My transformation: I cannot remember the last time I had a fever

The two photos below (click to enlarge) were taken 4 years apart. The one on the left was taken in 2006, when I weighed 210 lbs (95 kg). Since my height is 5 ft 8 in, at that weight I was an obese person, with over 30 percent body fat. The one on the right was taken in 2010, at a weight of 150 lbs (68 kg) and about 13 percent body fat. I think I am a bit closer to the camera on the right, so the photos are not exactly on the same scale. For a more recent transformation update, see this post.

My lipids improved from borderline bad to fairly good numbers, as one would expect, but the two main changes that I noticed were in terms of illnesses and energy levels. I have not had a fever in a long time. I simply cannot remember when it was the last time that I had to stay in bed because of an illness. I only remember that I was fat then. Also, I used to feel a lot more tired when I was fat. Now I seem to have a lot of energy, almost all the time.

In my estimation, I was obese or overweight for about 10 years, and was rather careless about it. A lot of that time I weighed in the 190s; with a peak weight of 210 lbs. Given that, I consider myself lucky not to have had major health problems by now, like diabetes or cancer. A friend of mine who is a doctor told me that I probably had some protection due to the fact that, when I was fat, I was fat everywhere. My legs, for example, were fat. So were my arms and face. In other words, I lot of the fat was subcutaneous, and reasonably distributed. In fact, most people do not believe me when I say that I weighed 210 lbs when that photo was taken in 2006; but maybe they are just trying to be nice.

If you are not obese, you should do everything you can to avoid reaching that point. Among other things, your chances of having cancer will skyrocket.

So, I lost a whopping 60 lbs (27 kg) over about 2-3 years. That is not so radical; about 1.6-2.5 lbs per month. There were plateaus with no weight loss, and even a few periods with weight gain. Perhaps because of that and the slow weight loss, I had none of the problems usually associated with body responses to severe calorie restriction, such as hypothyroidism. I remember a short period when I felt a little weak and miserable; I was doing exercise after long fasts (20 h or so), and not eating enough afterwards. I did that for a couple of weeks and decided against the idea.

There are no shortcuts with body fat loss, it seems. Push it too hard and the body will react; compensatory adaptation at work.

My weight has been stable, at around 150 lbs, for a little less than 2 years now.

What did I do to lose 60 lbs? I did a number of things at different points in time. I measured various variables (e.g., intake of macronutrients, weight, body fat, HDL cholesterol etc.) and calculated associations, using a prototype version of HealthCorrelator for Excel (HCE). Based on all that, I am pretty much convinced that the main factors were the following:

- Complete removal of foods rich in refined carbohydrates and sugars from my diet, plus almost complete removal of plant foods that I cannot eat raw. (I do cook some plant foods, but avoid the ones I cannot eat raw; with a few exceptions like sweet potato.) That excluded most seeds and grains from my diet, since they can only be eaten after cooking.

- Complete removal of vegetable oils rich in omega-6 fats from my diet. I cook primarily with butter and organic coconut oil. I occasionally use olive oil, often with water, for steam cooking.

- Consumption of plenty of animal products, with emphasis on eating the animal whole. All cooked. This includes small fish (sardines and smelts) eaten whole about twice a week, and offal (usually beef liver) about once or twice a week. I also eat eggs, about 3-5 per day.

- Practice of moderate exercise (2-3 sessions a week) with a focus on resistance training and high-intensity interval training (e.g., sprints). Also becoming more active, which does not necessarily mean exercising but  doing things that involve physical motion of some kind (e.g., walking, climbing stairs, moving things around), to the tune of 1 hour or more every day.

- Adoption of more natural eating patterns; by eating more when I am hungry, usually on days I exercise, and less (including fasting) when I am not hungry. I estimate that this leads to a caloric surplus on days that I exercise, and a caloric deficit on days that I do not (without actually controlling caloric intake).

