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Muscle Fiber Typing and Race: Redux

I recently blogged on Muscle Fiber Typing, HBD, and Sports. I showed that differences in which race wins at what competition comes down to ancestry, which then correlates with muscle fiber typing. I came across this paper, Black and White race differences in aerobic capacity, muscle fiber type, and their influence on metabolic processes, today which, of course, proved my point on muscle fiber typing.

The authors say that obesity is a known risk factor of cardiometabolic disease (though Blüher 2012 says that up to 30 percent of obese patients are metabolically healthy with insulin sensitivity on the same level as thin individuals) and that cardio can reduce excess adipose tissue (this isn’t true either), maintains weight (maybe) and reduces the risk of obesity (it doesn’t) and cardiometabolic disease (this is true). The two major determinants of aerobic capacity are muscle fiber typing and “the capacity of the cardiorespiratory system to deliver nutrient-rich content to the muscle”. As I said in my previous article on muscle fiber typing, depending on which fibers an individual has determines whether or not they are predisposed to being good at endurance sports (Type I fibers) or being good at explosive sports (Type II fibers). Recent research has shown that blacks fiber typing predisposes them to a lower overall VO2 max.

VO2 max comes down to a strong oxygen support system and the capacity to contract a large number of muscle fibers at once, both of which are largely genetic. Lactic acid makes us tired, the best way to train is to minimize lactic acid production and maximize lactic acid removal during exercise. High-Intensity Interval Training, or HIIT, achieves this. The more O2 consumed during exercise, the less of a reliance there will be on the anaerobic breakdown of CHO to lactic acid.

Along with inadequate exercise, these variables place blacks at an increased risk for obesity as well as other negative metabolic factors in comparison to other races/ethnic groups. The author’s purpose of the review was to show how skeletal muscle fiber typing contributes to obesity in non-“Hispanic” black populations.

The review indicates that the metabolic properties of Type II fibers (reduced oxidative capacity, capillary density, which is a physiological measure that takes a cross-section of muscle and counts the number of blood vessels within. The measurement can be considered an indicator of physical health and is also related to the ability to do strenuous activity) are related to various cardiometabolic diseases.

Since non-“Hispanic” blacks have more Type II fibers on average, they have a lower maximal aerobic capacity. Combined with low Resting Energy Expidenture (REE) and reduced hemoglobin concentration (hemoglobin is a protein in the red blood cells that shuttles oxygen to your tissues and organs and transports carbon dioxide from your organs and tissues back to your lungs), non-“Hispanic” blacks may be predisposed (they are when you look at what the differing skeletal muscle fibers do in the body and if you have a basic understanding of physiology) to a lower maximal aerobic capacity, which contributes to obesity and metabolic disease in the non-“Hispanic” black population.

I have written on ethnicity and obesity last year. In the two racial groups that were tested, American non-“Hispanic” whites and American non-“Hispanic” blacks, what the researchers say holds true.

On the other hand, Kenyans have an average BMI of 21.5. Since we know that a high VO2 max and low BMI are correlated, this is why Kenyans succeed in distance running (along with VO2 max training, which only enhances the genetic effects that are already there).

Moreover, I wrote an article on how Black American Men with More African Ancestry Less Likely to Be Obese. How do we reconcile this with the data I have just written about?

Simple. The population in the study I’m discussing in this article must have had more non-African ancestry than the population that was gathered showing that black American men with more African ancestry are less likely to be obese. The researchers in that study looked at  3,314 genetic markers. They then tested whether sex modifies the association of West African genetic ancestry and body mass index, waist circumference, and waist to hip ratio. Also, they adjusted for income and education as well as examined associations of ancestry with the phenotypes of males and females separately. They conclude that their results suggest that a combination of male gender and West African ancestry is correlated with protection against central obesity and suggests that a portion of the difference in obesity (13.2 percent difference) may be due, in part to genetic factors. The study also suggests that there are specific genetic and physiologic differences in African and European Americans (take that, race-denialists =^) ).

Since both black men and women in America share the same environment, some genetic factors are at play in the differences in obesity rates between the two sexes with more African ancestry for black American men being the main reason.

Finally, I wrote an article on BPA consumption and obesity. The sample was on blacks and Dominicans (they’re black as well) in NYC. It was discovered that babes who were exposed to BPA more in childhood and in the womb had higher chances of being obese. This goes with what the authors of the study I’m citing in this article say. There are numerous environmental factors that pertain to obesity that’s not kcal in/out (which the First Law of Thermodynamics is irrelevant to human physiology). BPA consumption is one of them (as well as a cause for the current and ongoing cucking of Europe). Whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. Bottled water has BPA in the plastic, and since they drink more bottled water, they run the risk of their children being more prone to obesity due to the negative effects of BPA in the human body.

In sum, blacks are more likely to be faster due to their fiber typing, but are also more likely to be obese (in this sample, anyway which I assume was a mix of men and women. I will update this article when I find and read the full paper). They also run a higher risk of having related diseases, most notably due to a lower REE (showing they don’t walk around as much, since too much sitting increases mortality EVEN WITH EXERCISE. So if you have a desk job and don’t do any other physical activity and enjoy living, do more LISS, low-intensity steady-state cardio). These factors also, in part, explain why blacks have higher rates of hypertension (with Sickle Cell Anemia being another cause since when the blood is sickle-shaped, they crowd in the blood vessels causing blockage in the veins which leads to strokes and other diseases). The more the genetic factors that predispose people to obesity are understood (let’s be real here, there ARE genetic correlates with obesity), the better we can help those who suffer from the condition.

