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.
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.
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.
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
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.
Concentrations of aldehyde per litre of oil when heated to 180 C (from Groosvelt et al, 2015)
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).
Comparison of Dietary Fats – linoleic acid content
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
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.
“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].
Ancient olive oil press
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 inthe 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 Panelof 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]
soybean extraction plant
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
Alfred Thomas (2002). “Fats and Fatty Oils”. Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH.
“Tentative Determination Regarding Partially Hydrogenated Oils”. Federal Register. 8 November 2013. 2013-26854, Vol. 78, No. 217.
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
Schaer, L., Grainews, Canola gets competition from soybeans, Feb 01, 2016, https://www.grainews.ca/2016/02/01/canola-gets-competition-from-soy/
Wall Street Journal, “Soybeans Are Ancient; Oil Is Not”, 2011, https://blogs.wsj.com/chinarealtime/2011/01/03/soybeans-are-ancient-oil-is-not/
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 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.
Keys et al – Epidemiological studies related to coronary heart disease: characteristics of men aged 40—59 in seven countries [1]
Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note [2]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 inthe 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 – yeta 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 sameDr. 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 withincreased 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.
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
Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118—139 (1953).
Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343—54
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.
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
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.
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
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
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
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
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.
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
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
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
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
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
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
Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
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
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
Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
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
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
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
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)
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
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/
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.
(reverse side) Comparison of Dietary Fats — ”Provided as a Professional Service by Proctor & Gamble”, 1989 – full size photo, below
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.
(front side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989
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“.
(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989
I’ve highlighted some of the wording that makes Proctor & Gamble’s bias apparent;
(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989 – red text mine
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.
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
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.
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.
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.
Recommended Daily Allowance (RDA) for Protein [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health]
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
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.
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
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
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
U.S. Department of Agriculture and U.S. Department of Health and Human Services, Dietary Guidelines for Americans, 2010. 7th Edition, Washington, DC.
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
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.
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
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.
Overall Results of Blood Glucose Monitoring Systems – Diabetes Technology Society 2018
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.
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.
Many people (including me) are sick with the flu and many are sipping soup, because it is warm and comforting and provides them with some protein, vitamins and minerals. I’m drinking chicken soup, made from my grandmother’s recipe and this isn’t any chicken soup, as you will soon find out.
Whenever someone in my family is sick, it’s me they turn to for chicken soup — but not just any chicken soup, but the one I learned how to make at my grandmother’s knee.
This soup is purported to have curative effects and it must have had something because my Bubby (‘grandmother’) lived until 104 years old and was in very good health until a few months before she passed away (2013).
My grandmother used to joke that she “didn’t lose her marbles” and to be honest, she had more “marbles” at 104 than many do at half that age.
Her chicken soup was amazing — nothing like any similarly named broths by Lipton®’s or Campbell®’s. Bubby’s Chicken Soup was made with love, care and the best of ingredients and was the epitome of what has become known as, “Jewish penicillin”. I still have vivid memories from when I was a little girl of going to the market with my grandmother to pick out a live chicken.
She always served her chicken soup in a “soup plate”, like this and the spoon was deep and round, like a miniature bowl with a handle.
Bubby’s Chicken Soup – served in a ‘soup plate’same soup – different way to serve
I wonder if she’d be horrified that I drink mine out of a coffee mug!
The first question many people ask me when I talk about my Bubby’s Chicken Soup is “what makes Jewish chicken soup different“?
No, the chickens aren’t “Jewish” (!) — although a kosher soup chicken does make the most amazing broth.
Bubby’s Chicken Soup was made with a special type of chicken and has a texture and a taste unlike any other. To illustrate my point, here is a photo of what Bubby’s Chicken Soup looks like when its chilled;
natural gelatin from the ‘soup chicken” results in this texture, when chilled
It is the special type of chicken that this soup is made from (and a few other special ingredients that I’ll tell you about shortly) that contribute collagen and natural gelatin and result in the chilled broth being like very firm Jello®.
