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Stress and Race Redux: A ‘Hispanic’ Paradox?

1500 words

American Renaissance published an article the other day titled “Is ‘Racism’ Killing Black People?” and, for the most part, I largely agree with it. However, there are a few faults in it that I need to address.

First, off, as the article rightly noted, it’s not only perceived ‘racism’ that is the cause for these health disparities, but stress from other blacks as well. Gregory Hood (the author of the AmRen article) cites a new study showing that blacks who move out of the ‘hood’ see a subsequent decrease in BP (Kershaw et al, 2017). They followed 2,290 people 974 were men and 1,306 were women. This is data collected from the CARDIA study which has helped us to understand racial disparities in all types of different health outcomes. Blacks who lived in high segregation neighborhoods had higher levels of SBP (systolic blood pressure), and saw a decrease in their SBP when they moved to less segregated neighborhoods. The authors conclude that “policies that reduce segregation may have meaningful health benefits.” What kind of policies will ‘reduce segregation’? Most races/ethnic groups group together in an area, so I don’t see how this would happen.

In regards to the argument on black maternal mortality and ‘racism’, I think it’s much more nuanced. Black women are 2 to 6 times more likely to die giving birth than white women; while the leading causes of maternal death in black women is pregnancy-induced hypertension, and embolism (Chang et al, 2003), though reasons for the mortality rate are not explainable at present (Flanders-Stepans, 2002). Further, in regards to preeclampasia, women who get pregnant at younger ages are more likely to acquire the disease while pregnant, and blacks and other non-whites are more likely to get pregnant at younger ages than whites (Main et al, 2015).

However, there are ways to reduce maternal mortality in black women. In a RCT undertaken between the years of 1990-2011 in Memphis, Tennesee, black women were followed with their live-in children and placed into one of four groups: “treatment 1 (transportation for prenatal care [n = 166]), treatment 2 (transportation plus developmental screening for infants and toddlers [n = 514]), treatment 3 (transportation plus prenatal/postpartum home visiting [n = 230]), and treatment 4 (transportation, screening, and prenatal, postpartum, and infant/toddler home visiting [n = 228])” (Olds et al, 2014). They conclude that pre- and post-natal care greatly reduces maternal/infant mortality in black women, “living in highly disadvantaged settings.”

Further, the racial disparity in post-term neonates is largely driven by “CHD among term infants with US-born mothers is driven predominately by the postneonatal survival disadvantage of African-American infants” (Collins et al, 2017). Though, as can be seen in the study by Olds et al (2014), pre- and post-natal care can greatly reduce both infant and maternal mortality.

Stress can also be measured in pregnant women by measuring the level of blood cortisol (Gillespie et al, 2017). They show that, independent of adulthood stress, stress during childhood may shape birth timing, with cortisol being the biological mediator. This may be an explanation for what Gregory Hood notes. He states in his article that there has to be an explanation for why black women birth earlier, and while I am sympathetic to biological models ala Rushton (1997), Gillespie et al (2017) drive a hard argument that stress during childhood using cortisol as a biological mediator makes a lot of sense.

There are a few studies that attest to pre- and post-natal care having a large effect on the morality of black women, and that having the carers being black women seems to have  a positive effect (Guerra-Reyes and Hamilton, 2017). They conclude that “Recognition, support, and increasing the number of African-American midwives and birth assistants is vital in tackling health inequalities.” In regards to infant mortality rate (IMR), 18 states will achieve racial equality by 2050 if current trends from 1999-2013 hold (Joedrecka et al, 2017).

Now for the main reason I decided to write this: the ‘Hispanic’ paradox. This paradox is that for the past twenty years, ‘Hispanics’ with low SES have similar or better health outcomes than whites (Franzini, Ribble, and Keddie, 2001). However, more recent analyses show that the ‘Hispanic’ paradox does not exist, mostly due to methodological problems and migrant selectivity (Crimmins et al, 2007; Teruya and Bazargan-Hezeji, 2013) and was not noticed in Chile either (Cabiesies, Tunstall, and Pickett, 2013). There is no migrant selectivity in regards to smoking, however (Fenelon, 2013, 2016).

Teruya and Bazargan-Hezejie (2013) write:

Studies which advocate the validity of the Immigrant Paradox are countered by those which report specific, negative physical and mental health outcomes, and higher rates of substance use, especially among immigrant adolescents. Findings may also be compromised by fundamental methodological concerns such as migrant health selectivity, and approaches that consider only selectively healthy groups. Moreover, the Immigrant Paradox’s benefits do not appear to extend evenly and consistently to all races, ethnicities and subgroups. Similarly, the Hispanic Paradox does not protect consistently across all Latino ethnicities, age groups and genders, with Puerto Ricans and Cubans in particular found to enjoy fewer health advantages.

This is good evidence that the people who migrate to America are healthier, and that the symptoms of low SES show in their children, but not in them because they are a self-selected population. There is no ‘Hispanic’ paradox (Smith and Bradshaw, 2006; Schoenthaler, 2016). Even a new meta-analysis on this ‘paradox’ states “Immigrant children and youth suffer from an immigrant mortality disadvantage” (Shor, Roelfs, and Vamg, 2017).

Lastly, Gregory Hood brings up stress and suicide, stating that if blacks were really more stressed than whites then blacks would have higher rates of suicide, but some studies show that whites have a higher rate of suicidal ideation, while others do not show this (Perez-Rodriguez et al, 2010). Though, as Balis and Postolache (2010) show, studies show that while there is conflicting evidence in regards to racial/ethnic differences in suicide, whites still attempt it the most. However, suicide for young black Americans is on the rise. Ahmedani et al (2016) show that “Nearly 27% of White individuals made a mental health visit versus less than 20% of Asian, Hawaiian/Pacific Islander, and Black individuals in this period. Within 4 weeks, all visits and mental health visits remained most common for White individuals (67.3% and 47.4%, respectively) and least common among Asian individuals (52.8% and 31.9%, respectively). Within 52-weeks, more than 90% made any visit. Alaskan Native/Native American (81.5%) and White individuals (79.5%) made mental health visits 10–25% more often than other groups.” However, at least in Fulton County, Georgia, black suicide decedents were less likely to report depression than white suicide decedents (Abe et al, 2008).

However, for whites, as noted in this 1982 New York Times article, suicidal feelings “reflects feelings of loneliness and hopelessness, which can be greater factors as one grows older; for instance, after loved ones have died” whereas for older white men, loss of status may be a cause, which would not be that prevalent in lower SES ethnicities. The article seems to implicate loss of status as a main cause for higher rates of suicide in white Americans, and states that as other, lower SES ethnies attain higher status, that suicide rates would rise for them as well.

Another cause could be prescription drugs, for instance in the Northeast which has been hit hard by the opiate/heroin crisis which leads to more white deaths. Robert Putnam puts this on “the links between poverty, hopelessness and health” and states that the suicide rate has declined for two groups, black males and males over the age of 75. Further, “divorce, economic strain, or political repression are often characterized as suicide risks.” Cheng et al (2010) show that “A high level of identification with one’s ethnic group was associated with lower rates of suicide attempts.” So, it seems that if one keeps their status, and has a high level of identification with their ethnic group, whites would then be protected against suicidal ideation. Nonmetropolitan counties also have higher rates of suicide than metropolitan counties (Ivey-Stephenson et al, 2017). People who livee in rural counties are less likely to seek help for mental problems (Carpenter-Song and Snell-Rood, 2016). Whites are also more likely to live in rural areas. This could explain higher rates of suicide in whites, along with loss of status, depression and drug use.

In conclusion, the ‘Hispanic’ paradox doesn’t exist; whites attempt/commit suicide more due to loss of status and since most whites live in rural areas, they do not seek help for their mental health problems which then leads to suicide. In regards to black maternal mortality/infant mortality rates, if they have midwives present during and after the birth, mortality rates have decreased. If these trends continue, there will be racial equality in terms of maternal/infant mortality in 18 states. The AmRen article was good and well written, but there were a few huge flaws. The author assumed that since the ‘Hispanic paradox’ exists, that this should have one disregard the effects of, say, stress on blood pressure in black Americans, as I have discussed in the past. But since the ‘Hispanic’ paradox does not exist, then you cannot say that (perceived) discrimination and ‘racism’ is not a cause for higher rates of mortality in blacks compared to whites.


Agriculture and Evolution: A Reply to The Alternative Hypothesis

2050 words

I love nutrition science. So much so that I read a new book on it every week. The Alternative Hypothesis has a pretty old video on agriculture and evolution. I strongly disagree with his main thesis. I strongly disagree with his denigration of Gary Taubes. Most of all, I strongly disagree with what he says about the East Asian rice eaters because since that video has been made, the carbohydrate/insulin hypothesis of obesity has changed to the insulin hypothesis of obesity.

In the very beginning of the video he brings up Gary Taubes’s research on low-carb diets and how people tend to be healthier than those who eat higher carb diets. He brings up the East Asians who eat a lot of rice. However, it’s clear he doesn’t know that the percent of carbohydrate intake is nowhere near as important as the absolute amount of carbohydrate consumed:

  1. They consume a fraction of the sugar we do.  More sugar consumption leads to greater insulin resistance, more fat creation, less fat breakdown, and more fat accumulation.
  2. They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
  3. They consume a ratio of omega-6 to omega-3 PUFA that is much lower than we do.  This mayfurther reduce any insulin resistance brought on by the glucose they do consume (in smaller doses and with less sugar).

The fact that East Asians didn’t have high rates of diabesity (diabetes and obesity) was a big blow to the carbohydrate insulin hypothesis. However, the East Asian rice paradox is simply explained by low, if non-existent, consumption of refined carbohydrates. Those populations actually consume fewer total carbohydrates than Western diets, and have lower levels of glycemic load as a result. To quote Mark Sisson:

Before recently, Asians ate less refined sugar and used animal fats for cooking. Sugar intake is rising now, of course, and cooking oils made from corn and soybean have largely replaced lard and tallow, but rice in the context of a low-sugar, no-HFCS (remember, the oft-cited 55/45 fructose/glucose breakdown for HFCS is highly misleading and actually quite often incorrect), low-vegetable oil, nose-to-tail nutrient-dense diet is (or was) acceptable. You can’t reduce a food down to its constituent parts and focus on, say, the bit of fructose in a blueberry and then condemn the entire berry because of it. Similarly, you can’t reduce a diet down to a single constituent food and condemn – or praise – it based on that single food. You have to look at the entire picture, and the Asian diet is largely a nutritious one.

