Boring is another word for satiating

Satiety is a common topic of discussion on this blog. In the last few posts it came up several times in the comments’ sections. Also, in my interview with Jimmy Moore, we did talk a bit about satiety. I told him what has been my perception and that of many people I know, which is that the least satiating foods tend to be foods engineered by humans.

(Source: Wellnessuncovered.com)

There is another component to satiety, which applies to natural foods, or foods that are not man-made. That other component is the nutrition value of those foods, and whether they meet our nutrition needs at a given point in time. If our body needs certain essential amino acids for tissue repair, subconscious mechanisms will make us crave those foods from which those amino acids can be extracted. In this context, eating is generally a good idea.

The problem is that we have not evolved mechanisms to differentiate “true” from “fake” nutrient starvation; one example of the latter would be fat starvation due to transient hyperinsulinemia induced by refined carbohydrate-rich foods.

Foods engineered by humans tend to lead to overeating because humans are good engineers. In modern society, business drives everything. Food business is predicated on consumption, so engineered foods are designed so that one person will want to consume many units of a food item – typically something that will come in a box or a plastic bag. There is no conspiracy involved; the underlying reason is profit maximization.

When we look at nature, we typically see the opposite. Prey animals do not want to be eaten; often they fight back. Eggs have to be stolen. Plants do not want their various parts, such as leaves and roots, to be eaten. Much less their seeds; so they have developed various defense mechanisms, including toxins. Fruits are exceptions to this rule; they are the only natural foods that are designed to be eaten by animals.

Plants want animals to eat their fruits so that they can disperse the plants’ seeds. So they must be somewhat alluring to animals. Sugar plays a role here, but it certainly is not the only factor. The chemical composition of fruits is quite complex, and they usually contain a number of health-promoting substances, such as vitamins. For example, most fruits contain vitamin C, which happens to be a powerful antioxidant, and also has the ability to reversibly bind to proteins at the sites where sugar-induced glycation would occur.

Many modern fruits have been bred to be resistant to diseases, more palatable, and larger (usually due to more water retention). But, fundamentally, fruits are products of evolution. So how come we don’t see fruits that are pure sugar? Watermelons, for example, are often referred to as “bags of sugar”, but they are only 6 percent sugar. Ice cream is 25 percent sugar.

Two things must be kept in mind regarding fruits and their evolution. One is that dead animals do not eat fruit, and thus cannot disperse seeds. Sick animals would probably not be good candidates for fruit dispersion either. So the co-evolution of fruits and animals must have led fruits to incorporate many health-promoting attributes. The other is that seed dispersion success is correlated with the number of different animals that consume fruits from a plant. In other words, plants do not want all of their fruits to be eaten by one single animal, which must have led fruits to incorporate satiety-promoting attributes.

Often combining foods, adding spices, and so on, is perceived as making those foods exciting. That is so even with natural foods. If you read the descriptions of the foods consumed by healthy isolated populations in Weston Price’s Nutrition and Physical Degeneration, you will probably find them a bit boring. A few very nutritious food items, consumed day in and day out, frequently without heavy preparation. Exciting foods, requiring elaborate and time-consuming preparation, were consumed in special occasions. They were not eaten regularly.

The members of those healthy isolated populations were generally thin and yet lacked no important nutrients in their diet. They were generally free from degenerative diseases. Their teeth were normally strong and healthy.

Just before writing this post, I took six whole sardines out of the freezer to thaw. I will prepare them as discussed on this post, and eat them with a side of steamed vegetables for lunch. (I tend to eat fruits only on the days I exercise; typically 3 days out of 7.) This lunch will be very nutrient-dense. I will be very hungry before lunch, since I’ll have been fasting for 16 hours, and after I’ll not be hungry until dinner. Frankly, eating the sardines will not be very exciting, since I’ve been doing this for years.

Boring is another word for satiating.

