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Our View of ‘Intelligence’ Needs to Change
900 words
What is intelligence? How would we define it? Would intelligence be reacting to what occurs in the immediate environment; having the ability to have behavioral plasticity or even communicating with others? Amazingly, bacteria have been found to do both things noted above: They have been found to be able to react to their environment, i.e., have the ability for plastic behavior and they have even been shown to communicate with one another. Hell, even something as simple as a slime mold has been found to navigate a maze to find food. Is that not intelligence?
Ken Richardson, author of the book Genes, Brains, and Human Potential: The Science and Ideology Behind Intelligence writes:
Living things, then, need to be good at registering those statistical patterns across everyday experience and then use them to shape the best response, including (in the cell) what genes to recruit for desired products. This is what intelligence is, and it’s origins coincide with the origins of life itself, and life is intelligence. (Richardson, 2017: 115)
In multicelluar systems, of course, the cells are not just responding to one another, but also collectively to the changing environment outside. That requires an intelligent physiology, as described in chapter 5. However, it is still the statistical structure of the changes that matters and that forms the basis of a living intelligence. Even at this level, closest to the genes, then, the environment is emphatically not a loose collection of independent factors to which the cells respond, in stimulus-response fashion, under gene control. This reality makes the additive statistical models of the behavioral geneticist quite unrealistic. (Richardson, 2017: 120)
Currently, our view of intelligence has an anthropometric lean. But, as I’ve been saying for months now, why should we view humans as a sort of ‘apex’ to evolution? Why should we be the measuring stick? If you really think about it to put us—our brains—at the top of a rank order as ‘the best’ and not recognize what other, smaller supposedly ‘archaic’ forms of life can do, then maybe it’s best to take off our human-centric glasses and look at the whole of the animal kingdom as intelligent—including bacteria, as they show the basic things necessary for what we would call intelligence, i.e., behavioral plasticity.
In this paper published just two months ago, the authors write:
Bacteria are far more intelligent than we can think of. They adopt different survival strategies to make their life comfortable. Researches on bacterial communication to date suggest that bacteria can communicate with each other using chemical signaling molecules as well as using ion channel mediated electrical signaling. (Majumdar and Pal, 2017)
Furthermore, looking at definitions of the term ‘behavior’ from ethology, we can see that bacteria exhibit these behaviors that we have deemed ‘human’ or ‘human-like’:
- “Externally visible activity of an animal, in which a coordinated pattern of sensory, motor and associated neural activity responds to changing external or internal conditions” (Beck et al. 1981)
- “A response to external and internal stimuli, following integration of sensory, neural, endocrine, and effector components. Behavior has a genetic basis, hence is subject to natural selection, and it commonly can be modified through experience” (Starr and Taggart 1992)
- “Observable activity of an organism; anything an organism does that involves action and/or response to stimulation” (Wallace et al. 1991)
- “What an animal does” (Raven and Johnson 1989)
Bacteria have been found to fit all of the criteria mentioned above. If organisms can react to how the environment changes, then that organism has—at least a semblance—of intelligence. Bacteria have also been found to be able to learn and they also have memories, so if this is true (and it is), then bacteria are intelligent.
Finally, Westerhoff et al (2014) write that leaving out the terms ‘human’ and our brains as measuring sticks for what is intelligent, that “all forms of life – from microbes to humans – exhibit some or all characteristics consistent with “intelligence.” For people with anthropocentric views of evolution, however, this is a hard pill to swallow. If the data says that bacteria have evidence of ‘cognition’ and an ability to react to outside environmental cues then bacteria have a semblance of intelligence. There is no denying it.
We clearly need to look at intelligence in a different way—one that’s free of any anthropocentric bias—-and if we do, we would recognize numerous species as intelligent that we would never have thought of before since we view ourselves as some sort of ‘apex’ of evolution, that we are supreme on this earth, when the bacteria—the modal bacter—reign supreme and will continue to remain supreme until the Sun explodes. So if bacteria show the ability to communicate with one another and the ability to change their behavior when their environment changes, i.e., that they learn and have ‘memories’ of past events, then maybe it’s time for us to change from our human-centric view of intelligence (which makes a ton of sense; viewing us as an ‘apex’ of evolution makes no sense and doesn’t allow us to appreciate the wide range of variation on earth).
As Gould wrote in Full House, looking at only the right tail we would believe that some sort of ‘progress’ reigns supreme, but looking at the whole sum of variation, we can see that the bacteria are the mode of all life, have been the mode of all life and will remain the mode of all life until the Sun explodes and all life forever perishes from Earth.
Testosterone and Aggressive Behavior
1200 words
Testosterone gets a bad rep. People assume that if one has higher testosterone than average, that they will be a savage, bloodthirsty beast with an insatiable thirst for blood. This, however, is not the case. I’ve documented how testosterone is vital for male functioning, and how higher levels don’t lead to maladies such as prostate cancer. Testosterone is feared for no reason at all. The reason that people are scared of it is that of the anecdotal reports that individual A had higher testosterone when he committed crime B so, therefore, anyone who commits a crime has higher testosterone and that is the ultimate—not proximate—cause of crime. This is erroneous. There is a positive—albeit extremely low—correlation between physical aggression and violence at .14. That’s it. Furthermore, most of these claims of higher levels of testosterone causing violence is extrapolated from animal studies to humans.
Testosterone has been shown to lead to violent and aggressive behavior, largely only in animal studies (Archer, 1991; Book et al, 2001). For years, the relationship between the two variables was thought to be causal, i.e., high levels of testosterone cause violent crimes, which has been called into question over recent years. This is due to how the environment can raise testosterone levels. I have documented how these environmental factors can raise testosterone—and after these events, testosterone stays elevated.
Largely, animal studies are used to infer that high levels of testosterone in and of themselves lead to higher rates of aggression and therefore crime. However, two important meta-analyses show this is not necessarily the case (Archer, 1991; Book et al, 2001). Book et al, 2001 showed that two variables were important in seeing the relationship between aggression and crime—the time of day that the assay was taken and the age of the participant. This effect was seen to be largest in, not unexpectedly, males aged 13-20 (Book et al, 2001: 594). So since age confounds the relationship between aggression and testosterone in males, that is a variable that must also be controlled for (which, in the meta-analyses and other papers I cite on black and white testosterone is controlled for).
More interestingly, Book et al (2001) showed that the nature of the measure of aggression (self-reported or behavioral) did not have any effect on the relationship between testosterone and aggression. Since there is no difference between the two measures, then a pencil-and-paper test is a good enough index of measure of aggression, comparable to observing the behavior of the individual studied.
Archer (1991) also showed the same low—but positive—correlations between aggression and testosterone. Of course, as I’ve extensively documented since there is a positive relationship between the two variables does not necessarily mean that high-testosterone men commit more crime—since the outcome of certain situations can increase and decrease testosterone, no causal factors have been detangled. Book et al (2001) confirmed Archer’s (1991) finding that the correlation between violent and aggressive behavior was positive and low at .14.
Valois et al (2017) showed there was a relationship between emotional self-efficacy (ESE) and aggressive and violent behaviors in a statewide sample of high school children in South Carolina (n=3,386). Their results suggested that there was a relationship between carrying a weapon to school within the past 30 days along with being injured with a club, knife or gun in the past 12 months was significantly associated with ESE for specific race and sex groups.
Black girls who reported a low ESE reported carrying a weapon to school 30 days prior to the survey were 3.22 times more than black girls with a high ESE who did not report carrying a weapon to school within the past 30 days prior to the questionnaire. For black boys with low ESE, they were 3.07 times more likely to carry a weapon to school within the past 30 days in comparison to black boys with high ESE who did not carry a weapon to school in the past 30 days. White girls who reported low ESE had the highest chance of bringing a weapon to school in comparison to white girls with low ESE—they were 5.87 times more likely to carry a weapon to school 30 days prior to the survey. Finally, white boys with low ESE were slightly more than 2 times more likely than white boys with high ESE to carry a weapon to school 30 days prior to the survey.
Low ESE in white and black girls is associated with carrying a weapon to school, whereas low ESE for white and black boys is associated with being threatened. Further, their results suggested that carrying a weapon to school was associated with low ESE in black and white girls suggesting that low ESE is both situation-specific and specific to the female sex. The mediator between these things is low ESE—it is different for both black boys and black girls, and when it occurs different courses of action are taken, whether it’s through bringing a weapon to school or being threatened. What this tells me is that black and white boys with low ESE are more likely to be threatened because they are perceived to be more meek, while black and white girls with low ESE that get provoked at school are more likely to bring weapons. So it seems that girls bring weapons when provoked and boys fight.
The two meta-analyses reviewed above show that there is a low positive (.14) correlation between testosterone and aggression (Archer, 1991; Book et al, 2001). Thusly, high levels of testosterone on their own are not sufficient enough to explain high levels of aggression/violence. Further, there are race- and sex-specific differences when one is threatened at high school with black and white boys being more likely to report being threatened more (which implies a higher rate of physical fighting) while black and white girls when threatened brought weapons to school. These race- and sex-specific differences in the course of action taken when they are physically threatened needs to be looked into more.
I’d like to see the difference in testosterone levels for a matched sample of black and white boys from two neighboring districts with different murder rates as a proxy for the amount of violence in the area. I’d bet that the places with a higher murder rate would have children 1) report more violence and instances of bringing weapons to school and 2) report more harm from these encounters—especially if they have low ESE as seen in Valois (2017) and 3) the children in the high schools along with the residents of the area would have higher testosterone than the place with less violence. I would expect these differences to be magnified in the direction of Valois (2017) in that areas with higher murder rates would have black and white girls report bringing weapons to school when threatened whereas black and white boys would report more physical violence.