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Myopia, IQ, and Race

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We’ve all heard of the nerd stereotype. One of the main ones is that nerds wear glasses. However, as most of my readers may know, stereotypes are based on fact more often than not. From the black criminal and sprinter, to the hyper-intelligent East Asian, to the intelligent and creative Europeans, we see that these so-called ‘stereotypes’ arise because stereotypes are actually average traits. Therefore, this ‘nerd stereotype’ that they always wear glasses is based on averages, so there must be a genetic component behind it. In this article I will talk about the genetics of myopia, reasons why researchers believe it arises, and racial differences in the prevalence of myopia.

Myopia, better known as nearsightedness, has a pleiotropic relationship with intelligence. Pleiotropy is the single gene or set of genes controlling multiple, possibly unrelated, phenotypic traits. So if the two traits are correlated, then there is a good chance that if one wears glasses they may have higher average intelligence.

Rosner and Belkin (1987) found that the prevalence of myopia was higher in more intelligent and educated groups. They found a strong association between the rate of myopia, years of schooling and intelligence level. Schooling and intelligence weigh equally with myopia, showing that those who are myopic tend to stay in school longer and are more intelligent than average.

Saw et al (2004) show that there may be similar genes associated with eye growth or size (myopia) and neocortical size (*possibly* correlated with IQ, we know it is). This is exactly what Cohn, Cohn, and Jensen found in 1987; that there was a pleiotropic relationship between IQ and myopia. One set of genes controls one or multiple phenotypic traits. They also say that nonverbal IQ is correlated with myopia in the Singaporean cohort independent of near work from the children (such as reading). Nonverbal IQ may be an independent risk factor of myopia independent of books read per week. They conclude that more research needs to be taken out to untangle the cause and effect of the myopia/intelligence/reading relationship.

Mirashi et al (2014) show in a sample of 4600 myopia-inflicted Germans between the ages of 35 and 74 that about 53 percent of the sample had graduated from college compared to 24 percent of the sample who didn’t go to school past high school. They, too, conclude that higher levels of myopia are associated with higher educational achievement and post-school professional achievement and that those who were myopic had higher levels of educational achievement than those in the sample who weren’t myopic.

More recently, Verma and Verma (2015) state that there is evidence that both genetic and environmental factors play a role in the prevalence of myopia. Moreover, Czepida, Lodykowska, and Czepita (2008) come to the same conclusion; that children with myopia have higher IQs and was verified in other countries (the USA, the Czech Republic, Denmark, Israel, New Zealand).

The correlation between myopia and IQ is between .2 and .25 (Jensen, 1998 b; 149). Jensen writes on page 150:

. . .the degree of myopia was measured as a continuous variable (refraction error) by means of optical techniques in a group of sixty adolescents selected only for high IQs (Raven matrices) and their less gifted full siblings, who averaged fourteen IQ points lower, a difference equivalent to 0.92o. The high-IQ subjects differed significantly from their lower-IQ siblings in myopia by an average of 0.39a on the measure of refraction error.1161 In other words, since there is a within-families correlation between myopia and IQ, the relationship is intrinsic. However, it is hard to think of any directly functional relationship between myopia and IQ. The data are most consistent with there being a pleiotropic relationship. The causal pathway through which the genetic factor that causes myopia also to some extent elevates g (or vice versa) is unknown. Because the within-family relationship of myopia and IQ was found with Raven’s matrices, which in factor analyses is found to have nearly all of its common factor variance on g ,n it leaves virtually no doubt that the IQ score in this case represents g almost exclusively. (emphasis his)

Therefore, as noted earlier, we would see a slight variation in the general population between those with high IQs and those who wear glasses and are myopic.

Jensen also talks about race and myopia. He says that Asians have the highest rates of myopia, while blacks have the lowest rate and whites have a rate slightly higher than blacks.

In a tribute to Arthur Jensen, edited by Helmuth Nyborg, it states that East Asians have the highest rates of myopia, with blacks having the lowest rate and whites being intermediate (Rushton’s Rule of Three).  Ashkenazi Jews have a rate of myopia two times higher than that of gentiles, on par with East Asians. These are yet other biological correlates with the g factor that also lend credence to the hereditarian hypothesis.

Glassescrafter.com also shows that East Asians have a higher rate of myopia with blacks having a lower rate:

Certain types of visual disturbances affect some races more frequently. Asian-Americans, for example, are more likely to be near-sighted than Caucasians or African-Americans. African-Americans have the lowest incidence of near-sightedness, but are more prone to cataracts and some other eye diseases. Eye problems, including the need to wear glasses, also can run in families.

Of course, if myopia is a pleiotropic trait (there is good evidence that there is), and wearing glasses runs in families as well as high intelligence, it can be safely hypothesized that the two indeed do have a relationship with each other. The biological correlates show enough that these traits, too, follow Rushton’s Rule.

Finally, Au, Tay and Kim (1993) present data that shows the prevalence and severity of myopia is associated with higher education. They also report on data that Rosner and Belkin reported the prevalence of myopia in males with and IQ of 80 or less was 8 percent while the rate increased up to 27.3 among those with an IQ of 128 or higher. Reported separately, it was concluded that the myopia rates in the cohort of 110,236 young Singaporean males correlated with race (Au, Tay, and Lim, 1993). The myopia rate for the Chinese was 48.5 (IQ 105), for Eurasians it was 34.7, for Indians it was 30.4 (IQ 82), and for Malays it was 24.5 (IQ 92). It’s worth noting that India’s IQ is depressed by disease and bad nutrition, and if this were to be ratified their IQ would be around 94. So this, again, shows the biological correlate with IQ and myopia as it’s showing on the Indians’ genotype.

The association between myopia and intelligence isn’t definite yet, however with more studies looking into the relationship between these variables I believe it will be concrete that those who are more myopic tend to have higher IQs due to the pleiotropic nature of IQ and myopia. Since reading is heritablethose with higher IQs as children tend to read more as adults, and the racial gradient is noticed in children, it’s pretty safe to say that myopia and IQ are linked pleiotropically and give more credence to the hereditarian hypothesis. Most studies find a statisically positive correlation between myopia and intelligence. Along with the racial disparities in myopia as well as intelligence, it’s pretty safe to say that the relationship is genetic and pleiotropic in nature since the races also differ in these variables.