These paradoxes where one population seems to disprove a certain hypothesis are pretty easily explainable with the existing data. There are numerous reasons why East Asian rice eaters have lower rates of diabesity. Dr. Jason Fung also explains why:

Wheat, particularly in the modern iteration may be particularly fattening for numerous reasons.  The high level of amylopectin means that most of the starch contained in flour is efficiently converted to glucose.  This deadly combination of wheat and sugar has been introduced into the Chinese diet.  The result is a Chinese diabetes catastrophe.  The prevalence of diabetes in China has now even outstripped the USA.

This is the answer to the paradox of the Asian Rice eater puzzle.  Why didn’t the Chinese have a diabetes epidemic in 1990 with all their white rice?  Well, because they didn’t eat any sugar (fructose), they were not developing insulin resistance.  Because they were not snacking all the time, they had periods of low insulin level that helped prevent the development of insulin resistance.  So the high rice intake by itself was not enough to cause either of diabetes or obesity.

Then he says that whites intake more total carbs in comparison to blacks and ‘Hispanics’ (1:32 in the video). This is wrong.

Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake.  Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.

Diaz et al state in the results of the study:

Dietary differences are seen by ethnicity, with non-Hispanic whites having higher
energy, saturated fat and total fat intake, while Hispanics had higher carbohydrate intake and African-Americans had lower fibre intake.Both African-Americans and Hispanics had higher levels of fasting insulin, demonstrating lower insulin sensitivity in comparison with non-Hispanic whites.
Non-‘Hispanic’ whites have higher overall energy and fat intake. This means that carbohydrates are less of a percent of the overall diet. In comparison, blacks had lower fiber intake. This means that they eat more processed foods. The same with ‘Hispanics’. Since they constantly spike their insulin with refined carbs, they have higher rates of fasted insulin and thus, have lower insulin sensitivity which is a risk factor for pre-diabetes.
Moreover, from my own personal work with people’s diets, whites eat less refined carbs than blacks or ‘Hispanics’, and while an anecdote, I’ve worked with hundreds of people.
Table 2 of the study shows that whites have a higher total kcal intake in comparison to blacks and ‘Hispanics’, ‘Hispanics’ have a statistically significant higher carb consumption, and blacks eat less fiber. Since whites eat more dietary fat and have a higher fiber intake, that protects them against higher rates of the *average population* that will be obese. Blacks consume less fiber. Dietary fiber actually protects against obesity, so the fact that blacks don’t eat more fiber shows that they eat more refined foods (it’s easily explainable why ‘Hispanics’ eat more fiber. They consume more beans and other fibrous, whole foods). However, since ‘Hispanics’ are more likely to be poor (correlated with low intelligence), they then cannot afford higher quality foods.
Drewnowski and Specter (2004) showed that 1) the highest rates of obesity are found in populations with the lowest incomes and education (correlated with IQ); 2) an inverse relationship between energy density and energy cost; 3) sweets and fats have higher energy density and are more palatable (food scientists work feverishly in labs to find out different combinations of foods to make them more palatable so we will eat more of them); and 4) poverty and food insecurity are associated with lower food expenditures, lower fruit and vegetable intake, and lower-quality diet. All of these data points show that those who are poor are more likely to be obese due to more energy-dense food being cheaper and fats and sugars being more palatable. it’s worth noting that dietary fat combined with carbohydrates and the subsequent insulin spike stores the dietary fat as body fat as well as the insulin telling the body to not burn fat.

I’ve written more on this here and here.

So now that I’ve established that blacks and ‘Hispanics’ consume more total carbohydrates from refined foods, now I’ll show the physiologic effects of insulin.

Insulin inhibits the breakdown of fat in the adipose tissue by inhibiting the lipase that hydrolyzes (the chemical breakdown of a compound due to a reaction with water) the fat out of the cell. Since insulin facilitates the entry of glucose into the cell, when this occurs, the glucose is synthesized into glycerol. Along with the fatty acids in the liver, they both are synthesized into triglycerides in the liver. Due to these mechanisms, insulin is directly involved with the shuttling of more fat into the adipocyte. Since insulin has this effect on fat metabolism in the body, it has a fat-sparing effect. Insulin drives most cells to prefer carbohydrates for energy. Putting it all together, insulin indirectly stimulates the accumulation of fat into the adipose tissue.

Do you see why blacks and ‘Hispanics’ are more susceptible to obesity?

Another glaring error he commits is not separating refined carb consumption with natural carb consumption. Refined carbs spike insulin much more than those foods with natural carbohydrates. East Asians do not have a “higher carbohydrate tolerance than Europeans” (2:06 in the video). This one huge error he commits completely discredits his hypothesis.

He then goes on to talk about India’s diabetes rates. But why is it increasing? Because of Western diets. It’s not about a “lower carbohydrate tolerance” as he says at 3:07, it’s about consuming more refined carbohydrates.

Then at 5:05, he says that he’s “solved Gary Taubes’s race problem in regards to diet”. He did nothing of the sort.

I, of course, have no problem with his IQ data. I have a problem with the conclusions he jumps to in regards to carbohydrates and diabetes. He clearly didn’t look at other factors that would explain why East Asians have lower rates of diabesity (which is increasing as they adopt a Western lifestyle… Weird…). The same thing explains it with the Australian Aborigines.

I have absolutely no problem with the second half of his video. My problem is the first half of it–his denigration of Taubes, non-understanding of insulin spikes in comparison to the quality of carbohydrate ingested and not controlling for refined carbs– as it’s clear he didn’t do extensive research into these populations (which Taubes and others have) to show why they don’t have higher rates of diabesity.

What he doesn’t touch on are “obesogenic environments” which is defined as “the sum of influences that the surroundings, opportunities, or conditions of life have on promoting obesity in individuals or populations”. What a huge coincidence that most of the populations he cited today with higher rates of diabesity live in first-world nations, otherwise known as obesogenic environments.

He should have spoken about the Pima Indians and their rates of diabesity. They didn’t have rates of diabesity as high 100 years ago. Why? The introduction of the obesogenic environment. Prisancho (2003) in his study on the Pima and reduced fat oxidation in first-world countries showed how the Pima preferentially burn carbs and not body fat for energy. Fat-burning would account for 9 kcal lost and CHO for 4. Since they preferentially burn carbs for energy and not fat, this shows why they have higher rates of diabesity. It’s not that it’s a genetic susceptibility to burn CHO for energy over fat (there may be a small genetic component, but it doesn’t override the effects of the actual diet). I’ve shown insulin’s role in fat storage above, do you see why the Pima have this diabesity epidemic after the introduction of refined carbohydrates and the obesogenic environment?

Added sugars and salts in foods causes us to want more of those foods. As I alluded to above, food scientists continuously work to find out which combinations of sugar, salt and fat will be more hyperpalatable to us and make us eat them more. Whites nor East Asians have a ‘higher carb tolerance’, they just eat different types of carbs (mostly unrefined, in comparison to blacks and ‘Hispanics’ anyway). If any individual were to overeat on high carb foods they would become diabetic and obese. Whites nor East Asians are exempt from that.

In sum, he didn’t look at where the carbs came from, only total carb intake. Refined carbs and unrefined carbs do different things in the body. The whiter a processed food is, the more it is refined. The more a food is processed, the more its natural nutrients such as fiber are taken out. These low-fat refined foods are one cause of obesity. However, it’s way too complicated to say that only refined carbohydrates cause diabesity.

I strongly recommend he read Taubes’s and Fung’s books. If he did, he wouldn’t have said what he said about Taubes’s theory and completely disregard the absolute total amount of carb intake and not the total amount of carbohydrates ingested.

Race, Obesity, Poverty, and IQ

2100 words

America has a current and ongoing obesity epidemic. Some ethnicities are more likely to be obese or overweight than others due to lower intelligence which means a lack of ability to delay gratification, lack of ability to think into the future, lower funds which translates to eating more refined carbohydrates which means more blood glucose spikes which then leads to obesity as I will show. Insulin has a causal relationship with obesity so those who lack funds to buy healthier food then turn to refined foods high in carbohydrates as they are cheaper and more abundant in low-income neighborhoods.

Adult obesity rate by State (top 5) is: 1) Louisiana (36.2 percent), 2) Alabama (35.6), West Virginia (35.6), and Mississippi (35.6), and 5) Kentucky (34.6) with the 5 least obese States being 51) Colorado (20.2), 49) Hawaii (20.7), 48) Montana (23.6), 47) California (23.2), and 46) Massachusetts (24.3). Notice how the States with higher rates of obesity are in the South and the States with the lower rates are in the North, give or take. The average IQ for these States as follows: Lousiana: 95.3, Alabama: 95.7, West Virginia 98.7, Mississippi 94.2 (lowest IQ State in the country, largest black population at 37 percent), and Kentucky at 99.4. The average IQ for those States is 96.66. The average IQs for the States with the lowest obesity rates are: Colorado 101.6, Hawaii 95.6, Montana 103.4, California 95.5, and Massachusets 104.3 (highest IQ State). The average for these States being 100.08. So there is a 4 point IQ difference between the top 5 States with the highest and lowest percentage of obese people, which goes with the North/South gradient of higher IQ people living in the North and lower IQ people living in the South. Back in 2014, a California real estate group took 500,000 Tweets using a computer algorithm and estimated intelligence based on spelling, grammar, and word choice and found a difference in State by State intelligence. Notice how the further North you go the higher the average intelligence is, which is then correlated with the obesity levels in that State.

With poverty rates by State, we can see how the States in the South have less intelligent people in them which then correlates to the amount of obesity in the State. Though, there are some anomalies. West Virginia and Kentucky have a super majority of whites. This is easily explained by the fact that less intelligent whites live in those States, and since both the poverty rates and obesity rates are high, it follows that the State will be less intelligent than States that have more intelligent people and less obesity.