High testosterone itself is not sufficient enough to explain violence as the correlation is extremely low at .14. Testosterone levels fluctuate depending on the time of day (Brambilla et al, 2009; Long, Nguyen, and Stevermer, 2015) to the time of year (Stanton, Mullette-Gillman, and Huettel, 2011; Demur, Uslu, and Arslun, 2016). How the genders/races react differently when threatened in adolescence is interesting and deserves further study.
You Are what you Eat, Including Brains
by Scott Jameson
850 words
I’ve been thinking about Omega 3 fatty acids (N3s) recently. We’re clearly adapted to getting more of them than we’re actually getting.
Children whose mothers took fish oil (chock full of N3s EPA and DHA) during pregnancy have higher coordination, and they are smarter, although that difference may not persist later in development. RaceRealist has written about N3s and PISA math scores before.
Here’s a paper summarizing many of the known benefits of fish oil supplementation. Goes over some of the aforementioned results regarding kids, and also shows random improvements such as helping people with Alzheimer’s maintain weight.
A lack of N3s is associated with depression, coronary artery disease, maybe even autism. N3s are known to lessen autism symptoms. This is probably an immune thing. Sulforaphane, an anti-inflammatory agent, is known to reduce autism symptoms, and other research has elucidated the relationship between N3s and the immune system.
This is delicious fodder for a post of its own. There’s a mass of papers about the relationship between autism and the immune system; N3s being neuroprotective and correlating negatively with likelihood of autism/severity of autism symptoms vindicates the idea that autism happens when your immune system cooks your brain (neuroinflammation). You would expect males to be whacked harder by this because they’re not good at producing the important N3 docosahexaenoic acid (DHA). Thus, males ought to have higher autism rates- and they do.
Anyway, here’s what I’m getting at. Either N3s are a counter-intuitive miracle drug, or they’re just an important nutrient of which many of us do not get enough. The latter, I should think! The lemonade that can and will be made from these lemons is that widespread N3 deficiency gives us an opportunity to understand one of the ways that a human brain can get messed up. But we still want to fix the problem- more on that in my next post.
Our ancestors probably got more N3s than we do. They’ve been estimated to, anyway. (Second study mentioning our ancestors’ higher N3 intake.) If they didn’t, they might’ve been selected for better processing of alpha linoleic acid into eicosapentaenoic acid and subsequently docosahexaenoic acid, which real-life humans aren’t great at. As it stands, humans need either a whole bunch of excess ALA to convert to EPA and DHA, or we could have EPA and DHA straight. The excess ALA idea probably isn’t something you can rely on for your N3 needs, but certainly ALAs are better than nothing.
Seeds would’ve been a part of the diet back in the Paleolithic. Flax, an example of a seed rich in ALA, was known to humans quite a darned while ago, so seeds might have been a source of these critical nutrients. It’s worth noting that the first paleolithic diet estimation study linked in the previous paragraph pegs hunter gatherers as getting way more ALA than modern folks do.
Of course, many populations would’ve lived near oceans or at least rivers and lakes, where they could’ve gotten N3s from fish and seafood.
Some of it must have come from insects, themselves actually having a decent amount of N3s.
I’ve got an even weirder guess, though: bioaccumulation in land animal tissue. This possibility must have been important for peoples like the Botai culture with extremely narrow (Tarpan-based) diets, which likely didn’t include enough seeds, insects, and/or seafood. Animals can’t produce N3s of their own, but they eat ALA, convert it into EPA and DHA, and send a lot of it up to the brain, where it’s needed, with the result being that the brain has a lot more and higher quality N3s than any of the plants from which the N3s were derived.
Grog the caveman could’ve gotten a bunch of N3s from his favorite treat: scrambled auroch brains. Many of his progeny carry the practice into the present day, to the disgust of other living humans. Being that humans and our relatives are disgusting in general, Neanderthals occasionally even ate each other’s brains, and according to CNN, they’re still at it!
Nonhuman brains had to be the more popular option, then as now; mentioning the whole cannibalism thing is a bit of a non sequitur I shoved in for sheer entertainment value. But I suspect that there are several reasons we Westerners don’t get enough N3s: we don’t eat brains anymore, we don’t eat bugs anymore, and we don’t get as many ALA-rich plant oils as we used to. Perhaps we’re not getting enough fish, or perhaps the fish we’re getting are less likely to be fatty (e.g. salmonids, tuna, schooling fish) and more likely to be lean (cod, pollock).
Somehow or other we ought to get N3s back in our diet. Could save some kids from autism or, failing that, improve their prognosis. Again, it could increase our math scores, too, particularly in women. Closing part of the gap with other nations and between our sexes- two birds with one stone for our educators- and a boon for our engineering departments as well. Which is a boon for everyone.
The stakes are high. Who can save us from our collective state of starved brains? I’ll post my ideas soon.
Race, Testosterone, and Prostate Cancer
1900 words
I have explicitly shown how the ‘black men have more T’ canard is false. I have provided sufficient evidence for this claim. People claim to be unbiased—like PumpkinPerson—and say they’re only ‘looking for the truth’. However, it’s clear that in all of my conversations with him on the matter, he’s reaching for anything that affirms his worldview when he is shown evidence to the contrary of his beliefs (Nyhan and Reifler, 2012). It’s so very easy to notice this. I will provide yet more robust data on the black/white testosterone ‘gap’ while also critiquing some other studies that didn’t control for some pretty important variables. The gist is: after controlling for the most important variables, (waist circumference, BMI) the ‘testosterone difference’ all but disappears—and I don’t think people will argue for .0068 ng/ml higher testosterone cause things like prostate cancer and higher rates of crime.
Gapstur et al (2002) studied 5,115 individuals from aged 18-30 who completed baseline examinations at one of four locations from 1985-86: Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California. Then, 4 follow-ups were completed (Year 2: 1987-88; year 5: 1990-91; year 7: 1992-93; and year 10: 1995-96).
The number of blacks who completed the baseline information was 1157 whereas for whites it was 1171. They measured waist circumference (WC) at the minimal abdominal girth. Whether or not one took medication was self-reported, so Gapstur et al (2002) separated medications into two categories: regulation or interfering with binding likely, or interfering with binding unlikely/impossible.
Now, before I discuss the results of Gapstur et al (2002) I must talk about why they controlled for BMI (body mass index) and WC along with age. Since the obesity rate differs by race/ethnicity, along with obesity frequently changing with age, all three of the variables need to be controlled for to get a clearer picture of what circulating testosterone looks like—on average—between blacks and whites. White men are slightly more likely than black men to be obese/overweight in America (being African-American seems to be a protector against obesity; African American men with more African ancestry are less likely to be obese), however the sample used by Gapstur et al (2002) had blacks who had a higher WC and BMI than whites.
At year 2, there was no significant difference in total serum testosterone between the races with or without adjustment for age, BMI and WC. The only part in this analysis that blacks had higher testosterone levels than whites was at year ten, with black ‘enjoying’ .0063 ng/ml higher levels than whites. Furthermore, there was no significant difference in testosterone between blacks and whites after adjustment for age. Only adjusting for BMI, blacks had substantially higher levels of testosterone (.21 ng/ml) however after including WC and the changes in WC between blacks and whites (blacks had a greater change over the study) this difference all but disappeared. The age-associated changes in testosterone between blacks and whites were similar after adjusting for waist circumference and BMI. Also, after adjusting for the relevant confounds, free testosterone did not differ between blacks and whites.
Measures of body size (i.e., BMI and WC) must be controlled for when comparing race/ethny since levels of obesity vary amongst them as well as obesity constantly changing with age. Furthermore, testosterone increased for both groups between the ages of 20-21 to 22-23 (blacks had a higher T level by .7 ng/ml at age 20-21), with the two groups diverging at age 22-23 with blacks having higher levels of total testosterone by .1 ng/ml.
The average ages for the cohort were 28.4 and 28.8 for blacks and whites respectfully. Thus, blacks (theoretically) had a slight advantage due to the age confound, which had to be controlled for. The unadjusted mean total testosterone, SHGB, and free testosterone were not statistically significant at any point in the study except at year 10 where blacks had slightly higher levels at 5.8 ng/ml compared to whites’ 5.69 ng/ml. The difference in year 2 (when testosterone levels raised for both groups) was a difference of 5.8 and 5.75 for blacks and whites respectfully. Free testosterone did not differ at all from years 2, 7, and 10 (.17 compared to .17 in year 2; .16 to .15 in year 7; and .16 to .15 in year 10; blacks and whites respectfully).
Levels of testosterone were also found to be lower in 12-13-year-old blacks compared to whites (Lopez et al, 2013). In this study, Mexican Americans had higher T levels, while after adjustments for confounds, blacks and whites did not differ. They conclude that testosterone levels were not higher in black compared to white adolescents. Black men have higher levels of estradiol than white men, not testosterone (Roerrmann et al, 2007; Lopez et al, 2013). These studies are done to see the relationship between PCa (prostate cancer) and certain hormones. These and other studies have shown that the black-white difference isn’t large (Richard et al, 1992; Roerrmann et al, 2007; Lopez et al, 2013; Richard et al, 2014) and that prostate cancer is not caused by abnormally high testosterone levels (Stattin et al, 2003; Michaud, Billups, and Partins, 2015).
