Lifeworld

Genes do not evolve, nor do traits that are coded for our genes. We say that they evolve to facilitate discourse, which is alright. Populations evolve. A new genotype appears in a population and then either spreads or disappears. If it spreads, then the population is said to be evolving with respect to that genotype. A genotype may spread to an entire population; in population genetics, this is called “fixation”.


Asexual reproduction is very uncommon among animals. The most accepted theory to explain this is that animal populations live in environments that change very quickly, and thus need a great deal of genetic diversity within them to cope with the change. Otherwise they disappear, and so do their genes. Asexual reproduction leads to dramatically less genetic diversity in populations than sexual reproduction.

Asexual reproduction is similar to cloning. Each new individual looks a lot like its single parent. This does not work well in populations where individuals live relatively long lives. And even 1 year may be too long in this respect. It is just too much time to wait for a possible new mutation that will bring in some genetic diversity. To complicate matters, genetic mutation does not occur very often, and most genetic mutations are neutral with respect to the phenotype (i.e., they don’t code for any trait).

This is not so much of a problem for species whose members reproduce extremely fast; e.g., produce a new generation in less than 1 hour. A fast-reproducing species usually has a short lifespan as well. Accordingly, asexual reproduction is common among short-lived and fast-reproducing unicellular organisms and pathogens that have no cell structure like viruses.

Bacteria and viruses, in particular, form a part of the environment in which animals live that require animal populations to have a large amount of genetic diversity. Animal populations with low genetic diversity are unlikely to be able to cope with the barrage of diseases caused by these fast-mutating parasites.

We make sex chiefly because of the parasites.

And what about death? What does it bring to the table for a population?

Let us look at the other extreme – immortality. Immortality is very problematic in evolutionary terms because a population of immortal individuals would quickly outgrow its resources. That would happen too fast for the population to evolve enough intelligence to be able to use resources beyond those that were locally available.

In this post I assume that immortality is not the same as indestructibility. Here immortality is equated to the absence of aging as we know it. In this sense, immortals can still die by accident or due to disease. They simply do not age. For immortals, susceptibility to disease does not go up with age.

One could argue that a population of immortal individuals who did not reproduce would have done just fine. But that is not correct, because in this case immortality would be akin to cloning, but worse. Genetic diversity would not grow, as no mutations would occur. The fixed population of immortals would be unable to cope with fast-mutating parasites.

There is so much selection pressure against immortality in nature that it is no surprise that animals of very few species live more than 60 years on average. Humans are at the high end of the longevity scale. They are there for a few reasons. One is that our ancestors had offspring that required extra care, which led to an increase in the parents’ longevity. The offspring required extra care chiefly because of their large brains.

That increase in longevity was likely due to genetic mutations that helped our ancestors extend a lifespan that was programmed to be relatively short. Immortality is not a sound strategy for population survival, and thus there are probably many mechanisms through which it is prevented.

Death is evolution’s main ally. Sex is a very good helper. Both increase genetic diversity in populations.

We can use our knowledge of evolution to live better today. The aging clock can be slowed significantly via evolutionarily sound diet and lifestyle changes, essentially because some of our modern diet and lifestyle choices accelerate aging a lot. But diet and lifestyle changes probably will not make people live to 150.

If we want to become immortal, as we understand it in our current human form, ultimately we may want to beat evolution. In this sense, only very intelligent beings can become immortal.

Maybe we can achieve that by changing our genes, or by learning how to transfer our consciousness “software” into robots. In doing so, however, we may become something different; something that is not human and thus doesn’t see things in the same way as a human does. A conscious robot, without the hormones that so heavily influence human behavior, may find that being alive is pointless.

There is another problem. What if the only natural way to achieve some form of immortality is through organic death, but in a way that we don’t understand? This is not a matter of faith or religion. There are many things that we don’t know for sure. This is probably the biggest mystery of all; one that we cannot unravel in our current human state.

This previous post looks at the amounts of protein needed to maintain a nitrogen balance of zero. It builds on data about individuals doing endurance exercise, which increases the estimates a bit. The post also examines the issue of what happens when more protein than is needed in consumed; including by people doing strength exercise.

What that post does not look into is whether strength exercise, performed at the anaerobic range, increases nitrogen balance. If it did, it may lead to a counterintuitive effect: strength exercise, when practiced at a certain level of intensity, might enable individuals in calorie deficit to retain their muscle, and lose primarily body fat. That is, strength exercise might push the body into burning more body fat and less muscle than it would normally do under calorie deficit conditions.



Under calorie deficit people normally lose both body fat and muscle to meet caloric needs. About 25 percent of lean body mass is lost in sedentary individuals, and 33 percent or more in individuals performing endurance exercise. I suspect that strength exercise has the potential to either bring this percentage down to zero, or to even lead to muscle gain if the calorie deficit is very small. One of the reasons is the data summarized on this post.

Two other reasons are related to what happens with children, and the variation in spontaneous hunger up-regulation in response to various types of exercise. The first reason can be summarized as this: it is very rare for children to be in negative nitrogen balance (Brooks et al., 2005); even when they are under some, not extreme, calorie deficit. It is rare for children to be in negative nitrogen balance even when their daily consumption of protein is below 0.5 g per kg of body weight.

This suggests that, when children are in calorie deficit, they tend to hold on to protein stores (which are critical for growth), and shift their energy consumption to fat more easily than adults. The reason is that developmental growth powerfully stimulates protein synthesis. This leads to a hormonal mix that causes the body to be in anabolic state, even when other forces (e.g., calorie deficit, low protein intake) are pushing it into a catabolic state. In a sense, the tissues of children are always hungry for their building blocks, and they do not let go of them very easily.

