low protein

The 811 overweight adults were randomly assigned to one of four diets:

1. Low Fat, Average Protein: fat: 20%, protein: 15%, carbohydrate: 65% (202 subjects)
2. Low Fat, High Protein: fat: 20%, protein: 25%, carbohydrate: 55% (202 subjects)
3. High Fat, Average Protein: fat: 40%, protein: 15%, carbohydrate: 45% (204 subjects)
4. High Fat, High Protein: fat: 40%, protein: 25%, carbohydrate: 35% (201 subjects)

Two Diets were Low Fat but Two were not High-Fat Diets

The researchers stated that “two diets were low-fat and two were high-fat”, but it is important to note that none of the diets were “low carb high fat”/ ketogenic diets, which are â‰¥ 65% fat (not 40% fat). Two of the diets were higher in fat than the recommended dietary intake (in both the US and Canada).

Two Diets were Average Protein but not High Protein

The researchers said that “two diets were average protein and two were high protein” and while the ‘average protein intake’ in the US in 2008 was ~15%  (16.1% for men and 15.6% for women), diets such as two of the ones in this study that have only 25% protein are really at the very lowest range of what are considered high-protein diets – which normally contain between  27 – 68 % protein. Also important to note, a “low carb high fat”/ ketogenic diet usually has ~20% protein (considered ‘moderate protein’) and are not high protein diets.

Two Diets were High Carb and One Diet was Moderate Carb

The first and second dietary interventions would both be considered high carb, as they fall within the range of the dietary recommendations in both  Canada and the USA, 45-65% carbohydrate, with one being higher protein and one being average protein.

The third diet would be consider “moderate carb” according to Diabetes Canada’s standards, at 45 % carbohydrate, and higher fat and higher protein.

One Diet was Low Carb but not Ketogenic – and not Low Carb High Fat

The fourth diet could be considered ‘low-carb’ at 35% carbohydrate, but it is not a ketogenic diet, as the percent of carbohydrate is too high. A ketogenic diet has between 5-10% carbohydrate.  It was not a “high fat diet”, as the fat is only 40%, not â‰¥ 65% fat.

None of the dietary interventions in this study was ‘low-carb high fat’ or ketogenic, however one diet was “low carb”.

Other Study Goals and Information

Other goals for all the dietary interventions were that the diets had;
– 8% or less of saturated fat
– 20 g or more of dietary fiber
– 150 mg or less of cholesterol per 1000 kcal

Each participant’s calories represented a deficit of 750 kcal per day
from baseline, as calculated from the person’s resting energy expenditure and activity level (which should have promoted a weight loss of ~ 1.5 pounds per week).

Blinding between the groups was maintained by the use of similar foods in each of the dietary interventions.

Staff as well as participants were taught that each diet adhered to principles of a “healthful diet” and that each had been recommended for “long-term weight loss”.

Group dietary counselling sessions were held once a week, 3 of every 4 weeks during the first 6 months and 2 of every 4 weeks from 6 months to 2 years; individual sessions were held every 8 weeks for the entire 2 years. Behavioral counseling was integrated into the group and individual sessions to promote adherence to the assigned dietary intervention.

Participants were instructed to record their food and beverage intake in a daily food diary and in a web-based self-monitoring tool that provided information on how closely their daily food intake met their dietary intervention’s goals for macronutrients and calories.

The goal for physical activity was 90 minutes of moderate exercise per week. Participation in exercise was monitored by questionnaire and by
the online self-monitoring tool.

Measurements

Body weight and waist circumference were measured in the morning before breakfast on 2 days at baseline, 6 months, and 2 years, and on a single
day at 12 and 18 months.

Levels of serum lipids, glucose, insulin, and glycated hemoglobin (HbA1C) were measured via fasting blood samples, and 24-hour urine samples, and measurement of resting metabolic rate were obtained on 1 day, and blood-pressure measurement on 2 days, at baseline, 6 months and 2 years.

Results

Weight loss and Waist Circumference

The amount of weight loss after 2 years was similar in participants assigned to a diet with 25% protein and those assigned to a diet with 15% protein.

Weight loss was the same in those assigned to a diet with 40% fat and those assigned to a diet with 20% fat.