Ross et al (1986) did not have a measure of central adiposity (WC), thusly the results were confounded. Further, the other study Rushton cited in Race, Evolution, and Behavior is and Nyborg (1992) on discharged army veterans stating a difference of 3 percent, Ellis and Nyborg did not control for WC nor BMI. As seen in the Gapstur et al (2002) study, WC is an extremely important variable to control for as decreases in testosterone are high when central adiposity is high (Wang et al, 2011) so if we are trying to compare two ethnies on one variable such as testosterone, all of the above variables MUST be controlled for, and if they are not then they can be safely disregarded.
The non-inclusion of a measure of WC is the most likely cause of the different results found in Gapstur et al (2002). If you don’t control for WC, then you cannot get an actual and reliable testosterone reading since the results will be confounded. Anyone who says otherwise that the aforementioned variables do not need to be controlled for literally have no idea what they’re talking about.
Lastly, a few more things must be addressed. In PumpkinPerson’s most recent article “Racial differences in testosterone“, he seems to now disavow testosterone as a useful measure since it can fluctuate due to winning sports games, to marriage, to anticipating confrontation, to being in a relationship, to honor culture. Now his thing is exposure to androgens (testosterone) in the womb. Supposedly, blacks have the lowest digit ratio, and low digit ratios signify higher levels of testosterone in vitro (Manning et al, 2004). However, the relationship is far from proven (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010) with these results, leaning towards no. Koheler, Simmons, and Rhodes (2004) failed to find any significant correlation between 2d/4d ratio and traits mediated by testosterone. So this is another claim that’s been put to bed as well.
There is a lot of bullshit to sift through out there; some things may seem simple at face value, but if you dig into it, it’s much more likely to be more complex than what it looks to be on the surface. This one singular variable (testosterone) is one of them. It does not differ between the races; exposure to androgens in the womb doesn’t affect digit ratio; high testosterone does not cause prostate cancer, but low testosterone does (Morgentaler, Brunning, and DeWolf, 1996) ; you can literally inject exogenous testosterone into a man with PCa and not effect this malady (Eisenberg, 2015; Boyle et al, 2016)
I hope this is the last time I have to say this: testosterone does not differ between blacks and whites. Testosterone is not the cause of differences in mortality rate in regards to PCa. (Diet is the much more likely factor) People still regurgitate Rushton’s bullshit from REB; Ross et al (1986) still gets cited to this day, when there are much more robust studies and samples that controlled for the relevant confounds that Ross et al (1986) did not control for. This is why that study is garbage and should not be looked at when assessing testosterone differences between the races. Much larger and robust samples show that there is no testosterone difference when the WC is controlled for.
Testosterone is not higher in black Americans; the data shows either an extremely negligible difference or no difference, not the huge 13 and 21 percent difference in free and total testosterone in black Americans in Ross et al (1986).
For the last time, and say it with me: testosterone does NOT differ by race, 2d:4d ratio is NOT influenced by androgens in vitro, and testosterone does NOT influence PCa rates. Testosterone is an extremely important hormone for vital functioning, so whoever believes the myths of the high testosterone savage and LIKES having low testosterone, have fun with a slew of maladies later in life.
References
Boyle, P., Koechlin, A., Bota, M., Donofrio, A., Zaridze, D. G., Perrin, P., . . . Boniol, M. (2016). Endogenous and exogenous testosterone and the risk of prostate cancer and increased prostate-specific antigen (PSA) level: a meta-analysis. BJU International,118(5), 731-741. doi:10.1111/bju.13417
Dobs, A., & Morgentaler, A. (2008). Does Testosterone Therapy Increase the Risk of Prostate Cancer? Endocrine Practice,14(7), 904-911. doi:10.4158/ep.14.7.904
Eisenberg, M. L. (2015). Testosterone Replacement Therapy and Prostate Cancer Incidence. The World Journal of Men’s Health, 33(3), 125–129. http://doi.org/10.5534/wjmh.2015.33.3.125
Gapstur, S. M., Kopp, P., Gann, P. H., Chiu, B. C., Colangelo, L. A., & Liu, K. (2006). Changes in BMI modulate age-associated changes in sex hormone binding globulin and total testosterone, but not bioavailable testosterone in young adult men: the CARDIA Male Hormone Study. International Journal of Obesity. doi:10.1038/sj.ijo.0803465
Koehler, N., Simmons, L. W., & Rhodes, G. (2004). How well does second-to-fourth-digit ratio in hands correlate with other indications of masculinity in males? Proceedings of the Royal Society B: Biological Sciences,271(Suppl_5). doi:10.1098/rsbl.2004.0163
Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
Medland, S. E., Zayats, T., Glaser, B., Nyholt, D. R., Gordon, S. D., Wright, M. J., . . . Evans, D. M. (2010). A Variant in LIN28B Is Associated with 2D:4D Finger-Length Ratio, a Putative Retrospective Biomarker of Prenatal Testosterone Exposure. The American Journal of Human Genetics,86(4), 519-525. doi:10.1016/j.ajhg.2010.02.017
Manning, J., Stewart, A., Bundred, P., & Trivers, R. (2004). Sex and ethnic differences in 2nd to 4th digit ratio of children. Early Human Development,80(2), 161-168. doi:10.1016/j.earlhumdev.2004.06.004
Morgentaler, A., Brunning, C. O., 3rd, & DeWolf, W. C. (1996). Occult Prostate Cancer in Men With Low Serum Testosterone Levels. JAMA: The Journal of the American Medical Association,276(23), 1904. doi:10.1001/jama.1996.03540230054035
Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions. Political Behavior,32(2), 303-330. doi:10.1007/s11109-010-9112-2
Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x
Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028
Wang, C., Jackson, G., Jones, T. H., Matsumoto, A. M., Nehra, A., Perelman, M. A., … Cunningham, G. (2011). Low Testosterone Associated With Obesity and the Metabolic Syndrome Contributes to Sexual Dysfunction and Cardiovascular Disease Risk in Men With Type 2 Diabetes. Diabetes Care, 34(7), 1669–1675. http://doi.org/10.2337/dc10-2339
Yan RHY, Malisch JL, Hannon RM, Hurd PL, Garland T Jr (2008) Selective Breeding for a Behavioral Trait Changes Digit Ratio. PLoS ONE 3(9): e3216. https://doi.org/10.1371/journal.pone.0003216
Dinosaurs, Brains, and ‘Progressive’ Evolution: Part II
1700 words
In part I, I showed how Dale Russel’s contention that the troodon would have evolved into a bipedal ‘dinosauroid’ with human locomotion and a human-sized brain was pure fantasy. I ordered the book of his that Rushton cited in his book Race, Evolution, and Behavior and I finally received it last week. When I read the relevant parts, I yawned because it’s the same old stuff that I’ve covered here on this blog numerous times. Since literally the only relevant part in the book about the troodon is the final 7 pages, that’s what I will cover today—along with a few more lines of evidence that large brains lie outside reptilian design (Gould, 1989).
First off, all of Rushton’s contentions in the final pages of his book (Rushton, 1997) need to be rebutted. Rushton (1997: 294) writes that dinosaur brains were ‘progressing’ in size for 140 million years, but neither of Russel’s writings that I have (Russel 1983; 1989) have the statement in them.
In the book Up From Dragons: The Evolution of Human Intelligence neuroscientist, evolutionary psychologist John Skoyles and science writer Dorian Sagan—the son of Carl Sagan—speak briefly about reptilian intelligence and why they wouldn’t have reached our levels of intellect:
But cold-bloodedness is a dead-end for the great story of this book—the evolution of intelligence. Certainly reptiles could evolve huge sizes, as they did over vast sweeps of Earth as dinosaurs. But they never could have evolved our quick-witted and smart brains. Being tied to the sun restricts their behavior: Instead of being free and active, searching and understanding the world, they spend too much time avoiding getting too hot or too cold. (Skoyles and Sagan, 2002: 12)
Hopson (1977: 443) writes:
I would argue, as does Feduccia (44), that the mammalian/avian levels of activity claimed by Bakker for dinosaurs should be correlated with a great increase in motor and sensory control and this should be reflected in increased brain size. Such an increase is not indicated by most dinosaur endocasts.
Most importantly, if some dinosaurs DID have bird-sized brains, the above contention would still hold. Hopson concludes that, except for coelurosaurs “the range of behaviors that existed in dinosaurs, as inferred from trackways and skeletal morphology, may not have lain much outside the observed range in ectothermic crocodilians” (Hopson, 1977: 444).
Since the conjecture/’thought experiment’ of the troodon was rebutted last week, it’s pretty conclusive that large brains lie outside of reptilian design; they need to spend so much time avoiding getting too hot or cold—as well as hunt and eat—so exploring the world and learning was not possible for them—along with the fact that they didn’t have a primate morphology and thus didn’t have the ability to fully manipulate their environment as we do which would further select for larger brains. However, as Hopson (1977) notes, animals with higher metabolic rates had larger brains; coelurosaurs had high metabolic rates and the largest dinosaur brains (Russel, 1983; 1989)—but that doesn’t mean they would have eventually evolved human-like intelligence, bipedalism or brain size and to say otherwise is fantasy.
Furthermore, there is large variation in encephalization and encephalization is not universal in mammals (Shultz and Dunbar, 2010).
Here is the thing about brain size increases: it is a local level trend. A local level trend is a trend that occurs within one or a few related species. This is exactly what characterized brain evolution; there is large variation depending on what the environment calls for (Boddy et al, 2012; Montgomery et al, 2012; see also island gigantism; Bromham and Cardillo, 2007; Welch, 2009; and also see the deep sea rule; Mcclain, Boyer, and Rosenberg, 2006). So these local trends differ by species—even one population split by, say, 50 miles of water will speciate and become evolve a completely different phenotype due to the environment of time. That is evolution by natural selection; local change, not any inherent or intrinsic ‘progress’ (Gould, 1996).