- A few minutes (15-20 min) of direct skin exposure to sunlight almost every day, when the sun is high, to get enough of the all-important vitamin D. This is pre-sunburn exposure, usually in my backyard. When traveling I try to find a place where people jog, and walk shirtless for 15-20 min.

- Stress management, including some meditation and power napping.

- Face-to-face social interaction, in addition to online interaction. Humans are social animals, and face-to-face social interaction contributes to promoting the right hormonal balance.

When I was fat, my appetite was a bit off. I was hungry at the wrong times, it seemed. Then slowly, after a few months eating essentially whole foods, my hunger seemed to start “acting normally”. That is, my hunger slowly fell into a pattern of increasing after physical exertion, and decreasing with rest. Protein and fat are satiating, but so seem to be fruits and vegetables. Never satiating for me were foods rich in refined carbohydrates and sugars – white bread, bagels, doughnuts, pasta etc.

Looking back, it almost seems too easy. Whole foods taste very good, especially if you are hungry.

But I will never want to each a peach after I have a doughnut. The peach will be tasteless!

Insulin responses to foods rich in carbohydrates and protein

Insulin is often presented as a hormone that is at the core of the diseases of civilization, particularly because of the insulin response elicited by foods rich in refined carbohydrates and sugars. What is often not mentioned is that protein also elicits an insulin response and so do foods where carbohydrates are mixed with fat. Sometimes the insulin responses are way more than one would expect based on the macronutrient compositions of the foods.

Holt et al. (1997; full reference at the end of this post) conducted a classic study of insulin responses. This study has been widely cited, and paints an interesting picture of differences in insulin responses to various foods. But you have to be careful where you look. There has been some confusion about the results because of the way they are often reported in places like Wikipedia and on various Internet sites that refer to the study.

The key thing to bear in mind when reviewing this study is that the amounts of food used were designed to have the same calorie content: 1000 kJ or 240 kcal (i.e., 240 calories). This led to wild variations in the size of the portions that are compared and their weight in grams. Also, some of the food portions are probably not what people usually eat in one sitting.

In Holt et al.’s (1997) study the participants were 41 lean and healthy university students. They were fed 1000 kJ (240 kcal) portions of the test foods on separate mornings after a 10-hour fast overnight. Blood insulin levels were measured at different times within a 120-minute period after each meal. An insulin score was then calculated from the area under the insulin response curve for each food; white bread was used as the reference food.

Part of Table 2 on page 1267 is shown below (the full text version of the paper is linked at the end of this post), just to illustrate the types and amounts of food served, and the macronutrient breakdown for each food. I hope you can see what I meant when I said that some of the food portions are probably not what people usually eat in one sitting. I don’t think it would be hard to find someone who would eat 158 g of beef steak in one sitting, but 333 g of fish is a little more difficult. Fish has a higher proportion of protein than beef steak, and thus is more satiating. The same goes for 625 g of orange, about 6 oranges. Foods that have more fat have more calories per gram; hence the smaller portions served for high-fat foods.

Table 4 of the article is a bit long, so I am providing it in two parts below. AUC stands for “area under the curve”. As you can see, for isocaloric portions of different foods (i.e., with the same amount of calories), there is a huge variation in insulin response. The insulin AUCs are shown on the second numeric column from the left. Also note that the insulin responses (AUC) for white bread varied in different meals. This complicates things a bit, but at least provides a more realistic view of the responses since each participant served as his or her own control.

Look at the third column from the right, which shows the insulin responses per gram of each food, compared with the response to white bread, always shown at the top for each group of related foods (e.g., protein-rich foods). The gram-adjusted response for whole-meal bread is rather high, and so is the glucose response. The gram-adjusted insulin response to potatoes is less than one-third of the response to white bread, even though the non-gram-adjusted glucose response is higher. The insulin response to beef is also less than one-third of the response to white bread, gram-for-gram. Even cheese leads to a gram-adjusted response that is about half the one for white bread, and I don’t think many people will eat the same amount of cheese in one sitting as they would do with white bread.