Muscle Fiber Typing, HBD, and Sports

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With the Olympics currently happening, I figured I’d talk about muscle fiber typing and how it plays a factor in who wins what competition. First I’ll go through both fiber typings and what they mean for each sport. Then I will go through some of the most well-known sports and show how and why certain races dominate in different sports.

Muscle fiber typing

There are two types of muscle fibers: Type I fibers (slow twitch) and Type II fibers (fast twitch). Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.

Type I fibers lead to more strength and muscular endurance as they are slow to fire off, while Type II fibers fire quicker and tire faster. Slow twitch fibers use oxygen more efficiently, while fast twitch fibers do not burn oxygen to create energy. Slow twitch muscles delay firing which is why the endurance is so high in individuals with these fibers whereas for those with fast twitch fibers have their muscles fire more explosively. Slow twitch fibers don’t tire as easily while fast twitch fibers tire quickly. This is why West African blacks and their descendants dominate in sprinting and other competitions where fast twitch muscle fibers dominate in comparison to slow twitch.

Usain Bolt, who just won the 100m dash the other day, has fast twitch fibers (Type II) due to a gene called ACTN3 which is associated with elite athletic performance. West African blacks and their descendants have this gene. For example, 70 percent of Jamaicans have the ACTN3 gene, and this gene is why Usain Bolt is the world’s fastest man.

Though at the same time, West Africans and their descendants suffer in competitions where muscular endurance is needed (swimming is one of them). Caucasians Asians and East Africans have more slow twitch fibers (Type I fibers) which allows them to dominate in competitions where endurance is needed (weightlifting, Strong Man, distance running, swimming).

There are physiological differences found in the winners of these competitions, and like most things, there is a racial basis to them.

Sports

As noted above, West Africans and their descendants dominate competitions in which their muscle fibers are best put to use (sprinting, football, basketball, etc) while they suffer in competitions in which Caucasians and Asians dominate in which muscular endurance is needed (weightlifting, powerlifting, distance running).

World’s Strongest Man

Muscle fiber typings play a major part in the winners of these competitions as does limb length. Generally, the winners of the World’s Strongest Man (WSM) are more stocky and have shorter limbs which translates into more power generated since the distance is shorter.

A white man has won the WSM competition every year since its inception. It’s always a Northern or Easter European who wins these competitions. The Russians and Slavs are known for their crazy squat programs, and muscle fiber typing is the reason why. They are able to generate more power than those with fast twitch fibers which translates into domination in strength-based competitions.

The same thing is noticed in powerlifting. Caucasians and Asians dominate. I’ve seen some incredibly strong East Asian powerlifters, and the reason is they are shorter and stockier with shorter limbs. More power is able to be generated with the shorter distance and Type II fibers which allow these populations to excel in these types of competitions.

I hypothesize that just like West Africans and their descendants consistently win sprinting competitions due to their genes and fiber typing, this is the same reason why Europeans consistently win WSM. Though, PumpkinPerson thinks differently about this.

PP believes that since Africans have higher testosterone, then they, therefore, should dominate in these types of competitions. His reasoning is based on Rushton’s Rule of Three, which all though it holds well for a wide variety of variables, it doesn’t hold with more complex traits such as muscle fiber typing.

PP cites a study stating that blacks out benched whites in the beginning and end of the study. However, it seems this is anomalous. The researchers say this is the only study looking at this, and from what I can tell, they didn’t ask about dietary and or exercise habits. They also say that blacks were heavier in BMI at the onset, but not in the follow-up.

I’d like to see another study like this before any conclusions are drawn. Because what I see in actual powerlifting competitions from people who go above and beyond their genetic potential when everyone is using, Caucasians (whites, MENA people) and East Asians are consistently always stronger than blacks. From what we see from actual competitions, Caucasians and Asians dominate these competitions. Africans are really nowhere to be found. In fact, Kenya is the only sub-Saharan African country to place in the top 3 in the WSM, which strengthens my theory on muscle fiber typing and strength-based competitions since they have slow twitch fibers.

PP then writes another article saying that from 1938 to 1953 the WSM was a black man named John Henry Davis. He was known as the WSM from those years, but as we know, exceptions don’t prove rules.

Mark Henry is a better example. Genetic freak of nature. World record total in squat, bench and deadlift; he was a squatting 600 pounds as a freshman; as a teenager, he had the 8th best total regardless of age group.

He’s a genetic freak of nature. He’s way stronger than the guy you cited. Mark Henry is one of the strongest people to ever live. He is a freak of nature. I can’t emphasize that enough.

Sprinting

West Africans and their descendants excel at sports where their muscle fiber typing is put to good use. The ACTN3 gene, as noted above, has a lot to do with their success in these competitions but it doesn’t tell the whole story. Sprinters have long limbs, which allow them to cover a greater distance with each stride in comparison to another with shorter limbs. Sprinters also have lower levels of body fat which translates to more speed. Where these lower levels of body fat make have them suffer in swimming competitions since fat floats, this helps in sprinting competitions due to less fat mass.

Swimming

For those of you who are keeping up with the Olympics, you may have heard of Robel Kiros Habte. He finished with the worst time out of the 59 contestants and was only there due to an invitation extended to him by the International Swimming Federation who chooses people from countries that are underrepresented in the Games. This invitation shows that even the ‘best’ in their country is nowhere near good enough versus the best in the world.

But on the other hand, for the first time in history, swimmer Simone Manuel became the first black American to win gold in the 100m freestyle. There’s a first time for everything and exceptions don’t disprove rules.

Of course, Michael Phelps speaks for himself, with his 23rd gold medal win which broke a record that was standing for 2168 years.