The same local level trend occurs with parasites. Now think about parasites. The get selected for ‘complexity’ or a decrease in ‘complexity’ depending on what occurs in their host. Now, looking at it from this perspective, the body is the host’s environment while the earth is ours; so my example for an environmental change would be, as usual, the asteroid impact hitting the earth blocking out the sun and decreasing high-quality food all throughout the earth. Surely I don’t need to tell you what would occur…
Russel (1989) writes:
Examples of evolutionary changes that occured at ever-increasing speeds include the initial diversification of animals in the sea 650 and 550 million years ago, the attainment of tree stature in land plants between 410 and 360 million years ago, and the diversification of mammals between 200 million years ago and the present. Changes like this have resulted in increased organismal complexity, which, in combination with a general increase in number of species, has made the biosphere of the modern Earth so much richer than it was several hundred million years ago. It is reasonable to suppose that animals living in a complex environment might find it advantageous to possess complex nervous systems in order to have access to a greater variety of responses. Indeed, the largest proportion of brain weight in an animal has also increased at an ever-increasing rate across geological time. The brain has become evidently larger in animals as diverse as insects, mollusks, and backboned creatures. Relative brain size can be taken as an indication of biotic interactions.
He references time periods that correspond with decimations (mass extinctions). Decimations lead to diversification. Think back to the Cambrian Explosion. During the Cambrian Explosion, many more lifeforms existed than can be currently classified. Therefore, according to the decimation and diversification model, greater diversity of life existed in the past. When decimations (defined as a reduction in the anatomical forms of life from mass extinction) occur, the niches that become extinct quickly become filled.
The time periods that Russel references are when mass extinctions occurred. This is how diversification occurs. What allowed for this ‘organismal complexity’ and increase in the number of species (though body plans are limited due to the Burgess Decimation) is due to the decimations. Decimation and diversification proves that evolution is not progressive.
A ‘trend’ in biology is directional change in a group stat using the mean, median or mode. Any existence of a trend from the mean (‘progress’) tells us nothing about the underlying mechanisms behind it.
To wrap this all up, even if a trend in X were to be discovered, it still wouldn’t tell us a thing about the underlying mechanisms causing it, nor will it tell us about any increasing tendency.
The analogy of the drunkard’s walk (Gould, 1996) is why ‘progress’ doesn’t make sense. Further, niche construction matters as well. When organisms construct their own niches, change occurs based on those niche constructions. Milk-drinking 8kya in Europe and African farmers diverting water for their crops having mosquitoes come by and gaining a resistance to malaria are two examples of niche construction (Laland et al, 2009). That’s another barrier to progress!
In sum, Dale Russel says nothing I’ve not heard before in regards to ‘progressive’ evolution. He only describes ever-increasing ‘complexity’ which is due to decimations and further diversification by organisms to fill empty niches. Any type of ‘progress’ would have been stymied by mass extinctions.
Further, the fact that species can consciously—in a way—guide their own evolution through the manipulation of the environment once again shows how evolution doesn’t mean progress—it literally only means local change and any type of local change, no matter to what type of environment, will cause concurrent increases/decreases on whichever relevant traits that will give the organism the best chance for survival in that environment.
This is why evolution is not progressive; and even if scientists were to identify one thing, still, a causal mechanism won’t be able to be inferred. Ruseel (1989) describes right and left walls of complexity—nothing more. Dinosaurs didn’t have the body plans to have our brain size, bipedalism and intelligence, nor did they have the right type of blood, nor did they have the time to search and learn about the world due to being constrained to their cold-blooded system—being a slave to the sun, always attempting to avoid overheating or getting too cold (Skoyles and Sagan, 2002). The so-called ‘dinosauroid’ is an impossibility and implies a teleological lean to evolution—as if our morphology (or something similar from an unrelated organism) will always evolve if we replay the tape of life again (Gould, 1989; 1996). This is what Russel is pretty much arguing, and he is 100 percent wrong as noted above.
References
Bromham, L., & Cardillo, M. (2007). Primates follow the ‘island rule’: implications for interpreting Homo floresiensis. Biology Letters,3(4), 398-400. doi:10.1098/rsbl.2007.0113
Boddy, A. M., Mcgowen, M. R., Sherwood, C. C., Grossman, L. I., Goodman, M., & Wildman, D. E. (2012). Comparative analysis of encephalization in mammals reveals relaxed constraints on anthropoid primate and cetacean brain scaling. Journal of Evolutionary Biology,25(5), 981-994. doi:10.1111/j.1420-9101.2012.02491.x
Gould, S. J. (1989). Wonderful life: the Burgess Shale and the nature of history. New York: Norton.
Gould, S. J. (1996). Full House: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Hopson, J. A. (1977). Relative Brain Size and Behavior in Archosaurian Reptiles. Annual Review of Ecology and Systematics,8(1), 429-448. doi:10.1146/annurev.es.08.110177.002241
Laland, K. N., Odling-Smee, J., Feldman, M. W., & Kendal, J. (2009). Conceptual Barriers to Progress Within Evolutionary Biology. Foundations of Science, 14(3), 195–216. http://doi.org/10.1007/s10699-008-9153-8
Mcclain, C. R., Boyer, A. G., & Rosenberg, G. (2006). The island rule and the evolution of body size in the deep sea. Journal of Biogeography,33(9), 1578-1584. doi:10.1111/j.1365-2699.2006.01545.x
Montgomery, S. H., Capellini, I., Barton, R. A., & Mundy, N. I. (2010). Reconstructing the ups and downs of primate brain evolution: implications for adaptive hypotheses and Homo floresiensis. BMC Biology,8(1), 9. doi:10.1186/1741-7007-8-9
Russell, D. A. (1983). Exponential evolution: Implications for intelligent extraterrestrial life. Advances in Space Research,3(9), 95-103. doi:10.1016/0273-1177(83)90045-5
Russell, D. A. (1989). An Odyssey in Time: The Dinosaurs of North America. Minocqua, WI: Published by NorthWord Press in association with National Museum of Natural Sciences.
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Shultz, S., & Dunbar, R. (2010). Encephalization is not a universal macroevolutionary phenomenon in mammals but is associated with sociality. Proceedings of the National Academy of Sciences,107(50), 21582-21586. doi:10.1073/pnas.1005246107
Skoyles, J. R., & Sagan, D. (2002). Up From Dragons: The Evolution of Human Intelligence. New York: McGraw-Hill.
Welch, J. J. (2009). Testing the island rule: primates as a case study. Proceedings of the Royal Society B: Biological Sciences,276(1657), 675-682. doi:10.1098/rspb.2008.1180
Height and IQ Genes
1100 words
Genes account for about 80 percent of the variation in height and IQ, with both height and IQ correlating at .2. Therefore, genes must contribute largely to population variances in height. However, finding certain genes that contribute largely to these two traits is a problem, largely because both traits are polygenic in nature. Recent research has shown that most—or all–genes are height genes. If this is the case, are most—or all—genes IQ genes?
Height is around 80-90 percent heritable (Peeters et al, 2009). What this means is that the difference between the tallest and shortest 5 percent of the population is 11 inches, with 10 inches being accounted for by genes and 1 inch being accounted for by environment (Heine, 2017: 30). The gene that contributes the most to human height has been found to give 1/6th of an inch (Weedon et al, 2007). However, a recent meta-analysis shows that certain rare alleles give as much as 8/10ths of an inch (Hirschhorn, Deloukas, and Lettre, 2017). Furthermore, thousands of gene variants combined explain about 50 percent of human height (Yang et al, 2010). Yang et al (2010) also found 294,831 SNPs related to people’s height, which is—more or less—12 times the number of genes in our genome (Heine, 2017: 30; the number of genes in our genome is in the range of 19,000-20,000; Ezkurdia et al, 2014). Another meta-analysis found that 697 genetic variants explain about 20 percent of the genetic variation (Wood et al, 2014). Furthermore, according to geneticist David Goldstein, “most genes are height genes” (Goldstein, 2009).
Author of the book DNA is not Destiny and cultural and social psychologist Steven J. Heine writes:
“This means if you wanted to genetically engineer a designer baby who you would like to grow up to be tall, you would have to make almost 300,000 genetic alterations to the genome and you still would only be half way there. When the genetic evidence suggests that almost all genes are related to height, then in a way, we learn close to nothing about the genetic basis of height.” (Heine, 2017: 30)
Hirschhorn, Deloukas, and Lettre, (2017) found 83 rare and low-frequency genes that explain 1.7 percent of the adult heritability of height, along with newly identified and novel variants that explained 2.4 percent, “and all independent variants, known and novel together explained 27.4% of heritability. By comparison, the 697 known height SNPs explain 23.3% of height heritability in the same dataset (vs. 4.1% by the new height variants identified in this ExomeChip study)” (pg 7). So 27.4 percent of the variance is explained by known common variants and these new variants discovered.
Americans who drink more milk are, on average, half an inch taller than Americans who don’t recall drinking as much milk, even after controlling for race, income, and education (Wiley, 2005). This shows the importance milk has on skeletal muscle growth. This increase has even been noticed in Japan, where they increased their milk intake using school lunch programs (Takahasi, 1984), which increased their height by 4 inches (Funatogawa et al, 2009).
