As demonstrated in a previous article, a low carbohydrate or therapeutic ketogenic diet is a viable option for people to reduce their symptoms of Type 2 Diabetes, but does it increase the risk of cardiovascular disease such as heart attack and stroke?

Results of a peer-reviewed study of cardiovascular outcomes of people with Type 2 Diabetes (T2D) that was published at the beginning of May in the Journal of Cardiovascular Diabetology [1] found that those that followed a ketogenic diet (≤ 30 g carbohydrate per day) significantly improved in 22 of 26 cardiovascular disease risk factors, including biomarkers of cholesterol / lipoproteins, blood pressure, inflammation, and carotid intima media thickness (cIMT).

Previous published results from the same researchers and published in February of 2018 demonstrated that significant improvement of T2D symptoms was able to be achieved and sustained long term using a ketogenic diet [2,3]. A post reviewing that study can be read here.

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was not only a significant decrease in blood sugar and weight, but a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

The results of this most recent study do much to dispel the myth that a therapeutic ketogenic diet puts individuals at increased risk for heart attack and stroke. In fact, it reduces their risk.

Methods

Continuous Care Intervention (CCI) Group Participants

At the beginning of the study, there were 238 participants enrolled in the continuous care intervention (CCI) group and all had a diagnosis of Type 2 Diabetes (T2D) with an average HbA1c of  7.6%  ±1.5%.  They ranged in age from 46 — 62 years of age, 67% were women and 33% were men. Weight of the subjects ranged from 200 pounds to 314 pounds (117±26 kg) with an average weight of 257 pounds (117 kg) and Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.  The majority of participants (87%) were taking at least 1 medication for glycemic control medication.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention (CCI) group.

Intervention and Monitoring of CCI Group

Each participant in the CCI group received an Individualized Meal Plan which enabled them to attain and maintain nutritional ketosis. They also received behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates.

Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry.

Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and sufficient mineral and fluid intake.

Participants ability to achieve and maintain nutritional ketosis was determined by subjects monitoring their blood ketone level of β-hydroxybutyrate (BHB) using a portable, handheld device. Blood glucose and β-hydroxybutyrate (BHB) levels were initially tracked daily using a combination blood glucose and ketone meter and frequency of tracking was modified by the care team based based on each individual’s needs and preferences.

Participants with high blood pressure (hypertension) were provided with an automatic home blood pressure machine (sphygmomanometer) and they were instructed to record their readings daily to weekly in the supplied app, depending on recent blood pressure control. Antihypertensive medication prescriptions were adjusted based on home blood pressure readings and reported symptoms.

Downward Adjustment and/or Discontinuation of Medications

As blood pressure came down, diuretic medication was the first antihypertensive medication to be discontinued. This was followed by beta blockers (unless the participant had a history of coronary artery disease).

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) were generally continued due to their known protective effect on the kidneys in those with Type 2 Diabetes.

Statin medications were adjusted to maintain a goal of LDL-P under 1000 nmol L−1 (or based on participant preference after full risk/benefit discussion with the physician).

The Usual Care (UC) Group

For comparison purposes, an independent group of patients with Type 2 Diabetes were also recruited for the study and were referred to Registered Dietitians that provided dietary advice according to the American Diabetes Association Guidelines [4].

Laboratory Assessors

Since an abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) is a known risk factor for CVD [5] and is very common in people with Type 2 Diabetes, a number of laboratory tests were conducted at the beginning of the study and the end to determine if they improved, stayed the same or got worse.

Most common in people with Type 2 Diabetes is where there are increased triglycerides (TG), decreased high-density lipoprotein cholesterol concentration (HDL-C) and increased small low-density lipoprotein particle number (small LDL-P).

The authors of this study state that evidence suggests that increased very low-density lipoprotein particle number (VLDL-P) and a large VLDL-P in particular may be one of the key underlying abnormalities in this abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) associated with T2D.

The authors also outline how higher concentrations of small LDL are often associated with increased total LDL particle number (LDL-P) and increased ApoB which is the main protein constituent of  very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The authors provide previous study evidence that demonstrates that in people with insulin resistance and T2D, increased total LDL particle number (LDL-P) and increased ApoB may exist even with normal to low LDL-C concentrations values. For this reason, LDL-C alone was not relied on as a measure of abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) in this study as it could miss the impact of increased total LDL particle number (LDL-P) and/or ApoB.

The authors mentioned that in previous studies with carbohydrate restriction of up to 1 year, while triglycerides (TG) usually decrease and HDL-C often increase, LDL-C sometimes increased and other times decreases. The authors note that although higher LDL-C is a known risk factor for CVD, low LDL-C may also reflect higher small, dense LDL, total LDL particle number (LDL-P) or ApoB and thus be a risk factor, as well.

Since inflammation is involved at all stages of the atherosclerotic process, higher high-sensitivity C-reactive protein (CRP) and/or higher white blood cell count (WBC) were assessed as risk factors for CVD.

Finally, since high blood pressure (hypertension) is also an added risk factor for CVD in people with T2D, tighter blood pressure control was deemed to reduce the risk of DVD, stroke and other microvascular events.

Continuous Care Intervention (CCI) Group

Standard laboratory fasting blood draws of the CCI group were obtained at the start of the study (baseline), at 70 days (3 months) and at ~ 1 year follow-up.

Lipid/cholesterol-related tests included ApoB, ApoA1, total cholesterol, triglycerides, direct HDL-C concentrations and LDL was calculated using the Friedewald equation.

The LipoProfile3 algorithm was used to determine relationship of lipid subfractions to cardiovascular (CVD) risk – specifically the number of HDL particles (HDL-P) previously reported  to be associated with death, Myocardial Infarction (MI), stroke and hospitalization, HDL-C (HDL cholesterol) which is the amount of cholesterol those particles are carying, which is not associated with these negative outcomes and HDL-P subclasses [6].

Risk was also determined using the lipoprotein insulin resistance score (LP-IR) which was proposed to be associated with the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposal rate (GDR) [7].

Finally, risk was also determined using the 10-year atherosclerotic  cardiovascular disease (ACSVD) risk score of the American College of Cardiology [8].

Carotid ultrasonography (cIMT) measure was performed at baseline and 1 year to characterize atherosclerotic risk.

The Usual Care (UC) Group

Body measurements, vital signs and fasting blood draws for the Usual Care (UC) group were obtained at the start of the study (baseline) and at 1 year using the same clinical facilities and laboratory and data collection methods. Carotid ultrasonography (cIMT) measure was also performed at baseline and 1 year to characterize atherosclerotic risk.

Results

There were no significant difference in the baseline characteristics of the two sub groups of CCI participants (web-based on onsite-based) and no significant difference at 1 year, so for the purpose of analysis, data from both groups were combined.

As well, there were no significant difference in the baseline characteristics of the Usual Care (UC) group (which served as an observational comparison group) and the Continuous Care Intervention Group (CCI) except mean body weight and BMI were higher in the CCI versus the UC group.

The within-Continuous Care Intervention group changes in the following lipids and lipoproteins were all statistically significant and were as follows; ApoA1  [a component of high-density lipoprotein (HDL)] increase by +”‰9.8%) ApoB / ApoA1 ratio decreased by −”‰9.5% Triglycerides (TG) decreased by −”‰24.4% LDL-C increased by +”‰9.9% but LDL-particle size also increased by +”‰1.1% (that is, large fluffy LDL increased compared with small, dense LDL) HDL-C increased by +”‰18.1% total HDL-P increased by +”‰4.9% large HDL-P increased by 23.5% Triglyceride/ HDL-C ratio decreased by −”‰29.1% large VLDL-P decreased by −”‰38.9% small LDL-P decreased by −”‰20.8% There were no significant changes in total LDL-P or ApoB.

These results are impressive!