Bodybuilding

Blacks dominate in American bodybuilding. This is due to them having lower fat-free body (FFB) and being more mesomorphic on average.

The winner of Mr. Olympia for the five years in a row is Phil Heath (who will win a sixth title next month during the Olympia). Blacks have consistently been in the top running in the IFBB (International Federation of Bodybuilding). This is due to their muscle insertions and lower average fat-free body that allows a high percentage of blacks to compete. Moreover, I’d say that genetically speaking, blacks have a better chance to win over whites since they have a more sculpted physique naturally, which comes down to evolutionary selection

Some people may say that the above sports are tainted due to performance enhancing drug (PED) use. Though what they fail to realize is that drugs take you above and beyond your genetic limit. These people are already genetic freaks of nature and taking drugs just makes them that much better. You can’t take someone with garbage genetics, have him shoot up for years and bust his ass in the gym to be Mr. Olympia. Just like you can’t take someone with garbage genetics and the wrong proportions, inject them with PEDs and expect them to do well in powerlifting and Strongman competitions. The genetic potential is already there in these athletes and PEDs take them above and beyond what is naturally possible.

Strength and Mortality

Finally, to round this up, there is a correlation between strength and mortality. With a sample of 8762 men between the ages of 20 and 80, it was found that muscular strength was inversely and independently associated with death from all causes and cancer in men even after adjusting for cardiorespiratory fitness and other possible confounders. From the discussion of the paper:

The analysis on the combined effects of muscular strength and cardiorespiratory fitness with all cause mortality showed that the age adjusted death rate in men with high levels of both muscular strength and cardiorespiratory fitness was 60% lower (P<0.001) than the death rate in the group of unfit men with the lowest levels of muscular strength. These results highlight the importance of having at least moderate levels of both muscular strength and cardiorespiratory fitness to reduce risk of death from all causes and cancer in this population of men.

The point of bringing this paper up is that Caucasians and Asians are stronger than blacks, and also live longer. This is just like the correlation between IQ and life expectancy. Since men with higher levels of strength live longer than men with lower levels of strength, this strengthens my hypothesis for strength-based competitions and the racial mix of the competitions. Caucasians and East Asians, who have higher IQs than blacks, are also stronger than them on average, which also correlates with life expectancy.

(For more information see Steve Sailer’s post on West African and East Africans in sprinting and distance running as well as Razib Khan’s post on West Africans and their domination of sprinting competitions.)

Conclusion

HBD is evident in all of our lives. Though many of us don’t bring it up, it’s evident in the sports we watch to everyday life. The reason why there are racial disparities in the upper echelons of professional sports has to do with muscle fiber typing as well as those who are genetically predisposed to do well in these competitions. West Africans dominate in sprinting competitions and others where they are able to use their longer limbs and fast twitch fibers whereas Caucasians and Asians dominate in strength sports due to their limb length and slow twitch fibers. Professional sports proves what is evident in our everyday lives and, subconsciously at least, the average person sees this.

The Concept of “More Evolved”: A Reply to Pumpkin Person

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Recently, PumpkinPerson has been stating that one population can be ‘more evolved‘ than another which doesn’t make any biological sense. PP’s basic thesis is that since we are the last branch on the tree in comparison to the lifeforms that came before Homo Sapiens, that due to that, we are ‘more evolved’ than other organisms on the planet. I get where he’s coming from; he’s just extremely wrong.

Organisms evolve to better adapt to their environment through Natural Selection (NS). NS does select for positive traits, however, evolution is not a linear process. PP also claims that “evolution is progressive“. That couldn’t be further from the truth. Stating that evolution is “progressive” means that evolution through NS is progressing to an “endgame”. Though, we know there is no “endgame” with evolution, as evolution just happens.

Evolution is not progressive. NS may select for traits not suitable for that environment, as NS is “not all-powerful”. Selecting for one advantageous trait may change another trait for the worse. (See “Misconceptions on Evolutionary Trees“, which is what PP did, from Berkely).

PP asks “Who is most evolved?”

No organism is “more evolved” than another. NS selects for traits that are advantageous to that current environment (it selects for negative traits as well). Due to this, the word “superior”, the phrase “more evolved” is meaningless comparing human races to one another and humanity as a whole to the other lifeforms on the planet.

PP quotes Rushton as saying

One theoretical possibility is that evolution is progressive, and that some populations are more advanced than others.” J.P. Rushton, 1989

We know that evolution is not progressive, so due to this, some populations are not more advanced than others. Genetic superiority can be measured subjectively, but not objectively, as each organism has different strengths and weaknesses due to its environment.

PP then implies that bacteria are “less evolved” than we are. However, with recent breakthroughs in the HMP (Human Microbiome Project) we see the huge role that gut microbiota play when it comes to communicating with the brain, how antibiotics that kill gut microbiota also stop the growth of new brain cells, and how altered gut microbiota cause obesity. With more amazing uses and benefits we find involving gut microbiota and human health, can we really say that we’re “more evolved” than these organisms when they account for a huge amount of positive benefits for as a whole.

For another example, cows using their own genes wouldn’t be able to extract the fiber out of the food they eat. They would need special enzymes to break down the cell wall to extract the nutrients from the food. Though, evolving the genes to do this would take an extremely long time. This is where gut microbiota come in. Trillions of microbiomes live in the cows’ 4 stomachs.  The microbiomes living in the cows’ gut processes the food back and forth through the mechanical grinding of the cows’ mouth and thus, the nutrients are extracted by the microbiomes that way.

In this instance, is a cow superior to its microbiomes if a cow’s microbiomes make it possible for it to digest its food?

PP then asks “Does more evolved mean superior?”

No, it doesn’t. There is no way to quantify this, as evolution is not progressive. Furthermore, saying that one organism is “more evolved” than another doesn’t make any sense since, as noted earlier in this article, each organism is suited to the environment it evolved in through NS.