It is known that intelligence is correlated with obesity at around -.25 (Kanazawa, 2014). The negative correlation between intelligence and obesity means that they are inversely related so, on average, one with higher intelligence has less of a chance of being obese than one with lower intelligence. The States with the lowest IQ people having those with the highest BMIs corroborates this. In America, obesity rates by ethnicity are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for ‘Hispanics’.

Now that we know the average intelligence rates by State, the percentage of obese by State and the demographics by State, we can get into why obesity rates correlate with intelligence and race.

Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake.  Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.

Drewnowski and Specter (2004) showed that 1) the highest rates of obesity are found in populations with the lowest incomes and education (correlated with IQ), 2) an inverse relationship between energy density and energy cost, 3) sweets and fats have higher energy density and are more palatable (food scientists work feverishly in labs to find out different combinations of foods to make them more palatable so we will eat more of them), and 4) poverty and food insecurity are associated with lower food expenditures, lower fruit and vegetable intake, and lower-quality diet. All of these data points show that those who are poor are more likely to be obese due to more energy-dense food being cheaper and fats and sugars being more palatable.

Now that I’ve shown the relationship between race and IQ by state, obesity rates by state, insulin sensitivity by race, and that those in poverty are more likely to be obese, I can now talk about the actual CAUSE of obesity: insulin.

The conventional wisdom is that if you consume more kcal than you expend, you will gain weight, whereas if you consume less than your daily needs you will lose weight. This has been unchallenged for 50 years. Also known as Calories In and Calories Out (CICO), this mantra “eat less and move more!!!” has been bleated over and over with horrendous results. The CICO model only concerns itself with calories and not insulin which is a causal factor in obesity

In this study, participants in the basal insulin group which received the lowest average insulin dose gained the least average amount of weight at 4.2 pounds. Those on prandial insulin gained the most weight at 12.5 pounds. The intermediate group gained 10.3 pounds. More insulin, more weight gain. Moderate insulin, moderate weight gain. Low insulin, low weight gain.

Researchers compared a standard dose of insulin to tightly control blood sugars in type 1 diabetic patients. At the end of the 6 years, the study proved that intensive control of blood sugars resulted in fewer complications for those patients.

Though, in the high dose group, they gained on average 9.8 pounds more than those in the standard group.

More than 30 percent experienced major weight gain! Prior to the study, both groups were equal in weight. But the only difference was the amount of insulin administered. Were the ones given high levels of insulin all of a sudden more lazy? Were those who gained weight suddenly lacking in willpower? Were they lazier before the study? We’re they more gluttonous? No, no, and no!!



Finally, Henry et al (1993) took Type II diabetics and started them off with no insulin. They went from 0 units of insulin a day to 100 units at 6 months. As higher rates of insulin were administered, weight rose in the subjects. Insulin was given, people gained weight. A direct causal relationship (see figure above). However, what’s interesting about this study is that the researchers measured the amount of kcal ingested, the number of kcal ingested was reduced to 300 per day. Even as they took in less kcal, they gained 20 pounds! What’s going on here? Well, insulin is being administered and if you know anything about insulin it’s one of the hormones in the body that tells the body to either store fat or not burn it for energy. So what is occurring is the body is ramping down its metabolism in order for the subject to store more fat due to the exogenous insulin administered. Their TDEE dropped to about 1400 kcal, while they should have been losing weight on 1700 kcal! The CICO model predicts they should have lost weight, however, adaptive thermogenesis, better known as metabolic slow down, occurred which dropped the TDEE in order for the body to gain fat, as insulin directly causes obesity by signaling the body to store fat, so the body drops its metabolism in an attempt to do so. 

Putting this all together, blacks and ‘Hispanics’ are more likely to be in poverty, have lower intelligence, and have higher rates of obesity and diabetes. Furthermore, blacks are more likely to have metabolic diseases (adaptive thermogenesis aka metabolic slowdown is a metabolic disease) which are related with obesity due to their muscle fiber typing which leads to lower maximal aerobic capacity (less blood and oxygen get around the body). Type II skeletal muscle fibers’ metabolic profile contributes to lower average aerobic capacity in blacks. It also is related to cardiometabolic diseases, in my opinion because they don’t have the muscle fiber typing to run long distances, thus increasing their aerobic capacity and VO2 max.

Due to the diets they consume, which, due to being in poverty and having lower intelligence, they consume more carbohydrates than whites, which jacks their blood glucose levels up and the body then releases insulin to drive the levels glucose in the body down. As insulin levels are spiked, the body becomes insulin resistant due to the low-quality diet. Over time, even a change in diet won’t fix the insulin resistance in the body. This is because since the body is insulin resistant it created more insulin which causes insulin resistance, a vicious cycle.

Poverty, intelligence and race both correlate with obesity, with the main factor being lower intelligence. Since those with lower IQs have a lack of foresight into the future, as well as a lower ability to delay gratification which also correlates with obesity, they cannot resist low-quality, high-carb food the same way one with a higher IQ can. This is seen with the Diaz et al study I linked, showing that whites have higher levels of fat intake, which means lower levels of carbohydrate intake in comparison to blacks and ‘Hispanics’. As I’ve shown, those in poverty (code word for low intelligence) ingest more refined carbohydrates, they have higher levels of obesity due to the constant spiking of their insulin, as I have shown with the 3 aforementioned studies. Since blacks and ‘Hispanics’ have lower levels of intelligence, they have lower levels of income which they then can only afford cheap, refined carbs. This leads to insulin being constantly spiked, and with how Americans eat nowadays (6 times a day, 3 meals and snacks in between), insulin is being spiked constantly with it only dipping down as the body goes into the fasted state while sleeping. This is why these populations are more likely to be obese, because they spike their insulin more. The main factor here, of course, is intelligence.

Another non-CICO cause for obesity is exposure to BPA in the womb. Researchers carried out BPA testing in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period. The sample was of blacks and Dominicans from New York City. Whites drink less bottled water, which has higher levels of BPA. Blacks and ‘Hispanics’ consume more, and thus have higher levels of obesity.

In conclusion, blacks and ‘Hispanics’ are more likely to be in poverty, have lower intelligence, higher rates of obesity and lower incomes. Due to lower incomes, cheap, refined carbohydrates is what they can afford in bulk as that’s mostly what’s around poor neighborhoods. Ingesting refined carbohydrates more often consistently jacks up blood glucose which the body then releases insulin to lower the levels. Over time, insulin resistance occurs, which then leads to obesity. As I’ve shown, there is a direct causal relationship between the amount of insulin administered and weight gain. With the aforementioned factors with these two populations, we can see how the hormonal theory of obesity fits in perfectly with what we know about these ethnic groups and the obesity rates within them. Since people in poverty gravitate more towards cheap and refined carbohydrates, they’re constantly spiking their insulin which, over time, leads to insulin resistance and obesity.

Obesity and Intelligence

1600 words

[Edit: My view here has changed, read my recent article Is Diet an IQ Test?  It isn’t and it is, of course, much more nuanced than ‘IQ’ (which is a proxy for social class’ leading to obesity which would imply lack of funds and education on what and when to eat. Obesity is much more complex than ‘IQ’, numerous other variables come into play and since ‘IQ’ (which is just a proxy for general knowledge ‘is low then the individual in question won’t know what and when to eat and since this occurs in low income families more often than not who have low IQs then this effects them the most.] 

The relationship between intelligence and obesity is often misinterpreted. Numerous studies have concluded that becoming obese leads to a drop in IQ. This mistake happens due to improper interpretation of cross-sectional studies. However, analyses of population-based, longitudinal data show that low intelligence from birth causes obesity. No credible evidence exists for obesity lowering intelligence. There are, however, mountains of evidence showing that low intelligence from childhood leads to obesity (Kanazawa, 2014).

Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ. Those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs to learn how to manage their weight.  Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).

Less intelligent individuals are more likely to become obese than those who are more intelligent. With what we know about low IQ people and how there is a strong relationship between low intelligence and lack of ability to delay gratification, we can see how this lack of thought for future problems for their actions in the present can manifest itself in obesity.

This study claims that there is a link between morbid obesity and a drop in IQ. The researchers compared 24 children who weighed 150 percent of their bodyweight before age 4 with 19 children and adults with Prader Willi’s Syndrome, using 24 siblings as controls as “they share the same socioeconomic environment and genetics”. Prader Willi’s Syndrome (PWS) is a chromosomal disorder in which chromosome 15 is deleted. They have an almost insatiable desire to eat,which can cause one suffering from PWS to eat themselves to death. Those with PWS were found to have an IQ of 63, while those who became obese were found to have an IQ of 78 with the control siblings having an IQ of 106. The researchers were surprised to see such a difference in IQ between siblings. They then state that this could be one facet of obesity that could be irreversible. MRI scans of the cohort discovered white matter lesions on the subjects with PWS and early-onset obesity. The researcher says that these lesions could affect food seeking centers in the brain leading to a want to gorge on food. Seeing how those with PWS eat when unsupervised, this is an interesting hypothesis.

This study compared 49 teens with metabolic syndrome and 62 peers without the disorder, while controlling for socioeconomics status. They found significantly lower scores in arithmetic, attention and attention span, spelling, mental flexibility and regions of the brain with lower volumes of matter in the hippocampus and white matter integrity.

There are a few problems with these two studies. In a population-representative birth cohort study of 1037 children, it was found that cohort members who became obese had a low IQ, as expected. But, contrary to what your study said, cohort members didn’t exhibit a decline in IQ from becoming obese, they instead had a lower IQ since childhood. There is no evidence of obesity contributing to a decline in IQ, even in obese individuals and those on the verge of metabolic syndrome. Another problem is that they wrongly conclude that obesity leads to lowered intelligence, completely misinterpreting the extremely strong negative correlation between obesity and intelligence.

This study shows how obese mothers give birth to less intelligent children. In an observational study (already garbage), the researchers took 3412 participants and found a strong relationship with pre-pregnancy obesity and math and reading scores in children. For math, a 3 percent reduction was observed. There was a 3-point drop in reading scores with math scores showing a decline of 2 points. These differences are within the normal variation between tests, so it’s nothing to take note of. Also, this is an observational study. I have shown above that longitudinal studies are superior for this, as well as researchers misinterpreting the results found from their studies.