Maybe you should stop trying to be someone you are not

Many people struggle to lose body fat, and never quite make it to their optimal. Fewer people manage to do so successfully, and, as soon as they do, they want more. It is human nature. Often they will start trying to become someone they are not, or cannot be. That may lead to a lot of stress and frustration, and also health problems.

Some women have an idealized look in mind, and keep losing weight well beyond their ideal, down to anorexic levels. That leads to a number of health problems. For example, hormones approach starvation levels, causing fatigue and mood swings; susceptibility to infectious diseases increases significantly; and the low weight leads to osteopenia, which is a precursor to osteoporosis.

In men, often what happens is the opposite. Guys who are successful getting body fat to healthy levels next want to become very muscular, and fast. They have an idealized look in mind, and think they know how much they should weigh to get there. Sometimes they want to keep losing body fat and gaining muscle at the same time.

I frequently see men who already look very healthy, but who think that they should weigh more than they do. Since muscle gain is typically very slow, they start eating more and simply gain body fat. The reality is that people have different body frames, and their muscles are built slightly differently; these are things that influence body weight.

There are many other things that also influence body weight, such as the length of arms and legs, bone density, organ mass, as well as the amount of glycogen and water stored throughout the body. As a result, you can weigh a lot less than you think you should weigh, and look very good. The photo below (from MMAjunkie.com) is of Donald Cerrone, weighing in at 145 lbs. He is 6 ft (183 cm) tall.

Mr. Cerrone is a professional mixed martial arts (MMA) fighter from Texas; one of the best in professional MMA at the moment. Yes, he is a bit dehydrated on the photo above. But also keep in mind that his bone density is probably well above that of the average person, like that of most MMA fighters, which pushes his weight up.

A man can be 6 ft tall, weigh 145 lbs, and be very healthy and look very good. That may well be his ideal weight. A woman may be 5’5”, weigh 145 lbs, and also be very healthy and look very good. Figuring out the optimal is not easy, but trying to be someone you are not will probably be a losing battle.

Alcohol intake increases LDL cholesterol, in some people

Occasionally I get emails from people experiencing odd fluctuations in health markers, and trying to figure out what is causing those fluctuations. Spikes in LDL cholesterol without any change in diet seem to be a common occurrence, especially in men.

LDL cholesterol is a reflection of many things. It is one of the least useful measures in standard lipid profiles, as a predictor of future health problems. Nevertheless, if one’s diet is not changing, whether it is high or low in fat, significant fluctuations in LDL cholesterol may signal a change in inflammatory status. Generally speaking, the more systemic inflammation, the higher is the measured LDL cholesterol.

Corella and colleagues (2001) looked into alcohol consumption and its effect on LDL cholesterol, as part of the Framingham Offspring Study. They split the data into three genotypes, which are allele combinations. Alleles are genes variations; that is, they are variations in the sections of DNA that have been identified as coding for observable traits. The table below summarizes what they have found. Take a look at the last two columns on the right.

As you can see, for men with the E2 genotype, alcohol consumption significantly decreases LDL cholesterol. For men with the E4 genotype, alcohol consumption significantly increases LDL cholesterol. No significant effects were observed in women. The figure below illustrates the magnitude of the effects observed in men.

On average, alcohol consumption was moderate, around 15 g per day, and did not vary significantly based on genotype. This is important. Otherwise one could argue that a particular genotype predisposed individuals to drink more, which would be a major confounder in this study. Other confounders were also ruled out through multivariate controls - e.g., fat and calorie intake, and smoking.

Alcohol consumption in moderation seems, on average, to be beneficial. But for some individuals, particularly men with a certain genotype, it may be advisable to completely abstain from alcohol consumption. Who are those folks? They are the ones for whom LDL cholesterol goes up significantly following moderate alcohol consumption.

Interview with Jimmy Moore, and basics of intima-media thickness and plaque tests

Let me start this post by telling you that my interview with Jimmy Moore is coming up in about a week. Jimmy and I talk about evolution, statistics, and health – the main themes of this blog. We talk also about other things, and probably do not agree on everything. The interview was actually done a while ago, so I don’t remember exactly what we discussed.