In summary, insulin responses to protein-rich foods are often 50 to 70 percent lower than responses to equivalent amounts of refined carbohydrate-rich foods. Also, insulin responses to unrefined carbohydrate-rich foods (e.g., potato, fruits) are often 70 to 90 percent lower than responses to equivalent amounts of refined carbohydrate-rich foods.

Why do insulin levels go up in response to dietary protein?

One of the reasons is that insulin is needed for tissue protein synthesis. That is, increased circulating protein (as amino acids) and insulin have a net anabolic effect, promoting muscle growth and inhibiting muscle breakdown. (Muscle protein synthesis and breakdown happen all the time; the net effect defines whether muscle grows or shrinks.) In this respect, insulin acts in conjunction with other hormones, such as growth hormone and insulin-like growth factor 1.

Reference:

Holt, S.H., Miller, J.C., & Petocz, P. (1997). An insulin index of foods: The insulin demand generated by 1000-kJ portions of common foods. American Journal of Clinical Nutrition, 66, 1264-1276.

PepsiCo to reduce sugar and fat in products

I guess PepsiCo is moving ahead of the competition, but in a snail pace and in a very, very politically correct way. Will this help in any way? I doubt. It is just too little, too late. See article here.

The article states that:

The company also set two goals for the next 10 years: to cut the average added sugar per serving by 25 percent and saturated fat per serving by 15 percent, in addition to adding more whole grains, fruits, vegetables and low-fat dairy into its array of products.

While it is nice to see more of a focus on sugar than on saturated fat, I would have preferred to see something like this:

The company also set two goals for the next 5 years: to cut the average added sugar per serving by 95 percent and increase saturated fat per serving by 50 percent, in addition to adding more vegetables and full-fat dairy into its array of products.

What would happen? Well, Indra Nooyi is a very smart CEO, and the company has many competent people. They know that they would probably lose enough customers to go out of business … or become the Apple of their industry.

The bottom line is that, if you want to improve your health, you should generally avoid any food or liquid that is highly industrialized.

Maybe PepsiCo should add unprocessed coconut water to their portfolio of drinks.

Want to improve your cholesterol profile? Replace refined carbs and sugars with saturated fat and cholesterol in your diet

An interesting study by Clifton and colleagues (1998; full reference and link at the end of this post) looked at whether LDL cholesterol particle size distribution at baseline (i.e., beginning of the study) for various people was a determinant of lipid profile changes in each of two diets – one low and the other high in fat. This study highlights a few interesting points made in a previous post, which are largely unrelated to the main goal or findings of the study, but that are supported by side findings:

- As one increases dietary cholesterol and fat consumption, particularly saturated fat, circulating HDL cholesterol increases significantly. This happens whether one is taking niacin or not, although niacin seems to help, possibly as an independent (not moderating) factor. Increasing serum vitamin D levels, which can be done through sunlight exposure and supplementation, are also known to increase circulating HDL cholesterol.

- As one increases dietary cholesterol and fat consumption, particularly saturated fat, triglycerides in the fasting state (i.e., measured after a 8-hour fast) decrease significantly, particularly on a low carbohydrate diet. Triglycerides in the fasting state are negatively correlated with HDL cholesterol; they go down as HDL cholesterol goes up. This happens whether one is taking niacin or supplementing omega 3 fats or not, although these seem to help, possibly as independent factors.

- If one increases dietary fat intake, without also decreasing carbohydrate intake (particularly in the form of refined grains and sugars), LDL cholesterol will increase. Even so, LDL particle sizes will shift to more benign forms, which are the larger forms. Not all LDL particles change to benign forms, and there seem to be some genetic factors that influence this. LDL particles larger than 26 nm in diameter simply cannot pass through the gaps in the endothelium, which is a thin layer of cells lining the interior surface of arteries, and thus do not induce plaque formation.

The study by Clifton and colleagues (1998) involved 54 men and 51 women with a wide range of lipid profiles. They first underwent a 2-week low fat period, after which they were given two liquid supplements in addition to their low fat diet, for a period of 3 weeks. One of the liquid supplements contained 31 to 40 g of fat, and 650 to 845 mg of cholesterol. The other was fat and cholesterol free.