There is a strong relationship between parental years of education and childhood obesity. Since the mother’s IQ is the most important predictor of a child’s IQ *, that passes on to the child as well. (BMI is also 80 percent heritable). **.

So because of those factors involving the mother and child, that is what accounts for it. Not the environmental factors brought up.

This study claims that overweight parents are more likely to fail. This is all due to the fact that low IQ people are more likely to be obese or overweight, with heritability of BMI being .8, you can see how low IQ is the cause of both of those variables. 

This shows that binge eating is linked to memory loss. I heard about a study a few months ago actually like this. Rats were fed high fat diets and they noticed that the brain microglia actually started to eat neuronal pathways actually leading to a decrease in cognitive ability. But they said that returning to a new diet will stop its effects. Researchers say the negative cognitive effects are reversible, but I already gave the citstion about obesity not being linked to decreased IQ. I should also note that this study was carried out on rats and while this may be a factor for humans as well, a few studies need to be done.

Binge eating, however, actually has a genetic component. Though this was only observed in girls. One reason I can think of for this is that women need higher body fat for a leptin release so puberty can begin so they can bear children.

This article purports to show 5 ways obesity affects the brain. Obesity does cause food addiction, however, those who lack the ability to delay gratification are more likely to not be able to control their impulse to overeat. I always link to the MRI scan showing the control, obese and cocaine user’s brain. Interesting to see that sugar is just as addictive as cocaine. Obesity doesn’t make us more impulsive. Check out the Marshmallow Experiment, as well as its follow-up studies. Those who are more impulsive are more likely to be obese, as well as have lower SAT scores.

Satoshi Kanazawa also noted that childhood IQ predicted whether or not one would become obese at the age of 51. General intelligence in childhood has a direct effect on weight gain, BMI, and obesity, net of parents education and SES, parents BMI, the child’s social class, and sex. More intelligent children grew up to make healthier choices, and therefore stayed leaner than those children who were less bright. The link between childhood obesity and intelligence also shows that the effect between childhood is unmediated by education of income. Meaning, those with lower IQs in a higher socioeconomic bracket STILL have the same chance of becoming obese as those in the lower socioeconomic bracket. Finally, parental BMI itself is a consequence of parental general intelligence, which the parents pass on to their children. This shows the extremely high heritability of obesity as well as showing how intelligence plays a factor in the causes of obesity.

The known differences in ethnic obesity rates generally mirror the intelligence of those populations. All populations are showing a sharp dysgenic decline, which coincides with a more obese population as well. Sociologists and the like may say that those who are poor cannot afford the same types of food that those who have more wealth can. However, this is a false statement. Whole foods are not more expensive. The conclusion that was (obviously) reached is that there is expensive and non-expensive junk food as well as whole foods. Natural diets will not cost more, all things being equal. If you know how to eat and how to buy food, you will avoid spending too much money. This goes back to intelligence. One with a higher IQ will be able to think of what his present actions will lead to in the future while those with a lower IQ live in the now without a care for the future, which then manifests itself in their obesity.

There are numerous articles showing that the causality for low intelligence is not becoming obese, but that those who become obese have a lower IQ since childhood. Longitudinal studies show the relationship, while observational studies show that obesity drops intelligence. Clearly, observational studies are inferior for seeing the relationship between IQ and obesity. This then leads to researchers misinterpreting the data and drawing wrong conclusions.

The IQ of the mother is the most important factor in determining the future intelligence of the child.

** This is a great one. In a meta-analysis of twin and family studies, including mono and dizygotic twin studies, with a sample of 140,525 people, heritability of BMI was found to be between .75 and .82. Both extremely high correlations. Since the heritability of intelligence as well as height (another good predictor of intelligence), there is good evidence for the claim that becoming obese is due to lower childhood IQ, which is genetic in nature.

Towards a Theory of Everyone: Chanda Chisala Rebuttal on the Nature of the Black-White IQ Gap

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Chanda Chisala has been writing a series of articles for the Unz Review for almost a year now. They are on the nature of the black-white IQ gap. I’ve been eagerly awaiting his theory on the cause of the gap, as I always welcome any and all new information concerning this. Well, I was pretty underwhelmed by his theory.

Sowell has always used two arguments to cast doubt on the genetic hypothesis: the first one is the Flynn Effect or prior versions of it that he had noted himself, which shows that IQs have been rising with time for blacks and other people all over the world.

The “Flynn Effect” is rubbish. PumpkinPerson says:

It turned out Rushton was one of those “The Flynn effect is irrelevant” people. He found it prima facie absurd that we could have been a nation of mentally disabled people a century ago. It simply didn’t make any sense to him, given the outstanding achievements of early 20th century society. But it didn’t make any sense to me why the same tests that were culture reduced enough to measure the intelligence of South Africans could be so wrong when measuring Victorian intelligence. I needed an explanation. The Flynn effect is unrelated to g (general intelligence) and that was enough for him to just dismiss it and move on.

So even though Rushton and Jensen rebutted Flynn, as well as Flynn and Dickens, Chisala still chooses to use the Flynn Effect argument. Here is why it is irrelevant:

Let’s say Flynn is right. The average black now is as intelligent as the average white in 1945. That’s supposed to show that the race difference in IQ is environmentally caused because there hasn’t been that much genetic change in the white population and the IQ has allegedly gone up 15 points. So, you can have a 15 point difference created by just an environmental change, no one knows why. Some think better nutrition or malnourished brain, etc. That’s also a fallacy. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. The Flynn Effect make’s that highly unlikely and here’s why.

The Flynn Effect, assuming it’s real, has been acting completely uniformly in every population. Any country you ask, the rate of increase is 3 per decade. That means it’s an environmental factor that affects whites and blacks the same way as well as the whole world. And as a result of this uniform environmental factor, you have a difference in IQ that’s being preserved. That would suggest that the response on the parts of blacks and whites is due to some non-environment factors, a genetic factor, which is making the difference in IQ remain constant as the Flynn Effect goes into effect.

What makes it even more unlikely, in the last 60 years, their environments have become very similar since segregation. These differences don’t exist now, they go to the same schools by court order, same TV shows, same movies, basically same environment for both, and yet, that increasing similarity in the environment, the Flynn Effect, the IQ gap has remained intact. Which means whatever counts for the gap is genetic and not environmental. The more and more similar the environment, the less and less of the difference can be due to the environment and the more and more it must be due to genes. So this 15 point gap surviving these changes in the environment, seems more and more likely to be genetic in origin.

So because this ‘Effect’ is the same across all populations and the gap didn’t close, that means it’s genetic. If the gap persisted even when IQs were rising 3 points per year, the B-W gap has still persisted, proving that it’s genetic.

That is why the Flynn Effect is irrelevant. This “Effect”, has been a slight upward trend in IQ, around 3 points per decade, which, in my opinion, has to do with the advent of better nutrition and an industrialized society. The rise in IQ started around 1880, almost perfectly coinciding with the industrial revolution in America. Along with a more industrialized society, it’s possible to give most citizens in the country good enough nutrition to where they are not iodine deficient (adding iodine to our salt boosted Americans IQs), as well as being deficient in zinc, iron, protein and certain B vitamins which the effects of not getting enough leads to the brain not growing to its full potential, which in turn leads to a lower IQ.

One more point on the Flynn Effect. The Flynn Effect does not occur on g, as it is not a Jensen Effect. Rushton defines Jensen Effect as follows:

Significant correlations occurring between g-factor loadings and other variables have been dubbed “The Jensen eff€ect”.

Thus the secular increase in test scores (the “Lynn±Flynn e€ffect”) is not a “Jensen e€ffect” nor is this the first time the discriminating power of the Jensen eff€ect has been shown.

The Flynn Effect is not on actual g. The black-white IQ gap is most heritable on those sub-tests that correlate highly with g. Through correlations on scores on inbreeding depression, Rushton and Jensen (2005) conclude that the magnitude of the black-white IQ gap is 80 percent genetic and 20 percent environmental.

Now to get to this other part of his theory.

The second very unique and original argument he has used is the differential IQ performance of black males and females, which seems to favor the females. He charges that the genetic hypothesis can not explain this, but it is explainable under an environmental hypothesis.

Sowell’s second argument is much stronger than the Flynn Effect argument because it is very difficult for hereditarians to explain why there should be a gender difference in African American IQ, especially one favoring females (let’s call this the “Sowell Effect,” to avoid repetition). This is very problematic for hereditarians, particularly since the trend is normally for male IQ to exceed female IQ, especially at the higher levels of the IQ distribution curve. We can see this unique trend among blacks even in the applications to medical school, a field that is considered a good metric for group intellectual comparisons.

This is very simply explained. Occam’s Razor anyone?

Even today in Africa, the women did the hunting and gathering, giving them more selective power. The same holds true for Eurasian men, who have a slight advantage in IQ over Eurasian women. Because of the colder climate in Eurasia, meat was one of the staples they had. So that shifted selection pressure from women over to men. Since men had the food, and the ability to hunt for it for that matter, men had more selection power to select the best possible mates. This led to Eurasian women being selected for beauty, whereas this led to African men being selected for physical attractiveness.

To quote from Erectus Walks Amongst Us:

In Africa, the women, even today, farm and gather food, so they have more selection power, but in the colder climates more of the food was meat, especially in the winter, and hunting was done by men, shifting some selection power to men. (Miller, 1994a). As a result of selection by men, Eurasian women have become more beautiful and, as a result of selection by women, Eurasian men have become workaholics and slightly more intelligent than Eurasian women (more intelligence = a better provider in Eurasia). African women have become slightly more intelligent than African men, however, who have become the more physically attractive sex.

So more intelligence led to a better provider. Being able to farm for and or hunt for food gave those who did it the selection ability to be able to sexually select to their liking.

Sowell (2013) claims this empirical victory in Intellectuals and Race (page 79):

Further evidence that the male-female difference in IQs among blacks is cultural is that black orphans raised by white families show no such female superiority in IQs, in addition to both sexes having higher average IQs than other black children.

Chisala says the Sandra Scarr data from the Minnesota Study does not back up this claim.