We also grow more in the spring and summer than in the fall and winter. This is due to ultraviolet radiation from the sun’s rays that synthesize some of the vitamin D we drink that is in the cow’s milk. Clearly, environmental factors (UV rays, milk consumption, overall nutrition, etc) all have a part to play in human height variation (Heine, 2017: 30). However, if all genes may be height genes, may all genes be IQ genes?
In regards to IQ, 3 genetic variants explain .3 IQ points (Rietvald et al, 2014):
After adjusting the estimated effect sizes of the SNPs (each R2 ∼ 0.0006) for the winner’s curse, we estimate each as R2 ∼ 0.0002 (SI Appendix), or in terms of coefficient magnitude, each additional reference allele for each SNP is associated with an ∼0.02 SD increase in cognitive performance [or 0.3 points on the typical intelligence quotient (IQ) scale].
This is the gene with the highest known effect that we currently know of. No “but undiscovered X means Y!!”, because science isn’t based on ‘what ifs’.
To predict one’s intelligence, you would need all genes on an SNP chip—which contains about 500,000 SNPs—to be able to predict half of the individual variation in IQ (Davies et al, 2011; Chabris et al, 2012; Heine, 2017: 175). Just as is the case with height, it seems that it’s possible that most—if not all—genes are IQ genes.
So, clearly, intelligence is highly polygenic, and, contrary to what Plomin says, it’s doubtful that we’ll be able to genotype one to guesstimate their intelligence level.
This is because you need more than 500,000 SNPs on a gene chip and even still, that would only explain half of the variance. So it’s reasonable to assume—as is the case with height—that all genes are IQ genes.
Chabris et al (2012) write:
One SNP, rs2760118 in SSADH (also known as ALDH5A1), exhibited a nominally significant association with g (t = 2.01, p = .04), but this association did not survive a Bonferroni correction. The mean g values (transformed to the IQ scale) by genotype for this SNP were 98.3, 99.7, and 100.6 for genotypes TT, TC, and CC respectively.
So it seems that all genes are height genes and all genes could possibly be IQ genes (that is, having a small effect). If most genes are height genes, and height is linked to IQ, then most genes should be IQ genes as well. Therefore, it is plausible that all genes are IQ genes.
Finally, I need to talk about the study that everyone is talking about, the study that found 52 new genes for intelligence (Sniekers et al, 2017). However, Razib Khan cautions: “My plain words are this: do not trust, and always verify“. A Google search for “gene found for” brings up 26,300,000 hits. As can be seen with the study that was published the other day on the supposed ‘new hominin’ found in Europe, science journalists use fancy and catchy headlines. “Genes for ___ and ___” is a bad way to put it—few traits are caused by a single gene, and most traits are highly polygenic, height and IQ included.
Do I think we’ll disentangle the intricacies involved with height and IQ? One day. But since at the moment, 500,000 SNPs need to be loaded on a gene chip to explain half of the variation in individual IQ.
Since most—or all—genes are related to height and the same may be so for IQ, we don’t really learn anything knowing the genes that control for these two traits. In regards to Heine’s (2017) example of genetic engineering 300,000 SNPs for height and you’d only be halfway there, I’d assume the same would be true for IQ. Both traits are highly polygenic, with thousands of genes controlling these traits. Genetic engineering a human for high intelligence or height looks to be a long shot—at least until far into the future.
Rebutting Heartiste on the Twinkie Diet
1300 words
Nutritional myths run amok everywhere. One of the most persistent is that ‘a calorie is a calorie’, that is, every macronutrient will be processed the same by the body. Another assumption is that the body doesn’t ‘care’ about where the calories come from—they can come from fat, protein, or carbs and the response will be the same: bodyweight will be reduced until one reaches their goal. However, it’s not as simple as that. He also has the assumption that “diets work”, when the best meta-analysis I know of on the matter shows the opposite (Mann et al, 2007, see especially table 1). They control for studies where weight was self-reported. They conclude that dieting does not work. This is what, as Heartiste says, “iScience!” says on the matter, so he should believe everything I state in this article, which is backed by “iScience!”.
Chateau Heartiste published an article back in 2010 titled The Twinkies Diet Proves Fatty Fats Are Fat Because They Eat Too Much. He is referring to professor of human nutrition Mark Haub and his success on ‘the twinkies diet’, where 2/3rds of his caloric intake came from junk food such as Twinkies. He lost 27 pounds in a two month period while his LDL cholesterol decreased by 20 percent and his HDL cholesterol increased by 20 percent. His level of triglycerides also decreased by 37 percent, with his body fat decreasing from 33.4 to 24.9 percent. So he ate 1800 kcal per day—2/3rds of it being junk food—for two months and lost 27 pounds. Case closed, right? Eat junk food at a deficit and lose weight? A calorie is a calorie? There are a few problems with this contention which will be addressed below.
Heartiste writes:
Big bottom line: Being fat itself is bad for your health. “Fat and fit” is a myth. The change that counts the most is losing the weight, which can only be done by PUSHING AWAY FROM THE TABLE.
Except fit and overweight and obese individuals have similar mortality rates than their normal weight counterparts (Barry et al, 2014). However, more recently a study was published purporting that overweight and obese individuals being healthy despite excess weight is a myth. The researchers state that in a sample of millions of Britons that overweight and obese individuals had a higher risk of heart disease than their normal-weight counterparts. Unfortunately, I cannot locate the study since it wasn’t published in a journal (and thusly not peer reviewed). I wonder if variables such as diet, smoking and other lifestyle factors were taken into account. Nevertheless, the debate on fitness and fatness continues.
Another large meta-analysis shows that grade 1 obesity (BMI 30->35) had the same mortality risk as normal-weight individuals with grade 2 obese (BMI +35) having a significantly higher risk of death (Flegal, Kit, and Orpana, 2013).
Heartiste claims that ‘a calorie is a calorie’. This is a common fallacy. This suggests that the body will process all foods the same way—that is, processing them the same metabolically. This, however, is not the case. Haub himself is a sample size of 1. If Heartiste can use a sample size of 1 to make a claim, then I can too.
Sam Feltham ate +5,000 kcal per day for 21 days and only gained 1.3 kg when he should have gained 7.3 kg based on the amount of kcal he ate. A calorie is a calorie, right? This is a fallacious statement. The statement “a calorie is a calorie” violates the second law of thermodynamics (Feinman and Fine, 2004). Heartiste writes:
That first law of thermodynamics looms large over everything.
The first law of thermodynamics is irrelevant to human physiology. It only states that an organism gets bigger if it consumes more energy; it doesn’t state why this occurs, which is due to the hormone insulin which causes weight gain.
He does rightly state that an omega 3/6 imbalance is part of the reason but then handwaves it away. Western-like high-fat diets (i.e., diets with an imbalance of linoleic acids (LA; and n-6 fatty acid) with n-3) are sufficient enough to induce gradual enhancement in fat mass across the generations (Massiera et al, 2010). This obviously includes the average 55 percent carbohydrate diet that the AHA recommends (Eckel et al, 2014). The Standard American Diet (aptly named the “SAD diet”) has the n-3/n-6 imbalance along with being high in carbohydrates which spike insulin which impedes fat being unlocked from the adipocyte.
Heartiste doesn’t understand that if you reduce the ‘in’, the ‘out’ also decreases. This was noted in the famous starvation experiment headed by Ancel Keys. They took 36 healthy men who ate normally for three months while being their behavior and personality was monitored. In the next six months, they were reduced to eating half of their initial intake (they started at 2000 kcal and dropped to 1000 kcal; some individuals going lower than that) and their metabolic rate decreased by 40 percent (Keys et al, 1945). This is proof for the contention that the body decreases its metabolic rate due to what is ingested. A similar study was done on Vermont prisoners, except they were told to gorge on food. Since they were in a controlled setting, the prisoners could be monitored to ensure they ate all of the food.
At the end of the study, their metabolic rates had increased by 50 percent. This is evidence that the body was trying to get back to its original weight. In six months, the prisoners went back to their normal weight as they ate normally (Salas, Horton, and Sims, 1971) One man only gained ten pounds eating all of those calories. Clearly, the body was resisting weight gain and when they were allowed to eat normally, they effortlessly regained their normal weights.
Finally, on the topic of Haub, Big Food shill, I will address a few things about him and his ‘research’ that recently came to light.
Intermittent fasting and obesity expert Dr. Jason Fung showed that in 2016 after Coca-Cola released their funding reports after criticisms of transparency, Mark Haub was found to be one of the many researchers that were backed by Coca-Cola. This is an attempt to show that ‘a calorie is a calorie’ and that ‘all calories are created equal’. This has been rebutted above.
In 2016—six years after his ‘experiment—it was revealed that he was funded by Coca-Cola. No doubt in order to ‘prove’ that ‘a calorie is a calorie’ and have people continue to gorge on high carbohydrate/insulinogenic foods. However, the human body is a lot more complex than to just reduce it to simply calories in and calories out—which I have written about in depth.
People like Heartiste need to get an actual understanding of the literature and what Coca-Cola has been trying to do for years, which is to make eating junk food ‘OK’ because ‘it doesn’t cause obesity’. Children consume 45 percent more food when exposed to advertisements (Harris, Bargh, and Brownell, 2009). So to begin to curb obesity rates we don’t need to ‘eat junk food’, we need to not eat junk food and eat a diet more ancestral to us—that is, one lower in processed carbs and higher in animal fat and protein. Big Food shills like Haub need to be exposed for what they are—people who do ‘research’ for a quick buck, i.e., not furthering our understanding of a complex issue as he would like you to believe. Exercise also doesn’t induce weight loss. So the claims of ‘eat less and move more’ (eat less according to the 55 percent carbohydrate recommendations) is bound to fail.