Studies that adopt a particular diet at baseline have the advantage of departing from a uniform diet across conditions. They also typically have one common characteristic: the baseline diet reflects the beliefs of the authors about what an ideal diet is. That is not always the case, of course. If this was indeed the case here, we have a particularly interesting study, because in that case the side findings discussed below contradicted the authors’ beliefs.

The table below shows the following measures for the participants in the study: age, body mass index (BMI), waist-to-hip ratio (WHR), total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, and three subtypes of high-density lipoprotein (HDL) cholesterol. LDL cholesterol is the colloquially known as the “bad” type, and “HDL” as the good one (which is an oversimplification). In short, the participants were overweight, middle-aged men and women, with relatively poor lipid profiles.

At the bottom of the table is the note “P < 0.001”, following a small “a”. This essentially means that on the rows indicated by an “a”, like the “WHR” row, the difference in the averages (e.g., 0.81 for women, and 0.93 for men, in the WHR row) was significantly different from what one would expect it to be due to chance alone. More precisely, the likelihood that the difference was due to chance was lower than 0.001, or 0.1 percent, in the case of a P < 0.001. Usually a difference between averages (a.k.a. means) associated with a P < 0.05 will be considered statistically significant.

Since the LDL cholesterol concentrations (as well as other lipoprotein concentrations) are listed on the table in mmol/L, and many people receive those measures in mg/dL in blood lipid profile test reports, below is a conversion table for LDL cholesterol (from: Wikipedia).

The table below shows the dietary intake in the low and high fat diets. Note that in the high fat diet, not only is the fat intake higher, but so is the cholesterol intake. The latter is significantly higher, more than 4 times the intake in the low fat diet, and about 2.5 times the recommended daily value by the U.S. Food and Drug Administration. The total calorie intake is reported as slightly lower in the high fat diet than in the low fat diet.

Note that the largest increase was in saturated fat, followed by an almost equally large increase in monounsaturated fat. This, together with the increase in cholesterol, mimics a move to a diet where fatty meat and organs are consumed in higher quantities, with a corresponding reduction in the intake of refined carbohydrates (e.g., bread, pasta, sugar, potatoes) and lean meats.

Finally, the table below shows the changes in lipid profiles in the low and high fat diets. Note that all subtypes of HDL (or "good") cholesterol concentrations were significantly higher in the high fat diet, which is very telling, because HDL cholesterol concentrations are much better predictors of cardiovascular disease than LDL or total cholesterol concentrations. The higher the HDL cholesterol, the lower the risk of cardiovascular disease.

In the table above, we also see that triglycerides are significantly lower in the high fat diet, which is also good, because high fasting triglyceride concentrations are associated with cardiovascular disease and also insulin resistance (which is associated with diabetes).

However, the total and LDL cholesterol were also significantly higher in the high fat compared to the low fat diet. Is this as bad as it sounds? Not when we look at other factors that are not clear from the tables in the article.

One of those factors is the likely change in LDL particle size. LDL particle sizes almost always increase with significant increases in HDL; frequently going up in diameter beyond 26 nm, and thus passing the threshold beyond which an LDL particle can penetrate the endothelium and help form a plaque.

Another important factor to take into consideration is the somewhat strange decision by the authors to use the Friedewald equation to estimate the LDL concentrations in the low and high fat diets. Through the Friedewald equation, LDL is calculated as follows (where TC is total cholesterol):

    LDL = TC – HDL – Triglycerides / 5

Here is one of the problems with the Friedewald equation. Let us assume that an individual has the following lipid profile numbers: TC = 200, HDL = 50, and trigs. = 150. The calculated LDL will be 120. Let us assume that this same individual reduces trigs. to 50, from the previous 150, keeping all of the other measures constant. This is a major improvement. Yet, the calculated LDL will now be 140, and a doctor will tell this person to consider taking statins!