There was no effect on weight loss of carbohydrate level through the target range of 35 to 65%.

Most of the weight loss occurred in the first 6 months, however 23% of the participants continued to lose weight from 6 months to 2 years.

The change in waist circumference did not differ significantly among the diet groups.

At 2 years, 31 to 37% of the participants had lost at least 5% of their initial body weight, 14 to 15% of the participants in each diet group had lost at least 10% of their initial weight, and 2 to 4% had lost 20 kg or more.

Risk Factors for Cardiovascular Disease and Diabetes

All the diets reduced risk factors for cardiovascular disease and Diabetes at 6 months and 2 years.

At 2 years, the two low-fat diets and the highest-carbohydrate diet decreased low-density lipoprotein (LDL) cholesterol levels more than did the high-fat diets or the lowest-carbohydrate diet, 5% vs 1%. And at 2 years, the highest carbohydrate decreased LDL more (6%) versus the lowest carbohydrate diet (1%).

The lowest-carbohydrate diet increased HDL cholesterol levels more (9%) compared with the highest-carbohydrate diet (6%).

All the diets decreased triglyceride (TG) levels similarly, by 12 to 17%.

All the diets except the one with the highest carbohydrate content decreased fasting serum insulin levels by 6 to 12% – and the decrease was larger with
the high-protein diet than with the average-protein diet (10% vs. 4%).

Blood pressure decreased from baseline by 1 to 2 mm Hg, with no significant differences among the groups.

The metabolic syndrome (defined as elevated fasting blood glucose, elevated blood pressure and abnormal triglycerides or cholesterol levels) was present in 32% of the participants at baseline, and the percentage at 2 years ranged from 19 to 22% in the four diet groups.

Diet Adherence

Mean reported intakes at 6 months and at 2 years were not at the target levels for macronutrients (fat, protein and carbohydrate). This limits the applicability of the data.

In the Low Fat, Average Protein group (fat: 20%, protein: 15%, carbohydrate: 65%), carbohydrate intake decreased from baseline by 12.8% and by 9.3% from baseline at 2 years and fat intake decreased from baseline by 11.8% at 6 months and 12.0% at two years. As it should have, protein intake hardly changed at 6 months (0.2%) but by 2 years it had increased by 2.1% to 19.6%.

In the Low Fat, High Protein group (fat: 20%, protein: 25%, carbohydrate: 55%) at 6 months carbohydrate intake decreased from baseline by 7.4% and at 2 years, it decreased from baseline by 6.8%. Protein intake increased from baseline by 3.9% at 2 years it had increased by 2.5% – but it is important to note that such a modest increase meant that this group did not consume a diet of 25% protein (but slightly less than 19% at 6 months and 17.5% at 2 years). Fat intake decreased from baseline by 11.8% at 6 months and 12.0% at two years.

In the High Fat, Average Protein group (fat: 40%, protein: 15% carbohydrate: 45%), at 6 months carbohydrate intake  decreased from baseline by 5.0% and at 2 years, it decreased from baseline by 2.4%. Protein intake hardly increased from baseline at 6 months (0.5%), but at 2 years it had increased from baseline by 2.1%. Fat intake in this group was supposed to have increased, but actually decreased from baseline by 3.8% at 6 months and decreased from baseline by 2.1% at two years.

In the High Fat, High Protein group (fat: 40%, protein: 25%, carbohydrate: 35%) – which was the only intervention that was “low carb”, at 6 months carbohydrate intake only decreased from baseline by 0.2% and at 2 years, it decreased from baseline by 0.4%. In fact, carbohydrate remained at ~ 43% the entire time. Protein intake was supposed to increase substantially, but only increased from baseline by 4.3%, and at 2 years it had had only increased from baseline by 3.4%. It is important to note that such a modest increase in protein meant that this group did not consume a diet of 25% protein but ~19.3 % at 6 months and ~18.4% at 2 years. Fat intake in this group was supposed to have increased, but actually decreased from baseline by 3.7% at 6 months and decreased from baseline by 3.4% at two years.

Neither of the “high protein” groups achieved anywhere near 25% of daily calories as protein.

Despite the intensive behavioral counseling in this study, participants did not achieve the goals for macronutrient intake of their assigned group and while some data in this study is helpful, the one group that was supposed to be “low carb” (high fat, high protein) was none of those!

