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There is evidence to show that over-fatness and obesity is a problem involving both sugar and fat metabolism, resulting in fat deposition and an inability to mobilize fat from the fat tissue.

In the two previous tips here and here I have been trying to suggest that there is a fair bit of evidence showing that low calorie, low fat diets don’t work, and that historically speaking, we have eaten meat and saturated fat for millennia, whereas grains are relatively new to our diet. Once farming began, some traditional cultures did eat grains, but they were soaked first (probably to soften them up and make them easier to chew), reducing the amount of sugar in them and increasing their digestibility. Only in the last 150-200 years or so have our diets included growing amounts of processed sugar and such huge and growing quantities of baked goods, pasta, and other foods that contain unfermented flour. To me, just knowing that information alone is enough to make me suspect that perhaps it is the sugar, flour products and alcohol that are the cause of the rise of modern diseases of civilization (obesity, type 2 diabetes, heart disease, osteoporosis, cancer, etc.), as opposed to saturated fat and cholesterol, as we have been told by medical/nutritional pundits.

According to Gary Taubes in his book Good Calories Bad Calories, much of the research on the metabolism of obesity occurred prior to World War 2 in Germany, and for the most part, has not been considered much since. In the 1920s, biochemists such as Rudolf Schoenheimer realized that our fat tissue is very metabolically active, and not simply a place to store fat like a safety deposit box, that only gets looked at once in a blue moon. Instead Hilda Bruch suggested that fat metabolism works more like a coin purse, where free fatty acids are continually being deposited into our adipose (fat) tissue and turned into triglycerides for storage, and also are continually being broken back down into fatty acids, and sent into the bloodstream to be burned as fuel depending on the requirements of the moment. Fat provides the ready coin for the momentary energy needs of the body.

Triglycerides are a combination of 3 fatty acids held together with glycerol, and they come from the fat in the diet and they are made in the liver and fat tissue from the carbohydrate in the diet. Triglycerides are the form in which fats are stored, and free fatty acids are the form in which fats are burned as fuel. So, people become over-fat when their body is very good at storing triglycerides, and not good at breaking down the triglycerides into free fatty acids to be sent into the bloodstream to be burned. It is not so much about the quantity of food being consumed, but rather about whether the environment in the body is forcing deposition or mobilization of the triglycerides in the fat tissue. Ernst Wertheimer said in 1948 in a review of the science of fat metabolism at that time, that “The ‘classic theory’ that fat is deposited in the adipose tissue only when given in excess of the caloric requirement has been finally disproved”.

In 1956, it became possible to measure free fatty acids in the bloodstream, and it was discovered that after a meal, blood sugar levels tend to be high, and fatty acid levels are low, but fatty acid levels rise in the hours after the meal. If sugar or insulin is injected into the bloodstream, fatty acid levels plummet. This is the key. When sugar is available for fuel, fats get stored as triglycerides. When no sugar is available, fats get mobilized into free fatty acids to be used as fuel. Robert Gordon of the NIH published this information in 1956. Why have we forgotten it today??? The more carbohydrate consumed, the more triglycerides get made and stored. The more glucose/insulin in the bloodstream, the more "stuck" the fat is in the fat cells. When blood glucose/insulin is low, free fatty acids can escape from the fat cells into the bloodstream to be burned. Therefore, how many free fatty acids can be burned depends entirely on the amount of glucose and insulin in the bloodstream.

Furthermore, in order for triglycerides to be manufactured, the molecule glycerol phosphate is required, and that molecule is supplied only by carbohydrates. So, if there is little or no carbohydrates in the diet, little or no glycerol phosphate is available to make triglycerides and store fat, so little or no fat deposition can occur.

So a diet high in starchy carbohydrates (baked goods, pasta, other flour products, sugar, fruit and alcohol) leads to fat accumulation in two ways. First, it sharply increases blood sugar which increases insulin, our storage hormone, which in turn controls the production of glycerol phosphate and therefore the conversion of sugar into triglycerides and the storage of fat in the fat cells, causing fat deposition. Secondly, when blood sugar and blood insulin levels are high, fat is stuck in the fat cells and cannot be mobilized, resulting in an inability to use fat as a fuel. A combination of fat deposition and an inability to mobilize our fat for fuel leads to fat accumulation, over-fatness and obesity. Some of us can tolerate more carbohydrate in our diet than others without suffering negative consequences (biochemical individuality), and those that can't tend to develop problems like over-fatness, type 2 diabetes, heart disease etc.