By the way, most people who do a blood test and get their lipid profile report also get their LDL calculated through the Friedewald equation. Usually this is indicated through a "CALC" note next to the description of the test or the calculated LDL number.

Finally, total cholesterol is not a very useful measure, because an elevated total cholesterol may be primarily reflecting an elevated HDL, which is healthy. Also, a slightly elevated total cholesterol seems to be protective, as it is associated with reduced overall mortality and also reduced mortality from cardiovascular disease, according to U-curve regression studies comparing mortality and total cholesterol levels in different countries.

We do not know for sure that the participants in this study were consuming a lot of refined carbohydrates and/or sugars at baseline. But it is a safe bet that they were, since they were consuming 214 g of carbohydrates per day. It is difficult, although not impossible, to eat that many carbohydrates per day by eating only vegetables and fruits, which are mostly water.

This is why when one goes on a paleo diet, he or she reduces significantly the amount of dietary carbohydrates; even more so on a targeted low carbohydrate diet, such as the Atkins diet. Richard K. Bernstein, who is a type 1 diabetic and has been adopting a strict low carbohydrate diet during most of his adult life, had the following lipid profile at 72 years of age: HDL = 118, LDL = 53, trigs. = 45. His fasting blood sugar was reportedly 83 mg/dl. Click here to listen to an interview with Dr. Bernstein on the The Livin' La Vida Low-Carb Show.

The lipid profile improvement observed (e.g., a 14 percent increase in HDL from baseline for men, and about half that for women, in only 3 weeks) was very likely due to an increase in dietary saturated fat and cholesterol combined with a decrease in refined carbohydrates and sugars. The improvement would probably have been even more impressive with a higher increase in saturated fat, as long as it was accompanied by the elimination of refined carbohydrates and sugars from the participants’ diets.

Reference:

Clifton, P. M., M. Noakes, and P. J. Nestel (1998). LDL particle size and LDL and HDL cholesterol changes with dietary fat and cholesterol in healthy subjects. J. Lipid. Res. 39: 1799–1804.

How much vitamin D? Vitamin D Council's recommendations

Since my recent post on problems related to vitamin D deficiency and excess I received several questions. I have also participated in several discussions in other blogs related to vitamin D in the past few days.

There is a lot of consensus about vitamin D deficiency being a problem, but not much about vitamin D in excess being a problem as well.

Some bloggers recommend a lot of supplementation, which may be dangerous because: (a) our body evolved to obtain most of its vitamin D from a combination of sunlight exposure and cholesterol, and thus body accumulation regulation mechanisms are not designed to deal with excessive oral supplementation; and (b) vitamin D, like many fat-soluble vitamins, accumulates in fat tissue over time, and is not easily eliminated by the body when in excess.

The Vitamin D Council has the following general recommendation regarding supplementation:

Take an average of 5,000 IU a day, year-round, if you have some sun exposure. If you have little, or no, sun exposure you will need to take at least 5,000 IU per day. How much more depends on your latitude of residence, skin pigmentation, and body weight. Generally speaking, the further you live away from the equator, the darker your skin, and/or the more you weigh, the more you will have to take to maintain healthy blood levels.

They also provide a specific example:

For example, Dr. Cannell lives at latitude 32 degrees, weighs 220 pounds, and has fair skin. In the late fall and winter he takes 5,000 IU per day. In the early fall and spring he takes 2,000 IU per day. In the summer he regularly sunbathes for a few minutes most days and thus takes no vitamin D on those days in the summer.

For those who have problems with supplementation, here is what Dr. Cannell, President of the Vitamin D Council, has to say:

For people who have trouble with supplements, I recommend sunbathing during the warmer months and sun tanning parlors in the colder months. Yes, sun tanning parlors make vitamin D, the most is made by the older type beds. Another possibility is a Sperti vitamin D lamp.

One thing to bear in mind is that if your diet is rich in refined carbohydrates and sugars, you need to change that before you are able to properly manage your vitamin D levels. You need to remove refined carbohydrates and sugars from your diet. No more white bread, bagels, doughnuts, table sugar, sodas sweetened with high-fructose corn syrup; just to name a few of the main culprits.