From what I remember from mine and other interviews (I listen to Jimmy's podcasts regularly), I think I am the guest who has mentioned the most people during an interview – Gary Taubes, Chris Masterjohn, Carbsane, Petro (a.k.a., Peter “the Hyperlipid”), T. Colin Campbell, Denise Minger, Kurt Harris, Stephan Guyenet, Art De Vany, and a few others. What was I thinking?

In case you listen and wonder, my accent is a mix of Brazilian Portuguese, New Zealand English (where I am called “Need”), American English, and the dialect spoken in the “country” of Texas. The strongest influences are probably American English and Brazilian Portuguese.

Anyway, when medical doctors (MDs) look at someone’s lipid panel, one single number tends to draw their attention: the LDL cholesterol. That is essentially the amount of cholesterol in LDL particles.

One’s LDL cholesterol is a reflection of many factors, including: diet, amount of cholesterol produced by the liver, amount of cholesterol actually used by your body, amount of cholesterol recycled by the liver, and level of systemic inflammation. This number is usually calculated, and often very different from the number you get through a VAP test.

It is not uncommon for a high saturated fat diet to lead to a benign increase in LDL cholesterol. In this case the LDL particles will be large, which will also be reflected in a low “fasting triglycerides number” (lower than 70 mg/dl). While I say "benign" here, which implies a neutral effect on health, an increase in LDL cholesterol in this context may actually be health promoting.

Large LDL particles are less likely to cross the gaps in the endothelium, the thin layer of cells that lines the interior surface of blood vessels, and form atheromatous plaques.

Still, when an MD sees an LDL cholesterol higher than 100 mg/dl, more often than not he or she will tell you that it is bad news. Whether that is bad news or not is really speculation, even for high LDL numbers. A more reliable approach is to check one’s arteries directly. Interestingly, atheromatous plaques only form in arteries, not in veins.

The figure below (from: Novogen.com) shows a photomicrograph of carotid arteries from rabbits, which are very similar, qualitatively speaking, to those of humans. The meanings of the letters are: L = lumen; I = intima; M = media; and A = adventitia. The one on the right has significantly lower intima-media (I-M) thickness than the one on the left.

Atherosclerosis in humans tends to lead to an increase in I-M thickness; the I-M area being normally where atheromatous plaques grow. Aging also leads to an increase in I-M thickness. Typically one’s risk of premature death from cardiovascular complications correlates with one’s I-M thickness’ “distance” from that of low-risk individuals in the same sex and age group.

This notion has led to the coining of the term “vascular age”. For example, someone may be 30 years old, but have a vascular age of 80, meaning that his or her I-M thickness is that of an average 80-year-old. Conversely, someone may be 80 and have a vascular age of 30.

Nearly everybody’s I-M thickness goes up with age, even people who live to be 100 or more. Incidentally, this is true for average blood glucose levels as well. In long-living people they both go up slowly.

I-M thickness tests are noninvasive, based on external ultrasound, and often covered by health insurance. They take only a few minutes to conduct. Their reports provide information about one’s I-M thickness and its relative position in the same sex and age group, as well as the amount of deposited plaque. The latter is frequently provided as a bonus, since it can also be inferred with reasonable precision from the computer images generated via ultrasound.

Below is the top part of a typical I-M thickness test report (from: Sonosite.com). It shows a person’s average (or mean) I-M thickness; the red dot on the graph. The letter notations (A … E) are for reference groups. For the majority of the folks doing this test, the most important on this report are the thick and thin lines indicated as E, which are based on Aminbakhsh and Mancini’s (1999) study.

The reason why the thick and thin lines indicated as E are the most important for the majority of folks taking this test is that they are based on a study that provides one of the best reference ranges for people who are 45 and older, who are usually the ones getting their I-M thickness tested. Roughly speaking, if your red dot is above the thin line, you are at increased risk of cardiovascular disease.