If Heartiste can make a claim using one man as an example then so can I. Read the above article by Sam Feltham in which he writes about hs experience eating 5,000 kcal per day for 21 days while only gaining 1.3 kg. I can use this example to say that eating low carb and high fat at 5,000 kcal per day will lead to negligible weight gain, however, I don’t use n=1 sample sizes to make claims and no one else should either.
Modern Man Did Not Begin in Europe
1300 words
A lot of buzz is going around about a recent study that purports that the human-chimp split occurred in the Mediterranean—not Africa as is commonly thought (Fuss et al, 2017). This claim, however, is based off of a few teeth and jawbone with one tooth in it of a supposed hominin named Graecopithecus freybergi. A lot of wild conclusions are being jumped to about this study and these claims need to be put to rest.
On altright.com, an article was written titled Recent Discovery Shows Humans Came From Europe. The article claims that the OoA hypothesis has been “debunked by hard evidence”. Though to disprove the OoA hypothesis, a lot more will be needed than a few teeth and a jawbone. This is similar to another article on the Dailystormer, New Discovery Shows Pre-Human Hominids in Europe Before Africa, which, again, makes more wild claims.
white people are just Negroes who have lighter skin because during the Ice Age, they were wearing more clothing and thus needed lighter skin to absorb more Vitamin D. needed lighter skin to absorb more Vitamin D.
So, the reasoning behind the theory is that we are all very close together, genetically, so there isn’t really any problem with mixing us all together, and pretty much, race is a social construct.
Race is a social construct of a biological reality. OoA is based on solid evidence. Just because ‘we are close together, genetically’, as egalitarians would say, doesn’t mean we should destroy the human diversity we currently have.
Much damage to evolutionary research was done by the Jew Stephen Jay Gould3, who argued in favor of the idea of rapid evolution
This is bullshit. Stephen J. Gould and Niles Eldredge proposed Puncuated Equilibria (PE). PE occurs when a species becomes as ‘adapted’ to its environment as possible and then remains in stasis. Species speciate when the environment changes (climate), or, say an earthquake occurs and splits a population of 100 peacocks in half. Fifty of the peacocks will change due to drift, natural and sexual selection. But if the environmental conditions stay the same then species cannot change.
Punctuated Equlibria is an alternative to phyletic gradualism.
What is punctuated equilibrium? What is macroevolution? A response to Pennell et al
The proposal was that after a long time in stasis that quick speciation would occur—that would be in response to the environmental change that drives the evolution of species.
He also made much damage to the field of sociobiology, literally arguing that evolution has no role in human behavior
He argued that many functions of the ‘higher’ functions of the human brain evolved for other reasons and were coopted for other reasons, which is why he coined the term ‘exaptation’.
And the debate about spandrels—which is a phenotypic trait that is a byproduct of the evolution of another trait and not due to adaptive selection. There is a tendency to assume that all—or most—traits are due to adaptive selection. This is not true.
PZ Myers – Bad Biology: How Adaptationist Thinking Corrupts Science
With this new discovery of prehumans in Europe, they are dating the European fossil as older, but we would basically end up with the same conclusions with regards to rapid evolution and thus “race not existing.” So I don’t see anything for racists to get all excited about, with the way it is currently being presented.
Punctuated Equilibria is a lot more nuanced than you’re making it out to be. It’s looking at the whole entire fossil record and noticing that for most of a species’ evolutionary history that it remains in stasis and that evolution then occurs in quick bursts.
This theory postulates that Africans, Asians, Europeans and Aboriginal Australians all evolved completely separately from different hominidae
This is not tenable. This isn’t even how it works. Neanderthals and Homo sapiens are derived from Heidelbergensis.
Erectus is in our family tree beginning 2 mya. He is an origin of AMH and us as well. However, what you’re talking about needs to be proven with genetic testing.
Africans of course are more violent (and larger) not so much because of IQ, but because of higher levels of testosterone, but no one has explained what caused this.
Claims about substantially higher levels of testosterone in blacks are not true.
Then, of course, the Asians who moved north developed higher IQs and lighter skin because of climate-related reasons.
East Asians needed bigger brains for expertise capcity; not IQ. Light skin did evolve for climatic reasons; not sexual selection as some claim.
People need to 1) learn the basics of evolutionary theory; 2) learn the basics of the OoA hypothesis; 3) stop jumping to conclusions based on little evidence and large conjecture; 4) never trust anything at face value; always do more research into something and put all ideas under intense scrutiny, even ones you strongly believe. That way, articles like the ones above don’t get writtent with complete disregard for modern-day evolutionary theory.
John Hawks, paleoanthropologist writes:
Here’s what I think: Paleoanthropology must move past the point where a mandibular fragment is accepted as sufficient evidence.
He also states that this may be a case of apes evolving “supposed hominin characters” in the Miocene, citing a study by him and his colleagues showing that features that supposedly link Ardipethicus and Sahelanthropus are also found in other Miocene fossils (Wolpoff et al, 2006). Graecopithecus shares few features with Australopithecus, so Hawks says that we should begin to think about the possibility of Graecopithecus being “part of a diversity of apes that are continuous across parts of Africa and Europe.”
Finally, there is not enough evidence to back the claim that humans originated in Europe. Vertebrate paleontologist and paleobiologist Dr. Julian Benoit states that the author’s claim of the fourth molar root in Graecopithecus being similar to hominins is unfounded because “This is not a character that is conventionally used in palaeoanthropology, especially because not all hominins have similar tooth roots. This character is rather variable – and the authors go on to acknowledge this – so it’s unreliable for classification.” Further, humans aren’t the only apes with small canines and the jawbone and teeth aren’t too well preserved.
We have found thousands of hominin fossils in Africa. We know that the LCA between apes and humans existed between 6-12 mya in Africa. Graecopithecus was probably an ape species not related to humans. Even if the claim were true, it wouldn’t completely disprove the hypothesis that Man originated in Africa. Extraordinary claims require extraordinary evidence; this is not it.
People need to stop letting their biases and political beliefs get in the way of rational thought. Never take claims at face value; always look at things objectively. There needs to be a lot more evidence for the claim that Man originated in Europe; and even then, there is a mountain of evidence that anatomically modern humans arose in Africa.
In order to prove that Graecopithecus was a hominin and not another species of non-human ape, more fossils need to be found and a phylogenetic analysis needs to be done on the jawbone, comparing it with other species to see the closest relationship on the phylogeny. I assume when this is done it will show that it is related to non-human apes; not humans. Nevertheless, extraordinary claims require extraordinary evidence and people need to stop believing and agreeing with everything that ‘agrees’ with their worldviews as a fact without taking an objective look at the data. Never trust claims and always attempt to verify that what someone claims has a basis in reality. Only ask yourself what the facts are and what they show—without bias.
Dinosaurs, Brains, and ‘Progressive Evolution’
1800 words
Would dinosaurs have reached human-like intellect had the K-T extinction (an asteroid impact near the Yucatan peninsula) not occurred? One researcher believes so, and he believes that a dinosaur called the troodon would have evolved into a bipedal, human-like being. This is, of course, the old progressive evolution shtick. This assumes that a man-like being is an inevitability, and that sentience is a forgone conclusion.
This belief largely comes from Rushton’s citation of one Dale Russel, the discoverer of the dinosaur the troodon:
Paleontologist Dale Russell (1983,1989) quantified increasing neurological complexity through 700 million years of Earth history in invertebrates and vertebrates alike. The trend was increasing encephalization among the dinosaurs that existed for 140 million years and vanished 65 million years ago. Russell (1989) proposed that if they had not gone extinct, dinosaurs would have progressed to a large-brained, bipedal descendent. For living mammals he set the mean encephalization, the ratio of brain size to body size, at 1.00, and calculated that 65 million years ago it was only about 0.30. Encephalization quotients for living molluscs vary between 0.043 and 0.31, and for living insects between 0.008 and 0.045 but in these groups the less encephalized living species resemble forms that appeared relatively early in the geologic record, and the more encephalized species resemble those that appeared later. (Rushton, 1997: 294)
This argument is simple to rebut. What is being described is complexity. The simplest possible organism are bacteria, which reside at the left wall of complexity. The left wall “induces right-skewed distributions”, whereas the right wall induces “left-skewed distributions” (Gould, 1996: 55). Knowing this, biological complexity is a forgone conclusion, which exists at the extreme end of the right tail curve. I’ve covered this in my article Complexity, Walls, 0.400 Hitting and Evolutionary “Progress”
Talking about what Troodons may have looked like (highly, highly, doubtful. The anthropometric bias was pretty strong) is a waste of time. I’ve stated this a few times and I’ll state it yet again: without our primate body plan, our brains are pretty much useless. Our body needs our brain; our brain needs our body. Troodons would have stayed quadrupedal; they wouldn’t have gone bipedal.
He claims that some dinosaurs would have eventually reached an EQ of humans—specifically the troodon. They had EQs about 6 times higher than the average dinosaur, had fingers to grasp, had small teeth, ate meat, and appeared to be social. Dale Russel claims that had the K-T extinction not occurred, the troodon would look similar to us with a brain size around 1100 cc (the size of erectus before he went extinct). This is what he believes the dinosauroid troodon would look like had they not died out 65 mya:
When interviewed about the dinosauroid he imagined, he stated:
The “dinosauroid” was a thought experiment, based on an observable, general trend toward larger relative brain size in terrestrial vertebrates through geologic time, and the energetic efficiency of an upright posture in slow-moving, bipedal animals. It seems to me that such speculation remains acceptable, particularly if directed toward non-anthropoid anatomical configurations. However, I very nearly decided not to publish the exercise because of the damaging effects it might have had on the credibility of my work in general. Most people remained polite, although there were hostile reactions from those with “ultra-quantitative” and “ultra-intuitive” world views.
