Wednesday, March 21, 2018

Compensatory adaptation as a unifying concept: Understanding how we respond to diet and lifestyle changes

Trying to understand each body response to each diet and lifestyle change, individually, is certainly a losing battle. It is a bit like the various attempts to classify organisms that occurred prior to solid knowledge about common descent. Darwin’s theory of evolution is a theory of common descent that makes classification of organisms a much easier and logical task.

Compensatory adaptation (CA) is a broad theoretical framework that hopefully can help us better understand responses to diet and lifestyle changes. CA is a very broad idea, and it has applications at many levels. I have discussed CA in the context of human behavior in general (Kock, 2002), and human behavior toward communication technologies (Kock, 2001; 2005; 2007). Full references and links are at the end of this post.

CA is all about time-dependent adaptation in response to stimuli facing an organism. The stimuli may be in the form of obstacles. From a general human behavior perspective, CA seems to be at the source of many success stories. A few are discussed in the Kock (2002) book; the cases of Helen Keller and Stephen Hawking are among them.

People who have to face serious obstacles sometimes develop remarkable adaptations that make them rather unique individuals. Hawking developed remarkable mental visualization abilities, which seem to be related to some of his most important cosmological discoveries. Keller could recognize an approaching person based on floor vibrations, even though she was blind and deaf. Both achieved remarkable professional success, perhaps not as much in spite but because of their disabilities.

From a diet and lifestyle perspective, CA allows us to make one key prediction. The prediction is that compensatory body responses to diet and lifestyle changes will occur, and they will be aimed at maximizing reproductive success, but with a twist – it’s reproductive success in our evolutionary past! We are stuck with those adaptations, even though we live in modern environments that differ in many respects from the environments where our ancestors lived.

Note that what CA generally tries to maximize is reproductive success, not survival success. From an evolutionary perspective, if an organism generates 30 offspring in a lifetime of 2 years, that organism is more successful in terms of spreading its genes than another that generates 5 offspring in a lifetime of 200 years. This is true as long as the offspring survive to reproductive maturity, which is why extended survival is selected for in some species.

We live longer than chimpanzees in part because our ancestors were “good fathers and mothers”, taking care of their children, who were vulnerable. If our ancestors were not as caring or their children not as vulnerable, maybe this blog would have posts on how to control blood glucose levels to live beyond the ripe old age of 50!

The CA prediction related to responses aimed at maximizing reproductive success is a straightforward enough prediction. The difficult part is to understand how CA works in specific contexts (e.g., Paleolithic dieting, low carbohydrate dieting, calorie restriction), and what we can do to take advantage (or work around) CA mechanisms. For that we need a good understanding of evolution, some common sense, and also good empirical research.

One thing we can say with some degree of certainty is that CA leads to short-term and long-term responses, and that those are likely to be different from one another. The reason is that a particular diet and lifestyle change affected the reproductive success of our Paleolithic ancestors in different ways, depending on whether it was a short-term or long-term change. The same is true for CA responses at different stages of one’s life, such as adolescence and middle age; they are also different.

This is the main reason why many diets that work very well in the beginning (e.g., first months) frequently cease to work as well after a while (e.g., a year).

Also, CA leads to psychological responses, which is one of the key reasons why most diets fail. Without a change in mindset, more often than not one tends to return to old habits. Hunger is not only a physiological response; it is also a psychological response, and the psychological part can be a lot stronger than the physiological one.

It is because of CA that a one-month moderately severe calorie restriction period (e.g., 30% below basal metabolic rate) will lead to significant body fat loss, as the body produces hormonal responses to several stimuli (e.g., glycogen depletion) in a compensatory way, but still “assuming” that liberal amounts of food will soon be available. Do that for one year and the body will respond differently, “assuming” that food scarcity is no longer short-term and thus that it requires different, and possibly more drastic, responses.