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

In addition, the Continuous Care Intervention group had a significant reduction in; systolic blood pressure decreased −”‰4.8% diastolic blood pressure decreased −”‰4.3% C-Reactive Protein (CRP) decreased almost 40% (i.e. −”‰39.3%) white blood cell (WBC) count decreased −”‰9.1%

Below are graphs of the changes in biomarkers for the Continuous Care Intervention (CCI) group (figure 1) and the Usual Care (UC) Group;

 

Below is a comparative graph of the two groups, the Continuous Care Intervention (CCI) Group and the Usual Care (UG) Group

Some Final Thoughts…

This study demonstrates that a therapeutic ketogenic diet followed over the course of 1 year significantly improved 22 of 26 cardiovascular disease risk markers in those with Type 2 Diabetes. This is huge!

The size of the study group was large and had an 83% retention rate over the course of the year – which in and by itself demonstrates that the intervention diet was one that people had no difficulty staying with in their day-to-day lives, without the use of meal replacements (shakes or bars).

While not a randomized control trial between CCI and UG groups, this study supports that a ketogenic diet is both safe and effective for periods of up to a year (and in other studies has been documented to be safe and effective for up to two-years). Not only can a well-designed ketogenic diet reverse many of the symptoms of Diabetes it can also significantly improve risk markers for cardiovascular disease.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes and lower markers of risk factors for cardiovascular disease? Please send me a note using the ”Contact Me” form above to find out more.

References

1. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
3. Hallberg SJ, McKenzie AL, Williams, PT et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.
4. America Diabetes Association, Lifestyle management. Diabetes Care. 2017;40 (Suppl 1):S33—S43
5. Fruchart J-C, Sacks F, Hermans MP, Assmann G, Brown WV, Ceska R, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in patients with dyslipidemia. Am J Cardiol. 2008;102:1K—34K.
6. May HT,  Anderson JL, Winegar DA, Utility of high density lipoprotein particle concentration in predicting future major adverse cardiovascular events among patients undergoing angiography, Clinical Biochemistry, 2016;49(15): 1122-1126
7. Shalaurova I, Connelly MA, Garvey WT, Otvos JD. Lipoprotein insulin resistance index: a lipoprotein particle-derived measure of insulin resistance. Metabol Syndr Relat Disord. 2014;12:422—9.
8. Goff DC, Lloyd-Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, et al. ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;2014:S49—73 (tool: http://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate/)

Copyright ©2018 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 Part 1 of the new series on “Are Some Carbs Better Than Others” I explained what Glycemic Index (GI) is; how it 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. That is, 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 one 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!  Insulin Index, which will be covered in a future article, will enable us to choose between carb-based foods based on the demand they put on our β-cells and this is the topic of the next article in this series.

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.

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  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 carbohydrate foods (“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.

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.

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];

REAKFAST CEREALS	Glycemic index (glucose = 100)
Cornflakes	81 ± 6
Wheat flake biscuits	69 ± 2
Porridge, rolled oats	55 ± 2
Instant oat porridge	79 ± 3
Muesli	57 ± 2

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;

VEGETABLES	Glycemic index (glucose = 100)
Potato, boiled	78 ± 4
Potato, instant mash	87 ± 3
Potato, french fries	63 ± 5
Carrots, boiled	39 ± 4
Sweet potato, boiled	63 ± 6
Pumpkin, boiled	64 ± 7

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.  Stay tuned.

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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.

 

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  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.

This article is Part 2 in a two-part series on concerns with Polyunsaturated Vegetable Oils. Part 1 can be read here.

There are a few key things about polyunsaturates vegetable oils that need to be understood to understand this article, so I’ll keep the science simple.

There are two class of polyunsaturated fats; (PUFAs); omega 3 (ρ‰-3 also written n-3) and omega 6 (ρ‰-6 / n-6) which compete with each other for enzymes, and which becomes significant at one branch point (marked with the red and green box).

At that junction point (where the red box is at Arachidonic acid and green box is at Eicosapentanoic acid) if there is more n-6 fats than n-3 fats, then the pathway will favour the n-6 pathway. If there are more n-3 fats than n-6 fats, then the pathway will favour the n-3 pathway. The issue, as I will elaborate on below, is that in the Western diet, the n-6 pathway is always favoured.

Of significance, the n-6 polyunsaturated fats are pro-inflammatory and the n-3 polyunsaturated fats are anti-inflammatory. This is important to understand why eating lots of foods high in n-6 fats can lead to health consequences.

When people take low-dose Aspirin® for example, to lower the risk of heart attack or stroke, it acts on Arachidonic acid in the n-6 polyunsaturated fat pathway, to keep it from making certain inflammatory products that can lead to heart attack or stroke.

In our evolutionary history it was thought that n-6 fats (from nuts and seeds that were gathered in the wild) and n-3 fats (from the fish and meat we hunted) were eaten in close to a 1:1 ratio – providing the two essential fatty acids from both classes. When man began domesticating grain and growing beans and lentils and nuts and seeds for food (all high in n-6 fats), the shift towards a diet higher in n-6 fats occurred. The modern Western diet is estimated to have an omega-6 to omega-3 fatty acids of 15—20:1 in favour of n-6 fats [6].

Many people take omega-3 fish oil capsules in an effort to protect their body from inflammation, but because the amount of n-6 fats in the diet is so much higher than the amount of n-3 fats, the n-6 pathway is still favoured.

Unless we significantly lower the amount of n-6 fats in the diet, taking fish oil doesn’t really help as the n-6 pathway will always be favoured.

Changing the Makeup of Cell Components

Industrial seed oils have very high levels of linoleic acid which is at the top of the n-6 pathway.  These industrial seed oils are pro-inflammatory and will elongate to Arachidonic acid, resulting in many pro-inflammatory products being produced.

When we eat a lot of food made with soybean oil or fried in soybean oil we eat way more linoleic acid then our body has evolved to handle.

A major problem with polyunsaturated fatty acids such as linoleic acid are that they are very unstable fats that are easily oxidized (similar to a fat becoming ‘rancid’ or a metal ‘rusting’). Even if we never buy these industrial seed oils to cook with at home, when we buy French fries at restaurants they are fried in either soybean or canola oil. When we pick up a donuts, same thing.  Bottle salad dressing and mayonnaise (even the one that is called ‘olive oil mayonnaise’) are made with one of these industrial seed oils. These oils are found in products one would never expect to find them, including peanut butter! Start reading labels and you will be shocked how many products they are in – or rather, how few products they are NOT in.

Industrial seed oils are in most of the prepared food we buy and almost all of the food we eat out in fast-food restaurants.

According to a 2011 journal article published in the American Journal of Clinical Nutrition;

“The most striking modification of the US food supply during the 20th century was the >1000-fold increase in the estimated per capita consumption of soybean oil from 0.006% to 7.38% of energy.” [7]

When the linoleic acid content of the diet is high because we are eating foods made with industrial seed oils, important components of our cells membranes incorporate higher amount of linoleic acid into them.

For example, cardioleptin is a phospholipid component found in the inner mitochondrial membrane, which is where all energy metabolism in our body occurs. Cardioleptin plays an important role in the function of several enzymes involved in mitochondrial energy metabolism.

When we eat a lot of pre-made and processed foods and food made in fast-food restaurants, cardioleptin’s fatty acid content becomes 90% linoleic acid, making it easily oxidized, affecting its function. If the diet is high in coconut oil and olive oil, cardioleptin will be higher in stearic and oleic acids and these fats are more stable fats than linoleic acid.

Literally, we are what we eat!

Cooking with Industrial Seed Oils

When industrial seed oils are heated such as they are in the making of commercial foods using them, they undergo rapid oxidation which means that they react with oxygen in the air to form toxic substances, including aldehydes and lipid peroxides.  Aldehydes are known neurotoxins and carcinogens, and are documented to contribute to DNA mutations, inflammation and hypersensitivity [8].