Next week we'll explore why the medical / scientific community has not endorsed low starchy-carb diets as being a healthy way to eat, do a cost / benefit analysis, and see what conclusions we come to.

I HIGHLY recommend the recent book by Gary Taubes, Good Calories, Bad Calories if you are interested in the topics of diets, obesity, heart disease and diabetes. Or watch this webcast of a lecture given by Gary Taubes at Berkeley last November on this topic.

Related tips
Obesity, Type 2 Diabetes and Heart Disease – what does history tell us?
Obesity – a behavioural or a metabolic problem?
Insulin, our storage hormone
Sugar, the disease generator
Another “healthy heart guide” that got it wrong
Saturated fat, the misunderstood nutrient
Cortisol, our stress hormone

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Rather than trying to ascertain the causes of modern diseases only by looking through a microscope, it can often be extremely enlightening to back up and look at the big picture through the lens of history.

When one considers that the earliest hominid (prehistoric human) fossils found appear to be between 3.8 and 4 million years old, and it is believed that we were nomadic until the advent of agriculture about 10,000 years ago, it becomes obvious that in the scheme of things, growing food is a relatively new idea. When we were nomadic, we probably followed the meat in order to survive, supplementing with plant foods that were available wherever the meat was. Can you imagine taking a handful of whole oat kernels or wheat berries, throwing them in your mouth and chewing them as part of your meal? There isn't much evidence that nomadic cultures carted around pots to cook grains with, and in fact, there isn't much evidence that we cooked our food at all until relatively recently. I think it is fairly safe to assume that humans ate very little or no grain for the vast majority of our existence.

It is said that it takes 100,000 years to change our genes one tenth of one percent through the evolutionary process, so therefore as of today, one can argue that our bodies have not yet adapted well to eating whole grain, let alone grain that has been ground into flour (which makes it act like sugar in the body), or grain that has been genetically modified (who knows what that is doing to us).

In many previous tips I have discussed the research of Dr. Weston A. Price who travelled the world in the 1930s comparing the health of traditional cultures that had not yet come in contact with “white man’s food” to those that had, and consistently found that when cultures replaced their native diet with white flour, white sugar, and canned food, their health deteriorated. Dr. Price was by no means alone in making this connection. The British, in their colonization of India noticed that the incidence of obesity and diabetes varied depending on the sect or caste examined, and that generally diabetes and obesity were diseases that struck the rich who ate European diets and were more sedentary, and was pretty much nonexistent in those that ate their traditional diet. Similar patterns were noticed in Thailand, China, Sri Lanka, and Tunisia. The correlation between the increase in sugar and white flour consumption and the incidence of diabetes was forgotten after the 1930s in the US, even though similar findings were being noted in other parts of the world, such as the studies of Dr. Cohen who compared the Yemenite Jews who had lived in Israel since the early '30s, and those that arrived after 1949, and found that those that had lived in Israel longer had a diet much higher in sugar, and also had far higher incidence of type 2 diabetes, heart disease, obesity, hypertension and gout. Similar findings were found in the Maoris of New Zealand by Dr. Ian Prior, and in South Africa by Dr. George Campbell, who was the first person to propose an "incubation period" between the onset of sugar consumption and the diseases of civilization that follow.

In 1966, British Royal Navy Surgeon Dr. T.L. Cleave published a book called Diabetes, coronary thrombosis, and the saccharine disease, suggesting that all the modern diseases had a common cause – the consumption of refined flour, refined rice and sugar. "Saccharine" refers to sugar, as opposed to the artificial sweetener. He noted that disease was absent in both meat eaters like the Inuit or the Masai as well as plant-based cultures like the Hunza or the Kikuyu, until the time that these cultures began to add nutritionally depleted, "high saccharine" foods (refined carbohydrates) to their diet. He was unable to successfully convince the medical establishment that his theory had merit, even though it was generally acknowledged that those with diabetes were far more prone to heart disease and obesity.