Among other things, prolonged severe calorie restriction will lead to a significant decrease in metabolism, loss of libido, loss of morale, and physical as well as mental fatigue. It will make the body hold on to its fat reserves a lot more greedily, and induce a number of psychological responses to force us to devour anything in sight. In several people it will induce psychosis. The results of prolonged starvation experiments, such as the Biosphere 2 experiments, are very instructive in this respect.

It is because of CA that resistance exercise leads to muscle gain. Muscle gain is actually a body’s response to reasonable levels of anaerobic exercise. The exercise itself leads to muscle damage, and short-term muscle loss. The gain comes after the exercise, in the following hours and days (and with proper nutrition), as the body tries to repair the muscle damage. Here the body “assumes” that the level of exertion that caused it will continue in the near future.

If you increase the effort (by increasing resistance or repetitions, within a certain range) at each workout session, the body will be constantly adapting, up to a limit. If there is no increase, adaptation will stop; it will even regress if exercise ceases altogether. Do too much resistance training (e.g., multiple workout sessions everyday), and the body will react differently. Among other things, it will create deterrents in the form of pain (through inflammation), physical and mental fatigue, and even psychological aversion to resistance exercise.

CA processes have a powerful effect on one’s body, and even on one’s mind!

References:

Kock, N. (2001). Compensatory Adaptation to a Lean Medium: An Action Research Investigation of Electronic Communication in Process Improvement Groups. IEEE Transactions on Professional Communication, 44(4), 267-285.

Kock, N. (2002). Compensatory Adaptation: Understanding How Obstacles Can Lead to Success. Infinity Publishing, Haverford, PA. (Additional link.)

Kock, N. (2005). Compensatory adaptation to media obstacles: An experimental study of process redesign dyads. Information Resources Management Journal, 18(2), 41-67.

Kock, N. (2007). Media Naturalness and Compensatory Encoding: The Burden of Electronic Media Obstacles is on Senders. Decision Support Systems, 44(1), 175-187.

Sunday, February 25, 2018

Baked cod and lobster


Many years ago I lost 60 lbs (27 kg) over a period of about 2-3 years, and kept it off. Often people are surprised when I show them an old picture of myself, where I am visibly obese ().

I have always felt that one of the keys to losing a significant amount of body fat without triggering body starvation responses is to eat a diet that has a high nutrient-to-calorie ratio. The baked cod and lobster dish below, with photos before and after baking, is a good example of a meal in such a diet.





This is a fairly simple meal to prepare; simple and delicious. The cost of this dish goes down significantly if you do not include the lobster. Below is a recipe. I used it to prepare the baked cod and lobster shown on the photos above.

- Cut and spread on two sheet pans about 4 tomatoes, 1 cup of onion, 1 cup of spinach, 2 lbs of cod, and 4 lobster tails (approx. 4 oz each).

- Add some butter to the mix. I recommend more butter on the lobster than on the cod.

- Preheat the oven to 350 degrees Fahrenheit.

- Add seasoning to taste. I suggest using a small amount of salt, and some chili powder, garlic powder, cayenne pepper, and herbs.

- Bake for about 30 minutes, or until the lobster is soft.

Let us say you are hungry, so you eat about one-fourth of all of this. That is one lobster tail and about a quarter of the cod dish. The nutrition content of such a meal is shown below.



So you will be getting about 86 g of protein in this one single meal. The vitamins and mineral contents listed are mostly above 100 percent of the usually recommended intake. All of this while taking in only a little over 500 calories.

It is very difficult to get fat eating like this!

Thursday, January 25, 2018

Ketones and Ketosis: Physiological and pathological forms

Ketones are compounds that have a specific chemical structure. The figure below (from: Wikipedia) shows the chemical structure of various types of ketones. As you can see, all ketones share a carbonyl group; that is the “O=” part of their chemical structure. A carbonyl group is an oxygen atom double-bonded to a carbon atom.


Technically speaking, many substances can be classified as ketones. Not all of these are involved in the same metabolic processes in humans. For example, fructose is technically a ketone, but it is not one of the three main ketones produced by humans from dietary macronutrients (discussed below), and is not metabolized in the same way as are those three main ketones.