There are other studies that could possibly back Sowell up if he is right and we should check those too. For example, there is the well-known Eyferth Study in Germany which monitored the IQs of illegitimate children of black and white American soldiers who were stationed there at the end of the Second World War.

The Eyferth Study is a joke.

Wikipedia got its data from The g Factor, a book by Arthur Jensen (1998) that is probably the most cited in the racial intelligence debate. I went to the cited page and indeed found that Wikipedia had correctly reported Jensen’s data. The Sowell Effect had apparently disappeared among the black children born in Germany and the strong culture hypothesis seemed to be vindicated.

Arthur Jensen explains the cause for the mixed race children (and at the same time the cause for black female children having a higher IQ) on pp 483 of The g Factor: The Science of Mental Ability:

Finally, heterosis (the outbreeding effect; see Chapter 7, p. 196) probably enhanced the IQ level of the interracial children, thereby diminishing the IQ difference between the interracial children and the white children born to German women. A heterotic effect equivalent to about + 4 IQ points was reported for European-Asian interracial offspring in Hawaii.

This means that we can also resolve the debate about whether the black soldiers in this experiment were more selected than the white soldiers. It appears that the hereditarians were probably right on this point: the black soldiers had to have been significantly more intelligent than the white soldiers because the presence of a Sowell Effect indicates that the IQ of the black children has received extra depression (through an abnormal lowering of the male IQ, as usual.) However, it’s another Pyrrhic victory for hereditarians: the continued existence of apparent extra depression for black male IQ makes their simple models impotent, just as it does for standard environmentalist models.

Yet another point that Rushton and Jensen shoot down in their magnum opus paper:

Second, 20% to 25% of the “Black” fathers were not African Americans but French North Africans (i.e., largely Caucasian or “Whites” as we have defined the terms here). Third, there was rigorous selection based on IQ score in the U.S. Army at the time, with a rejection rate for Blacks on the preinduction Army General Classification Test of about 30%, compared with 3% for Whites (see Davenport, 1946, Tables I and III).

Huge error. About one-quarter of the ‘black fathers’ were French North Africans! Because North Africans have a higher genetic potential for IQ (nowhere near that of SSA), this is not a true representation of black fathers and white mothers.

Thus, racial hereditarians can not explain why the race of the mother matters

Is he being serious right now? It’s easily explained. We know that the mother’s IQ is the most important predictor of the child’s IQ. The prenatal environment is better in the white mother than in the black mother. Due to the mother’s IQ being the most important predictor of a child’s IQ, doesn’t that end the black-white IQ debate right there? Due to the fact that mixed race black and white children with white mothers show higher IQs than those with a black mother and white father, doesn’t that end the black-white IQ debate?

We racial hereditarians can definitely explain why the race of the mother matters. You should have done a bit more research into this matter.

And now on to my favorite part of this article. It’s so out there in its propensity for being a possibility for the cause of this gap between the races.

In Black Rednecks and White Liberals, Sowell (2006) theorizes that the modern ghetto culture of black Americans came from their association with white rednecks during the time of slavery and he believes it is the preservation of this detrimental culture – preserved with the intellectual help of “white liberals” – that keeps the black IQ low due to its anti-educational, anti-intellectual disposition. Sowell convincingly demonstrates some very uncanny similarities between ghetto black culture today and some aspects of white redneck culture that was more dominant in the South in the past than it is today, as more and more whites have decided to abandon it.

One huge problem with this. If that’s the case, if the cause of lower intellectual achievement is due to black Americans association with white rednecks during the time of slavery, all we need to do is look at Africa to see how they did without the “association with white rednecks during the time of slavery”! We can also look at those countries never touched by colonialism to see that they’re the same backwards countries.

Of course there will be “uncanny similarities”. When you have two groups who have lived amongst each other for a certain period of time, traits of both groups will rub off on each other. This is not a genetic cause, but an environmental cause. The similarities come down to being around other groups.

And here it is, here is the kicker:

Although I agree that the case for a cultural transfer from some groups of Southern whites is very strong, I think it is more likely that this “culture” was actually passed to blacks genetically rather than through mere influence and imitation. If that is the case, then it was in fact the presence of relatively strong mutations in that sub-population of whites that was affecting the stranger aspects of their behavior and intelligence, and they passed on the same genetic condition to blacks through mating with the black women.

THIS is his big reveal? No. Way. This has to be one of the funniest things I’ve heard in the black-white IQ debate. Hey, Chanda, there is something called Regression to the Mean (nice post, Jayman), which throws your theory out of the water.

blacks in fact had more stable families and even had less out-of-wedlock children than whites. He uses this to show that if slavery was the root of these problems, they could have started much earlier.


In this paper by Steven Ruggles, he says that analysis confirms that the high incidence of black Americans of single parenthood and children residing without their parents is not a recent phenomenon. Data shows that from 1880 through 1960, black children were two to three times more likely to reside without one or both children than white parents. This directly goes in the face of what liberals say is the cause of the demise of the black family structure. Ever since blacks have been free from slavery has this begun to happen.

What explains this perfectly, is Rushton’s r-K Selection Theory (now known as Life History Theory). Those who are more r selected (Africans), will have more children but spend less energy caring for them. Conversely on the other side, those more K-selected (Orientals and whites in the middle of K and r), will have fewer children but show more attention to them.

Some of Sowell’s strongest critics on this theory also suffer from the same progressional problem. Scholar and investigative journalist, Steve Sailer, for example,argued that much of the negative behavioral tendencies in black ghetto culture must have come with them from Africa. His theory is also unlikely to be true if the statistics about marriage and out-of-wedlock births etc are true. If their culture came with them from Africa they would not have had a long period where that culture seems to have been almost absent only to forcefully show up much later, in generations that had the least connection to or memory of Africa.

Sailer is correct. See my above cite showing that from 1880 through 1960 black children were two to three times more likely to reside with one or both children than white parents.

So we can see that it’s not a recent phenomenon.

Our theory thus explains a paradox that is difficult to explain by present environmental or hereditarian models: when blacks from Africa, the Caribbean and the US are compared, it is the least white-admixed black group that apparently performs best (the Africans), followed by Caribbean blacks who are in between; the most white-admixed group, the native black Americans, do worst. And yet within these communities, it is not necessarily true that the more white-admixed individuals perform worse; they may actually be over-represented on the highest levels of academic or social performance.

Dr. James Thompson says the sample for the Caribbean blacks in the UK is not a representative sample. Also, the hereditarian theory does not say that ALL Africans and African-descended peoples have a lower average IQ. It’s perfectly within the hereditarian hypothesis to have some African countries, as well as peoples, descended from African countries around the world, show a genetically higher IQ.

The evidence of such deleterious mutations still existing among modern day poor whites can be seen, not just from their low intellectual performance (going even lower than poor Caribbean boys), but even from their violent reactions against their fellow well-performing students, a culture that is also seen among ghetto black Americans, which is further evidence of a mutational rather than an imitational cause.

Wow, you mean to tell me that American whites aren’t a monolith and that there are some white groups in America with a lower average IQ? News to me!!

This solves one of the stronger challenges raised against the Unzian Asian Exception conjecture, asking why it was not East Asians who produced the greatest epochs of human intellectual achievements in history if it is true that their average IQs have consistently been stubbornly high for most of modern human history. It would be because the same canalization that protected them from low intelligence also “protected” them from producing the numbers of super-creative intellects that would be required for such revolutionary achievements in a concentrated period of time. They have a small creative smart fraction, in short.

The cause for lack of East Asian creativity is due to conforming in East Asian societies, which Rushton says in Race, Evolution and Behavior that it’s a genetic trait. Rushton did say that a larger average brain size means more creativity and that with social restrictions lifted, that East Asians may possibly become more creative than whites.

From time to time Lynn notes anomalies in his theory that require explanations. One of these is that Europeans made most of the great intellectual discoveries, while the East Asians, despite having a higher IQ, made relatively few—a paradox extensively documented by Charles Murray in his 2003 book, Human Accomplishment. Lynn proposes an explanation for this: it may be that East Asians are more conformist than Europeans and this inhibits creative achievement. (In Race, Evolution, and Behavior, I presented evidence that this personality trait has genetic roots.)

Winters Are Good For Your Genes: Lynn Book Finds World Average IQ 90, Declining From North To South

And yet the same hereditarians admit the conspicuous paucity of highly significant originators and innovators among East Asians, despite showing over-representation in high intellectual aptitude, sometimes very precociously so. East Asian women, who have the highest canalization coming from gender and race, are the most exemplary of this contrast. The shortage of such super-creative phenotypes can not be because they lack the numbers of people with the right genotype, but because the genotype is “buffered” from phenotypic expression by canalization.

See above.

Ashkenazi Jews, on the other hand, may be the most over-represented at the top of creative achievements in different intellectual fields (from chess to physics to literature, etc) simply because they happen to also be quite lowly canalized.

No. No way. Ashkenazi Jews are over-represented at the top of creative achievements in different intellectual fields because they mated with Roman women thousands of years ago. I have already noted about the mother being the best predictor of child’s intelligence. That’s the cause for high Ashkenazi IQ, not canalization.

Lower canalization also means that their improvement will be more rapid when such environmental conditions positively change (as can also be seen among recent black African immigrants, whose radical improvements begin even in children who were born under bad conditions in Africa, thus defying all kinds of hereditarian limitations.)

This is a case of super-selection. Only the most intelligent peoples leaving the country to immigrate.

In short, there is basically false assortative mating among black elites on average. This also explains why the mixed black male children have lower IQ when their mother is black than when their mother is white, as we demonstrated above.

I went over this earlier. Black mothers have a worse prenatal environment than do white mothers.

This obviously would not mean that the usual theories of environmentalists are correct either, since it should also not make a difference to them if the boys are included or excluded from the black American samples, especially in elite families. However, as we have faithfully acknowledged, both environmentalists and hereditarians also have some empirically confirmed arguments. Our present hypothesis, taking account of differential gender and racial canalization in human populations, can hopefully help to unify the valid aspects of the environmental and hereditarian frameworks.

I’ve noticed that Chisala used a hybrid environmentalist-hereditarian position to explain his theory on the black-white IQ gap.

