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What are the problems associated with low-carb diets, and do the benefits outweigh the risks?

I want to make it fundamentally clear from the outset that I am NOT suggesting that we eat no carbohydrates, or an “all meat and eggs” diet. So eat your veggies!! The foods I am suggesting we all remove from the diet are the ones that we didn’t eat 10,000 years ago, like products that contain sugar, flour, processed grain like white rice, and alcohol (the body treats alcohol like sugar). These are the foods that cause the biggest insulin response. Sugar drives insulin, which drives fat deposition. Vegetable oils are also a brand new food that entered our diet less than 100 years ago and need to be avoided, but that is not a part of this low-carb discussion. Those that are sensitive to carbs may also need to limit or avoid starchy below ground veggies, fruit and whole grains at least until weight and blood sugar are under control. At that point, these healthy foods can be added back in very gradually up to the level tolerated before weight starts to increase again.

Last week's tip on fat accumulation was over-simplistic, and dealt only with fat accumulation where poor blood-sugar control is the driver. Someone who gets fat due to poor blood-sugar control tends to put fat on all over - fat ankles and wrists, fat neck, fat legs and arms, and trunk. But some people put on fat in the hips and legs and are quite slender, sometimes even emaciated in the upper body, a pattern commonly seen in women. This fat pattern is probably more driven by imbalances in estrogen/progesterone, although insulin may play a role. Then there is the big gut, skinny legs and arms pattern, quite common in men. I think cortisol plays a role in this pattern (also food allergy/sensitivity and gut dysbiosis), although blood sugar control is also important. But the bottom line is that much of the time, fat deposition is hormone driven, not calorie driven in my opinion. (I'm not saying that chronic overeating is not a cause of obesity, but rather that people do commonly become over-fat without overeating.) Use functional testing to correct the hormone imbalances, enable the body to lose the fat.

Okay. Back to the low-carb safety question. The health concerns raised with respect to low carb diets are:

• Low carb = high fat = increased risk of heart disease
• increased risk of stomach/intestinal cancer
• kidney disease
• kidney stones
• calcium leaching which leads to osteoporosis
• ketosis - an increase of ketone bodies in the blood
• constipation
• decreased energy levels
• possible decrease in lean body mass shown is some studies
• decreased physical performance
• headache

The benefits of a low-carb diet are:

• Decreased blood-sugar levels
• Decreased insulin levels
• Decreased triglyceride levels
• Decreased VLDL levels (Very "bad" cholesterol)
• Increased HDL levels ("Good" cholesterol)
• Lower blood-pressure
• Less hunger
• Weight loss
• Decreased body inflammation (decreased C reactive protein and plasma
  serum amyloid A)
• Possible decrease in food sensitivity problems, because the foods that
  are eliminated are the processed foods containing food additives, gluten
  grains.

In my opinion, if a low carb diet decreases blood sugar, insulin, triglycerides, bad cholesterol, blood pressure, body weight, body inflammation, and increases good cholesterol, that would indicate a lessened risk of heart disease, not an increased one.

In trying to back up the increased risk of stomach / intestinal cancer from a low carb diet, I found studies that indicated that processed and salted meat were a problem. I found one study that indicated that red meat consumption increased the risk of gastric cancer, but I was unable to determine whether the animals consumed were grass-fed or grain-fed. Although I can't back this up with studies, my feeling would be that if the meat consumed is from animals that are eating their natural diet, it is less likely to create a problem. Also it looks like it is an interaction between the ulcer-causing bacteria H. Pylori and the meat that increased the risk of gastric cancer more than red meat alone.

There are lots of studies that seem to indicate that high protein diets can be damaging to the kidneys, in particular through the production of AGEs (Advanced Glycation Endproducts). But by definition AGES are actually glycated proteins, or the bonding of a sugar with a protein.  So, is it the high protein or the high blood-sugar that is the real culprit here?  AGEs are formed in greater numbers if meat is cooked at high temperatures, so lightly cooking meat may be a viable way to reduce the risk. Low carbohydrate diets do not necessarily mean a huge increase in protein intake in the absolute sense, but rather an increase of percentage of calories from protein relative to carbohydrate.