PP then says that he prefers a 3 race model, when a 5 race model makes more sense. These populations are “Africa, Europe, Asia, Melanesia and the Americas.”

I assume he would put ‘Natives’ with Asian Mongoloids, but ‘Natives’ have been genetically isolated in the Americas for so long that they formed their own distinct clade away from other populations due to no introgression between them, when other populations have admixture from other parts of the world:

Significant genetic input from outside is not noticed in Meso and South American Amerindians according to the phylogenetic analyses; while all world populations (including Africans, Europeans, Asians, Australians, Polynesians, North American Na-Dene Indians and Eskimos) are genetically related. Meso and South American Amerindians tend to remain isolated in the Neighbor-Joining, correspondence and plane genetic distance analyses.

Hence, a 5 race model makes more sense as these populations show genetic differentiation between each other.

Still, others may take the concept of “more evolved” and believe that one race is “more evolved” than another. That’s another wrong statement.

The assumption here is that populations that evolved closer to the equator had evolution “stop” for them due to “ease of lifestyle” (life is easy nowhere). That too makes no evolutionary sense. If that were so, how did Africans evolve the sickle cell trait? Evolution is a constant, ongoing process and does not ‘speed up or slow down’ based on the environments in which ancestral evolution has occurred.

Moreover, r/K selection theory does dictate fast and slow life history strategies, but it has nothing to do with ‘fast or slow evolution within human populations’.

To state that evolution ‘is faster or slower’ in certain populations of humans is like saying ‘evolution has slowed for man since 50kya’ as anti-human-evolutionists have said:

“Something must have happened to weaken the selective pressure drastically. We cannot escape the conclusion that man’s evolution towards manness has suddenly come to a halt.” – Ernst Mayr

“There’s been no biological change in humans in 40,000 or 50,000 years. Everything we call culture and civilization we’ve built with the same body and brain.” – Stephen Jay Gould

Stating that evolution occurs faster in certain populations is on the complete opposite of the “evolution stopped for humans 50kya” camp, which we know is not true and evolution has sped up in the last 10kya.

To say that one organism, or population for that matter, is more evolved than another makes no biological sense. Each organism is suited to its own environment and where it evolved. Even then, different organisms evolve different traits depending on what they have to do in that ecosystem to survive. Darwin’s finches are a perfect example of that.

Misconceptions on Calories In and Calories Out

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(To those from “myproana.com”, DO NOT misconstrue what I wrote here. What I wrote here is perfectly understandable. I am NOT saying that “you have no metabolism”. My point is, low kcal dieting CAN and WILL destroy your metabolism. The literature is vast on this subject and it’s waiting for you to read it. Any further confusions, please comment and I will answer your questions.)

“Eat Less and move more!!! That’s how you lose weight!” What people who don’t understand about human metabolism and homeostasis is that when caloric reduction occurs, the body drops the metabolism to match the amount of kilocalories (kcal) it is receiving. Thus, weight will plateau and you will need to further decrease caloric consumption to lose more weight. In this article, I will go through what a calorie is, common misconceptions of Calories In and Calories Out, the reasons for metabolic slow down,  the process of thermodynamics that people who don’t understand this research cry out whenever it’s said, and finally starvation experiments that prove metabolic slow down occurs during a decrease in caloric intake and how this metabolic slow down persists after the diet is over.

A kilocalorie is the heat required to raise 1 kilogram of water 1 degree celsius. This definition is used whenever people say ‘Calorie’.

Misconceptions on kcal in/kcal out

  1. One of the biggest misconceptions people have on Calories In/Calories out is that these variables are independent of each other. However, they are extremely dependent variables.  When you decrease Calories In, your body decreases Calories Out. Basically, a 20 percent reduction in kcal will result in a 20 percent reduction in metabolism which the end result ends up being minimal weight loss.
  2. The next big assumption people have about Calories In and Calories Out is the assumption that the Basal Metabolic Rate (BMR) remains stable. Of course, measuring the caloric intake is simple. However, measuring caloric outtake is a much more complicated process. When ever the Total Daily Energy Expidenture (TDEE) is spoken of, that involves the BMR, thermic effect of food, nonexercise activity thermogenesis (the energy expidenture of all activities sans sports), excess post-exercise consumption (EPOC, a measurably increased rate of oxygen intake following increased oxygen depletion), as well as exercise. the TDEE can increase or decrease by as much as 50 percent depending on caloric intake as well as the aforementioned variables.
  3. The third misconception people have is that we have conscious control over what we eat. We decide to eat when we are hungry (obviously). But numerous hormonal factors dictate the decision on when to eat or when to stop. We stop eating when we are full, which is hormonally mediated. Like breathing, the regulation of body fat is under automatic control. Just like we don’t have to remind ourselves to breath or remind our heart to beat, we don’t need to remind ourselves to eat. Thus, since hormones control both Calories In and Calories Out, obesity is a hormonal, not caloric disorder.
  4. The fourth misconception is that fat stores are essentially unregulated. However, every single system in the body is regulated. Height increases come from growth hormones; blood sugar is regulated by insulin, glucagon, and numerous other hormones; sexual maturation is regulated by testosterone and estrogen (as well as the hormone leptin which I will return to later); body temperature is mediated by a thyroid-stimulating hormone, among numerous other biologic factors. Though, we are told that the production of fat cells is unregulated. This is false. The best researched hormone on the storage of fat cells that we know of is the hormone leptin which was discovered in 1994. So if hormones dictate fat gain, obesity is a hormonal, not caloric disorder.
  5. And the final misconception is that a calorie is a calorie. This implies that the only important variable on weight gain is caloric intake and thus all foods can be reduced to how much caloric energy they have. But a calorie of potatoes doesn’t have the same effect on the body as a calorie of olive oil. The potatoes will increase the blood glucose level, provoking a response from the pancreas, which olive oil will not. Olive oil is immediately transported to the liver and has no chance to induce an insulin response and so there is no increase in insulin or glucose.