Researcher’s Conclusion

The researchers concluded;

“we did not confirm previous findings that low-carbohydrate or high protein diets caused increased weight loss at 6 months”

High Protein Diet “Fail”

The reason that this study failed to confirm whether a high protein diet causes increased weight loss at 6 months is because neither of the two “high protein” diet groups in this study ate anywhere near the target protein level of 25%, but rather ate between 17.5%-19% protein,  which is remarkably close to the average protein intake of 15%  (16.1% for men and 15.6% for women). Subjects also ate no where near the lower limits of a “high protein” diet, which is 27-68% of daily calories as protein.

Low Carbohydrate Diet “Fail”

The reason that this study failed to confirm that a low carbohydrate diet causes increased weight loss is because the one group of the four diet interventions that was supposed to eat what the researchers defined as “low carb” (35% of calories as carbohydrate) ate ~43% of calories as carbohydrate the entire duration of the study. This as a moderate carb diet, not a low carb diet.

Final Thoughts

In this long term study, researchers set out to look at the effectiveness of four dietary interventions including a “low carb” diet group, however poor study design failed to produce even one of the four groups that ate low carb.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Sacks FM, Bray GA, Carey VJ et al, Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates, N Engl J Med. 2009 Feb 26;360(9):859-73

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.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

1942-2015 Canada Food Guides: https://www.canada.ca/en/health-canada/services/food-nutrition/canada-food-guide/background-food-guide/canada-food-guides-1942-1992.html

Canadian Medical Association Journal, Early Releases (May 11, 2015), Food Guide Under Fire at Obesity Summit:  www.cmaj.ca/site/earlyreleases/11may15_food-guide-under-fire-at-obesity-summit.xhtml

2015 Acceptable Macronutrient Distribution Ranges:  https://www.canada.ca/en/health-canada/services/food-nutrition/reports-publications/eating-well-canada-food-guide-resource-educators-communicators-2007.html#a9

1970-1972 Obesity Rates:  https://lop.parl.ca/content/lop/ResearchPublications/prb0511-e.htm

2014 Obesity Rates, Statistic Canada – Overweight and obese adults (self-reported), 2014 http://www.statcan.gc.ca/pub/82-625-x/2015001/article/14185-eng.htm

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.
Gardner et al. http://jama.jamanetwork.com/article.aspx?articleid=205916

[14] Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive
performance. Halyburton et al. http://ajcn.nutrition.org/content/86/3/580.long

[15] A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic
and non-diabetic subjects. Dyson et al. http://onlinelibrary.wiley.com/doi/10.1111/j.1464-
5491.2007.02290.x/full

[16] The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in
type 2 diabetes mellitus. Westman et al. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633336/

[17] Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. Shai et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa0708681

[18] Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of
cardiovascular disease risk in subjects with abdominal obesity. Keogh et al.
http://ajcn.nutrition.org/content/87/3/567.long
www.PublicHealthCollaboration.org

[19] Metabolic Effects of Weight Loss on a Very-Low-Carbohydrate Diet Compared With an Isocaloric HighCarbohydrate
Diet in Abdominally Obese Subjects. Tay et al.
http://www.sciencedirect.com/science/article/pii/S0735109707032597

[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
after 12 mo. Brinkworth et al. http://ajcn.nutrition.org/content/90/1/23.long

[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
al. http://link.springer.com/article/10.1007/s00125-012-2567-4/fulltext.html

[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.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0091027

[25] Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial. Bazzano et al.
http://annals.org/article.aspx?articleid=1900694

[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
www.PublicHealthCollaboration.org

[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

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.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

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.

To our good health,

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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.

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 from insulin to 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 and low 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.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 

References

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.

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:

1. cerebrovascular disease (stroke)
2. cardiovascular disease (heart disease)
3. lower respiratory infection
4. 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:

1. 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.
   

   ---

2. 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.
   

   ---

3. 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.
   

   ---

4. 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;

1. smoking
2. diet
3. being overweight
4. physical inactivity
5. exposure to ionizing radiation (x-rays)
6. use of oral contraceptives
7. 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.