A “soup chicken” (also known as a “stewing hen“) is essential for making this soup. A “roaster” or “broiler” simply won’t do! They are too young and have too much fat, too much ‘meat’ and too little flavor.
A soup chicken is an old bird that has outlived its usefulness for laying eggs and it’s the age of the chicken that makes it perfect for making soup, because although the meat is tough it makes the best soup. Old laying hen hav lots of connective tissue and collagen, and it’s this which makes the resulting broth very different. This, and the addition of chicken feet. Yes, chicken feet. As my grandmother did, I chop the nails off of them before making soup, but many butchers that sell them, will do this for you, if you ask. One can often find ‘soup chickens’ or ‘stewing chickens’ at independent ethnic butchers or at small supermarkets with a large ethnic clientele and these same markets often sell chicken feet, too.
As you can see from the photo above, soup chickens are small and don’t have hormone-enlarged breasts- in fact, they have very little meat at all, and have almost no fat under the skin. It’s these factors (plus the addition of the feet) that result in the the chilled broth being so gelatinous, with the minimum of fat on it. Jewish Chicken Soup is the original “bone broth”.
Bubby’s Chicken Soup (aka “Jewish Penicillin)
Most people would never give out their grandmother’s family recipe, but since not everyone had a Jewish grandmother, I thought I’d share mine with you, along with her wonderful recipe for soup!
Bubby’s Chicken Soup
3 soup chickens / stewing fowl
8 chicken feet (nails removed), cleaned
1 lg onion, just the outermost skin removed, whole
2 very large carrots, peeled and cut in chunks
1 parsley root, peeled (I can’t find this in Vancouver, so I use the stems from a bunch of Italian parley plus a very tiny parsnip)
1 stalk of celery, with leaves
Salt to taste
cracked black pepper
Sprig of fresh dill (for garnish)
1 – Put two of the stewing chickens at the bottom of a very large stock pot.
2- Toss the vegetables on top, then the chicken feet. Cover with very cold water and add salt. Be careful not to put in too much water, otherwise the broth won’t have the correct taste, body or colour. Gently slip in the 3rd soup chicken.
3 – Bring to a boil over medium high heat, skimming off foam with a small mesh designed for this purpose, until it stops producing foam.
4 – Lower heat to medium low and simmer soup for at least 8-10 hours, overnight if possible.
5- Strain the broth through a large colander into another pot (so you only have the rich golden liquid). Pick out the carrot chunks from the colander, and serve with the clear broth. Garnish with fresh dill.
Note: for those that are not following a low carbohydrate / ketogenic lifestyle, this soup can also form the basis for “matzoh ball soup”.
Since 1977, the dietary recommendations in Canada and the US has been for people to consume a diet with limited fat and where ”complex carbohydrates” (starches) comprise the main source of calories.
From 1949 until 1977, the dietary recommendations of Canada’s Food Guide were for people to consume
~20-30% of their daily calories as carbohydrate
~40-50% of daily calories as fat
~20-30% of daily calories as protein
From 1977 onward, Canada’s Food Guide recommended that people consume:
55-60% of daily calories as carbohydrate
<30% of daily calories as fat, with no more than 1/3 from saturated fat
15-20% of daily calories as protein
The US recommendations since 1977 have been similar to those in Canada, with the Dietary Goals for the United States recommending that carbohydrates are 55-60% of daily calories and that calories from fat be no more than 30% of daily calories (of which no more than 1/3 comes from saturated fat).
Eating Well with Canada’s Food Guide which came out in 2015, recommends that people eat even more of their daily calories as carbohydrate;
45-65% of daily calories as carbohydrate
20-35% of daily calories as fat, with no more than 1/3 from saturated fat
Health Canada recommends limiting fat to only 20-35% of calories while eating 45-65% of daily calories as carbohydrates and currently advise adults to eat only 30-45 mL (2 — 3 Tbsp) of unsaturated fat per day (including that used in cooking, salad dressing and spreads such as margarine and mayonnaise).