I refuted the “Flynn Effect”, as well as the part of the Eyferth Study that talks about higher black female IQ, refuted the section about Caribbean blacks in the UK, and finally, I refuted his claim that we hereditarians “have no explanation for a mother’s IQ being the best predictor of the child’s IQ”.

In conclusion, this is just an extremely long-winded way of saying “whites are the cause of low black achievement, crime, IQ and anything else negative that affects blacks in Western countries”.

If that’s the case, Mr. Chisala, why is Africa so backwards?

“Race is a Social Construct”: Part 1

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“Race is a social construct”. You may hear that a lot from uneducated people. They may say that since the definition of race is ‘ever-changing’, that race doesn’t exist and that it only exists in our minds. They obviously have no understanding of genetics and how we came to be today. If you want to get technical, everything is a social construct. The Universe is a social construct. We’re only giving definitions to what we perceive something to be, so with the logic of ‘race being a social construct’, then everything is a social construct. With that logic, the Universe doesn’t exist because it’s a social construct.

I will look at 3 articles in the first of many articles on this subject. One from Angela Onwuachi-Willig, Bill Nye and Ta-Nehisi Coates. All 3 have extremely wrong views on the biological reality of race, and I will prove that here. I will quote from each article and show how they are wrong with scientific studies as well as point out their bad logic.

I will begin with Angela Onwuachi-Willig. In her article for The New York TimesRace and Racial Identities Are Social Constructs, she says that because of the ever-changing definition of the term race, that it is a social construct and not a biological one.

Race is not biological. It is a social construct. There is no gene or cluster of genes common to all blacks or all whites. Were race “real” in the genetic sense, racial classifications for individuals would remain constant across boundaries. Yet, a person who could be categorized as black in the United States might be considered white in Brazil or colored in South Africa.

Race is not biological, it is a construct. There are no clusters of genes or one gene that is common in blacks or whites. That is correct, but her statement about race being social and not a biological construct is clearly ignorant as I will show below.


You can see in the picture above that races clearly do cluster in different clusters from other races. She is right about the changing definitions, especially Brazil, but Brazil is a special case. So much mixing has gone on in Brazil that there is evidence of skin color becoming independent of ancestry. One outlier example doesn’t make race a ‘social construct’. South Africa is also another one. They classify race in South Africa with four categories: black, colored, Indian/Asian or white. Obama would have been called ‘colored’ in South Africa today. But, again, just because there are changing definitions of race throughout the globe, doesn’t mean that race doesn’t exist.

Like race, racial identity can be fluid. How one perceives her racial identity can shift with experience and time, and not simply for those who are multiracial. These shifts in racial identity can end in categories that our society, which insists on the rigidity of race, has not even yet defined.

Is she making an argument for being ‘trans-racial’? I bet Rachel Dolezal would be happy.

In a society where being white (regardless of one’s socioeconomic class background or other disadvantages) means living a life with white skin privileges — such as being presumed safe, competent and noncriminal — whites who begin to experience discrimination because of their intimate connection with someone of another race, or who regularly see their loved ones fall prey to racial discrimination, may begin to no longer feel white. After all, their lived reality does not align with the social meaning of their whiteness.

I always hear about ‘white privilege’ but never get an actual definition of what it means. People complain about ‘white privilege’ because they, of course, don’t understand the biological reality of race. Anything that may prove innate differences between individuals or races they just can’t imagine exists because of what they’ve been taught their whole lives. She is talking about those whites who are in the BLM movement. The false ideals of egalitarianism are the cause of this.

More than 50 years ago, Congress enacted the most comprehensive antidiscrimination legislation in history, the Civil Rights Act of 1964. Half a century later in 2015, the same gaps in racial inequality remain or have grown deeper. Today, the unemployment rate for African-Americans remains more than double that for whites, public schools are more segregated now than they were in the 1950s and young black males are 21 times more likely to be shot and killed by the police than their white male peers. Even a white fourth-grade teacher in Texas, Karen Fitzgibbons, openly advocated for the racial segregation of the 1950s and 1960s on her Facebook page.

Right. IQ is the cause of the unemployment rate of African Americans. Not any imaginary forces such as ‘white privilege’. Public schools are more segregated today due to people wanting to be with others genetically similar to themselves. Blacks cause themselves to get shot and killed by police due to their actions during altercations with police officers. Oh no, someone has not politically correct opinions!! She should lose her job and never work a good job again!

That’s what the Left does. They attempt to shout you down with buzzwords so you can’t calmly and intellectually prove your case.

She is clearly wrong. Good thing this is called an ‘opinion piece’, there were few actual facts in it.

Now to touch on Bill Nye’s views on race. It’s funny. I loved his show when I was a kid. Now, knowing the truth about racial differences, hearing him say that made me lose all respect for him. He’s a mechanical engineer with a Bs from Cornell University. People only take what he says because he is ‘The Science Guy’ when he has no training in what he is talking about.

“We obsess about whether our dog is a pug-Jack Russell terrier mix with corgi overtones and an oaky finish. ‘An approachable little dog,’ whatever. They’re all dogs, okay? And so the idea of a purebred is just a human construct. There’s no such thing – in a sense there’s no such thing as a purebred dog.”

That right there is a fallacy. As with the woman’s article above, they both use the ‘continuum fallacy‘. The continuum fallacy is when someone rejects a vague claim because it’s not as precise as they want it to be. ‘There are no pure races’ or ‘there are no pure breeds of dog’, that doesn’t mean that genes don’t cluster differently, showing genetic differentiation.

“If a Papua New Guinean hooks up with a Swedish person all you get is a human.  There’s no new thing you’re going to get. You just get a human. Japanese woman jumping the African guy, all you get is a human. They’re all humans. So this is a lesson to be learned. There really is, for humankind there’s really no such thing as race. There’s different tribes but not different races. We’re all one species.”

Right. That doesn’t mean there is no such thing as race. Grizzly bears and polar bears can mate to create a prizzly bear. Does that mean species doesn’t exist? (I will touch on speciation at the end of this article.) Once again, that statement doesn’t deny the biological reality of race, as you can see from the picture above.


Researchers have proven, scientifically, that humans are all one people. The color of our ancestors’ skin is a consequence of ultra-violet light, of latitude and climate.

We all belong to the same genus, Homo, but again, that doesn’t disprove race. He’s correct in saying that our ancestors’ skin is a consequence of UV light of latitude and climate, and right there he proves us correct in stating that sunlight differences depending on where your ancestors evolved in the world are the cause of racial differences.

Despite our recent sad conflicts here in the U.S., there really is no such thing, scientifically, as race. We are all one species. Each one of us more alike than different.

In this statement, he is saying the first sentence because of recent racial relations in the U.S. A clear politically-motivated statement.

“Each one of us more alike than different.’ That is correct, but, yet again, doesn’t disprove the reality of race. Geneticists estimate that humans will differ, on average, at 3 million base pairs in their DNA. That’s more than enough for distinct racial classification, as well as enough to differentiate us.

Is that supposed to mean anything? Cats have 90 percent homologous genes with humans, 82% with dogs, 80% with cows, 79% with chimpanzees, 69% with rats and 67% with mice.

90% of the mouse genome could be lined up with a region on the human genome.

99% of mouse genes turn out to have analogues in humans.

As you can see from the links above, we are all extremely genetically related to animals that are clearly extremely physically different from us humans. This shows, that the differences in humans are down to not how genetically distant we are from other animals in the animal kingdom, but how the differing genes we have are expressed.

We all came from Africa. We’re all made from the same star dust. We’re all going to live and die on the same planet – a pale blue dot in the vastness of space. We have to work together!

And finally, you can see his way of saying that racial differences mean nothing because ‘we all come from Africa’ and ‘ we’re all made from star dust’. That may be true, but that doesn’t do anything to acknowledge, or even show that racial differences are meaningless.

Bill Nye has absolutely no authority to speak on this matter. Liberals then eat this up and cite Bill Nye as proof that race doesn’t exist, which is clearly untrue as I have shown.

Finally, I will get to Ta-Nehisi Coates’ ‘The Social Construction of Race‘. He cites my favorite blogger/geneticist Razib Khan, so this should be good.

Ancestry — where my great-great-great-great grandparents are from — is a fact. What you call people with that particular ancestry is not. It changes depending on where you are in the world, when you are there, and who has power.

Right with the first sentence, and with the second. It seems he’s attempting to use what the first article I cited says: that due to ever-changing racial definitions that race doesn’t exist as we believe it to be. He says that ancestry is a fact, well wouldn’t that same ancestry be your racial classification? I am not following his logic. Just because there are differing views on the definition of race throughout the globe, doesn’t mean that there is no biological reality of race.

He cites someone else who states:

“Race” as a term is very nebulous. But human subgroups with similar ancestries can have group differences in DNA — and intelligence is highly unlikely to have no genetic basis at all (although most now believe its impact is greatly qualified by cultural and developmental differences).

Cultural and developmental differences. The cultural differences are thrown out. According to the editorial ‘Mainstream Science on Intelligence’, which came out shortly after The Bell Curve was published, one of their points is that IQ tests are not culturally biased if the individual speaks English. If they are not English speakers, they will either get a test in their native language or get Raven’s Progressive Matrices, which is a ‘culture free’ IQ test as it’s based on pattern recognition and has no writing involved. Developmental differences, yes. White mothers have a better prenatal environment then do black mothers, which is biological. Developmental differences are innate within the two populations.

I do not know. Andrew is more inclined to believe that there is some group-wide genetic explanation for the IQ difference. I am more inclined to believe that the difference lies in how those groups have been treated. One thing that I am not convinced by is controlling for income and education.