To your good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 The Low Carb High Fat Dietitian (a division of BetterByDesign Nutrition Ltd).  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 

References

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

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 and 107.7 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.

To your health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 The Low Carb High Fat Dietitian ( a division of BetterByDesign Nutrition Ltd).  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 

you can follow me at:

 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/

References

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

Weight gain is not caused simply by taking in more calories than you burn (the so-called ”calorie-in / calorie-out” model).  Calories in and calories out are interdependent factors, so when calories are restricted the body actually slows its metabolism, lowering the energy it uses for vital bodily functions. Basal Energy Expenditure (BEE) can decrease by as much as 30-50% in order to spare calories!

On the opposite end, when too many calories are taken in by someone who is already overweight, the body will try to get rid of them by increasing its Basal Energy Expenditure, usually by speeding up respiration, increasing heart rate and breathing and generating more heat.

The body does this because its set point’; the weight at which your body likes to be and will tend to stay with very little effort, is highly regulated. It really isn’t that easy to gain or lose weight if we haven’t already compromised this built-in homeostatic mechanism.

That is why trying to control calories doesn’t work for long term weight loss. When we restrict calories, and increase our exercise, our body responds by increasing hunger, initiating craving (especially for foods such as simple carbs that can be broken down quickly to glucose for your blood) and by decreasing the amount of energy it uses.

Have you ever skipped a meal or lowered your calories so much that you feel cold; even though the room is at an adequate temperature and you are dressed appropriately? You are shivering because your body is sparing calories it would normally use for heat generation.

Body Weight is Regulated by Hormones

Body weight is not really under our control as much as we’d like to believe.  It is a tightly regulated process that involves a variety hormones including leptin (a hormone that regulates fat stores by inhibiting hunger), ghrelin (a hormone that increase hunger when your stomach is empty) and insulin, which plays a very significant role in hunger, eating behavior and fat management.

To understand how significant a role insulin plays in weight regulation, let’s look at a situation where there is insufficient insulin. Type I diabetes results from the destruction of the insulin-producing pancreatic islet cells stemming from an autoimmune disorder. One of the hallmarks of this disease and it’s very low levels of insulin is severe weight loss. Type I diabetics need to take insulin injections to correct for the insulin deficiency but the more insulin that is taken, the more weight gain there is. As insulin levels go up, hunger is triggered and we feel the urge to eat.

Insulin is one of the major controllers of the body set point.

As mentioned, if we don’t take in sufficient calories, then our body decreases our Basal Energy Expenditure so that we end up maintaining our body weight in response to whatever the number of calories are that we take in.  The issue in weight gain is not how to reduce calories but how to reduce insulin.

Insulin as the Main Factor in Weight Gain

When we eat food, our body releases insulin in response to the rise in glucose in our blood, coming from the digested food. Insulin acts as a messenger to instruct the body’s cells to absorb glucose, in effect reducing blood glucose levels.

Insulin resistance is a condition in which the cells of the body become resistant to insulin and fail to respond normally to normal levels insulin, leading to higher blood sugar. The pancreas tries to compensate to this condition by producing more and more insulin.  As long as the pancreas is able to produce enough insulin to overcome this resistance, blood glucose levels remain normal but when the pancreas can no longer produce enough insulin, the blood glucose levels begin to rise.

Initially, this added rise in blood glucose happens after meals (when glucose levels are already at their highest) and more insulin is needed – but eventually these higher levels of glucose are seen first thing in the morning when the person hasn’t eaten for 8 or 10 hours. When blood sugar rises abnormally above specific clinical levels, the person is diagnosed as having Type 2 diabetes. Insulin resistance is often called ”pre-diabetes” because it precedes the development of Type 2 Diabetes.

Consistently high blood glucose levels along with insulin resistance lead to cells that are starved of glucose even though there is plenty of glucose in the blood. Since the cells aren’t getting any of the glucose even though it is there, it is not available to the cells because insulin is not binding it and taking it in. As a result, hunger signals are sent to the brain, leading to eating, even though the person has recently eaten.

As more and more glucose accumulates (both from the food being eaten and as you will see in a minute, through the making of glucose due to the effect of cortisol, another hormone) the high levels of glucose trigger the body to store the excess glucose as body fat.