Most people will fall in between the thick and thin lines. Those below the thick line (with the little blue triangles) are at very low risk, especially if they have little to no plaque. The person for whom this test was made is at very low risk. His red dot is below the thick line, when that line is extended to the little triangle indicated as D.

Below is the bottom part of the I-M thickness test report. The max I-M thickness score shown here tends to add little in terms of diagnosis to the mean score shown earlier. Here the most important part is the summary, under “Comments”. It says that the person has no plaque, and is at a lower risk of heart attack. If you do an I-M thickness test, your doctor will probably be able to tell you more about these results.

I like numbers, so I had an I-M thickness test done recently on me. When the doctor saw the results, which we discussed, he told me that he could guarantee two things: (1) I would die; and (2) but not of heart disease. MDs have an interesting sense of humor; just hang out with a group of them during a “happy hour” and you’ll see.

My red dot was below the thick line, and I had a plaque measurement of zero. I am 47 years old, eat about 1 lb of meat per day, and around 20 eggs per week - with the yolk. About half of the meat I eat comes from animal organs (mostly liver) and seafood. I eat organ meats about once a week, and seafood three times a week. This is an enormous amount of dietary cholesterol, by American diet standards. My saturated fat intake is also high by the same standards.

You can check the post on my transformation to see what I have been doing for years now, and some of the results in terms of levels of energy, disease, and body fat levels. Keep in mind that mine are essentially the results of a single-individual experiment; results that clearly contradict the lipid hypothesis. Still, they are also consistent with a lot of fairly reliable empirical research.

The China Study II: Wheat may not be so bad if you eat 221 g or more of animal food daily

In previous posts on this blog covering the China Study II data we’ve looked at the competing effects of various foods, including wheat and animal foods. Unfortunately we have had to stick to the broad group categories available from the specific data subset used; e.g., animal foods, instead of categories of animal foods such as dairy, seafood, and beef. This is still a problem, until I can find the time to get more of the China Study II data in a format that can be reliably used for multivariate analyses.

What we haven’t done yet, however, is to look at moderating effects. And that is something we can do now.  A moderating effect is the effect of a variable on the effect of another variable on a third. Sounds complicated, but WarpPLS makes it very easy to test moderating effects. All you have to do is to make a variable (e.g., animal food intake) point at a direct link (e.g., between wheat flour intake and mortality). The moderating effect is shown on the graph as a dashed arrow going from a variable to a link between two variables.

The graph below shows the results of an analysis where animal food intake (Afoods) is hypothesized to moderate the effects of wheat flour intake (Wheat) on mortality in the 35 to 69 age range (Mor35_69) and mortality in the 70 to 79 age range (Mor70_79). A basic linear algorithm was used, whereby standardized partial regression coefficients, both moderating and direct, are calculated based on the equations of best-fitting lines.

From the graph above we can tell that wheat flour intake increases mortality significantly in both age ranges; in the 35 to 69 age range (beta=0.17, P=0.05), and in the 70 to 79 age range (beta=0.24, P=0.01). This is a finding that we have seen before on previous posts, and that has been one of the main findings of Denise Minger’s analysis of the China Study data. Denise and I used different data subsets and analysis methods, and reached essentially the same results.

But here is what is interesting about the moderating effects analysis results summarized on the graph above. They suggest that animal food intake significantly reduces the negative effect of wheat flour consumption on mortality in the 70 to 79 age range (beta=-0.22, P<0.01). This is a relatively strong moderating effect. The moderating effect of animal food intake is not significant for the 35 to 69 age range (beta=-0.00, P=0.50); the beta here is negative but very low, suggesting a very weak protective effect.

Below are two standardized plots showing the relationships between wheat flour intake and mortality in the 70 to 79 age range when animal food intake is low (left plot) and high (right plot). As you can see, the best-fitting line is flat on the right plot, meaning that wheat flour intake has no effect on mortality in the 70 to 79 age range when animal food intake is high. When animal food intake is low (left plot), the effect of wheat flour intake on mortality in this range is significant; its strength is indicated by the upward slope of the best-fitting line.