Heating polyunsaturated vegetable oils for just 20 minutes produces 20 times the permitted levels of ldehydes recommended as a maximum limit by the World Health Organization [8].

Keep in mind that at fast-food restaurants and in the preparation of commercial donuts and other fried food products, these industrial seed oils are used for frying everything from French fries to donuts and are heated over and over for extended periods of time, creating alarming levels of aldehydes and lipid peroxidation products.

When heated, industrial seed oils produce oxidized metabolites known as oxidized linoleic acid metabolites (OXLAMs) which have been also been implicated in the development of non-alcoholic fatty liver disease (NAFLD)[9].

In the body cell components such as cardioleptin with high amounts of linoleic acid are easily oxidized producing an oxidation product known as 4-hydroxynonenal (4-HNE) which has been implicated in the development of cancer [10].

Increasing Appetite

The high linoleic acid content of industrial seed oils also act on two endo-cannibinoids in the body (2-AG and Anandamide) which results in us feeling hungry, even when we have recently eaten –  in much the same way as cannabis (marijuana) does [11-12].  As a result, these industrial seed oils are believed to contribute to obesity and the associated health risks such as Type 2 Diabetes and high blood pressure.

Final Thoughts…

For fifty years, the public ate industrially-created trans fats in place of natural saturated fats and we only found out later that they were a major contributor to heart disease.

For the last forty years we have been eating industrial seed oils in greater and greater quantities place of natural saturated fat, but (a) given how these industrial seed oils are produced (solvents, high heats for extended period of time, bleach, etc.) and (b) given what is known about the very toxic products they produce when heated in production and how they are oxidized in the body and oxidized through heating when cooking, it is warranted to be very cautious about eating prepared foods made with them.

To avoid these industrial seed oils will take a concerted effort as they are in virtually everything we buy ready-made and many of the foods we eat out, but one solution is to cook real food using healthy sources of fat and to avoid these industrial seed oils that were created and marketed to us as supposedly healthy substitutes for natural fats.

The butter, lard and tallow of years gone by were made from animals that were pasture raised, not fed soybeans and corn as commercial animals are now, but in light of the mounting number of studies that indicate that saturated fat is not associated with increased risk of cardiovascular disease, perhaps it might be preferable to buy grass fed butter or render tallow or lard from the fat of pasture-raised animals for some cooking applications – rather than use these industrial seed oils that were created as substitutes.  Butter, lard and coconut oil (a vegetarian saturated fat) are all very low in linoleic acid and thus are very stable.  They are not easily oxidized in the body or by heating and produce very low levels of aldehyde and lipid peroxidation products when heated, compared with many of the industrial seed oils.

These are all factors we need to consider when deciding which fats our food should be made with.

The chart below shows the linoleic content of some common fats in blue.  Keep in mind that fats with the smallest amount of linoleic acid are the most stable and the least prone to oxidation (either in the body or when heated).

A personal note: For non-heating uses, I use natural sources of monounsaturated fat such as cold pressed macadamia nut oil, hazelnut oil, avocado oil, and extra virgin olive oil and for cooking and heating uses I use a mixture of olive oil and coconut oil (to raise the smoke point), clarified butter (ghee) at higher temperatures and butter at lower temperatures and for baking. I read labels of all products I buy and deliberately avoid purchasing any food products that contain soybean oil, canola oil or sunflower oil and when I eat out, I ask that my food be prepared with coconut oil, butter or ghee.

While the jury is still “out” when in comes to saturated fat, it is my opinion that with the mounting evidence that eating saturated fat does not contribute to heart disease, using moderate use of butter, ghee (clarified butter) and coconut oil seems to me to be a more acceptable risk than eating foods made with, or fried in industrial seed oils.

I trust having the information contained in this article will help you make an informed choice for yourself and for those you cook for.

If you have questions about how I might be able to help you follow a low carb lifestyle -including selecting appropriate fats for use in your own cooking, please feel free to send me a note using the “Contact Me” form located on the tab above.

References

(continued from Part 1)

6. A.P. Simopoulos, Evolutionary aspects of the dietary omega-6:omega-3 fatty acid ratio: medical implications,World Rev Nutr Diet, 100 (2009), pp. 1-21

7. Tanya L Blasbalg, Joseph R Hibbeln, Christopher E Ramsden, Sharon F Majchrzak, Robert R Rawlings; Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century, The American Journal of Clinical Nutrition, Volume 93, Issue 5, 1 May 2011, Pages 950—962.

8. Grootvelt M, Rodada VR, Silwood CJL, Detection, monitoring, and
deleterious health effects of lipid oxidation products generated in culinary oils during thermal stressing episodes, Lipid Oxidation, November/December 2014, Vol. 25 (10)

9. Maciejewska, Dominika & Ossowski, Piotr & Drozd, Arleta & Karina, Ryterska & Dominika, Jamioł & Banaszczak, Marcin & Małgorzata, Kaczorowska & Sabinicz, Anna & Wyszomirska, Joanna & Stachowska, Ewa. (2015). Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease-A pilot study. Prostaglandins & other lipid mediators.

10. Zhong H, Yin H. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: Focusing on mitochondria. Redox Biology. 2015;4:193-199. doi:10.1016/j.redox.2014.12.011.

11. Alvheim AR, Malde MK, Hyiaman DO et al; Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity, Obesity (2012) 20;1984-1994

12. Alveim AR, Torstensen BE, Lin YH et al, Dietary Linoleic Acid Elevates the Endocannabinoids 2-AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet, Lipids (2014) 49:59—69

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Copyright ©2018 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: Both the US and Canadian Dietary Guidelines encourage us to limit saturated fat in order to reduce the risk of heart disease and to eat unsaturated fat, including polyunsaturated vegetable oils instead but what are these fats, where do they come from and what role might these play in development of obesity, Type 2 Diabetes, non-alcoholic fatty liver disease and even cancer?  This article is part 3 in the series titled Bad Fats and Enduring Beliefs.

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“Polyunsaturated vegetable oils” is really a misnomer, as neither soybeans nor rapeseed / Canola are “vegetables”.  More accurately these should be called “industrial seed oils”, as they are seed crops that have been deliberately engineered for food use.  These are created oil products which are quite unlike natural oils that can be easily expressed from nuts, seeds and fruit using a millstone, as has been done since the Bronze Age [1].

If you simply press olives, almonds, sesame or poppy seeds between your fingers you will be able to express a little bit of their oil on your fingers.

Not so with soybeans!

You can squeeze a soybean as hard as you like and for as long as you like and you are not going to get any oil out of it!

The first attempt at trying to express oil from soybeans occurred in the United States, a few years after the creation of Crisco® shortening in 1911.  For 3 long years (1922 – 1925) scientists tried over and over again to extract oil from soybeans  imported from Manchuria using hydraulic presses,  and time and time again they failed. Finally, in 1925 scientists turned to the use of chemical solvents  to get oil from soybeans and solvent extraction of soybean oil has been used ever since.

Trans Fats and Industrially Produced Shortening

In days gone by, deep-fat frying in restaurants (e.g. for French fries) was done in beef tallow, sometimes in lard. Pastry crusts were made with lard or butter, and baked goods such as cakes and brioches were usually made with butter – that is until 1911 when Crisco® shortening was invented. When it was noticed that hardened cottonseed oil used in the soap-making industry had an appearance like lard, scientists decided to further process it to remove the strong odor inherent with cottonseed oil, and market it to housewives as the ‘modern’ way to bake.

Beginning in the 1950s, trans fats (which occurs naturally in very small quantities) were industrially produced from other industrial seed oils such as soybean oil for use in other natural fat substitutes, including  margarine, fat for commercial baked goods and fat for deep-fat frying in the fast food industry [2]. Unfortunately, it was only in the late 1990s and early 2000s that it became widely-accepted by the scientific community that eating foods made with trans fats or fried in trans fats raised LDL-cholesterol while lowering protective HDL cholesterol, and also raised triglycerides; promoting systemic inflammation and contributing to the development of heart disease.