The Effect of Stress on Weight Gain

Cortisol, the so-called stress hormone also plays a role in weight gain. Let’s look at another medical conditions to illustrate the effects of cortisol. In Cushing Syndrome, cortisol is over-produced by the body and weight gain results.  When we give people a synthetic form of cortisol as a medication (e.g. prednisone) they get something called Cushinoid Syndrome.  That is, they look like they have Cushing ’s disease. Not only do they gain weight, but there is a particular distribution of this weight gain called truncal obesity which means that fat is gained around the belly, rather than on the arms and legs.

In adrenal insufficiency (also known as Addison’s disease) which produces the opposite effect, the adrenal gland becomes damaged due an autoimmune condition and is unable to produce cortisol.  The hallmark of Addison’s disease is weight loss.

So what role does cortisol play in healthy individuals? Cortisol is released as a result of ordinary events such as waking up in the morning or exercising, but also is released in response to physiological and psychological stress.  Physiological stress might be an illness or injury and the release of cortisol services a needed function to make sure we have enough glucose to heal.

Under stressful conditions, cortisol also plays the role of providing the body with glucose by tapping into protein stores via gluconeogenesis in the liver. This energy can be helpful in a ”fight or flight” type of stressor, such as when one is being chased by something however under constant levels of psychological stress, elevated cortisol over leads to higher levels of glucose being made from protein in the body the long term.  So in addition to glucose coming from the food we eat (exogenous sources), we now have the body making its own glucose (endogenous sources).  The combined exogenous glucose from good and the endogenous glucose triggered by cortisol, now leads to even higher blood sugar levels that without the long term stress.

With continually high levels of cortisol, the body will take fat that is stored as triglycerides in our liver and relocate them to visceral fat cells — those under the muscle, deep in the abdomen. Just like in Cushing’s syndrome, we now see truncal obesity triggered by stress, mediated by cortisol.

Weight Gain is due to Hormonal Triggers and not a Lack of Will-Power

Cortisol also directly influences appetite and cravings by binding to hypothalamus receptors in the brain, triggering us to eat and crave foods that are easily broken down to glucose.  Cortisol also indirectly influences appetite by modulating other hormones that stimulate appetite. Simple carbohydrates like bread, pasta, candy and pop are common foods that people reach for in response to these craving because they are easily broken down to simple sugars. So, it is actually the higher levels of cortisol that lead to increased appetite and in particular cravings for high-calorie foods, not simply a lack of will-power.

As you can see, we don’t really control our body weight any more than we control our heart rates.  To a large degree, body weight is regulated automatically under the influence of hormones; hormones that indicate to eat and indicate when we are satiated.  Hormones signal our bodies to increase energy expenditure and when calories are restricted, hormones will slow energy expenditure.

Why All Diets Work and often All Diets Fail

It doesn’t really matter which diet people follow, whether it is Atkins, South Beach, or the good old fashioned low fat, low calorie diet, all diets in the short term produce weight loss. Yes, some are healthier than others, but they all “work”.

One would hope that by continuing to eat according to what ever diet we’ve chosen and by exercising, that our body’s set point would reset at a lower level, but this doesn’t happen.

Insulin levels stay high, continuing to drive hunger and eating.

How does this affect weight loss?

A few months into our diet, regardless what diet we follow, weight loss begins to plateau.  As the plateau continues, people get discouraged, and think to themselves if I’m not losing weight, then I may as well eat — fill in the blank’. This is either followed by an abandoning of the diet completely and a regaining of the weight previously lost (or more) or by a stubborn insistence to restrict calories and fat even further — leading to a downshifting of basal energy expenditure. It’s a vicious cycle.

But why does Body Weight Plateau in the First Place?

In response to weight loss, the body tries to return to its original set point.  First it slows metabolism to try and slow down weight loss — resulting in slowed weight loss and eventual plateauing.

The reason is because we’ve done nothing to lower insulin levels.

Think of set point like a body weight thermostat’. With a thermostat, when the air is hot enough, the furnace turns off and when it is too cool, the thermostat turns the furnace on.  Regardless what kind of diet a person follows, there will be weight loss effects in the short term, but eventually, even with continued compliance, body weight plateaus and in time, the person begins to regain the weight.

What about exercise?

Surely exercise will help us lose weight, right?