In fact, a diet rich in refined carbohydrates and sugars, in and of itself, may be one of the reasons of a person''s vitamin D deficiency in the case of appropriate sunlight exposure or dietary intake, and even of excessive levels of vitamin D accumulating in the body in the case of heavy supplementation.

The hormonal responses induced by a diet  rich in  refined carbohydrates and sugars promote fat deposition and, at the same time, prevent fat degradation. That is, you tend to put on body fat easily, and you tend to have trouble burning that fat.

This causes a "hoarding" effect which leads to an increase in vitamin D stored in the body, and at the same time reduces the levels of vitamin D in circulation. This is because vitamin D is stored in body fat tissue, and has a long half-life, which means that it accumulates (as in a battery) and then slowly gets released into the bloodstream for use, as body fat is used as a source of energy.

It should not be a big surprise that vitamin D deficiency problems correlate strongly with problems associated with heavy consumption of refined carbohydrates and sugars. Both lead to symptoms that are eerily similar; several of which are the symptoms of the metabolic syndrome.

Applied evolutionary thinking: Darwin meets Washington

Charles Darwin, perhaps one of the greatest scholars of all time, thought about his theory of mutation, inheritance, and selection of biological traits for more than 20 years, and finally published it as a book in 1859.  At that time, many animal breeders must have said something like this: “So what? We knew this already.”

In fact George Washington, who died in 1799 (many years before Darwin’s famous book came out), had tried his hand at what today would be called “genetic engineering.” He produced at least a few notable breeds of domestic animals through selective breeding. Those include a breed of giant mules – the “Mammoth Jackstock” breed. Those mules are so big and strong that they were used to pull large boats filled with coal along artificial canals in Pennsylvania.

Washington learned the basic principles of animal breeding from others, who learned it from others, and so on. Animal breeding has a long tradition.

So, not only did animal breeders, like George Washington, had known about the principles of mutation, inheritance, and selection of biological traits; but they also had been putting that knowledge into practice for quite some time before Darwin’s famous book “The Origin of Species” was published.

Yet, Darwin’s theory has applications that extend well beyond animal breeding. There are thousands of phenomena that would look very “mysterious” today without Darwin’s theory. Many of those phenomena apply to nutrition and lifestyle, as we have been seeing lately with the paleo diet movement. Among the most amazing and counterintuitive are those in connection with the design of our brain.

Recent research, for instance, suggests that “surprise” improves cognition. Let me illustrate this with a simple example. If you were studying a subject online that required memorization of key pieces of information (say, historical facts) and a surprise stimulus was “thrown” at you (say, a video clip of an attacking rattlesnake was shown on the screen), you would remember the key pieces of information (about historical facts) much better than if the surprise stimulus was not present!

The underlying Darwinian reason for this phenomenon is that it is adaptively advantageous for our brain to enhance our memory in dangerous situations (e.g., an attack by a poisonous snake), because that would help us avoid those situations in the future (Kock et al., 2008; references listed at the end of this post). Related mental mechanisms increased our ancestors’ chances of survival over many generations, and became embedded in our brain’s design.

Animal breeders knew that they could apply selection, via selective breeding, to any population of animals, and thus make certain traits evolve in a matter of a few dozen generations or less. This is known as artificial selection. Among those traits were metabolic traits. For example, a population of lambs may be bred to grow fatter on the same amount of food as leaner breeds.

Forced natural selection may have been imposed on some of our ancestors, as I argue in this post, leading metabolic traits to evolve in as little as 396 years, or even less, depending on the circumstances.

In a sense, forced selection would be a bit like artificial selection. If a group of our ancestors became geographically isolated from others, in an environment where only certain types of food were available, physiological and metabolic adaptations to those types of food might evolve. This is also true for the adoption of cultural practices; culture can also strongly influence evolution (see, e.g., McElreath & Boyd, 2007).