Why does it look so human? Why does he assume that the ‘ideal body plan’ is what we have? It seems to be extremely biased towards a humanoid morphology, just as other reconstructions are biased towards what we think about certain areas today and how the people may have looked in our evolutionary past. Anthropocentric bias permeates deep in evolutionary thinking, this is one such example.
Thinking of this thought experiment of a possible ‘bipedal dinosauroid’ we need to be realistic in terms of thinking of its anatomy and morphology.
Let’s accept Russel’s contention as true; that troodontids or other ‘highly encephalized species’ reached a human EQ, as he notes, of 9.4, with troodontids at .34 (the highest), archaeopteryx at .32, triconodonts (early extinct mammal of the cretaceous) with a .29 EQ, and the diademodon with an EQ of .20 (Russel, 1983). Russel found that the troodontids had EQs 6 times higher than the average dinosaur, so from here, he extrapolated that the troodon would have had a brain our size. However, Stephen Jay Gould argued the opposite in Wonderful Life writing:
If mammals had arisen late and helped to drive dinosaurs to their doom, then we could legitimately propose a scenario of expected progress. But dinosaurs remained dominant and probably became extinct only as a quirky result of the most unpredictable of all events—a mass dying triggered by extraterrestrial impact. If dinosaurs had not died in this event, they would probably still dominate the large-bodied vertebrates, as they had for so long with such conspicuous success, and mammals would still be small creatures in the interstices of their world. This situation prevailed for one hundred million years, why not sixty million more? Since dinosaurs were not moving towards markedly larger brains, and since such a prospect may lay outside the capability of reptilian design (Jerison, 1973; Hopson, 1977), we must assume that consciousness would not have evolved on our planet if a cosmic catastrophe had not claimed the dinosaurs as victims. In an entirely literal sense, we owe our existence, as large reasoning mammals, to our lucky stars. (Gould, 1989: 318)
If a large brain was probably outside of reptilian design, then a dinosaur—or a descendant (troodon included)—would have never reached human-like intelligence. However, some people may say that dinosaur descendants may have evolved brains our size since birds have brains that lie outside of reptilian design (supposedly).
However, one of the most famous fossils ever found, archaeopteryx, was within reptilian design, having feathers and along with wings which would have been used for gliding (whether or not they flew is debated). Birds descend from therapods. Anchiornis, and other older species are thought to be the first birds. Most of birds’ traits, such as bipedal posture, hinged ankles, hollow bones and S-shaped neck in birds are derived features from their ancestors.
If we didn’t exist, then if any organism were to come close to our intelligence, I would bet that some corvids would, seeing as they have a higher packing density and interconnections compared to the “layered mammalian brain” (Olkowicz et al, 2016). Nick Lane, biochemist and author of the book The Vital Question: Evolution and the Origins of Complex Life believes a type of intelligent ocotopi may have evolved, writing:
Wind back the clock to Cambrian times, half a billion years ago, when mammals first exploded into the fossil record, and let it play forwards again. Would that parallel be similar to our own? Perhaps the hills would be crawling with giant terrestrial octopuses. (Lane, 2015: 21)
We exist because we are primates. Our brains are scaled-up primate brains (Herculano-Houzel, 2009). Our primate morphology—along with our diet, sociality, and culture—is also why we came to take over the world. Our body plan—which, as far as we know, only evolved once—is why we have the ability to manipulate our environment and use our superior intelligence—which is due to the number of neurons in our cerebral cortex, the highest in the animal kingdom, 16 billion in all (Herculano-Houzel, 2009). Why postulate that a dinosaur could have looked even anywhere close to us?
This is also ignoring the fact that decimation and diversification also ‘decide the fates’ so to speak, of the species on earth. Survival during an extinction event is strongly predicated by chance (and size). The smaller an organism is, the more likely it will survive an extinction event. Who’s to say that the troodon doesn’t go extinct due to an act of contingency, say, 50 mya if the K-T extinction never occurred?
In conclusion, the supposed ‘trend’ in brain size evolution is just random fluctuations—inevitabilities since life began at the left wall of complexity. Gould wrote about a drunkard’s walk in his book Full House (Gould, 1996) in which he illustrates an example of a drunkard walking away from a bar with the bar wall being the left wall of complexity and the gutter being the right wall. The gutter will always be reached; and if he hits the wall, he will lean against the wall “until a subsequent stagger propels him in the other direction. In other words, only one direction of movement remains open for continuous advance—toward the gutter” (Gould, 1996: 150).
I bring up this old example to illustrate but one salient point: In a system of linear motion structurally constrained by a wall at one end, random movement, with no preferred directionality whatever, will inevitably propel the average position away from a starting point at the wall. The drunkard falls into the gutter every time, but his motion includes no trend whatever toward this form of perdition. Similarly, some average or extreme measure of life might move in a particular direction even if no evolutionary advantage, and no inherent trend, favor that pathway (Gould, 1996: 151).
We humans are lucky we are here. Contingencies of ‘just history’ are why we are here, and if we were not here—if the K-T extinction never occurred—and the troodon or another dinosaur species survived to the present day, they would not have reached our ‘level’ of intelligence. To believe so is to believe in teleological evolution—which certainly is not true. Anthropometric bias runs deep in evolutionary biology and paleontology. People assume that since we are—according to some—the ‘pinnacle’ of evolution, that us, or something like us, would eventually have evolved.
Any ‘trends’ can be explained as life moving away from the left wall of complexity, with the left wall—the mode of life, the modal bacter-–being unchanged. We are at the extreme tail of the distribution of complexity while bacteria are at the left wall. Complex life was inevitable since bacteria, the most simple life, began at the left wall. And so, these ‘trends’ in brain size are just that, increasing complexity, not any type of ‘progressive evolution’. Evolution just happens, natural selection occurs based on the local environment, not any inherent or intrinsic ‘progress’.
References
Gould, S. J. (1989). Wonderful life: the burgess Shale and the nature of history. New York: Norton.
Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Herculano-Houzel, S. (2009). The human brain in numbers: a linearly scaled-up primate brain. Frontiers in Human Neuroscience,3. doi:10.3389/neuro.09.031.2009
Lane, N. (2015). The vital question: energy, evolution, and the origins of complex life. New York: W.W. Norton & Company.
Olkowicz, S., Kocourek, M., Lučan, R. K., Porteš, M., Fitch, W. T., Herculano-Houzel, S., & Němec, P. (2016). Birds have primate-like numbers of neurons in the forebrain. Proceedings of the National Academy of Sciences,113(26), 7255-7260. doi:10.1073/pnas.1517131113
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Russell, D. A. (1983). Exponential evolution: Implications for intelligent extraterrestrial life. Advances in Space Research,3(9), 95-103. doi:10.1016/0273-1177(83)90045-5
Traumatic Brain Injury and IQ
1900 words
What is the relationship between traumatic brain injury (TBI) and IQ? Does IQ decrease? Stay the same? Increase? A few studies have looked at the relationship between TBI and IQ, and the results may be quite surprising to some. Tonight I will look through a few studies and see what the relationship is between TBI and IQ—does IQ decrease substantially or is there only a small decrease? Does it decrease for all subtests or only some?
TBI and IQ
In a sample of 72 people with TBI who had significant brain injuries had an average IQ of 90 (study 1; Bigler, 1995). Bigler also says that whatever correlation exists between brain size and IQ “does not persist post injury” (pg 387). This finding has large implications: can there be a minimal hit to IQ depending on age/severity of injury/brain size/education level?
As will be seen when I review another study on IQ and brain injury, every individual in the cohort in Bigler (1995) was tested after 42 days of brain injury. This does matter, as I will get into below.
Table 1 in study 1 shows that whatever positive relationship between IQ and brain size that is there before injury does not persist after injury (Bigler, 1995: 387). Study 1 showed that, even with mild-to-severe brain damage, there was little change in measured IQ—largely because the correlation between brain size and IQ is .51 at the high end (which I will use—the true correlation is between .24 [Pietschnig et al, 2015] to .4 [Rushton and Ankney, 2009]), this means that if the correlation were to be that high, brain size would only explain 25 percent of the variation in IQ (Skoyles, 1999). That leaves a lot of room for other reasons for differences in brain size and IQ in individuals and groups.
In study 2 (Bigler, 1995: 389-391), he looked into whether or not there were differences in IQ between high and low brain volume people (95 men). Results summed in table 3 (pg 390). Those with low brain volume (1185), aged 28, had an IQ of 82.61 while those with high brain volume (1584), aged 34 had an IQ of 92 (both cohorts had similar education). Bigler showed in study 1 IQ was maintained post injury, so we can say that this was their IQ preinjury.
In table 2, Bigler (1995) compares IQs and brain volumes of mild-to-moderate and moderate-to-severe individuals with TBI. Brain volume in the moderate-to-severe group was 1289.2 whereas for the mild-to-moderate TBI-suffering individuals had a mean brain volume of 1332.9. Amazingly, both groups had IQ scores in the normal range (90.0 for moderate-to-severe TBI and 90.7 for individuals suffering from mild-to-moderate TBI. In study 3, Bigler (1995) shows that trauma-induced atrophic changes in the brain aren’t related to IQ postinjury, nor to the amount of focal lesion volume.