What these results seem to be telling us is that wheat flour consumption contributes to early death for several people, perhaps those who are most sensitive or intolerant to wheat. These people are represented in the variable measuring mortality in the 35 to 69 age range, and not in the 70 to 79 age range, since they died before reaching the age of 70.

Those in the 70 to 79 age range may be the least sensitive ones, and for whom animal food intake seems to be protective. But only if animal food intake is above a certain level. This is not a ringing endorsement of wheat, but certainly helps explain wheat consumption in long-living groups around the world, including the French.

How much animal food does it take for the protective effect to be observed? In the China Study II sample, it is about 221 g/day or more. That is approximately the intake level above which the relationship between wheat flour intake and mortality in the 70 to 79 age range becomes statistically indistinguishable from zero. That is a little less than ½ lb, or 7.9 oz, of animal food intake per day.

Book review: Biology for Bodybuilders

The photos below show Doug Miller and his wife, Stephanie Miller. Doug is one of the most successful natural bodybuilders in the U.S.A. today. He is also a manager at an economics consulting firm and an entrepreneur. As if these were not enough, now he can add book author to his list of accomplishments. His book, Biology for Bodybuilders, has just been published.

(Source: www.dougmillerpro.com)

Doug studied biochemistry, molecular biology, and economics at the undergraduate level. His co-authors are Glenn Ellmers and Kevin Fontaine. Glenn is a regular commenter on this blog, a professional writer, and a certified Strength and Conditioning Specialist. Dr. Fontaine is an Associate Professor at the Johns Hopkins University’s School of Medicine and Bloomberg School of Public Health.

Biology for Bodybuilders is written in the first person by Doug, which is one of the appealing aspects of the book. This also allows Doug to say that his co-authors disagree with him sometimes, even as he outlines what works for him. Both Glenn and Kevin are described as following Paleolithic dieting approaches. Doug follows a more old school bodybuilding approach to dieting – e.g., he eats grains, and has multiple balanced meals everyday.

This relaxed approach to team writing neutralizes criticism from those who do not agree with Doug, at least to a certain extent. Maybe it was done on purpose; a smart idea. For example, I do not agree with everything Doug says in the book, but neither do Doug’s co-authors, by his own admission. Still, one thing we all have to agree with – from a competitive sports perspective, no one can question success.

At less than 120 pages, the book is certainly not encyclopedic, but it is quite packed with details about human physiology and metabolism for a book of this size. The scientific details are delivered in a direct and simple manner, through what I would describe as very good writing.

Doug has interesting ideas on how to push his limits as a bodybuilder. For example, he likes to train for muscle hypertrophy at around 20-30 lbs above his contest weight. Also, he likes to exercise at high repetition ranges, which many believe is not optimal for muscle growth. He does that even for mass building exercises, such as the deadlift. In this video he deadlifts 405 lbs for 27 repetitions.

Here it is important to point out that whether one is working out in the anaerobic range, which is where muscle hypertrophy tends to be maximized, is defined not by the number of repetitions but by the number of seconds a muscle group is placed under stress. The anaerobic range goes from around 20 to 120 seconds. If one does many repetitions, but does them fast, he or she will be in the anaerobic range. Incidentally, this is the range of strength training at which glycogen depletion is maximized.

I am not a bodybuilder, nor do I plan on becoming one, but I do admire athletes that excel in narrow sports. Also, I strongly believe in the health-promoting effects of moderate glycogen-depleting exercise, which includes strength training and sprints. Perhaps what top athletes like Doug do is not exactly optimal for long-term health, but it certainly beats sedentary behavior hands down. Or maybe top athletes will live long and healthy lives because the genetic makeup that allows them to be successful athletes is also conducive to great health.