This is why it is arguably a good idea for people to look at their background (i.e., learn about their ancestors), because they may have inherited genes that predispose them to function better with certain types of diets and lifestyles. That can help them better tailor their diets to their genetic makeup, and also understand why certain diets work for some people but not for others. (This is essentially what medical doctors do, on a smaller time scale, when they take a patients' parents health history into consideration when dispensing medical advice.)

By ancestors I am not talking about Homo erectus here, but ancestors that lived 3,000; 1,000; or even 500 years ago. At times when medical care and other modern amenities were not available, and thus selection pressures were stronger. For example, if your no-so-distant ancestors have consumed plenty of dairy, chances are you are better adapted to consume dairy than people whose ancestors have not.

Very recent food inventions, like refined carbohydrates, refined sugars, and hydrogenated fats are too new to have influenced the genetic makeup of anybody living today. So, chances are, they are bad for the vast majority of us. (A small percentage of the population may not develop any hint of diseases of civilization after consuming them for years, but they are not going to be as healthy as they could be.) Other, not so recent, food inventions, such as olive oil, certain types of bread, certain types of dairy, may be better for some people than for others.

References:

Kock, N., Chatelain-Jardón, R., & Carmona, J. (2008). An experimental study of simulated web-based threats and their impact on knowledge communication effectiveness. IEEE Transactions on Professional Communication, 51(2), 183-197.

McElreath, R., & Boyd, R. (2007). Mathematical models of social evolution: A guide for the perplexed. Chicago, IL: The University of Chicago Press.

Go see your doctor, often

As I blog about health issues, and talk with people about them, I often notice that there is a growing contempt for the medical profession.

This comes in part from the fact that many MDs are still providing advice based on the mainstream assumption that saturated fat is the enemy. Much recent (and even some old) research suggests that among the main real enemies of good health are: chronic stress, refined carbs, refined sugars, industrial trans-fats, and an omega-6/omega-3 imbalance caused by consumption of industrial vegetable oils rich in omega-6 fats.

Because of this disconnect, some people stop seeing their doctors regularly; others avoid doctors completely. Many rely exclusively on Internet advice, from health-related blogs (like this) and other sources. In my opinion, this is a BIG mistake.

A good MD has something that no blogger who is not an MD (like me) can have. He or she has direct access to a much larger group of people, and to confidential information that can clarify things that would look mysterious to non-MDs. They cannot share that information with others, but they know.

For example, often I hear from people that they did this and that, in terms of diet a lifestyle, and that their lab tests were such and such. Later I find out that what they told me was partially, or completely, wrong. That is, they distorted the truth, maybe subconsciously.

I have never met an MD who completely ignored hard facts, such as results of lab tests and common health-related measurements. I have never met an MD who tried to force me to do anything either; although I have to admit that some tend to be a bit pushy.

I see a doctor who does not agree with me; e.g., he wanted me to take statins. No problem; that is the way I like it. If my doctor will agree 100% with all I say, do I need to see that doctor?

My doctor does not question lab results though, and maybe I am changing a bit the way he thinks. He wanted me to take statins, but once I told him that I wanted to try a few other things first, he said: no problem. When the results came, he had that look on this face - maybe u wuz royt eh!?

Many, many patients are under the mistaken assumption that they need to please their doctors. A subconscious assumption for most, no doubt. I guess this is part of human nature, but I don’t think it is helpful to doctors or patients.

Patients actually need to work together with their doctors, see them often, do their own research, ask questions, and do those things that lead to health improvements – ideally measurable ones.

Refined carbs, sugar, and cholesterol: My own experience

A few years ago I went to the doctor for a routine appointment, and I was told that my LDL cholesterol was elevated. I was in my early 40s. My lipid profile was the following - LDL: 156, HDL: 38, triglycerides: 188. The LDL was calculated. I was weighing about 210 lbs, which was too high for my height (5 ft 8 in). My blood pressure was low, as it has always been - systolic: 109, diastolic: 68.