Humans, as well as most other vertebrates, produce three main ketones (also known as ketone bodies) from dietary macronutrients. These are acetone, acetoacetate and beta-hydroxybutyrate. Low carbohydrate diets tend to promote glycogen depletion, which in turn leads to increased production of these ketones. Glycogen is stored in the liver and muscles. Liver glycogen is used by the body to maintain blood glucose levels within a narrow range in the fasted state. Examples of diets that tend to promote glycogen depletion are the Atkins Diet and Kwaśniewski’s Optimal Diet.

A search for articles on ketosis in scientific databases usually returns a large number of articles dealing with ketosis in cows. Why? The reason is that ketosis reduces milk production, by both reducing the amount of fat and glucose available for milk synthesis. In fact, ketosis is referred to as a “disease” in cows.

In humans, most articles on ketosis refer to pathological ketosis (a.k.a. ketoacidosis), especially in the context of uncontrolled diabetes. One notable exception is an article by Williamson (2005), from which the table below was taken. The table shows ketone concentrations in the blood under various circumstances, in mmol/l.


As you can see, relatively high concentrations of ketones occur in newborn babies (neonate), in adults post-exercise, and in adults fed a high fat diet. Generally speaking, a high fat diet is a low carbohydrate diet, and a high carbohydrate diet is a low fat diet. (One occasionally sees diets that are high in both carbohydrates and fat; which seem excellent at increasing body fat and thus reducing life span. This diet is apparently popular among sumo wrestlers, where genetics and vigorous exercise usually counter the negative diet effects.)

Situations in which ketosis occurs in newborn babies (neonate), in adults post-exercise, and in adults fed a high fat diet are all examples of physiological, or benign, ketosis. Ketones are also found in low concentrations in adults fed a standard American diet.

Ketones are found in very high concentrations in adults with untreated diabetes. This is an example of pathological ketosis, even though ketones are produced as part of a protective compensatory mechanism to spare glucose for the brain and red blood cells (which need glucose to function properly). Pathological ketosis leads to serum ketone levels that can be as much as 80 times (or more) those found in physiological ketosis.

Serum ketone concentrations increase proportionally to decreases in stored glycogen and, when glycogen is low or absent, correlate strongly (and inversely) with blood glucose levels. In some individuals glycogen is practically absent due to a genetic condition that leads to hepatic glycogen synthase deficiency. This is a deficiency of the enzyme that promotes glycogen synthesis by the liver. The figure below (also from Williamson, 2005) shows the variations in glucose and ketone levels in a child with glycogen synthase deficiency.


What happened with this child? Williamson answers this question: “It is of interest that this particular child suffered no ill effects from the daily exposure to high concentrations of ketone bodies, underlining their role as normal substrates for the brain when available.”

Unlike glucose and lipoprotein-bound fats (in VLDL, for example), unused ketones cannot be converted back to substances that can be stored by the body. Thus excess ketones are eliminated in the urine; leading to their detection by various tests, e.g., Ketostix tests. This elimination of unused ketones in the urine is one of the reasons why low carbohydrate diets are believed to lead to enhanced body fat loss.

In summary, ketones are present in the blood most of the time, in most people, whether they are on a ketogenic diet or not. If they do not show up in the urine, it does not mean that they are not present in the blood; although it usually means that their concentration in the blood is not that high. Like glucose, ketones are soluble in water, and thus circulate in the blood without the need for carriers (e.g., albumin, which is needed for the transport of free fatty acids; and VLDL, needed for the transport of triglycerides). Like glucose, they are used as sources of energy by the brain and by muscle tissues.

It has been speculated that ketosis leads to accelerated aging, through the formation of advanced glycation endproducts (AGEs), a speculation that seems to be largely unfounded (see this post). It is difficult to believe that a metabolic process that is universally found in babies and adults post-exercise would have been favored by evolution if it led to accelerated aging.

References:

Williamson, D.H. (2005). Ketosis. Encyclopedia of Human Nutrition, 91-98.