How ironic that the fats that were created to replace naturally-occurring saturated fats ended up being so detrimental to health!

After trans fats were discontinued due to their adverse health effects, industrial seed oils such as soybean oil and canola oil became the number one and number two oils of the food industry. These unsaturated (liquid) industrial seed oils have replaced saturated (solid) trans fat industrial oils in our food supply, however there is considerable evidence emerging which should cause us to question whether these fats are any safer (more on that below).

The Created Market for Industrial Seed Oils

The market for industrial trans fats and liquid industrial seed oils was itself created based a belief that ‘dietary saturated fat led to heart disease’.  Much  of what we have come to believe about this originated with a pathologist named Ancel Keys who proposed his ‘diet-heart hypothesis’ in the 1950s.

In 1967, Keys published his “Seven Country  Study” that reported that populations that consumed large amounts of saturated fats in meat and dairy had high levels of heart disease but when data from 22 countries that was available since 1957 was plotted, it was a great deal more scattered, indicating a much weaker association than Keys’ Seven Country  Study data indicated.

In August of 1967, just as Ancel Keys published his study, Stare, Hegsted and McGandy, 3 Harvard researchers paid by the sugar industry published their reviews in the New England Journal of Medicine which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (previous article on that topic here). Sponsorship of this research by the sugar industry certainly casts a dark shadow over their findings.

These 3 researchers insisted in their conclusion that there was a link between dietary cholesterol and heart disease and that there was “major evidence” which suggested that there was “only one avenue for diet to contribute to hardening of the arteries and the development of heart disease”,  but as covered in the previous article, it is known that a year after their publications (1968), the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done.

Just 10 years after the sugar industry paid Stare, Hegsted and McGandy to write their reviews, Hegsted was directly involved with developing and editing the 1977 US Dietary Guidelines which recommended that Americans decrease intake of saturated fat and cholesterol and increase dietary carbohydrate – entrenching the belief that saturated fat caused heart disease into American public health policy. That same year (1977), based on the same body of literature, Canada adopted very similar dietary guidelines around saturated fat…and the rest is history.

Public Health Policy Based Rooted in a Belief

For the last forty years Americans and Canadians have shunned natural fats such as butter, cream and lard in place of man-made margarine, non-dairy creamer and Crisco® – all in the enduring belief that ‘saturated fat is “bad” and leads to heart disease’.  Given that published reports vilifying saturated fat were funded by the sugar industry and that Ancel Keys study left out 2/3 of the nutrition and health data available at the time, it has become evident that public health policy was founded on what is now questionable data.

In addition, more and more current peer-reviewed published studies are concluding that saturated fat is not associated with an increased risk of developing cardiovascular disease.

If saturated fat is not associated with increased risk of heart disease then should we be eating industrial seed oils that were created and marketed as a replacement for them?

Creation of Industrial Seed Oils

Inexpensive soybean oil has been the leading oil used in food production in the United States since 1945 [3]. It was previously made into a hard fat through hydrogenation and sold to consumers as trans-fat based shortening and margarine and came into wide-spread use as both synthetic hard fat and as a food-based oil product in the late-1960s.

In Canada, soybean oil is just behind canola oil in terms of the most used, and canola is another industrial seed oil that was created by science. In 1978 rapeseed, a prairie weed was specially bred in Canada to produce a novel plant that was lower in erucic acid (a toxin found in rapeseed) and this new plant was named “canola” (‘Canadian Oil’).

A 2015 study on Canadian vegetable oil purchased and eaten in Canada found that in 2013, 42% was canola oil (a Canadian bio-engineered industrial seed oil) and 20% was soybean oil, an industrially-engineered seed oil developed in the US [4]. Keep in mind this figure excludes food products available in Canada that are manufactured in the US, which uses predominantly soybean oil.

Soybean Oil is a Modern, Industrial Product

According to an article titled “Soybeans Are Ancient; Oil Is Not” published in the Wall Street Journal in 2011 [5], soybeans as the basis for tofu and soy sauce is an ancient food in China, but soybean oil was virtually unknown until global food oil shortages during World War I created an interest to extract the fatty part of the soybean for oil. Soybean oil is a modern creation.

How is oil made from seeds such as soybean and canola?

“Soybeans are first crushed into crude oil and then refined to remove impurities like free fatty acids. Over days, the crude is ”neutralized” of acidity with phosphoric acid, ”winterized” through filters that remove wax, bleached at high heat to lighten the color and finally vacuum ”deodorized” to eliminate impurities.” [5]

The extraction of soybean oil involves the industrial processing of soybeans with solvents at very high heats over an extended length of time in order to have the soybean give up its small amount of oil.

Solvent extraction of canola oil occurs in a similar method, beginning with an hour or more ‘wash’ of the rapeseed with a hexane solvent, then a sodium hydroxide wash. Bleach is then used to lighten the cloudy color of the processed oil and then it is steamed injected at high temperatures to
remove the bitter smell.

Yummy! Now this oil is ready to sell to the public to cook with and eat!

Should we even be eating these industrial seed oils?

Are they any safer than trans fats that were approved for consumption for 50 years and later found to contribute to heart disease?

Part 2 of this article will continue in Concerns with Polyunsaturated Vegetable Oils – Part 2.

References

1. Alfred Thomas (2002). “Fats and Fatty Oils”. Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH.
2. “Tentative Determination Regarding Partially Hydrogenated Oils”. Federal Register. 8 November 2013. 2013-26854, Vol. 78, No. 217.
3. Dutton, HJ. Journal of the American Oil Chemists Society, Vol. 58, No.3 Pages: 234-236 (1981),  https://pubag.nal.usda.gov/pubag/downloadPDF.xhtml?id=26520&content=PDF
4. Schaer, L., Grainews, Canola gets competition from soybeans, Feb 01, 2016, https://www.grainews.ca/2016/02/01/canola-gets-competition-from-soy/
5. Wall Street Journal, “Soybeans Are Ancient; Oil Is Not”, 2011, https://blogs.wsj.com/chinarealtime/2011/01/03/soybeans-are-ancient-oil-is-not/

Copyright ©2018 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.

The Diet-Heart Hypothesis

The diet-heart hypothesis is the belief that eating foods high in saturated fat contributed to heart disease was first proposed in the 1950s by a scientist named Ancel Keys who believed that by replacing saturated fat from meat, butter and eggs with newly-created industrial polyunsaturated vegetable oil (such as soybean oil) that heart disease and the deaths allegedly associated with it would be reduced by lowering blood cholesterol levels.

In 1952, Keys suggested that Americans should reduce their fat consumption by 1/3 – while at the same time acknowledged that he had no idea whether he was right;

“Direct evidence on the effect of the diet on human arteriosclerosis is very little and likely to remain so for some time” [1].

In 1953, Ancel Keys published the results of his ”Six Countries Study” [1], where he said that he had demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease.

Four years later, in 1957, Yerushalamy published a paper with data from 22 countries [2], which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s Six Countries Study data.

 

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Nevertheless, in 1970, Keys went on to publish his Seven Countries Study in which maintained there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease -basically ignoring the data presented in Yerushalamy’s 1957 study and failing to study countries where Yerushalamy found no relationship, such as France. In a paper published in 1989 based on food consumption patterns in the 1960s in the seven countries [3], Keys said that the average consumption of animal foods (with the exception of fish) was positively associated with 25 year CHD mortality (death) rates and the average intake of saturated fat was strongly related to 10 and 25 year CHD mortality rates. Keys knew of Yerushalamy’s data from 1957 and ignored it.

Keys methodology has been widely criticized for selecting data only from the 7 countries that best fit his hypothesis.