As for the idea that diets high in protein cause calcium leaching which may lead to osteoporosis, I actually see more evidence to the contrary in my cursory search. Many studies seem to indicate that higher protein levels are important for bone preservation, especially in the elderly who may be malnourished. This review published in the Journal of the American College of Nutrition examines the claims of the dangers of high protein intake on bone mass, and lays them all to rest.

Even studies that show positive results always end with the caveat that it is too early to advocate long term use of low carb diets, as the long term studies have not yet been done. Does the fact that humankind has been eating low starch/low sugar diets for all time up until a couple of centuries ago not count? Although there are some problems with low starch diets, I think they can be very helpful for those trying to lose weight, type 2 diabetics, and those with blood-sugar regulation issues. I think that for many, high starch diets can be far less healthy than low starch diets, but to suggest that everyone needs to follow an Atkin's style diet would be an exaggeration, as long as the food consumed is whole and unprocessed. It will be interesting to see what the long-term studies show.

If you decide to try a low starch /no sugar diet, check with your doctor, particularly if you have health concerns like kidney problems or diabetes, and watch for negative reactions that might indicate you have pushed your metabolism too far - lethargy, constipation, feel full but hungry, heavy gut, mentally sluggish, inability to do the physical activity you are accustomed to doing (the reduction in glycogen stores will cause this), suddenly painful menstruation etc. Make sure that your protein source is real food, and not protein powders etc. If you are having negative reactions, increase the ratio of above-ground vegetables to protein/fat, and make sure you are consuming half your bodyweight in pounds, in ounces of pure water each day, and see if you feel better. If this still doesn't resolve the problem, add whole grains or starchy veggies one tablespoon per meal at a time, until you feel great. Sugar, flour products, processed grains (like white rice) and alcohol however, are not good for anyone and should not be consumed at all, in my opinion.

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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.

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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.

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Another “healthy heart guide” that got it wrong
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Is obesity caused by an unwillingness or inability to limit food consumption and increase activity levels, or is it a defect in fat metabolism causing the nutrients consumed to be converted into fat as opposed to being used for energy, resulting in cell starvation and lethargy?

Personally, I no longer believe in the law of thermodynamics when it comes to human metabolism and obesity. I don’t believe that a calorie is a calorie, and that to lose fat one has to eat fewer calories than one burns, and to gain weight one must eat more calories than one burns. I am a rather small person, yet I eat like a horse. Many people have asked me where I put it, and if I have a hollow leg. I eat much more than many who are three times my size, yet I remain quite slim, whereas others only have to be in the same room as a pastry and it winds up on their hips. I don’t do a crazy amount of physical activity either. I see many people in the gym that are trying to lose weight who exercise a lot more than I do, and the weight does not move much. My observations do not a scientific study make, but there is a fair bit of science, albeit mostly ignored, that does make a strong case for a problem with metabolism being the root cause of obesity as opposed to slovenly behaviour.

Much of the obesity research was done in Germany prior to World War 2, and large strides were made in delineating the metabolic problems that led to obesity. Perhaps because the research was done in the German language rather than English or because the war was essentially against Germany, somehow after the war, that important research was not taken up again, and the behavioural view of obesity took hold. Even today, physicians commonly refer their obese patients to psychiatrists, psychologists and/or dietitians who try and get to the bottom of why they can't control their eating, put them on low fat, low calorie diets, and tell them to move more. Very little weight is lost on these plans - losing 8 to 10 pounds if one weighs 300+ does not resolve the problem. Suggesting to someone that it is their fault that they are overweight, and they only need to pick up their socks, stop eating so much and exercise more just adds guilt and frustration. It makes sense to assume that most obese people have already tried to lose weight through calorie restriction. Those people will tell you that it is NOT that easy. I think that suggesting that obesity is a psychological problem and it is simply a matter of will power, does not make sense.

Does controlling calories actually lead to weight loss? Well, no. Calorie restriction rarely leads to substantial weight loss in the obese. If we look at rat studies where it is easy to control the number of calories consumed, we see that calories consumed does not determine whether or not the rat becomes obese. Jean Mayer noticed in the 1950s, that a genetically obese kind of mouse would put on fat weight no matter how few calories they were given. Even when semi-starved, the metabolism of the mice would result in organ and muscle wasting rather than a reduction in the fatty tissue. In 1981, Greenwood found the same thing using Zucker rats, a genetically obese kind of rat. She actually found that the Zucker rats that were calorie restricted from birth wound up fatter than those who could eat what they wanted, leading one to wonder if calorie restriction causes obesity.