Oh, the old ‘Stereotype Threat‘ canard. The paper, which was cited more than 5000 times, states that African-Americans do worse on tests in which they are told that they are being judged on their race. Well, a meta-analysis of 55 published and unpublished studies came out and what was found that the it shows clear publication bias. Either due to people not knowing how to read scientific papers or more insidious tactics. The effect varies across studies and is small. Though elite university undergrads may underperform on tests of cognitive tests due to Stereotype Threat, this effect doesn’t generalize to non-adapted standardized tests, high-stakes settings and less academically gifted test takers. Stereotype Threat cannot explain the difference in mean cognitive test performance between African Americans and European Americans. (pg 68)

In the mid-20th century, as we have been documenting, it was the policy of this country to deny African-Americans access to the same methods of wealth-building, that it was making available to whites.
African-Americans can’t build the same type of wealth due to mean genetic differences in IQ.
This is not merely a problem for your local  diversity and sensitivity workshop. It is a problem of wealth and power. When you create a situation in which a community has a disproportionate number of poor people, and then you hyper-segregate that community, you multiply the problems of poverty for the entire community–poor or not. That is to say that black individuals are not simply poorer and less wealthier than white individuals.  Because of segregation, black individuals and white individuals of the same income and same wealth, do not live in communities of equal wealth.
Wealth and power are directly related to IQ. Communities have a disproportionate amount of poor people due to them being low-IQ, blacks, whites or Asians, you can’t get away from low-IQ being the cause of poverty. People hyper-segregate themselves, see my Genetic Similarity article. Again, segregation is due to GST, not any insidious plot to hold anyone down. I’ve spoken multiple time on how oxytocin is responsible for ‘racism’ (ethnocentrism), and everything he is saying is just proving my point.
What bearing does segregation have on IQ differential? I don’t know. My skepticism of genetics is rooted in the fact that arguments for genetic inferiority among people of African ancestry are old, and generally have not fared well. My skepticism is also rooted in the belief that power generally seeks to justify itself. The prospect of actual equality among the races is frightening. If black and white people truly are equal on a bone-deep level, then the game might really be rigged, and we might actually have to do something about it. I think there’s much more evidence of that rigging, then there is evidence of cognitive deficiency .
There is no evidence for racial/ethnic equality. Any ‘evidence’ is shoddy and has NOT and NEVER WILL BE replicated because any studies that show racial equality are either badly administered or they never do a follow-up study at adulthood.  Blacks and whites are not equal ‘on a bone-deep level’. What kind of statement is that? There is WAY MORE evidence for cognitive deficiency than for ‘rigging’ of the game to hold blacks down in America.
I must add that I can not pretend to be a dispassionate, nor impartial observer. I come from a particular place. I’ve now been out in the world, and seen how other people in other places live. They don’t strike me as more intelligent. They strike me as better armed. There’s nothing scientific about that. But I think we all have core faiths. These are mine. You’ve been warned.
“My personal anecdotal experiences mean more to scientific studies on race and intelligence.” Where have we all heard that before? Too bad your ‘core faiths’ are just that Mr. Coates: FAITH.

Regardless of the method used in the analyses, all researchers reached estimated very close to that obtained by Lewontin: The differences observed by the subdivisions (populations, groups of populations, races) represented 10 to 15 percent of the total genetic variation found within the human species. Formally, these findings demonstrate, first, that the species is indeed subdivided into genetically definable groups of individuals and, second, that atleast some of these groups correspond to those defined by anthropologists as races on the basis of physical characters. They do not however, settle the arguments regarding the methods of racial classification. Unfortunately, Lewontin did not specify before initiating his analysis how large the difference has to be in order to call the groups “races”.

Consequently, the results of the studies have led population geneticists to two diametrically opposite conclusions. Lewontin called the observed differences trivial, and proclaimed that “racial classification is now seen to be of no genetic or taxonomic significance” so that “no justification can be offered for its continuance.” This view is echoed by authors of similar studies, who seem to be surprised that genetic variation within populations is greater than that between them. By contrast, Sewell Wright who can hardly be taken for a dilettante in questions of population genetics, has stated emphatically that if differences of this magnitude were observed in any other species, the groups they distinguish would be called subspecies.

One can extend Wright’s argument even further. The more than 200 species of haplochromine fishes in Lake Victoria differ from each other much less than the human races in their neural genes, although they are presumably distinguished by genes that control differences in their external appearances. The same can be said about atleast some of the currently recognized species of Darwin’s finches and other examples of recent adaptive radiations. In all these cases, reproductively isolated groups are impossible to tell apart by the methods used to measure differences in human races. Obviously, human races are not reproductively isolated (interracial marriages are common and the progenies of such marriages are fully fertile) but the external differences between them are comparable to cichlid fishes and Darwin’s finches. Under these circumstances, to claim that the genetic differences between the human races are trivial is a more political statement than a scientific argument. Trivial by what criterion? How much difference would Lewontin and those who side with him consider non-trivial?

By mixing science with politics, geneticists and anthropologists are committing the same infraction of which they are accusing other scientists, who they themselves label as racist. Even worse, by labelling the genetic differences as insignificant, they play into the hand of genuine racists who can demolish this claim and so further their own agenda. It is intellectually more honest to acknowledge and then point out that by no means imply supremacy of one race over others. This can be done by demonstrating that the differences are in genes that cannot be linked to any features that would be required for the preeminence of a particular race.

It’s clear that racial classification does exist. The creator of Fst, Sewall Wright, says that a Fst distance of .15 is more than enough for speciation (differing racial classifications). It directly refutes Lewontin, who put his political ideology of Marxism over science. Those cichlids in Lake Victoria are a perfect example that though the definition of ‘species’ does change depending on which researcher you speak to, it doesn’t discount that there are real and physical genetic differences between races and ethnicities.

In conclusion, the term “race is a social construct” is a deliberately intellectually dishonest statement, or a statement used to hide the truth for more insidious things to happen due to the non-acknowledgement of race.

IQ, Nutrition, Disease and Parasitic Load

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There are some environmental factors that have negative effects on IQ. Three I will touch on today are nutrition, disease and parasitic load. All three mean decreased cognitive ability as well as a slew of other negative effects on their lifestyle.

To start, nutrition of the mother is one of the most important and telling things for the health as well as IQ of the child. Prenatal nutrition is very important to a developing fetus. What the mother eats has a big effect on the fetus. For instance, vitamins and minerals are extremely important. A pregnant mother needs two times the amount of folic acid than a non-pregnant mother. A pregnant woman needs 400 mcg per day to prevent defects to the babies brain and spine called neural tube defects. A pregnant woman also needs double the amount of iron than a non-pregnant woman.

We can see here that if a pregnant woman is protein deficient, it passes on to the baby. Protein is more important in the second and third trimester due to the fetus developing more rapidly. It can also lead to growth retardation, due to reduced nutrient supply to the fetus. The authors end up concluding that the women who ingested 50-70 grams of protein per day and 156 to 465 ml of milk had children with significant and better tendency in femur length, bi-parietal diameter, abdomen circumference and head circumference. It’s important for a mother to get the right amount of protein for optimal fetal growth.

It’s also known how malnutrition in early years can lead to antisocial and aggressive behavior as well as lower cognition. It’s due to what I touched on above. They state that malnutrition in early childhood years such as lack of iron, zinc, B vitamins as well as being protein deficient leads to the 3 aforementioned things. As I have shown in the previous paragraph, the lack of the same nutrients during fetal development causes the same problems.

Now that I have touched on how prenatal nutrition is important for the fetus, I will talk about parasitic load.

According to a paper by Eppig et al, the prevalence of parasites is the cause of worldwide differences in cognitive ability. They state that from an energetics standpoint, that a developing human would have a hard time developing a brain while fighting infectious disease, as both are very metabolically demanding. They go through all of the theories of differences in cognitive ability, such as the cold winter hypothesis of Lynn, Rushton and Kanazawa, to studies of inbreeding depression by Saadat and Woodley. They state that Lynn has argued that nutrition is important to high degrees of mental development, that nutrition is the cause of the ‘Flynn Effect’ and that he showed that undernourished children have smaller heads, smaller brains and lower cognitive function than adequately nourished children. They end up concluding that as nations develop, they should be monitored for a decrease in parasitic infection to see if it correlates with a rise in IQ and whether any gain would be able to account for the ‘Flynn Effect’ (which the rate is 3 points per decade, no matter what population you look at).

To touch quickly on what Lynn said about undernourished children having smaller heads, smaller brains, and, therefore, lower cognitive function, all 3 of those variables are related. Brain size is correlated with cognitive ability at .44. So, we can see there is a pretty good relationship with brain size and IQ. So, those who don’t get adequate nutrition will, in turn, have a smaller head size and a smaller brain, which both lead to depressed intelligence.

There is evidence that Sickle Cell Anemia leads to a decrease in IQ. The authors conclude with MRI scans, that those with SCA have a decrease in total brain volume, which of course has a negative effect on cognitive ability. Though, that happened due to an increase in age. It’s known that brain size and the amount of neurons in the brain decrease with age. I won’t discount that SCA lowers cognitive ability, it’s a good hypothesis, along with the paper by Eppig et al, but I still think that Rushton, Lynn and Kanazawa’s Cold Winter Theory is the best evolutionary model for differences in intelligence found across the globe.


In the map above you can see the rate of malaria in the world. It’s concentrated around the equator as mosquitoes are the main transmitters of the parasites. Though, is it the parasitic load that causes low IQ or evolution in hot climates, which lead to low IQ and, in turn, makes them able to not be able to figure out how to cure the diseases due to low intellect? I believe it’s both, leaning more to the side of evolution in hot climate obviously, but I won’t discount that malaria, and therefore, SCA, has something to do with lower cognitive ability in those populations with higher rates of malaria.

So with all of the above factors, let’s talk about Africa.

We know they have the lowest IQs in the world (IQ 67 to 70), and we know they have the highest rates of malaria in the world, and also some of the worst nutritional standards of any geographic region in the world.

What is the cause? IQ? Disease? Parasitic load? Nutrient deficiencies?

All of the above. The last 3 are environmental effects that retard IQ. IQ drives most all development for a country, so with the last 3 points being there, obviously since they retard IQ, the QoL in the country will suffer.

Lynn states that with better nutrition that Africans will be able to reach their phenotypic IQ of 80. There is some good evidence for his claim as he also states that blacks with low to no white admixture have an IQ of 80. Rushton and Jensen also say that since psychologists don’t venture into the lowest income neighborhoods in the South, that the black IQ may be 78 in America, and not 85. Right there by the African phenotypic IQ of 80. So, that would mean that those with the highest amount of African ancestry have an IQ of around 80, plus or minus a few points. So if those African-Americans with low amount of white admixture have an IQ of 80, then it’s a good bet to take that if Africans themselves had proper nutrition that they would hit 80 as well, just as Lynn has stated.