In the US, at the McGovern Senate Select Committee on Nutrition and Human Needs in April '73, the scientific community debated whether it was a high fat diet or a high processed carbohydrate diet that was disease causing. Cohen, Campbell, Peter Bennett who discussed the obesity/diabetic plight of the Pima Indians, Walter Mertz, T.L. Cleave, Carol Berdanier and John Yudkin all demonized sugar, yet Ancel Keys' cholesterol-heart disease hypothesis won out, despite the fact that there was far more evidence implicating refined carbohydrates. The McGovern Committee sided with the saturated fat hypothesis, and in 1977 put out their Dietary Goals to lower saturated fat intake, and the public was led to believe that there was overwhelming consensus on the evils of fat, when in fact the scientific community was very much divided. In 1980, once the debate entered the political arena and the USDA published their Dietary Guidelines for Americans, the scientific debate around saturated fat vs. refined carbohydrate was pretty much silenced in favour of the wrong hypothesis, in my opinion. And unsurprisingly since that time, despite the decline in consumption of saturated fats, obesity, type 2 diabetes and heart disease rates have continued to rise along with the continued increase in consumption of processed sugar, high-fructose corn syrup, and products made of flour.

Today, obesity, type 2 diabetes and heart disease are more common in the poor. Unfortunately, the least expensive foods available are those that are highly processed, and frequently contain refined flour and sugar. The poor often find it difficult to afford quality meat and vegetables, and frequently rely on packaged food and fast food outlets for cheap, nutritionally deplete food that satisfies hunger. But the poor are not the only ones that partake in breads, pastries, pastas, and sugar-laden desserts, and they are certainly not the only ones to suffer from overfatness, heart disease, hypertension, gout, type 2 diabetes, osteoporosis, arthritis and cancer, all which have been linked to refined carbohydrates and sugar consumption.

My apologies in the delay in discussing the metabolic cause of obesity – what happens in the body when one consumes sugar, flour products and other refined grains that leads to fat accumulation. It's coming …

I HIGHLY recommend the recent book by Gary Taubes, Good Calories, Bad Calories if you are interested in the topics of diets, obesity, heart disease and diabetes.

Related tips
Obesity – a behavioural or a metabolic problem?
Insulin, our storage hormone
Sugar, the disease generator
Another “healthy heart guide” that got it wrong
Saturated fat, the misunderstood nutrient
Cortisol, our stress hormone

www.wellnesstips.ca

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I promised a couple of weeks ago to comment on the ACCORD type 2 diabetes study, part of which was halted due to increased deaths in the arm of the study that was trying to aggressively lower blood-sugar levels to those of non-diabetics. This result was surprising to many, as it was widely expected that very low blood-sugar levels would improve health outcomes rather than increase risk of death.

The ACCORD trial (ACCORD stands for Action to Control Cardiovascular Risk in Diabetes) was launched in 2001, and involved over 10,000 people from the US and Canada that had suffered from Type 2 Diabetes for at least 10 years, and were at high risk for heart disease. One of the questions asked by the study was whether or not lowering blood-glucose (sugar) aggressively was more effective than lowering it less aggressively, using hemoglobin A1c as the measure. One group was asked to try and maintain an HbA1c reading of less than 6%, and another group, between 7 and 7.9%, which is the current diabetic treatment goal. Hemoglobin A1c is a useful measure because it can tell a physician how well blood-sugar levels have been controlled over a period of weeks. There were 20% more deaths in the group that were asked to maintain a hbA1c of 6%, and as such, that part of the study was halted.

So, what might explain these surprising results? I think it is important to remember that Type 2 Diabetes is not only a disease of high blood-sugar and of triglycerides being inappropriately deposited in muscle and liver cells, but also
a disease of high blood insulin levels due to insulin resistance. Insulin is damaging to arteries, and paving the way for heart disease. Those in the “aggressive” arm of the study were asked to lower blood-sugar to very low levels, and many used insulin and insulin pumps to be successful at that task. Type 2 Diabetics by definition have high insulin levels, and to achieve the goals of the study, some were taking more. I think that it is very plausible that very high insulin levels may have accelerated the cardiovascular disease, possibly prompting more deaths. Not only that, but we also know that high insulin levels promote the conversion of carbohydrates into triglycerides in the liver, further increasing insulin resistance and obesity. In my opinion, treating Type 2 Diabetes with insulin would make the whole cycle worse.

In the next few weeks I want to look more closely at obesity, heart disease, and diabetes as I am becoming more and more convinced that these are different manifestations all coming from a similar cause.

Related tips
Insulin, our storage hormone
Breakthrough on the food-guide front
The cause of Type 2 Diabetes
Sugar, the disease generator
Blood-sugar regulation
Customized nutrition

www.wellnesstips.ca