The Sugar Industry Funding of Research Vilifying Fat

In August of 1967, just as Ancel Keys had published his Seven Country Study, Stare, Hegsted and McGandy – the 3 Harvard researchers paid by the sugar industry published their review in the New England Journal of Medicine, titled ”Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (see previous article on that topic).

Stare, Hegsted and McGandy concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis) and resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids;

”Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol…the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.” [4]

These researchers concluded that there was major evidence available at the time which suggested that there was only ONE avenue for diet to contribute to hardening of the arteries and the development of heart disease – yet a year later in 1968 the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done [5];

”the committee strongly recommended to the National Heart Institute that a major definitive study of the effect of diet on the primary prevention of myocardial infarction be planned and put into operation as soon as possible. “

This is an important point; prior to a major study having ever been conducted to determine whether changes in dietary cholesterol impacts heart disease, 3 Harvard researchers paid by the sugar industry concluded that there was “only one avenue” by which diet contributed to the development and progression of atherosclerosis (i.e. “hardening of the arteries”) and heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids.

Researcher Paid by the Sugar Industry Helps Develop the 1977 US Dietary Guidelines

Only ten years after the sugar industry paid Stare, Hegsted and McGandy to write their reviews, the same Dr. Hegsted was directly involved with  developing and editing the 1977 US Dietary Guidelines [6] which recommended an increase in dietary  carbohydrate and a decrease in saturated fat and cholesterol in the diet.

Historic changes in the Dietary Recommendation in Canada have largely been based on changes to the Dietary Recommendations in the US, and as a result both stemmed from a belief that eating saturated fat increases total cholesterol and therefore increases the risk of heart disease.

The problem is this belief is just that, a belief.

There have been many studies that have disproved this including a  randomized, controlled dietary intervention trial from 2008 which compared a low calorie, low in fat with a low carbohydrate, high fat diet of the same number of calories. This study found that overall heart health is significantly improved when carbohydrate is restricted, rather than fat [7,8].

Not all LDL cholesterol is “bad” cholesterol.

Small, dense LDL (“Pattern B”)  causes more “hardening of the arteries” than the large, fluffy LDL particles (“Pattern A”)[9].

It has been reported that when dietary fat is replaced by carbohydrate, the percentage of the small, dense LDL particles  (the ones that cause hardening of the arteries) is increased, increasing risk for heart disease.  Furthermore,  the low carb diet increased HDL (so-called “good” cholesterol), which are protective against heart disease and HDL and small, dense LDL were made worse on the low fat diet. Quite opposite to the “Diet-Heart Hypothesis, this study demonstrated improvements in the risk of heart disease for those eating a low carbohydrate, high fat diet compared to those eating a low fat, low calorie diet – which is not all that surprising given that it had been reported previously that a diet high in saturated fat actually lowers small, dense LDL (the type of LDL that causes hardening of the arteries) and raises the large fluffy LDL; actually improving risk factors for heart disease [15].

There are also other randomized controlled trials from 2004-2008 which demonstrate that a low carb diet improves blood cholesterol test results more than a low fat diet [10,11,12,13,14] – yet despite this, the belief that eating saturated fat increases blood cholesterol, persists.

Both the American and Canadian governments are in the process of revising their Dietary Guidelines and what is clear is that what is needed is an external, independent scientific review of the current evidence-base for the enduring false belief that dietary fat, especially saturated fat contributes to heart disease.

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [16-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

”Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [24].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.

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The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [25]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [26]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [26].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

Have questions about which types of fats are best to include in your diet and which are best to limit? Please send me a note using the “Contact Me” tab above and I will reply shortly.

References

1. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118—139 (1953).
2. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343—54
3. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
4. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242—47
5. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
6. Introduction to the Dietary Goals for the United States — by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
7. Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008;47:307—18
8. Forsythe CE, Phinney SD, Fernandez ML, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008;43:65—77
9. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189—99
10. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082—90.
11. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778—85
12. Gardner C, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women. JAMA 2007;297:969—77
13. Yancy WS Jr., Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769—77
14. Shai I, Schwarzfuchs D, Henkin Y, et al. Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229—41
15. Dreon DM, Fernstrom HA, Campos H, et al. Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am J Clin Nutr 1998;67:828—36
16. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
17. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
18. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
19. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
20. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
21. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
22. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
23. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
24. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
25. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
26. Sigurdsson, AF, The Fate of the PURE Study — Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

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Copyright ©2018 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.

 

Yesterday, in preparing to begin a new series of articles on the relationship between polyunsaturated vegetable fats to obesity, I came across an old, yellowed sheet titled “Comparison of Dietary Fats” that I was given as an undergrad Dietetic student at McGill, in 1989.

It was designed to help us teach consumers how to choose the “healthiest” dietary fats.

As indicated at the bottom of both sides of the handout (see full size photos, below), it was “provided as a Professional Service by Proctor and Gamble“.

Why would Proctor and Gamble, a soap company provide future Dietitians with a teaching handout on choosing healthy oils for cooking? A bit of understanding about how soap is made, will help.

At the time, the making of soap required a mixture of animal fats and lye, however William Procter and James Gamble (brothers-in-law living in Cincinnati in the late 1800s and who formed Proctor and Gamble) needed to find an inexpensive replacement for animal fat for the creation of individually wrapped bars of soap.

The source of soap fat they turned to was a waste-product of the cotton industry – cottonseed oil. It was literally the garbage leftover when cotton was produced and is cloudy, red and bitter to the taste, and toxic to most animals.

They needed to make cottonseed oil solid in order to make bar soap and utilized a newly patented technology to produce a creamy, pearly white substance out of cottonseed oil. This fat resembled lard (the most popular natural animal fat baking and frying fat at the time), so with a little more tweaking, this hydrogenated cottonseed oil was then sold in 1911 by Procter & Gamble to home cooks as Crisco® shortening.

All that was needed now was for Proctor and Gamble to market this industrially-produced seed oil fat, and market it they did. They hired America’s first full-service advertising agency, the J. Walter Thompson Agency that employed graphic artists and professional writers.

“Samples of Crisco were mailed to grocers, restaurants, nutritionists, and home economists. Eight alternative marketing strategies were tested in different cities and their impacts calculated and compared.

Doughnuts were fried in Crisco and handed out in the streets.

Women who purchased the new industrial fat got a free cookbook of Crisco recipes. It opened with the line, “The culinary world is revising its entire cookbook on account of the advent of Crisco, a new and altogether different cooking fat.” [1]

From the very beginning, Proctor and Gamble marketed their industrially-created solid fat (Crisco®) to “nutritionists” and “home economists” – the forerunners to Dietitians.

When Procter & Gamble introduced Puritan Oil® in 1976, a liquid cooking oil made of sunflower oil which became 100% canola oil by 1988, it was natural for them to market their newly created oil to Dietitians.

Proctor & Gamble now had a lucrative business manufacturing industrial seed oils as dietary fats and they wanted to make sure that we, as Dietitians encouraged people to use their “healthy” fats.

I’ve scanned in both sides of the handout (it’s old and yellowed, having been kept in the back of my “new” 1988 Canada’s Food Guide book for almost 30 years). As can be seen, in first place on the front side of the handout is canola oil identified by the trade name “Puritan Oil®”, a registered trademark of Proctor and Gamble.

On the reverse side, is what consumers should know about these oils, including that canola oil is “better than all other types of vegetable oil“.

I’ve highlighted some of the wording that makes Proctor & Gamble’s bias apparent;

Some Final Thoughts…

From the very beginning, industrially-produced seed  fats and oils have been marketed to nutritionists, home economists and Dietitians by the companies that created them, in some cases as a “Professional Service”.

As will become clear in the next article we, as Dietitians were tasked by the Dietary Guidelines in both Canada and the US with promoting “polyunsaturated vegetable oils” to the public as ‘healthful alternatives’ to presumably unhealthy saturated animal fats. The manufacturers were there to ‘assist’ as a ‘Professional Service’.