The second reason is an interesting variation in the patterns of spontaneous hunger up-regulation in various athletes. The increase in hunger is generally lower for strength than endurance activities. The spontaneous increase for bodybuilders is among the lowest. Since being in a catabolic state tends to have a strong effect on hunger, increasing it significantly, these patterns suggest that strength exercise may actually contribute to placing one in an anabolic state. The duration of this effect is approximately 48 h. Some increase in hunger is expected, because of the increased calorie expenditure during and after strength exercise, but that is counterbalanced somewhat by the start of an anabolic state.

What is going on, and what does this mean for you?

One way to understand what is happening here is to think in terms of compensatory adaptation. Strength exercise, if done properly, tells the body that it needs more muscle protein. Calorie deficit, as long as it is short-term, tells the body that food supply is limited. The body’s short-term response is to keep muscle as much as possible, and use body fat to the largest extent possible to supply the body’s energy needs.

If the right stimuli are supplied in a cyclical manner, no long-term adaptations (e.g., lowered metabolism) will be “perceived” as necessary by the body. Let us consider a 2-day cycle where one does strength exercise on the first day, and rests on the second. A surplus of protein and calories on the first day would lead to both muscle and body fat gain. A deficit on the second day would lead to body fat loss, but not to muscle loss, as long as the deficit is not too extreme. Since only body fat is being lost, more is lost on the second day than on the first.

In this way, one can gain muscle and lose body fat at the same time, which is what seems to have happened with the participants of the Ballor et al. (1996) study. Or, one can keep muscle (not gaining any) and lose more body fat, with a slightly higher calorie deficit. If the calorie deficit is too high, one will enter negative nitrogen balance and lose both muscle and body fat, as often happens with natural bodybuilders in the pre-tournament “cutting” phase.

In a sense, the increase in protein synthesis stimulated by strength exercise is analogous to, although much less strong than, the increase in protein synthesis stimulated by the growth process in children.

References

Ballor, D.L., Harvey-Berino, J.R., Ades, P.A., Cryan, J., & Calles-Escandon, J. (1996). Contrasting effects of resistance and aerobic training on body composition and metabolism after diet-induced weight loss. Metabolism, 45(2), 179-183.

Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.

The figure below, from Brooks et al. (2005), shows a graph relating nitrogen balance and protein intake. A nitrogen balance of zero is a state in which body protein mass is stable; that is, it is neither increasing nor decreasing. The graph was taken from this classic study by Meredith et al. The participants in the study were endurance exercisers. As you can see, age is not much of a factor for nitrogen balance in this group.


Nitrogen balance is greater than zero (i.e., an anabolic state) for the vast majority of the participants at 1.2 g of protein per kg of body weight per day. To convert lbs to kg, divide by 2.2. A person weighing 100 lbs (45 kg) would need 55 g/d of protein; a person weighing 155 lbs (70 kg) would need 84 g/d; someone weighing 200 lbs (91 kg) would need 109 g/d.

The above numbers are overestimations of the amounts needed by people not doing endurance exercise, because endurance exercise tends to lead to muscle loss more than rest or moderate strength training. One way to understand this is compensatory adaptation; the body adapts to endurance exercise by shedding off muscle, as muscle is more of a hindrance than an asset for this type of exercise.

Total calorie intake has a dramatic effect on protein requirements. The above numbers assume that a person is getting just enough calories from other sources to meet daily caloric needs. If a person is in caloric deficit, protein requirements go up. If in caloric surplus, protein requirements go down. Other factors that increase protein requirements are stress and wasting diseases (e.g., cancer).

But what if you want to gain muscle?

Wilson & Wilson (2006) conducted an extensive review of the literature on protein intake and nitrogen balance. That review suggests that a protein intake beyond 25 percent of what is necessary to achieve a nitrogen balance of zero would have no effect on muscle gain. That would be 69 g/d for a person weighing 100 lbs (45 kg); 105 g/d for a person weighing 155 lbs (70 kg); and 136 g/d for someone weighing 200 lbs (91 kg). For the reasons explained above, these are also overestimations.

What if you go well beyond these numbers?

The excess protein will be used primarily as fuel; that is, it will be oxidized. In fact, a large proportion of all the protein consumed on a daily basis is used as fuel, and does not become muscle. This happens even if you are a gifted bodybuilder that can add 1 lb of protein to muscle tissue per month. So excess protein can make you gain body fat, but not by protein becoming body fat.

Dietary protein does not normally become body fat, but will typically be used in place of dietary fat as fuel. This will allow dietary fat to be stored. Dietary protein also leads to an insulin response, which causes less body fat to be released. In this sense, protein has a fat-sparing effect, preventing it from being used to supply the energy needs of the body. As long as it is available, dietary protein will be favored over dietary or body fat as a fuel source.

Having said that, if you were to overeat anything, the best choice would be protein, in the absence of any disease that would be aggravated by this. Why? Protein contributes fewer calories per gram than carbohydrates; many fewer when compared with dietary fat. Unlike carbohydrates or fat, protein almost never becomes body fat under normal circumstances. Dietary fat is very easily converted to body fat; and carbohydrates become body fat when glycogen stores are full. Finally, protein seems to be the most satiating of all macronutrients, perhaps because natural protein-rich foods are also very nutrient-dense.

It is not very easy to eat a lot of protein without getting also a lot of fat if you get your protein from natural foods; as opposed to things like refined seed/grain products or protein supplements. Exceptions are organ meats and seafood, which generally tend to be quite lean and protein-rich.

References

Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.

Wilson, J., & Wilson, G.J. (2006). Contemporary issues in protein requirements and consumption for resistance trained athletes. Journal of the International Society of Sports Nutrition, 3(1), 7-27.