All five of these assumptions have been proven false.

[9/21/16 edit:]


Calories in/out implies that during extended caloric restriction no matter the type of kcal (fat, CHO, protein, alcohol, except when alcohol is ingested your body puts fat storage on hold until all alcohol is metabolized from the body. You can see how wiith chronic drinkers as they are obese a lot of the time, with there being a strong link between alcoholism and obesity as there are nunmerous pathways related with each other that lead to excessive eating as well as dependance on alcohol and other drugs) ingested, as long as caloric restriction is continued that weight (fat) loss will be achieved. CICO adherents say that “a calorie is a calorie”, but what’s funny with that statement is that is violates the Second Law of Thermodynamics. Naturally, to CICO adherents since “a calorie is a calorie”, kcal would be restricted from fat since it’s the most calorie dense macro (alcohol coming in second at 7 kcal per gram). By doing this, CHO will be increased, as is recommended by all of the ‘experts’. “Increase CHO, fat leads to CD!!!” This isn’t true, that’s another reason for cutting fat, the supposed ‘increased risk of heart disease”. However, when this occurs, insulin is spiked and when insulin is spiked the body doesn’t use the fat stores for energy it uses the glucose from the carbs.

Putting this all together, let’s say someone’s TDEE is 2000 kcal per day (for a 14k kcal per week average) and they reduce it to 1200 kcal and go on a LFHC diet like is commonly recommended. Insulin remains high and therefore fat cannot be tapped into. This is due to the CICO mantra (which violates the 2nd LoT) “a calorie is a calorie” that leads people to believe that all calories are ‘equal’ in terms of hormonal responses in the body. Let’s take a piece of bread and a teaspoon of olive oil. When you eat the piece of bread, insulin is spiked in response to the glucose from the carbohydrate. When you drink the olive oil, it’s immediately absorbed by the liver eliciting no insulin spike. Clearly, with a long term LFHC diet, this will consistently occur and the body will be continuously using CHO for energy and not the fat stores as insulin is continuously spiked in the body. Insulin either tells the body to store fat or not burn it for energy. Eventually, over time, this leads to insulin resistance (however, insulin resistance may precede obesity and diabetes) and more metabolic problems amongst a myriad of other variables.

As kcal is reduced to 1200 per day, the body is forced to match its metabolism to what your intaking as it can’t get energy from anywhere else since “a calorie is a calorie”. This happens during any calorie restricted diet and is why diets are doomed to fail. This same thing happened with The Biggest Loser contestants. Notice how The First Law of Thermodynamics isn’t broken? It’s irrelevant.

See how the mantra “a calorie is a calorie” violates the Second law of thermodynamics and fails because the CICO model doesn’t take insulin into the equation, which is a causal factor with obesity?


[End edit]

The correlation between weight gain and caloric consumption has recently been discovered. Ladabaum, et al (2014) examined trends in obesity from 1988 to 2010. The trends they observed were: obesity, abdominal obesity, physical activity and caloric consumption in US adults. They discovered that the obesity rate increased at .37 percent per year while caloric intake remained virtually the same.

The Law of Thermodynamics

The first law of thermodynamics states that energy can not be created nor destroyed in an isolated system (this is important). People often invoke the LoT to support the Calories In and Calories Out model. Dr. Jules Hirsch says in this NYT article:

There is an inflexible law of physics – energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content – reduce obesity – one must reduce calories taken in, or increase output by increasing activity, or both. This is true whether the calories come from pumpkins or peanuts or pâtés de foie gras.

To quote MD Jason Fung, author of The Obesity Code:

But thermodynamics, a law of physics, has minimal relevance to human biology for the simple reason that the human body is not an isolated system. Energy is constantly entering and leaving. In fact, the very act we are most concerned about-eating-puts energy into the system. Food energy is also excreted from the system in the form of stool Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight gain were mentioned even a single time. (Fung, 2016: 33)

We assume with the model of the calorie-balancing scale that fat gain or fat loss is unregulated, however, no system in the body is unregulated like that. Hormones tightly regulate all bodily functions. Body fat is no exception. The body actually has numerous ways in which to control body fat. Distribution of energy is the problem with fat accumulation. Too much energy is diverted to fat creation as opposed to body-heat production. Most of this is under automatic control, except exercise (which even then, there is a genetic basis for motivated exercise). We can’t decide whether or not to allocate calories to nail production or increase stroke volume. These metabolic processes are almost impossible to measure, and thus most assume that it’s relatively constant. Particularly, Calories In is not assumed to change in response to Calories Out. We assume these are independent variables. Reducing calories in only works if calories out remains constant. However what we find is that a sudden reduction of Calories In leads to a similar reduction of Calories Out and no weight is lost as the body balances its energy budget.

Starvation experiments

In 1919, a landmark study was carried out by Francis Benedict. The volunteers in the study agreed to a semi-starvation diet ranging from 1400 to 2100 kcal, approximately 30 percent of the subject’s bodyweight. The question was whether or not decreased caloric intake lead to a decrease in metabolism. The results were shocking.

The subjects experienced a 30 percent reduction in metabolism, with their initial caloric expidenture being 3000 kcal dropping to 1950 kcal. A 30 percent reduction in kcal resulted in a 30 percent decrease in metabolism. The First Law of Thermodynamics is not broken. 

Towards the end of WWII, Dr. Ancel Keys wanted to improve understanding of starvation and better help Europe after the War. With an average height of 5 feet 10 inches and an average weight of 153 pounds, these were normal men, which Dr. Keys wanted to see the effects of a semi-starvation diet on those with a normal weight. For the first three months of the study, they were given slightly over 3000 kcal. Though over the next six months, they were given 1570 kcal. Eventually, some men were decreased to less than 1000 kcal a day. They were given a diet of foods high in carbs and low to no animal meat as that was the condition in Europe at the time. Moreover, they also had to walk 22 miles a week as exercise. Again, the results were shocking.