Satoshi Kanazawa also said this back in 2006. Of course the media made him out to be someone who just said that without any backing of his claims. He compared IQ scores with indicators of ill health in 126 countries. He found that those countries with the lowest IQs have higher rates ill health. They accuse him of attempting to ‘revive the politics of eugenics by publishing the research which concludes that low IQ levels, rather than poverty and disease, are the reason why life expectancy is low and infant mortality high’. We know that poverty goes out the window because of the relationship between IQ and poverty. But as seen above, disease does have an effect on IQ. They only threw buzzwords at him and, of course, didn’t attempt to say anything meaningful to him.

The link between life expectancy and IQ is well studied. Those with lower IQs live shorter lives and those with higher IQs live longer lives. The studies and information I cite in that article corroborate what Kanazawa says about IQ and ability to fight disease.

IQ is affected by environmental factors such as disease, nutrition and parasitic load. I have given good evidence that with better nutrition, Africans can reach their phenotypic IQ of 80. But, they can’t learn how to farm because of their low IQ. They can’t get a higher IQ because they can’t learn how to farm.

The cause of this is evolution. When they say, as seen in Kanazawa’s article, that poverty (malnutrition) and disease are the causes of low IQ, low IQ causes those 2 things because those with lower IQ don’t have the abstract ability to think into the future that what they’re doing to their bodies can and will have negative effects in the future, which leads to decreased life span as I have noted in the article I have linked. It also leads to them not being able to farm, due to not having a high enough intellect due to evolving in the hot climates of the sub-Saharan desert. The only thing that holds wight, in my opinion, for the case for an environmental effect for lowered IQ is the case for parasitic load. So, I posit that if Africans were to some how to get it in to shape on their own and take care of those things on their own, they will be able to reach their phenotypic IQ of 80. We also know that immigrants from European countries with lower IQs, their descendants in America have IQs closer to average to the white average (100). 33 million people in Europe are at risk for malnutrition, so those who do come to America who are at risk for malnutrition, get the IQ boost due to living in America with better nutrition. This is also supported by African immigrants to America having a higher rate of collegiate attainment than white Americans, though that may be due to super-selection, only the smartest African populations coming here.

In conclusion, those African-Americans with low to no white admixture have an IQ of around 80, so it’s well supported that, with better nutrition, lower parasitic load and lower disease rate, Africans, and all other low IQ countries for that matter, can get a boost of around 10 to 15 points with all 3 things I have noted in this article taken care of.

“Differences in brain structure development may explain test score gap for poor children” Maybe not….

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Summary: They would have to explain why whites in poorer families score higher than blacks in all other income brackets except blacks in families making over 200,000 dollars per year, which even then blacks only score 3 points higher in the 200,000 dollar plus per year income bracket. They say that frontal and temporal lobes are smaller in poorer children, which whites have bigger frontal and temporal lobes on average as well as having more activity in the frontal lobes, which is thought to be the seat of intelligence. Blacks having smaller brains than whites on average explains the size differences between the differences in the different parts of the brain mentioned.

Low-income children had atypical structural brain development and lower standardized test scores, with as much as an estimated 20 percent in the achievement gap explained by development lags in the frontal and temporal lobes of the brain, according to an article published online by JAMA Pediatrics.

If true, only 20 percent of the achievement gap affected by poverty. I doubt it seeing as poor whites in families making less than 20,000 dollars a year still have 180 points over blacks in the same income bracket and blacks in families making more than 200,000 dollars per year have a 981 score, only 3 points higher than whites in families making less than 20,000 dollars per year. Whites in families making less than 20,000 dollars per year still outperform all negro families in all other income brackets except in negro families making over 200,000 dollars per year by only 3 points. Not even worth talking about.

20 percent of the achievement gap is apparently explained by developmental lags in the front and temporal lobes of the brain. Blacks have a smaller PFC (prefrontal cortex) which may explain it.

Socioeconomic disparities in school readiness and academic performance are well documented but little is known about the mechanisms underlying the influence of poverty on children’s learning and achievement.

It’s well documented that even in poor whites and poor blacks, poor whites are still on average more intelligent and have higher standardized test scores than do blacks.

Seth D. Pollak, Ph.D., of the University of Wisconsin-Madison, and colleagues analyzed magnetic resonance imaging (MRI) scans of 389 typically developing children and adolescents ages 4 to 22 with complete sociodemographic and neuroimaging data. The authors measured children’s scores on cognitive and academic achievement tests and brain tissue, including gray matter of the total brain, frontal lobe, temporal lobe and hippocampus.

I wonder what the breakdown was. Will revise when the full paper comes out. Hippocampal differences are also explained by whites having larger brains than blacks as well as the other parts they state.

The authors found regional gray matter volumes in the brains of children below 150 percent of the federal poverty level to be 3 to 4 percentage points below the developmental norm, while the gap was larger at 8 to 10 percentage points for children below the federal poverty level. On average, children from low-income households scored four to seven points lower on standardized tests, according to the results. The authors estimate as much as 20 percent of the gap in test scores could be explained by developmental lags in the frontal and temporal lobes.

On frontal lobes from this Rushton paper decimating Gould’s garbage *Mismeasure of Man*, which also states they have smaller frontal lobes than whites:

“Bean also reported that the 103 Negro brains were less convoluted than were 49 White brains and that Whites had a proportionately larger genus to splenium ratio (front to back part of corpus callosum), implying that Whites may have more activity in the frontal lobes which were thought to be the seat of intelligence. Consider the following statistically significant comparisons (sexes combined) from recently conducted studies using the four techniques mentioned above. Using brain mass at autopsy, Ho et al. (1990) summarized data for 1,261 individuals. They reported a mean brain weight of 1,323 grams for White Americans and 1,223 grams for Black Americans. Using endocranial volume, Beals et al. (1984) analyzed about 20,000 skulls from around the world and found that East Asians, Europeans, and Africans averaged cranial volumes of 1,415, 1,362, and 1,268 cm3 respectively. Using external head measurements from a stratified random sample of 6,325 U.S. Army personnel, Rushton (1992) found that Asian Americans, European Americans, and African Americans averaged 1,416, 1,380, and 1,359 cm3, respectively. Using external head measures from tens of thousands of men and women from around the world collated by the International Labour Office, Rushton (1994) found that Asians, Europeans, and Africans averaged 1,308, 1,297, and 1,241 cm3, respectively. Finally, an MRI study in Britain found that people of African and of Caribbean background averaged a smaller brain volume than did those of European background (Harvey et al., 1994). Contrary to most purely environmental theories, racial differences in brain size show up early in life. Data from the U.S. National Collaborative Perinatal Project on 19,000 Black children and 17,000 White children showed that Black children had a smaller head perimeter at birth and, although Black children were born shorter in stature and lighter in weight than White children, by age 7 ‘catch-up growth’ led Black children to be larger in body size than White children. However, Blacks remained smaller in head perimeter (Broman et al., 1987). Further, head perimeter at birth, 1 year, 4 years, and 7 years correlated with IQ scores at age 7 in both Black and White children (r = 0.13 to 0.24).”

On temporal lobes, from the scientist that Rushton cited above:

“The size of the pole of the temporal lobe is less in the Negro than in the white, and less in the Negro female than in the Negro male…The shape of the pole of the temporal lobe is different in the two races, being slightly more slender in the Negro, and almost the same size in the two races antero-posteriorly. The differences are not only absolute but are also relative to the to the weight and size of the entire cerebral hemispheres.”

.”Development in these brain regions appears sensitive to the child’s environment and nurturance. These observations suggest that interventions aimed at improving children’s environments may also alter the link between childhood poverty and deficits in cognition and academic achievement,” the study concludes.

“Appears sensitive”. I doubt it. See the table on test scores and income above.

In a related editorial, Joan L. Luby, M.D., of the Washington University School of Medicine, St. Louis, writes: “Building on a well-established body of behavioral data and a smaller but expanding body of neuroimaging data, Hair et al provide even more powerful evidence of the tangible detrimental effects of growing up in poverty on brain development and related academic outcomes in childhood. … In developmental science and medicine, it is not often that aspects of a public health problem’s etiology and solution become clearly elucidated. It is even less common that feasible and cost-effective solutions to such problems are discovered and within reach. Based on this, scientific literature on the damaging effects of poverty on child brain development and the efficacy of early parenting interventions to support more optimal adaptive outcomes represent a rare roadmap to preserving and supporting our society’s most important legacy, the developing brain. This unassailable body of evidence taken as a whole is now actionable for public policy.”

I’m assuming they have never seen the SAT score gaps and how whites in families making less than 20,000 dollars a year score the same as blacks in families making over 200,000 dollars a year.


It’s well-known that IQ is the best predictor of success in life. Blacks have a lower a lower average IQ, and smaller brains than whites and Asians which explains the achievement test score gaps. I would like to see a study that separates rich blacks, rich whites and poor blacks and poor whites with controls and see how they differ. I’m assuming it’ll be the same as the SAT score gaps which I have linked above.

The difference in brain size between blacks and whites perfectly describe what is being shown above. More blacks live in poverty because they have lower IQ. IQ is correlated with poverty, crime, illegitimacy, and chronic welfare status. G, or general intelligence, is highly correlated with most things in life. Excerpt from THE g FACTOR The Science of Mental Ability by Arthur Jensen:

The well-established correlation of IQ and similar cognitive measures with a number of social variables, such as poverty, crime, illegitimacy, and chronic welfare status, makes it almost a certainty that g itself is the major cognitive component in the relationship. However, I have not found a study that directly addresses the extent to which just g itself, rather than IQ or other highly gloaded measures, is related to social variables. The repeated finding that verbal test scores are somewhat more highly correlated with delinquent and criminal behavior than are nonverbal performance tests (generally loaded on the spatial factor) suggests that other cognitive factors in addition to g are probably responsible for the correlation of IQ with these most common forms of antisocial behavior. pg 294

In conclusion, they need to have studies that have poor whites and poor blacks, rich blacks and rich whites, rich whites and poor blacks, poor whites and rich blacks and controls to see what the differences really are, and we know there will be differences between the above-mentioned groups, and that poor whites still perform better academically than poor blacks.