This is what people have come to call a ”balanced diet”.
But is it?
For the past 40 years, the public has come to believe that eating fat made you fat’ and that eating saturated fat caused heart disease. This however is not what evidence-based research shows. More on that in future articles.
Our society has become ”fat phobic”. People guzzle skim or 1% milk with little regard to the fact that just 1 cup (250 ml) has almost the same amount of carbs as a slice of bread. And who drinks only one cup of milk at a time? Most people’s ”juice glasses” are 8 oz and the glasses they drink milk from are 16 oz, which is 2 cups. Who ever stops to think of their glass of milk as having the same amount of carbs as almost 2 slices of bread?
In addition, carbs are hidden in the 7-10 servings of Vegetables and Fruit they are recommended to eat — with no distinction made between starchy- and non-starchy vegetables. Many people eat most of their vegetable servings as carbohydrate-laden starchy vegetables such as peas, corn, potatoes and sweet potatoes and then have a token serving of non-starchy vegetables (like salad greens, asparagus or broccoli) on the ”side” at dinner. Who stops to think that just a 1/2 cup serving of peas or corn has as many carbs as a slice of bread — and often those vegetables are eaten with a cup of potatoes, adding the equivalent number of carbs as another 2 slices of bread?
People drink fruit juice and ”smoothies” with no regard for all of the extra carbs they are consuming (not to mention the effect that all of that fructose has). A ”small juice glass” is 8 oz, so just a glass of orange juice has the equivalent number of carbs as another 2 slices of bread! Many grab a smoothie at lunch or for coffee break without even thinking that the average smoothie has the same number of carbs as 5 slices of bread!
Then there is the toast, bagels and cereal or bars that people eat for breakfast, the sandwiches or wraps they eat for lunch and the pasta or rice they have for supper. These are carbs people know as carbs — which are added to all the carbs they consumed as vegetables, fruit and milk.
What has been the outcome of people following these dietary recommendations to eat a high carb diet since 1977 ?
Obesity Rates
In 1977, obesity rates* were 7.6% for men and 11.7% for women, with the combined rate of < 10 % for both genders.
* Obesity is defined as a Body Mass Index (BMI) ≥30 kg/(m)2
In 1970-72 the obesity rate in Canadian adults was 10% and by 2009-2011, it increased two and a half times, to 26%.
In 1970-72, only 7.6% of men were obese but by 2013, 20.1% of men were categorized as obese. In 1970-72, only 11.7% of women were obese but by 2013, 17.4% of women were obese.
In 1978 in Canada, only 15% of children and adolescents were overweight or obese, yet by 2007 that prevalence almost DOUBLED to 29% of children and adolescents being overweight or obese. By 2011 obesity prevalence alone (excluding overweight prevalence) for boys aged 5- to 17 years was 15.1% and for girls was 8.0%.
The emphasis since 1977 on consuming diets high in carbohydrates and low in fat has taken its toll.
Effect on Health
Non-alcoholic liver disease is rampant and not surprisingly, considering 37% of adults and 13% of youth are abdominally (or truncally) obese — that is, they are carrying their excess body fat around and in the internal organs, including the liver.
Since the 1970’s, Diabetes rates have almost doubled.
In the 1970s, the rate of Type 2 Diabetes in women was 2.6% and in men was 3.4 %. In the 1980s that number rose in women to 3.8% and in men to 4.5%. In the 1990s the rate was almost double what it was in 1970; in women it was 4.7% and in men, 7.5%.
If people eating a high carb, low fat diet has corresponded to an increase in obesity, overweight and Diabetes, then what’s the alternative?