Looking back on the role of fat manufacturers and the sugar industry (outlined in the preceding article) on which foods were recommended and promoted, it makes me question what I was taught and who affected what I was taught. Given that it was known at the time the sugar industry funded the researchers that implicated saturated fat as the alleged cause of heart disease, I wonder what we don’t know about which industry funded which research.  After all, the knowledge about the sugar industry having funded the researchers that implicated saturated fat only ‘came out’ in November 2016 when it had occurred decades earlier.

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NOTE: It is increasingly my conviction that the simultaneous (1) marketing of polyunsaturated vegetable oil (soybean oil, canola oil) along with (2) changes in the Dietary Recommendations for people to (a) eat no more than 20- 30% of calories from fat and to (b) limit saturated fat to no more than 10% of calories, combined with the recommendations for people to (c) eat 45-65% of calories as carbohydrate was the “perfect storm” that may well explain the current obesity crisis and associated  increase in metabolic health problems that we now see 40 years later.

In subsequent articles I’ll elaborate on why I believe this is the case.

References

1. Ramsey, D*., Graham T., The Atlantic. How Vegetable Oils Replaced Animal Fats in the American Diet, April 26 2012 (www.theatlantic.com/health/archive/2012/04/how-vegetable-oils-replaced-animal-fats-in-the-american-diet/256155/)

*Dr. Drew Ramsey, MD is an assistant clinical professor of psychiatry at Columbia University.

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Copyright ©2018 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.

 

 

A year ago, I found out from a fellow Dietitian that a recently published article in the Journal of the American Medical Association revealed that the sugar industry had secretly funded a group of renowned Harvard researchers to write an influential series of articles which downplayed, discredited or outright ignored research known at the time, and which demonstrated that sugar was a contributor to heart disease.

I read the article and was stunned at its significance.

As I am in the midst of a new series of articles on the role of saturated fat and polyunsaturated fat in health and disease, I felt it’s important that people understand the sugar’s industry involvement in potentially skewing of the scientific evidence at the very time that the original 1977 low-fat high carb Dietary Guidelines were being formulated and so I researched further and wrote this article.

Two of the prominent Harvard researchers that were paid by the sugar industry and who wrote articles dismissing that sugar was a significant contributor to heart disease and implicating saturated fat as the cause were the late Dr. Fredrick Stare, chair of Harvard’s School of Public Health Nutrition Department and the late Dr. D. Mark Hegsted, a professor in the same department [2].

POST PUBLICATION NOTE (March 12 2018): Dr. Hegsted, one of the 3 Harvard researchers paid by the sugar industry to write these review articles was directly involved in developing and editing the 1977 US Dietary Guidelines [6].

A commentary in the Journal of Accountability in Research [4] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that  dietary fat and cholesterol was the primary contributor.”

In the mid-1960’s, the Sugar Research Foundation (which is the predecessor to the Sugar Association) wanted to counter research that had been published at the time which suggested that sugar was a more important cause of atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose[2].  Letters exchanged between the parties were brought to light in the November 2016 article published by Kearns et al [1] maintained that the Sugar Research Foundation tasked the researchers with preparing ”a review article of the several papers which find some special metabolic peril in sucrose [sugar] and, in particular, fructose [3].”

This would seem akin to the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled ”Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which stated;

”Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol”

The report concluded;

”the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

”there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet.”

The Harvard researchers concluded;

“on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

Stare, Hegsted and McGandy did not disclose that they were paid by the Sugar Research Foundation for the two-part review [4].

In response to Kearns et al article in the Journal of the American Medical Association in November 2016 [1], the Sugar Association responded [5] by stating that it;

”should have exercised greater transparency in all of its research activities, however, when the studies in question were published funding disclosures and transparency standards were not the norm they are today.” [5]

Some final thoughts…

The reviews written by these influential Harvard School of Public Health Nutrition Department researchers and paid for by the sugar industry have the appearance of being a deliberate manipulation of the perception of the scientific evidence known at the time. 

Whether deliberate or inadvertent, the fact that such sponsorship occurred at the very period in time when the Dietary Guidelines were under revision to emphasize that saturated fat intake must be reduced and carbohydrate consumption must be increased cannot be understated — a move which certainly benefited the sugar industry.

POST PUBLICATION NOTE (March 12 2018): Discovered after publication of this article, one of the three Harvard researchers funded by the sugar industry, Dr. D.M Hegsted was one of the scientists that worked on the 1977 US Dietary Guidelines[6].

How has this turned out for us?

For the last 40 years, Americans and Canadians have diligently eaten more carbohydrate (including foods containing sucrose and fructose) and more polyunsaturated fats (especially soybean and canola oil) just as the Harvard researchers paid for by the sugar industry recommended — and to what end?

Obesity rates have gone from ~10% in the 1950’s and 60’s in both countries to 26.7% in Canada (2015) and ~34% in the US (2017) and Diabetes and high blood pressure (hypertension) rates have risen exponentially.

What’s going on?

Could it be that the shift to a diet abundant in omega-6 polyunsaturated fat (such as soyabean oil) and which supplies 45-65% of daily calories as carbohydrate created the ‘perfect storm‘ which inadvertently fueled the obesity and health epidemic we now see?

This will be the subject of future articles.

Have questions?

Please send me a note using the “Contact Me” tab above and I will reply shortly.

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Copyright ©2018 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.

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).

People understand it’s important for children to eat enough protein because they’re growing but adults and older adults need to eat enough protein each day, as well.

After youth have finished growing, they are at their maximum physical capacity between age 20 and 30 years old and after the age of 30 years old, adults begin to lose muscle mass at the rate of 1% per year [1].

We’ve come to expect that as people age, they will gain more fat, loose bone mass and that they’ll have decreased muscle strength and that in time, these will lead to difficulty getting around, a greater risk of falls and eventually to physical disability. We commonly see older people with spindly legs and bony arms and we think of this as ‘normal’, but as discussed in a recent “A Dietitian’s Journey” article, we’ve mixed up what is “common” with what is “normal”.  When we look at seniors in Okinawa, Japan for example, we don’t see this. They continue to do manual jobs and practice martial arts well into their 80’s and 90’s. Aborigine elders in Australia also remain lean, fit and active as seniors. This is normal.

The physical deterioration that we associate with aging including weak bones (osteoporosis) and the loss of skeleton muscle mass (sarcopenia) don’t develop suddenly, but take place over an extended period of time – brought on by less than optimal practices in early middle age.

How Much Protein?

The Recommended Dietary Allowance (RDA) for protein is set at 0.8 g protein/kg per day and describes the minimum quantity of protein that needs to be eaten each day to prevent deficiency. Protein researchers propose that while sufficient to prevent deficiency, this amount is insufficient to promote optimal health as people age[2].

There have been several recent “position statements” issued by those that work with an aging population indicating that protein intake between 1.0 and 1.5 g protein / kg per day may provide optimal health benefits during aging [3, 4]. This seems at odds with the 2010 Dietary Guidelines Advisory Committee report [5] which states that ‘protein intake in the US is more than adequate’ and that ‘inadequate protein intake is rare’ [5]. These seemingly contradictory positions are largely due to a difference in terms of how protein adequacy is determined.

The RDA – more specifically the Estimated Average Requirement (EAR) is the minimum amount of protein intake required to prevent deficiency and is based on nitrogen balance studies (since nitrogen is the main component of the amino acids which make up proteins). The EAR is set at the amount of protein that allows the body to achieve nitrogen balance (protein making and protein breakdown is equal) and evaluates overall protein intake.  Evaluation of optimal protein intake not only considers total amount of protein eaten, but also evaluates the metabolic roles of individual amino acids. While the EAR may be enough protein for healthy younger adults, higher intakes of specific Essential Amino Acids (ones the body can’t make, e.g.  Leucine and Isoleucine and Valine) have been reported to improve body composition (muscle mass and increased strength) in older adults.