Nevertheless, Bigler (1995) shows that those with bigger brains had less of a cognitive hit after TBI than those with smaller brains. PumpkinPerson pointed me to a study that shows that TBI stretches far back into our evolutionary history, with TBI seen in australopithecine fossils along with erectus fossils found throughout the world. This implies that TBI was a driver for brain size (Shivley et al, 2012); if the brain is bigger, then if/when TBI is acquired, the cognitive hit will be lessened (Stern, 2002). This is a great theory for explaining why we have large brains despite the negatives that come with them—if we were to acquire TBI in our evolutionary past, then the hit to our cognition would not be too great, and so we could still pass our genes to the next generation.
The fact that changes in IQ are minimal when brain damage is acquired shows that brain size isn’t as important as some brain-size-fetishists would like you to believe. Though, preinjury (PI) IQ was not tested, I have one study where it was.
Wood and Rutterford (2006) showed results similar to Bigler (1995)—minimal change to IQ occurs after TBI. The whole cohort pre-injury (PI) had a 99.79 IQ. T1 (early measure) IQ for the cohort was 90.96 while T2 (late measure) IQ for the cohort was 92.37. For people with greater than 11th-grade education (n=30), IQ decreased from 106.57 PI to 95.19 in T1 to 100.17 in T2. For people with less than an 11th-grade education (n=44), IQ PI was 95.16 and decreased to 86.99 in T1 and increased to 87.96 in T2. Male (n=51) and female (n=23) were similar, with male PI IQ being 99.04 to women’s 101.44 with a 90.13 IQ in T1 for men with a 90.72 IQ in T1 for women. In T2 for men it was 92.94 and for women, it was 92.83. So this cohort shows the same trends as Bigler (1995).
The most marked difference in subtests post-injury was in vocabulary (see table 3) with similarities staying the same, and digit symbol, and block design increasing between T1 and T2. Neither group differed between T1 and T2. The only significant association in performance change over time was years of education. Less educated people were at greater risk for cognitive decline (see table 2).
The difference for PI IQ after T2 for less educated people was 7.2 whereas for more educated people it was 6.4. Though more educated people gained back more IQ points between T1 and T2 (4.98 points) compared to less educated people (.97 IQ points). And: “The participants in our study represent a subgroup of patients with severe head injury reported in a larger study assessing long‐term psychosocial outcome.”
Bigler (1995) didn’t have PI IQ, but Wood and Rutterford (2006) did, and from T1 to T2 (Bigler 1995 tested what would be equivalent to T1 in the Wood and Rutterford 2006 study), IQ hardly increased for those with lower education (.97 points) but substantially increased for those with higher education (4.98 points) with there being a similar difference between PI IQ and T2 IQ for both groups.
Brain-derived neurotrophic protective factor (BDNF) also promotes survival and synaptic plasticity in the human brain (Barbey et al, 2014). They genotyped 156 Vietnam War soldiers with frontal lobe lesion and “focal penetrating head injuries” for the BDNF polymorphism. Though they did find differences in the groups with and without the BDNF polymorphism, writing that there were “substantial average differences between these groups in general intelligence (≈ half a standard deviation or 8 IQ points), verbal comprehension (6 IQ points), perceptual organization (6 IQ points), working memory (8 IQ points), and processing speed (8 IQ points) after TBI” (Barbey et al, 2014). This supports the hypothesis that BDNF is protective against TBI; and since BDNF was important in our evolutionary history which is secreted by the brain while endurance running (Raichlen and Polk, 2012), this could have also been another protective factor against hits to cognition that were acquired, say, during hunts or fights.
Nevertheless, one study found in a sample of 181 children Crowe et al (2012) found that children with mild-to-moderate TBI had IQ scores in the average range, whereas children with severe TBI had IQ scores in the low average range (80 to 90; table 3).
Infants with mild TBI had IQ scores of 99.9 (n=20) whereas infants with moderate TBI has IQs of 98.0 (n=23) and infants with severe TBI had IQs of 90.7 (n=7); preschoolers with mild TBI had IQ scores of 103.8 (n=11), whereas preschoolers with moderate TBI had IQ scores of 100.1 (n=19) and preschoolers with severe TBI had IQ scores of 85.8 (n=13); middle schoolers with mild TBI had IQ scores of 93.9 (n=10), whereas middle schoolers with moderate TBI had IQ scores of 93.5 (n=21), and middle schoolers with severe TBI had IQ scores of 86.1 (n=14); finally, children with mild TBI in late childhood had a mean FSIQ of 107.3 (n=17), while children with moderate TBI had IQs of 99.5 in late childhood (n=15), and children with severe TBI in late childhood had FSIQs of 94.7 (Crowe et al, 2012; table 3). This shows that age of acquisition and severity influence IQ scores (along with their subtests), and that brain maturity matters for maintaining average intelligence post-TBI. Königs et al (2016) also show the same trend; the outlook is better for children with mild TBI, while children faired far worse with severe TBI compared to mild when compared to adults (also seen in Crowe et al, 2012).
People who got into motor vehicle accidents suffered a loss of 14 IQ points (n=33) after being tested 20 months postinjury (Parker and Rosenblum, 1996). The WAIS-IV Technical and Interpretive Manual also shows a similar loss of 16 points (pg 111-112), however, the 22 subjects were tested within 6 to 18 months within acquiring their TBI, with no indication of whether or not a follow-up was done. IQ will recover postinjury, but education, brain size, age, and severity all are factors that contribute to how many IQ points will be gained. However, adults who suffer mild, moderate, and severe TBIs have IQs in the normal range. TBI severity also had a stronger effect on children aged 2 to 7 years of age at injury, with white matter volume and results on the Glasgow Coma Scale (which is used to assess consciousness after a TBI) were related to the severity of the injury (Levin, 2012).
Conclusion
TBI can occur with a minimal hit to IQ (Bigler, 1995; Wood and Rutterford, 2006; Crowe et al, 2012). IQs can still be in the average range at a wide range of ages/severities, however the older one is when they suffer a TBI, the more likely it is that they will incur little to no loss in IQ (depending on the severity, and even then they are still in the average range). It is interesting to note that TBI may have been a selective factor in our brain evolution over the past 3 million years from australopithecines to erectus to Neanderthals to us. However, the fact that people with severe TBI can have IQ scores in the normal range shows that the brain size/IQ correlation isn’t all it’s cracked up to be.
References
Barbey AK, Colom R, Paul E, Forbes C, Krueger F, Goldman D, et al. (2014) Preservation of General Intelligence following Traumatic Brain Injury: Contributions of the Met66 Brain-Derived Neurotrophic Factor. PLoS ONE 9(2): e88733. https://doi.org/10.1371/journal.pone.0088733
Bigler, E. D. (1995). Brain morphology and intelligence. Developmental Neuropsychology,11(4), 377-403. doi:10.1080/87565649509540628
Crowe, L. M., Catroppa, C., Babl, F. E., Rosenfeld, J. V., & Anderson, V. (2012). Timing of Traumatic Brain Injury in Childhood and Intellectual Outcome. Journal of Pediatric Psychology,37(7), 745-754. doi:10.1093/jpepsy/jss070
Green, R. E., Melo, B., Christensen, B., Ngo, L., Monette, G., & Bradbury, C. (2008). Measuring premorbid IQ in traumatic brain injury: An examination of the validity of the Wechsler Test of Adult Reading (WTAR). Journal of Clinical and Experimental Neuropsychology,30(2), 163-172. doi:10.1080/13803390701300524
Königs, M., Engenhorst, P. J., & Oosterlaan, J. (2016). Intelligence after traumatic brain injury: meta-analysis of outcomes and prognosis. European Journal of Neurology,23(1), 21-29. doi:10.1111/ene.12719
Levin, H. S. (2012). Long-term Intellectual Outcome of Traumatic Brain Injury in Children: Limits to Neuroplasticity of the Young Brain? Pediatrics, 129(2), e494–e495. http://doi.org/10.1542/peds.2011-3403
Parker, R. S., & Rosenblum, A. (1996). IQ loss and emotional dysfunctions after mild head injury incurred in a motor vehicle accident. Journal of Clinical Psychology,52(1), 32-43. doi:10.1002/(sici)1097-4679(199601)52:1<32::aid-jclp5>3.3.co;2-1
Pietschnig, J., Penke, L., Wicherts, J. M., Zeiler, M., & Voracek, M. (n.d.). Meta-Analysis of Associations Between Human Brain Volume And Intelligence Differences: How Strong Are They and What Do They Mean? SSRN Electronic Journal. doi:10.2139/ssrn.2512128
Raichlen, D. A., & Polk, J. D. (2012). Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings of the Royal Society B: Biological Sciences,280(1750), 20122250-20122250. doi:10.1098/rspb.2012.2250
Rushton, J. P., & Ankney, C. D. (2009). Whole Brain Size and General Mental Ability: A Review. The International Journal of Neuroscience, 119(5), 692–732. http://doi.org/10.1080/00207450802325843
Shively, S., Scher, A. I., Perl, D. P., & Diaz-Arrastia, R. (2012). Dementia Resulting From Traumatic Brain Injury: What Is the Pathology? Archives of Neurology, 69(10), 1245–1251. http://doi.org/10.1001/archneurol.2011.3747
Skoyles R. J. (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society,8(03), 448-460. doi:10.1017/s1355617702813248
Wood, R. L., & Rutterford, N. A. (2006). Long‐term effect of head trauma on intellectual abilities: a 16‐year outcome study. Journal of Neurology, Neurosurgery, and Psychiatry, 77(10), 1180–1184. http://doi.org/10.1136/jnnp.2006.091553
NotPoliticallyCorrect 