That is where a ketogenic diet comes in , which is a low carbohydrate, high fat diet which supplies adequate, but not excess protein. Eating this way enables us to use our own fat stores for energy, and to make our own glucose and ketones to fuel our cells and organs. Since humans are designed to run on carbs (in times of plenty) and in our fat stores (when food is less plentiful), ketosis is a normal physiological state. By eating a low carb high fat diet when we’re hungry and delaying eating for short periods, we can mimic the conditions that were common to our ancestors. By eating this way over an extended period of time, we can bring down insulin levels and as a result, decrease the insulin resistance of our cells. We can improve our blood sugar, lower our blood pressure and see our LDL cholesterol and triglycerides come down to normal, healthy levels.
Want to know more?
Why not send me a note using the Contact Us form located above?
Long before the ‘hybrid car” there was the human body – a hybrid ‘machine’ perfectly designed to use either carbohydrates or fat for energy. Like a hybrid car, we can run on one fuel source or the other at any one time.
If we are eating a largely carbohydrate based diet, we will be in ‘carbohydrate mode’ by default. Carb-based foods will be broken down by our bodies to simple sugars and the glucose used to maintain our blood sugar levels. Our liver and muscle glycogen will be topped up, then the rest will be shuttled off to the liver where it will be converted into LDL cholesterol and triglycerides and stored in fat cells.
Historically, in times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen and thenswitch fuel sources to be in “fat-burning mode” — accessing our own fat stores, for energy.
The problem is now that we rarely, if ever access our stored fat because we keep eating a carb-based diet. So we keep getting fatter and fatter.
GLUCOSE OR FAT AS FUEL
When we are in “carb burning mode”, the carbs we eat are broken down by different enzymes in our digestive system to their simplest sugar form (monosaccharides) such as glucose, fructose and galactose.
Glucose is the sugar in our blood, so starchy foods such as bread and pasta and potatoes are broken down quickly so they are available to maintain our blood sugar levels.
Monosaccharides are the building blocks of more complex sugars such as disaccharides, including sucrose (table sugar) and lactose (the sugar found in milk), as well as polysaccharides (such as cellulose and starch). When we drink milk for example, the galactose found in it is broken down into lactose and glucose. When we eat something sweetened with ‘sugar’ (sucrose), it is quickly broken down to glucose and fructose.
Any glucose that is needed to maintain our blood sugar level is used immediately for that purpose and the remainder is used to “top up” our glycogen stores in our muscle and liver. There are only ~ 2000 calories of glycogen – enough energy to last most people one day, so when our glycogen stores are full, excess energy from what we eat is converted to fat in the liver and stored in adipocytes (fat cells).
One problem is that 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.
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This delicious low carb high fat Matcha Smoothie can help you lose weight & abdominal fat. The science behind it, the recipe & the nutritional info in this article.
Green tea is the unfermented leaves of the Camellia sinensis plantand contains a number of biologically active compounds called catechins of which epigallocatechin gallate (EGCG) makes up ~ 30% of the solids in green tea [Kim et al]. Studies have found that green tea catechins, especially EGCG play a significant role in both weight loss and lower body fat composition.
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].
Several large-scale population studies have linked increased green tea consumption with significant reductions in metabolic syndrome – a cluster of clinical symptoms which include insulin resistance or hyperinsulinemia (high levels of circulating insulin), Type 2 Diabetes, hypertension or high blood pressure, cardiovascular disease including coronary heart disease and atherosclerosis.
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 Type 2 Diabetes [Kao et al].
EGCG also lowers blood pressure almost as effectively as the ACE-inhibitor drug, Enalapril, having significant implications for people with hypertension (high blood pressure) and cardiovascular disease [Kim et al].
Research indicates that 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].
The most effective way to reduce the symptoms associated with metabolic syndrome is through a low carb high healthy fat diet, however the addition of green tea as a beverage – especially as matcha green tea powder, may provide a means to preferentially target abdominal weight loss.
GREEN TEA CATECHINS
Catechins make up ~ 30% of green tea’s dry weight (of which 60—80% are catechins) and oolong and black tea (which are produced from partially fermented or completely fermented tea leaves) contains approximately half the catechin content of green tea.