It seems that it is the type of calories that is more important than the number of calories. Blake Donaldson who worked with Robert Halsey, one of the founding four members of the American Heart Association, started working with obese patients in 1919. He abandoned semi-starvation diets after a year of trying in favour of a higher calorie, carbohydrate restricted diet of which fatty meat was the staple. His patients tended to lose 2-3 pounds a week without feeling hungry. He successfully treated obese patients on this diet for 40 years. Alfred Pennington also started out by trying low-calorie diets that restricted fats and carbs, but then found success when he tested Donaldson's higher calorie meat diet (over 3000 calories a day, but only 80 calories from carbohydrate a meal, and none from starch or sugar). Pennington's work was published in the New England Journal of Medicine in 1950. The low calorie advocates pushed back, suggesting that these diets were monotonous and therefore actually were low calorie, and that they were unhealthy due to the larger amount of fat being consumed. This was around the time that Ancel Keys was pushing his "fat causes heart disease" theory. John Thorpe suggested in 1957 that semi-starvation diets were unhealthy because they resulted in malnourishment, causing the body to reallocate its resources resulting in muscle and bone wasting, rather than targeting only fat loss. Thorpe also successfully prescribed Pennington's and Donaldson's diet to his obese patients. Other clinicians that had success with the carbohydrate-restricted diet with their obese patients include Margaret Ohlson, Charlotte Young (J. Am. Dietetic Ass.), Hilde Bruch, William Leith (McGill), George Blackburn (MIT and Harvard Med. School), Russell Wilder (Mayo Clinic), Heinrich Kasper & Udo Rabast (U. of Wurzburg), Edwin Astwood (Tufts U.), Willard Krehl (U of Iowa), Weldon Walker (Walter Reed Army Med Center), John LaRosa, (State U.), Robert Kemp (Walton Hospital Liverpool), and of course Robert Atkins, of Dr. Atkins' Diet Revolution fame. Clinicians tend not to be scientists, and clinical success does not usually make its way into medical journals. In 2003 a review study was done, published in JAMA, which concluded that the scientific data was "insufficient to recommend or condemn the use of these diets", because no long term controlled trials have been done to verify the safety of low carb diets. However, the lower carb diets did result in far greater weight loss - 37 pounds compared to 4 pounds when carbs were not restricted.

Many of you may object to me bringing up research that is almost a century old in dealing with this topic, but I think that sometimes lines of research get abandoned or forgotten simply because another idea becomes all the rage, and not because the first idea has no merit. And dismissing out of hand the experience of clinicians that have successfully treated thousands of obesity patients because their method has not yet been "proven" in the medical literature seems premature. I also think that because something is old does not mean it is irrelevant. After all, the theory of relativity is an old idea. Does that idea no longer have any credence simply because it is old? Thankfully, probably due to the Atkins craze, scientific research has resumed (see below) comparing low carbohydrate diets to low calorie / low fat diets, and most of the randomized controlled trials not only are showing more weight loss, but also better lipid profiles on the carbohydrate-restricted diets. I think it is time to realize that low-calorie diets don't seem to work, and to research more thoroughly why higher calorie, carbohydrate-restricted diets do seem to work. And by accepting that fact, we are also accepting the fact that the calories in vs. calories out hypothesis needs to be discarded with respect to weight gain and weight loss. I think that obesity is a disorder of fat accumulation as opposed to a disease of overeating (too many calories). Next week we will explore the metabolic hypothesis as the cause of obesity.

Although I have been coming to these conclusions based on my own studies over the last year, the recent book by Gary Taubes, Good Calories, Bad Calories lays out the research so vividly, and has been invaluable in clarifying various ideas, and in pointing me to different kinds of research that I had not considered before. I HIGHLY recommend this book if you are interested in the topics of diets, obesity, heart disease and diabetes.

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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.

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