Basal energy expenditure which is the amount of energy we use at rest is estimated to be approximately 12-15 calories per pound.  For someone confined to complete bed-rest, caloric needs are calculated as 1.2 times Basal energy expenditure (BEE).

To visualize the effect exercise has on calorie loss, let’s take a 140 pound person as an example, whose basal caloric needs are 2200 — 2500 calories per day. Say they start exercising.  They start walking at a moderate pace (2 miles/hour) for 45 minutes every day, and burn roughly 104 calories.  Let’s look at that in terms of basal energy expenditure — that is only 4% of the BEE.  Okay, so say the person starts working out at a more vigorous pace, calorie burning will go up, right?  But how much?  6% of BEE?  8% of BEE? That’s about it.

The bottom line is, the vast majority of calories you take it; about 95% of caloric intake is used to heat the body and other metabolic processes, including keeping your heart beating, breathing, digestion, brain function, liver and kidney function, etc.

Set point is a tightly regulated mechanism, like a thermostat.  When we burn more calories through exercise two things happen.  Studies show that people actually end up decreasing their activity outside of the period of exercise and the other is they increase their caloric intake in response to exercise. That’s where the phrase ”working up an appetite” comes from.

The reason exercise is not that effective for weight loss is because of metabolic compensation.  We understand this intuitively though, don’t we? When know when we cut calories, restrict certain foods and increase our exercise that our body responds by being more hungry and increasing cravings. We try to take extreme measures only to find that we don’t really have a chance at making the weight loss last long term.

Don’t misunderstand; exercise is good for you.  There are many benefits to regular exercise such as improved cardiovascular function, increased strength and flexibility, and lowering stress which will lower cortisol but weight loss is not one of the significant benefits of exercise.

So if restricting calories causes are energy usage to slow and results in us being more sedentary outside of the times we exercise or eating more in response to exercise, how do we lose weight and keep it off?

To keep weight off long term, we need to address the underlying hormonal trigger to hunger and appetite; mainly insulin. To lower weight and keep it off, we need to lower our insulin level.

There are two aspects to lowering insulin levels (1) the foods we eat and (2) when we eat and this will be the topic of the next blog.

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.

UPDATE: 

(April 25, 2017) Be sure get the recipe for a Low Carb High Healthy Fat Matcha Smoothie here: https://www.lchf-rd.com/2017/04/24/low-carb-green-tea-matcha-smoothie-role-in-weight-and-abdominal-fat-loss/.

Less than 3 gm of carbohydrate at all the health benefits of Matcha!

Introduction

Role of Green Tea Catechins in Weight Loss

Green tea is the unfermented leaves of the Camellia sinensis plant and contains a number of biologically active compounds called catechins and epigallocatechin gallate (EGCG) makes up almost 30% of the solids in green tea [Kim et al].  Recent studies have found that green tea catechins, especially EGCG play a significant role in both weight loss and body fat composition.

Green Tea Catechins and ”Metabolic Syndrome”

Several large-scale population studies have linked increased green tea consumption with significant reductions in ”metabolic syndrome” which is a cluster of diseases that include;

–          insulin resistance or diabetes

–          hyperinsulinemia (high levels of insulin in the blood)

–          cardiovascular diseases; high blood pressure & coronary heart disease

–          obesity

It is thought that epigallocatechin gallate (EGCG), the most abundant catechin in green tea, mimics the actions of insulin.  This has positive health implications for people with insulin resistance or diabetes [Kao et al] and EGCG also lowers blood pressure almost as effectively as the ACE-inhibitor drug, Enalapril, having significant implications for people with cardiovascular disease [Kim et al].

Green Tea in Population Studies

Population studies and several randomized controlled studies (where one group is ”treated” and the other group is not) have shown that waist circumference is smaller and levels of body fat is less the more green tea consumed  [Phung et al] .  The anti-obesity effects of green tea are usually attributed to the presence of catechins [Naigle].

Green Tea Catechins

While catechins make up ~ 30% of green tea’s dry weight (of which 60—80% are catechins) oolong and black tea, which are produced from partially fermented or completely fermented tea leaves contains approximately half the catechin content of green tea.