In this respect, however, Doug is one of the people who have gotten the closest to convincing me that genes do not influence so much what one can achieve as a bodybuilder. In the book he shows a photo of himself at age 18, when he apparently weighed not much more than 135 lbs. Now, in his early 30s, he weighs 210-225 lbs during the offseason, at a height of 5'9". He has achieved this without taking steroids. Maybe he is a good example of compensatory adaptation, where obstacles lead to success.

If you are interested in natural bodybuilding, and/or the biology behind it, this book is highly recommended!

Strength training plus fasting regularly, and becoming diabetic!? No, it is just compensatory adaptation at work

One common outcome of doing glycogen-depleting exercise (e.g., strength training, sprinting) in combination with intermittent fasting is an increase in growth hormone (GH) levels. See this post for a graph showing the acute effect on GH levels of glycogen-depleting exercise. This effect applies to both men and women, and is generally healthy, leading to improvements in mood and many health markers.

It is a bit like GH therapy, with GH being “administered” to you by your own body. Both glycogen-depleting exercise and intermittent fasting increase GH levels; apparently they have an additive effect when done together.

Still, a complaint that one sees a lot from people who have been doing glycogen-depleting exercise and intermittent fasting for a while is that their fasting blood glucose levels go up. This is particularly true for obese folks (after they lose body fat), as obesity tends to be associated with low GH levels, although it is not restricted to the obese. In fact, many people decide to stop what they were doing because they think that they are becoming insulin resistant and on their way to developing type 2 diabetes. And, surely enough, when they stop, their blood glucose levels go down.

Guess what? If your blood glucose levels are going up quite a bit in response to glycogen-depleting exercise and intermittent fasting, maybe you are one of the lucky folks who are very effective at increasing their GH levels. The blood glucose increase effect is temporary, although it can last months, and is indeed caused by insulin resistance. An HbA1c test should also show an increase in hemoglobin glycation.

Over time, however, you will very likely become more insulin sensitive. What is happening is compensatory adaptation, with different short-term and long-term responses. In the short term, your body is trying to become a more efficient fat-burning machine, and GH is involved in this adaptation. But in the short term, GH leads to insulin resistance, probably via actions on muscle and fat cells. This gradually improves in the long term, possibly through a concomitant increase in liver insulin sensitivity and glycogen storage capacity.

This is somewhat similar to the response to GH therapy.

The figure below is from Johannsson et al. (1997). It shows what happened in terms of glucose metabolism when a group of obese men were administered recombinant GH for 9 months. The participants were aged 48–66, and were given in daily doses the equivalent to what would be needed to bring their GH levels to approximately what they were at age 20. For glucose, 5 mmol is about 90 mg, 5.5 is about 99, and 6 is about 108. GDR is glucose disposal rate; a measure of how quickly glucose is cleared from the blood.

As you can see, insulin sensitivity initially goes down for the GH group, and fasting blood glucose goes up quite a lot. But after 9 months the GH group has better insulin sensitivity. Their GDR is the same as in the placebo group, but with lower circulating insulin. The folks in the GH group also have significantly less body fat, and have better health markers, than those who took the placebo.

There is such a thing as sudden-onset type 2-like diabetes, but it is very rare (see Michael’s blog). Usually type 2 diabetes “telegraphs” its arrival through gradually increasing fasting blood glucose and HbA1c. However, those normally come together with other things, notably a decrease in HDL cholesterol and an increase in fasting triglycerides. Folks who do glycogen-depleting exercise and intermittent fasting tend to see the opposite – an increase in HDL cholesterol and a decrease in triglycerides.

So, if you are doing things that have the potential to increase your GH levels, a standard lipid panel can help you try to figure out whether insulin resistance is benign or not, if it happens.

By the way, GH and cortisol levels are correlated, which is often why some associate responses to glycogen-depleting exercise and intermittent fasting with esoteric nonsense that has no basis in scientific research like “adrenal fatigue”. Cortisol levels are meant to go up and down, but they should not go up and stay up while you are sitting down.

Avoid chronic stress, and keep on doing glycogen-depleting exercise and intermittent fasting; there is overwhelming scientific evidence that these things are good for you.