My doctor gave me the standard advice in these cases: exercise, lose weight, and, most importantly, reduce your intake of saturated fat. I was also told that I would probably have to take statins, as my high LDL likely had something to do with my genetic makeup. Again, this is quite standard, and we see it all over the place, particularly in commercials for statins.

I told my doctor that I would do some research on the topic, which I am going to save for other posts. Let me get to the point, by telling you what my lipid profile is today - LDL: 123, HDL: 66, triglycerides: 46. Again, the LDL value is calculated. I am weighing about 152 lbs now, with about 13 percent of body fat.

The HDL and triglycerides numbers above are shown in bold font because my research convinced me that these two numbers are the ones most people should really worry about when trying to address what is known as dyslipidemia. Here I am assuming that only standard lipid profiles are available; there are better alternatives, such as particle type analyses, which are not yet standard.

Many people who suffer from cardiovascular disease have low LDL cholesterol, but very few of those have high HDL cholesterol, which is one of the best predictors of cardiovascular disease among lipids. More specifically, if you have an HDL higher than 60, you have a very small chance of developing cardiovascular disease. (It can happen, but it is very unlikely, with a percentage chance in the single digits.)

Interestingly, low HDL cholesterol is also associated with the metabolic syndrome. This syndrome is characterized by the following:

- High fasting serum glucose (hyperglycemia), which is one of many signs of insulin resistance, a precursor to diabetes type 2;
- High blood pressure;
- Abdominal obesity (also known as pot or beer belly);
- Low HDL cholesterol; and
- Elevated triglycerides.

Now, you may ask, how did you increase your HDL? Well, I tried a number of things - diet and lifestyle changes - and had a blood test every 3 months. After a while I was able to put all of the measures in a spreadsheet table, and correlate them using a statistical software that I developed, to give me an idea of what was going on.

Weight was a big factor on LDL, and I was able to bring my weight down to 150 lbs and my LDL to below 100 at some point. For me, and many other people, body weight and LDL cholesterol are strongly and positively correlated (the higher the weight, the higher the LDL cholesterol - actually body fat seems to be the real culprit). Moreover, my LDL seemed to decrease more markedly when my weight was on the way down, and not as much when it was stable, even if low.

But the HDL would only increase if I increased my saturated fat intake. The problem is that every time I increased my saturated fat intake my LDL would go up; it reached 162 at one point, when my HDL went up to a modest but encouraging 47. That was my highest HDL until I eliminated refined carbs and sugars (e.g., bread, pasta, cereals, doughnuts, bagels, regular sodas) from my diet.

When I brought my intake of refined carbs and sugars down to zero, my intake of protein and saturated fat went up. Either that would happen, or I would starve, because you have to eat something. (I figured that I would not die by doing a low carb/high fat-protein experiment for 3 months to see what happened.) Also, I dramatically increased my dietary cholesterol - two to four eggs per day, organ meats, and seafood.

That is when my HDL shot up, to 66, and my LDL went down. Yes, my LDL levels seem to be negatively correlated with dietary saturated fat and cholesterol amounts, as long as I do not consume refined carbs and sugars. Moreover, it is very likely that my LDL particle size increased, and large LDL particles DO NOT cause atherosclerosis because they cannot penetrate the artery walls.

So, the bottom line is that, at least for me, an INCREASE in saturated fat and a DECREASE in refined carbs and sugars, happening together, seem to have taken me out of my previous path toward the metabolic syndrome.

Moreover, I feel a lot more energetic than before, my immune system seems to have gotten better at fighting disease, and even my pollen allergies are not as bad as they were before. Admittedly, these benefits may be strongly associated with the weight loss and the related reduction in body fat percentage.

I hope this post is helpful to others. The standard advice that people with high LDL cholesterol receive, which usually focuses on reducing saturated fat intake, has a big problem. When you reduce your intake of a type of food, you usually increase your intake of other types of food. Most people who try to reduce their saturated fat intake invariably increase their carb intake, usually with the wrong types of carb-rich foods (the man-made ones), simply because they go hungry.