Drinking 8-10 cups of green tea per day is enough to increase blood levels of EGCG into a measurably significant range [Kim et al]. Matcha, a powdered green tea used in the Japanese tea ceremony and popular in cold green tea beverages such as bubble tea, contains 137 times greater concentration of EGCG than China Green Tips (Mao Jian) tea [Weiss et al].

 Green Tea Catechin Content of Brewed Green Tea vs Matcha Powder

A typical cup (250 ml) of brewed green tea contains 50—100 mg catechins and 30—40 mg caffeine, with the amount of tea leaves, water temperature and brewing time all affecting the green tea catechin content in each cup.

A gram (~1/3 tsp) of matcha powder contains 105 mg of catechins (of which 61 mg are EGCs) and contains 35 mg of caffeine. Most matcha drinks made at local tea and coffee houses are made and served cold and contain ~1 tsp of matcha powder which contains ~315 mg of catechins (of which ~183 mg are EGCs).  Since there is no brewing time involved in the preparation of cold matcha beverages, the amount of catechins remains relatively constant in each cup. Variation in catechin content in matcha powder is largely due to where the plant is grown and how it is processed.

Weight Loss Effect of Green Tea Catechins

A 2009 meta-analysis (combining the data from all studies) of 11 green tea catechin studies found that subjects consuming between 270 to 1200 mg green tea catechins / day (i.e. 1 — 4 tsp of matcha powder per day) lost an average of 1.31 kg (~ 3 lbs) over 12 weeks [Hursel].

 Decreased Body Fat & Abdominal Fat even without Significant Weight Loss

The effect of green tea catechins on body composition is significant even when the weight loss between ”treated” and ”untreated” groups is small (~5 lbs in 12 weeks).

Even with such small amounts of weight loss;

– the total amount of abdominal fat decreases 25 times more with green tea catechin consumption than without it (−7.7 vs. −0.3%)

and

– total amount of subcutaneous abdominal fat (the fat just below the skin of the abdomen) decreases almost 8 times more with green tea catechin consumption thank without it (−6.2 vs. 0.8%).

 How do Green Tea Catechins Work?

The mechanisms by which green tea catechins reduce body weight and reduce the amount of total body fat and in particular reduce the amount of abdominal fat are still being investigated.  It is currently thought that green tea catechins;

–          increased thermogenesis; i.e. increased heat production which would result in increased energy expenditure (or calorie burning)

–          increase fat oxidation (or using body fat as energy)

–          decrease appetite

–          down-regulation of enzymes involved in liver fat metabolism

–          decrease nutrient absorption

 Green Tea Absorption

Green tea catechins are absorbed in the intestine.  Since the presence of food significantly decreases their absorption, green tea catechins are best taken 1/2 an hour before meals or 2 hours after meals.

The timing of green tea catechin intake may also affect the absorption and metabolism of glucose.  A study by Park et al found that when green tea catechins were given one hour before to a glucose (sugar) load, glucose uptake was inhibited and was also accompanied by an increase in insulin levels. Taking green tea catechins an hour before consuming highly sweet foods may be beneficial for those with insulin resistance or diabetes.

Green Tea Catechins and Milk

There seems to be some dispute in the literature as to whether the casein (a protein) in milk binds green tea catechins, making them unavailable for absorption in the body, which is why matcha drinks are often made with non-milk beverages such as soy milk, almond milk or rice milk (that don’t have casein).

Conclusion

Consuming between 1 — 4 tsp of matcha powder per day (270 to 1200 mg green tea catechins / day) is sufficient to result in weight loss of approximately 3 lbs in 12 weeks (with no other dietary or activity changes) and to significantly decrease body fat composition and reduce the quantity of abdominal fat.
 

***Warning to pregnant women***

While EGCG has also been found to be similar in its effect to etoposide anddoxorubicin, a potent anti-cancer drug used in chemotherapy [Bandele et al], high intake of polyphenolic compounds during pregnancy is suspected to increase risk of neonatal leukemia. Bioflavonoid supplements (including green tea catechins) should not be used by pregnant women [Paolini et al].

Recipe for Iced Matcha 

For those of you that have been asking what I am always drinking in that thermos…this is it!