Dr. Keys showed that they had a 40 percent decrease in metabolic rate. The body decreased its metabolism to match the amount of calories consumed. They showed a 20 percent decrease in strength, a significant decrease in heart rate (55 to 35 beats per minute), stroke volume decreased by 20 percent, body temperature dropped to 95.8 degrees Fahrenheit (which makes sense since less caloric consumption means less energy for the body to convert into heat), physical endurance dropped by half, blood pressure dropped, they became tired and dizzy and finally their hair and nails grew extremely brittle. They couldn’t stop thinking about food. Some of them wrote cookbooks, others dreamed about food. They became obsessed with eating. All of these causes go directly back to decreased caloric consumption as the amount of heat produced by the body decreased due to an increase in caloric consumption. In sum, the body responds to a decrease in caloric intake by dropping metabolism.

Metabolic slow down

Recent data has come out on decreased energy expidenture due to dieting from contestants on the show The Biggest Loser. The contestants were followed for six years after the show ended. Fothergill, et al (2016) showed that after six years, most contestants gained back the original weight they lost, but their metabolism was still decreased by 600 kcal.

The mean metabolic adaptation had increased to 500 kcal per day, which explains why RMR remained 700 kcal per day below the baseline level despite a 90 lb body weight regain. The researchers even said that this large metabolic difference couldn’t be explained by the different calirometer used at the end of the six year period. 

Substantial weight loss induces biological changes that promote weight gain.

Moreover, after a period of dieting, your brain panics and thinks it’s starving. During this time, the the production of the hunger hormone ghrelin increases. Levels of this hormone increase right before a meal and steadily decrease after. This is one of the many hormones that control when we’re hungry and this is one of the many reasons why diets fail and do not work long term.

Our bodies have homeostatic mechanisms that cause us to gain back or lose weight whenever caloric consumption is increased or decreased. The main cause is the body weight set-point which I will cover in a future article.

And a quote from Sandra Aamodt’s book “Why Diets Make Us Fat“:

“Leibel finds that metabolic suppression persists in dieters who have kept weight off for one to six years, so he scoffs at claims that the successful weight loss story disproves his ideas. “If you talk to people who’ve done it – not the studies, but people who actually manage to lose weight and keep it off – they’ll tell you what I’m telling you,” he says: that the only way to achieve this goal was to allow themselves to be hungry all the time while increasing their physical activity substantially. Indeed, his point is supported by data on the eating and exercise habits of people listed in the National Weight Control Registry, who have lost at least thirty pounds and kept it off for one year. A calorie calculator says that Dennis Asbury should have needed 2,100 calories to maintain his weight at 150 pounds, but instead he found that he needed to eat 400 to 500 calories less than that. Such metabolic suppression is the difference between being within the defended range and being below it. Many people blame others for eating too much or exercising too little, assuming incorrectly that both are under voluntary control, but it’s much harder to justify holding people responsible for diet-induced changes in the way the body burns energy.” (Aamodt, 2016, pg. 68)

Conclusion

The fact of the matter is, kcal in and out is completely misunderstood due to a non-understanding of human metabolism. As we decrease our caloric intake, our body adjusts its metabolism down to match the amount of kcal we are currently consuming. This is why Calories In and Calories Out does not tell the whole story. Our body constantly fights to maintain what is normal, its set-point. When thrown out of what the brain considers ‘normal’ the brain through the hypothalamus does whatever it can to get us back to its set-point. Thus, obesity is a hormonal, not a caloric disorder.

The Evolution of Violence: A Look at Infanticide and Rape

1700 words

The pioneer of criminology was a man named Cesare Lombroso, an Italian Jew (a leftover remnant from the Roman days), who had two central theories: 1) that criminal behavior originated in the brain and 2) criminals were an evolutionary throwback, a more primitive type of human. Lombroso felt strongly about the rehabilitation of criminals, at the same time believing in the death penalty for “born criminals”. Though, with new advances in criminology and new insights to the brain, it looks like Lombroso was right with his theory of born criminals.

Why are you 100 times more likely to be killed on your birthday? Why are children 50 times more likely to be murdered by their stepfather than biological one? Why do some parents kill their children? Finally, why do men rape not only strangers, but also rape their wives? All of these questions can be answered with evolutionary psychology.

Evolutionarily speaking, antisocial and violent behavior wasn’t a random occurrence. When these actions occurred tens of thousands of years ago, they were because resources were being acquired from these actions. Thus, we can see some modern criminal acts as resource competition. The more resources one has, the easier it is for him to pass his genes on to the next generation (a big driver for violence). In turn, women are more attracted to males who can provide resources and protection (those who were more antisocial and violent). This also explains these prison romances, in which women get into romances with murderous criminals since they are attracted to the violence (protection) and resources (theft).

The mugger who robs for a small amount of money is increasing his odds of resource acquisition. Drive-by shootings in violent neighborhoods increase the status of those who survive the shootout. What looks like a simple brawl over nothing may be one attempting to increase social dominance. All of these actions have evolutionary causes. What drive these actions are our ‘Selfish Genes’.

The more successful genes are more ruthlessly selfish in their struggle for survival, which then drives individual behavior. The individual behaviors that occur due to our selfish genes may be antisocial and violent in nature, which in our modern society is frowned upon. The name of the game is ‘fitness’. The amount of children you can have in your time allotted on Earth. This is all that matters to our genes. Even those accomplishments you think of, such as completing college or attaining mass amounts of capital all fall back to fitness. With that, increasing your fitness and ensuring your genetic lineage passes on to the next generation is greatly enhanced.