Another factor is that nitrogen balance studies look at the total amount of protein eaten in a day but don’t look at the amount of protein eaten at each meal [6,7] nor the role of the Essential Amino Acid Leucine which is  required to be present for protein synthesis to begin (including synthesis of new protein for muscle and bone)[6].  Leucine is an indispensable amino acid in the making of all types of protein, but has a unique role in signaling the beginning of muscle protein synthesis. Much research has been done with large doses of free leucine, however a 2012 animal study[6] found that in small meals with limited protein intake (often the case for older adults), that there was a specific minimum amount of Leucine required to be be present, before protein synthesis took place. This “Leucine threshold” had to be met or exceeded before the body would even begin the energy-expensive process of making new proteins!

Typically, the average American eats only 10 g protein for breakfast, 15 g protein for lunch and has most of their daily protein at supper (65 g protein at supper) and since the minimum amount of Leucine that needs to be present in a meal (i.e. “Leucine Threshold”) is not enough at breakfast and lunch with this pattern of protein intake, protein synthesis is only triggered after the evening meal. As elaborated on below, it is recommended that this change.

A 2013 study of muscle protein synthesis in adults in their late 30’s found that when the amount of protein is distributed evenly throughout the day (30 g protein at breakfast, lunch and supper) that significantly more muscle protein was made. Of importance, the (a) making of new protein and (b) the threshold at which protein will be triggered to be made differ with age – with older people needing a higher intake of protein and specifically the amino acid Leucine, than younger adults [8]. This reduced muscle protein synthesis has been called “anabolic resistance” (anabolic means to ‘build’) and studies have shown that this “anabolic resistance” can be overcome with meals containing higher amounts of Essential Amino Acids and appears to be related to the Leucine content of the meal [8]. These findings led to Dietary Recommendations for older adults that emphasize a minimum of 20 g of protein per meal containing more than 2.3 g Leucine to optimize the building of new muscle protein [4].

Final Thoughts…

It is not only growing children and youth that need to eat adequate protein daily, but older adults as well. In many Indigenous cultures, the Elders eat first and eat the best of the animal proteins – which may factor in to the preservation of bone and muscle mass we see in many of these cultures.

The average protein intake for men >20 years old in the US is ~98 g per day and for women it is 68 g per day which may be adequate in total for healthy young adults, but is considered imbalanced in terms of distribution, as a minimum amount of Leucine is required for protein synthesis (specific amount in humans has not yet be determined). Dr. Layton recommends that until further research is conducted and the optimal amount of Leucine is determined that young adults and middle aged adults distribute their protein evening throughout the day with ~25 g (women) -30 g (men) of animal-based protein at each meal. The reason high biological value proteins from animal sources (meal, poultry, fish, egg, dairy) are recommended is because these are high in Leucine (rather than having only 10 g protein for breakfast, 15 g protein for lunch and 65 g protein at supper).

The recommendations above for older adults to eat 1.0 – 1.5 g protein / kg per day distributed evening over three meals which would be on average ~30-40g of animal-based protein at each meal to provide for optimal muscle protein synthesis, preventing sarcopenia – the muscle loss we’ve come to see as ‘normal’ in aging.

How much is too much protein?

According to Dr. Layton, the Upper Limit of Protein according to the Recommended Daily Allowance for Protein is set at ~ 2.5 g protein / kg per day which would put the maximum amount for most adult men at ~200 g protein per day.

Have questions?

Need help determining how much protein you should optimally be eating at each meal and from what sources? Please send me a note using the “Contact Me” form and I will reply as soon as possible.

To your good health!

Joy

References

1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350.
2. Volpi E, Campbell WW, Dwyer JT, et al. Is the optimal level of protein intake for older adults greater than the recommended dietary allowance? J Gerontol A Biol Sci Med Sci. 2013 Jun;68(6):677-81
3. Fielding RA, Vellas B, Evans WJ, Bhasin S, et al, Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J Am Med Dir Assoc. 2011 May;12(4):249-56
4. Bauer J1, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
5. U.S. Department of Agriculture and U.S. Department of Health and Human Services, Dietary Guidelines for Americans, 2010. 7th Edition, Washington, DC.
6. Norton LE, Wilson GJ, Layman DK, et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond). 2012 Jul 20;9(1):67
7. Mamerow MM, Mettler JA, English KL, et al. Dietary Protein Distribution Positively Influences 24-h Muscle Protein Synthesis in Healthy Adults. The Journal of Nutrition. 2014;144(6):876-880.
8. Layman DK, Anthony TG, Rasmussen BB, et al. Defining meal requirements for protein to optimize metabolic roles of amino acids, The American Journal of Clinical Nutrition, Volume 101, Issue 6, 1 June 2015, Pages 1330S—1338S

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Copyright ©2018 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.

Previous to today, I never gave the reliability of blood glucose monitors a second thought. I assumed that if they were sold in Canada, they were reliable. Not all are as good as others, it seems!

Yesterday morning, as I always do, I tested my morning fasting blood glucose with my glucometer. As someone with Type 2 Diabetes, this helps me understand the effect that the food I had for supper may have had and also helps guide me as to whether I may begin the day with time-delayed eating. For Type 1 Diabetics or insulin-dependent Type 2 Diabetics however, the accuracy of this information is critical! They base the dosage of insulin they take on this data and count on it being reliable and accurate.

Accuracy is how close the reading on the meter is to the actual blood glucose value and reliability is the likelihood of repeating the measure with the same meter at the same time and getting the same result.

Yesterday, I swabbed by thumb with an alcohol wipe, let it dry and took my blood glucose reading at 5:27 am and got a reading of 4.8 mmol/L (86 mg/dl) and thought “that can’t be!“, as I know that is a blood sugar reading that I only obtain after more than 18 hours of fasting.

 

I got another test strip from the same vial (recently opened and not expired) and tested the same thumb in a location immediately beside where I had just tested and got a reading of 5.8 mmol/L (105 mg/dl) and thought “that seems more reasonable, but what’s with the meter?”.

Ironically, only several hours prior a physician-friend sent me the link a report from August 14, 2017 that indicated that only 6 out 18 blood glucose meters tested passed the standard for meter accuracy which is for them to be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value in 95% of 100 trials. That means there was only a 1/3 pass rate!

Naturally, the first thing I did was look up to see how my meter – actually both my meters (which are identical) ranked.  It failed!

Even though I had brought my glucometer to the lab with me in July when I last had my fasting blood glucose measured and it matched the lab results exactly, my meter failed the test because when tested 100 times, it was NOT accurate 95% of the time.  

To pass a meter had to match or be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value on 95/100 trials.

I only tested my meter against the lab value ONCE and assumed it to be accurate. It was accurate on that one occasion, but it was not reliable, because when repeating the measure 100 times with the same meter it did not produce results within the 15% acceptable variation.

At 5:27 AM my blood glucose reading was 4.8 mmol/L and 2 minutes later with a new strip it was 5.8 mmol/L – on the same meter. That is a huge amount of variation, although depending on what the lab value actually would have been at that time, the results may or may not have fallen with range (see box below).

NOTE: The average of the two readings, 4.8 & 5.8 is 5.3 mmol/L and a ±15% tolerance would be ± 0.795 or ~ ± 0.8, for a range of 4.5 mmol/L to 6.1 mmol/L, so the readings would be within that range, ASSUMING the AVERAGE is the CORRECT result. While 0.8 is +16.7% more than the lower result and -13.8% less than the higher result, the actual ± 0.5 deviation from the mean is +10.4% and -8.6% of the lower & upper results. If either one result was correct, then 4.8 x 1.15 = 5.52 mmol/L, while 5.8 x 0.85 = 4.93 mmol/L, so the other would be erroneous. But, 4.8 í· 0.85 = 5.65 mmol/L, and  5.8 í· 1.15 = 5.04 mmol/L, so if the laboratory serum reading fell between 5.04 and 5.65 mmol/L then the meter’s two readings would be accurate to within ±15%. Now ± 15% is 30% of the value which means that (a) A serum glucose of 3.5 mmol/L (low end of normal) could mean a glucometer reading range of 1.05, or 3.04 mmol/L to 4.12 mmol/L A serum glucose of 11 mmol/L (way too high!) would be a 3x larger range of 3.3, or 9.56 mmol/L to 12.94 mmol/L. [thanks to Dr. L De Foa for the calculations]

Unfortunately, I know that my device(s) are not reliable based on this study data and for people who are insulin-dependent Type 1 or Type 2 Diabetics, they rely on the readings from their blood glucose monitors in order to dose their insulin. When their meters have been proven unreliable, it is cause for major concern.