Matcha, a powdered green tea used in the Japanese tea ceremony and popular in cold green tea beverages contains 137 times greater concentration of EGCG than China Green Tip tea (Mao Jian) [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 EGCGs 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.
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 (1 — 4 tsp of matcha powder per day) lost an average of 1.31 kg (~ 3 lbs) over 12 weeks with no other dietary or activity changes [Hursel].
Body composition EFFECT OF GREEN TEA CATECHINS
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 decreased 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 than 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 i.e. using body fat as energy. For those on a low fat high fat diet, this is good!
– decrease appetite
– down-regulation of enzymes involved in liver fat metabolism (fat storage)
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].
Low Carb Green Tea Matcha Smoothie Recipe
Total carbs: 2.5 gm per serving – contains ~315 mg catechins
Ingredients
1 tsp matcha (green tea) powder * (1 tsp = 2 gm)
12 cubes ice, crushed
1/2 cup (125 ml) coconut milk
optional: 1/2 tsp Silan (Middle Eastern date syrup) – will add an additional 3.5 g carbs to the recipe
Method
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
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)
With a bamboo whisk (available at Japanese and Korean grocery stores) or a plain spoon, whisk 3 Tbsp boiled and cooled water into the matcha powder, until all the lumps are gone and the mixture is smooth
Place a whole tray of ice cubes (12) into a blender
Pour matcha and water mixture over ice in the glass
Pour coconut milk on top of ice and matcha
Pulse until desired texture is achieved*
*I blend mine just fine enough to be able to drink it through a straw.
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.
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.
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
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
Less than 3 gm of carbohydrate at all the health benefits of Matcha!
Introduction
Recent estimates indicate that about 1/3 of the adult population in the US is obese [Centers for Disease Control and Prevention, 2009] and while 2011 estimates in Canada indicate that approximately 1/5 of Canadians adults are classified as obese based on self-reported height and weight [Statistics Canada], studies have found that obesity rates in self-reported weight is ~7.4% higher when based on measured height and weight [Shields et al]. Adjusting for this under self-reporting of weight, > 1/4 (25.6%) of the adult population in Canada would be considered obese. Recent literature suggests that obesity and the related diseases of ”metabolic syndrome” associated with obesity are not just a North American problem either, but a global health problem [Popkin].Although there are many genetic and environmental factors that may predispose people to weight gain, the main cause of overweight and obesity is believed to be animbalance between dietary intake and energy expenditure(i.e. calories in > calories out). Excess fat mass develops over time from a very small positive energy imbalance i.e. just taking in slightly more calories than needed. In general, average weight gain per year is small; approximately 1 pound per year across all race, economic, and sex groups[Brown].There are many strategies used to address weight gain, including;-
Dietary approaches;whichusually focus on decreasing caloric intake through a variety of means and while some people go on self-chosen ”diets” that are bizarre and even dangerous, weight loss will occur as long as energy intake is less than energy expenditure (i.e. calories in < calories out).
– Lifestyle strategies that help individuals identify and modify their eating behaviour and patterns of eating. When people understand why they eat and when they eat, it is easier for them to make long-term lifestyle changes.
– Exercise and increased physical activity to help people attain and maintain a healthy body weight.
– Food intake is sometimes addressed pharmacologically by doctors by using drugs such as Orlistat (which blocks lipase, an enzyme involved in fat absorption).
– Surgical approaches provide the most dramatic weight loss and outside of the cosmetic value, may have a role in reducing long-term mortality and the incidence of diabetes [Bray].
Role of Green Tea Catechins in Weight Loss
Green tea is the unfermented leaves of the Camellia sinensis plantand contains a number of biologically active compounds called catechinsand 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;
– thetotal 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!
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
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)
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
Place 1/4 cup of crushed ice in the bottom of a tall (16 oz / 500 ml) glass
Pour matcha and water mixture over ice in the glass
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.
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
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
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.
Rice noodles, such as those in Pho (Vietnamese Beef Noodle soup) are even higher, at 53 ± 7.
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?”.
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.
Ingredients