Biological fitness can be enhanced in one of two ways. You can have as many children as possible, giving little parental care to each, or you can have fewer children but show more attention and care to them. This is known as r/K Selection Theory. Rushton’s r/K Selection Theory compliments Dawkins Selfish Gene theory in that the r-strategist is maximizing his fitness by having as many children as possible, while the K-strategist increases his fitness by having fewer children in comparison to the r-strategist but showing more parental attention. There are, however, instances in which humans kill children, whether it’s a mother killing a newborn baby or a stepfather killing a child. What are the reasons for this?

Killing Kids

The risk of being a homicide victim in the first year of life is highest in the first year of life. Why? Canadian Psychologists Daly and Wilson demonstrated in inverse relationship between degree of genetic relatedness and being a victim of homicide. Daly and Wilson discovered that the offender and victim are genetically related in only 1.8 percent of all homicides. Therefore, 98 percent of all murders are killings of people who do not share the killer’s genes.

Many stories have been told about ‘wicked stepparents’ in numerous myths and fairytales. But, as we know, a lot of stories have some basis in reality. Children of stepparents are 40 times more likely to suffer abuse at the hands of a stepparent. People who are living together who are unrelated to one another are more likely to kill one another. Even adoptions are more successful when the adopting parents view the child as genetically similar to themselves.

In this study carried out by Maillart, et al, it was discovered that for mothers, the average age of offense for filicide was 29.5 years for the mother and 3.5 years for the babe. Bourget, Grace, and Whitehurst, 2007 showed that a risk factor for infanticide was a second child born to a mother under 20-years of age. The reasoning for this is simple: at a younger age the mother is more fertile, and thus, more attractive to potential mates. The older the woman is the more sense it makes to hold on to the genetic investment since it’s harder to make up for the genetic loss late in her reproductive life.

Genetic relatedness, fitness, and parental investment show, in part, why filicides and infanticides occur.

Raping Your Wife

There are evolutionary reasons for rape as well. The rape of a non-relative can be looked at as the ultimate form of ‘cheating’ in this selfish game of life. One who rapes doesn’t have to acquire resources in order to attract a mate, he can just go and ‘take what he wants’ and attempt to spread his genes to the next generation through non-consensual sex. It’s known that rape victims have a higher chance of getting pregnant, with 7.98 percent of rape victims becoming pregnant. (News article) One explanation for this is that the rapist may be able to possibly detect how fertile a woman is. Moreover, rapists are more likely to rape fertile women rather than infertile women.

One rapist that author of the book The Anatomy of Violence, Adrian Raine interviewed said that he specifically chose ugly women to rape (Raine, 2013: 28). He says that he’s giving ugly women ‘what they want’, which is sex. There is a belief that women actually enjoy sex, and even orgasm during the rape, even though they strongly resist and fight back during the attack. Reports of orgasm during rape are around 5 to 6 percent (Raine, 2013: 29), but the true number may be higher since most women are embarrassed to say that they orgasmed during a rape.

Men, as we all know, are more likely to engage in no-strings-attached sex more than women. This is due to the ‘burden’ of sex: children. Women are more likely to carefully select a partner who has numerous resources and the ability to protect the family. Men don’t have the burden of sticking around to raise the child.

Men are more likely to find a sexual relationship more upsetting in comparison to women who are more likely to find an emotional infidelity as more distressing. This data on Americans still held true for South Korea, Germany, Japan, and the Netherlands. Men are better than women at detecting infidelity, and are more likely to suspect cheating in their spouses (Raine, 2013: 32). Unconscious reason being, a man doesn’t want to raise a child who is not genetically similar to themselves.

But this begs another question: why would a man rape his wife? One reason is that when a man discovers his spouse has been unfaithful, he would want to inseminate her as quickly as possible.

There has never in the history of humankind been one example of women banding together to wage war on another society to gain territory, resources or power. Think about it. It is always men. There are about nine male murderers for every one female murderer. When it comes to same-sex homicides, data from twenty studies show that 97 percent of the perpetrators are male. Men are murderers. The simple evolutionary reason is that women are worth fighting for. (Raine, 2013: 32)

A feminist may look at this stat and say “MEN cause all of the violence, MEN hurt women” and attempt to use this data as ‘proof’ that men are violent. Yes, we men are violent, and there is an evolutionary basis for it. However, what feminists who push the ‘all sexes are equal’ card don’t know, is that when they say ‘men are more likely to be murderers’ (which is true), they are actively accepting biological differences between men and women. Most of these differences in crime come down to testosterone. I would also assume that men would be more likely to have the ‘warrior gene’, otherwise known as the MAOA-L gene, which ups the propensity for violence.

The sociobiological model suggests that poorer people kill due to lack of resources. And one reason that men are way more likely to be victims of homicide is because men are in competition with other men for resources.

Going back to the violence on stepchildren that I alluded to earlier, aggression towards stepchildren can be seen as a strategic way of motivating unwanted, genetically dissimilar others out of the home and not take up precious resources for the next generation bred by the stepfather (Raine, 2013: 34).

Women also have a way to increase their fitness, which a brunt of it is through sexual selection. Women are known to be ‘worriers’. That is, they rate dangerous and aggressive acts higher than men. Women are also more fearful of bodily injury and more likely to develop phobias of animals. In these situations, women are protecting themselves and their unborn (or born) children by maximizing their chances for survival by being more fearful of things. This can help explain why women are less physically violent than men and why those murder stats are so heavily skewed towards men: biology.

Women compete for their genetic interests with beauty and childbearing. The more beautiful the woman, the better resources a woman can acquire from a male and this will ensure a healthy life for the offspring.

Evolutionary psychology can help explain the differences in murder between men and women. It can also explain why young mothers kill their children and why stepparents are so abusive to, and are more likely to murder stepchildren. Of course, a social context is involved but we need to look at evolutionary causes for what we think we may be able to simply explain. Because it’s, more often than not, more complex than we could imagine. And that complexity is our Selfish Genes doing anything possible to reproduce more copies of itself through its vehicle: the human body.