I am reproducing the main data from this study because it is imperative that people know whether the monitor they are relying on is indeed, reliable.

The full testing protocol and results can be found here.

The rated accuracy from Bayer of the number one rated meter above, the Contour Next USB is 100% within ±0.56 mmol/L for glucose < 5.55 mmol/L and 98.1% within ±10% and 100% within ±15% for blood glucose > 5.55 mmol/L and it was accurate 100% of the time in the tests.

As for me, I have gone back to using a glucometer that I had on hand (which also tests blood ketones), as it is one of the models that passed.

While I am left with almost 1/2 a package of new test strips from the unreliable meter, how much worse could it be for someone who is dosing insulin based on unreliable blood glucose meter reading.

Type 2 Diabetes?

If you have Type 2 Diabetes and have struggled to lower your HbA1C or achieve your weight loss goals please send me a note using the “Contact Me” form above about how I can help and I’ll be happy to reply.

Copyright ©2018 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.

Long before the ‘hybrid car” there was the human body – a hybrid ‘machine’ perfectly designed to use either carbohydrates or fat for energy. Like a hybrid car, we can run on one fuel source or the other at any one time.

If we are eating a largely carbohydrate based diet, we will be in ‘carbohydrate mode’ by default. Carb-based foods will be broken down by our bodies to simple sugars and the glucose used to maintain our blood sugar levels. Our liver and muscle glycogen will be topped up, then the rest will be shuttled off to the liver where it will be converted into LDL cholesterol and triglycerides and stored in fat cells.

Historically, in times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen and then switch fuel sources to be in “fat-burning mode” — accessing our own fat stores, for energy.

The problem is now that we rarely, if ever access our stored fat because we keep eating a carb-based diet.  So we keep getting fatter and fatter.

GLUCOSE OR FAT AS FUEL

When we are in “carb burning mode”, the carbs we eat are broken down by different enzymes in our digestive system to their simplest sugar form (monosaccharides) such as glucose, fructose and galactose.

Glucose is the sugar in our blood, so starchy foods such as bread and pasta and potatoes are broken down quickly so they are available to maintain our blood sugar levels.

Monosaccharides are the building blocks of more complex sugars such as disaccharides, including sucrose (table sugar) and lactose (the sugar found in milk), as well as polysaccharides (such as cellulose and starch). When we drink milk for example, the galactose found in it is broken down into lactose and glucose.  When we eat something sweetened with ‘sugar’ (sucrose), it is quickly broken down to glucose and fructose.

Any glucose that is needed to maintain our blood sugar level is used immediately for that purpose and the remainder is used to “top up” our glycogen stores in our muscle and liver. There are only ~ 2000 calories of glycogen – enough energy to last most people one day, so when our glycogen stores are full, excess energy from what we eat is converted to fat in the liver and stored in adipocytes (fat cells).

One problem is that our diets are high in fructose – naturally found in fruit but also as high fructose corn syrup in many processed foods. Fructose can’t be used “as is”, so it is brought to the liver.  If our blood sugar is low, it will be used to make glucose for the blood (via gluconeogenesis) otherwise it will be converted into LDL cholesterol and triglycerides and stored as fat.

Feasting and Fasting

When we don’t eat for a while, such as would have occurred when our ancestors were hunter-gatherers, we’d use up our glycogen stores hunting for an animal to eat, or gathering other edible foods and if we weren’t successful at finding food to eat, then our bodies would access our fat stores, for energy.  This is known as lipolysis. This process is regulated mainly by a hormone called glucagon, but other hormone such as epinephrine (the “fright and flight” hormone), cortisol (the “stress hormone”) as well as a few others (ACTH, growth hormone, and thyroxine) also play a role.

In times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen, switch into “fat-burning mode” and then rely on our stored fat for energy.

The problem for most of us in North America and Europe is that we have access to food in our homes, in stores and at fast food restaurants 24/7. We can’t go for a walk without passing places selling or serving food and if the weather is bad or we are too tired, food is just a phone call or web-click away. So we just keep storing up our fat for ‘lean times’ that never come.

In addition, irrespective of our cultural background, our eating style is carb based; pasta, pizza, sushi, curry and rice or naan, potato, pita – you name it.  Every meal has bread or cereal grains, pasta, rice or potatoes – and even what we consider “healthy foods” such as fruit and milk have the same number of carbs per serving as bread, cereal, pasta, rice and potatoes. That wasn’t always so. Our indigenous cultural foods were very different.

Compounding that, many “low-fat” products have added sugar (sucrose) in order to compensate for changes in taste from reducing naturally occurring fat, which then adds to excess carb intake.  Sucrose (ordinary table sugar) is made up of half fructose, so a diet high in sugar adds even more fructose transport to the liver, for conversion to cholesterol and fat.

The vilification of fat

In 1977, both the Canadian and US food guides changed in response to the promoted belief that eating diets high in saturated fat led to heart disease. Multiple studies and reanalysis of the data of older studies indicates that saturated fat is not the problem, but that diets high in carbohydrate combined with chronic inflammation and stress, is.

In 2016, it came to light that the sugar industry funded the research in the 1960’s that downplayed the risks of sugar in the diet as being related to heart disease and highlighted the hazards of fat instead – with the results having been published in the New England Journal of Medicine in 1967 with no disclosure of the sugar industry funding*. The publication suggested that cutting fat out of the American diet was the best way to address coronary heart disease, and which resulted in the average American and Canadian as inadvertent subjects in an public health experiment gone terribly wrong. Overweight and obesity has risen exponentially and with that Diabetes, hypertension (high blood pressure) and high cholesterol.

*(Kearns CE, Schmidt LA, Glantz SA. Sugar Industry and Coronary Heart Disease Research A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016;176(11):1680-1685. doi:10.1001/jamainternmed. 2016. 5394).

Over the last 40 years the promotion of “low fat eating” by governments and the food industry has resulted in carbohydrate-intake skyrocketing. Every high-carb meal is followed by another high-carb meal, and if we can’t wait, a snack, too. We eat every 2-3 hours, and eating carb-based foods every 2 or 3 hours all day, every day is quite literally killing us.

How do we get fat out of “storage”?

The “key” to unlocking our fat stores, is decreasing overall intake of carbohydrates by decreasing the amount of carbohydrates we eat, both by eating much less of it and on occasion, by delaying the amount of time between meals.

Decreasing carb intake lowers insulin, the fat-storage hormone. At first our bodies access liver and muscle glycogen for energy, but since that is only about a one day’s supply, our bodies then turn to our own fat stores as a supply of energy.

By eating a diet rich in fat and keeping protein at the level needed by the body but not in excess, dietary protein is not used to synthesize glucose, but fat is.

An added bonus is that since insulin also plays a role in appetite, as insulin falls, appetite decreases.

This is the role of a low carb high healthy fat diet, a topic covered in this article.

Have questions?

Why not send me a note, using the “Contact Us” form above?  I’d be happy to answer your questions.

To your health!

Joy

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. 

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(April 25, 2017) Be sure get the recipe for a Low Carb High Healthy Fat Matcha Smoothie here: https://www.bbdnutrition.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