Ingredients

–          1 tsp matcha (green tea) powder (contains ~315 mg catechins)

–          500 ml soy milk

–          crushed ice

Method

1. Place 1 tsp matcha powder in a small stainless steel sieve and gently press through the sieve into a small bowl with the back of a small spoon
2. Put the sieved matcha powder into a ceramic or glass bowl (not metal, as the tannins in the tea will react and give the beverage and ”off” metalic taste)
3. With a bamboo whisk (available at Japanese and Korean grocery stores), whisk 3 Tbsp boiled and cooled water into the matcha powder, until all the lumps are gone and the mixture is smooth
4. Place 1/4 cup of crushed ice in the bottom of a tall (16 oz / 500 ml) glass
5. Pour matcha and water mixture over ice in the glass
6. Fill glass with soy milk (or almond milk or rice milk) *

* I use 2/3 unsweetened soy milk and 1/3 sweetened soy milk

Note: once the matcha is blended with the soy milk, the tannins in the green tea are neutralized and no longer react with metal, so the beverage can then be put in an insulated stainless steel cup.

References

Bandele, OJ, Osheroff, N. Epigallocatechin gallate, a major constituent of green tea, poisons human type II topoisomerases”.Chem Res Toxicol 21 (4): 936—43, April 2008.

Bray GA. Lifestyle and pharmacological approaches to weight loss: efficacy and safety. J Clin Endocrinol Metab 2008;93:S81—88.

Brown WJ, Williams L, Ford JH, Ball K, Dobson AJ. Identifying the energy gap: magnitude and determinants of 5-year weight gain in midage women. Obes Res 2005;13:1431—41.

Centers for Disease Control and Prevention (CDC). Overweight and obesity. http://www.cdc.gov/obesity/index.html accessed Nov 20. 2009

Hursel R, Viechtbauer W, Westerterp-Plantenga MS. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obes (Lond) 2009;33:956—61.

Kao YH, Chang MJ, Chen CL, Tea, Obesity, and Diabetes, Molecular Nutrition & Food Research, 50 (2): 188—210, February 2006

Kim JA, Formoso G, Li Y, Potenza MA, Marasciulo FL, Montagnani M, Quon MJ., Epigallocatechin gallate, a green tea polyphenol, mediates NO-dependent vasodilation using signaling pathways in vascular endothelium requiring reactive oxygen species and Fyn, J Biol Chem. 2007 May 4;282(18):13736-45. Epub 2007 Mar 15.

Nagle DG, Ferreira D, Zhou YD. Epigallocatechin-3-gallate (EGCG): chemical and biomedical perspective. Phytochemistry 2006;67:1849—55.

Park JH, Jin JY, Baek WK, Park SH, Sung HY, Kim YK, et al. Ambivalent role of gallated catechins in glucose tolerance in humans: a novel insight into nonabsorbable gallated catechin-derived inhibitors of glucose absorption. J Phyisiol Pharmacol 2009;60:101—9.

Popkin BM. Recent dynamics suggest selected countries catching up to US obesity. Am J Clin Nutr 2010;91:284S—8S.

Phung OJ, Baker WL, Matthews LJ, Lanosa M, Thorne A, Coleman CI. Effect of green tea catechins with or without caffeine on anthropometric measures: a systematic review and meta-analysis. Am J Clin Nutr 2010;91:73—81.

Paolini, M, Sapone, A, Valgimigli, L, “Avoidance of bioflavonoid supplements during pregnancy: a pathway to infant leukemia?”. Mutat Res 527 (1—2): 99—101. (Jun 2003)

Rains, TM, Agarwal S, Maki KC, ”Antiobesity effects of green tea catechins; a mechanistic review” J or Nutr Biochem 22(2011):1-7

Shields M, Connor Gorber S, Trembaly MS, Estimates of obesity based on self-report versus direct measures, Statistics Canada (StatsCan), http://www.statcan.gc.ca/pub/82-003-x/2008002/article/10569-eng.htm

Statistics Canada(StatsCan) — Overweight and Obese Adults (self-reported), 2011 http://www.statcan.gc.ca/pub/82-625-x/2012001/article/11664-eng.htm

Weiss, DJ, Anderton CR, Determination of catechins in matcha green tea by micellar electrokinetic chromatography, Journal of Chromatography A, Vol 1011(1—2):173-180, September 2003