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Polar Bears, Inuits, Evolution and Fst
1150 words
The Daily Stormer published an article today that claimed that “Polar bears are miscegenating with grizzly bears“. When polar bears and grizzly bears mate, they produce a “pizzly bear“. Due to this, the polar bear population is shrinking and the grizzly bear population is growing.
Scientists say this doesn’t look good for the polar bears; though these hybridizations are not due to ‘climate change’, as is suggested. Using a computer model, the researchers generated a prediction of the Earth’s climate from 2071 to 2100. The model analyzed how different species of birds, mammals and amphibians would need to migrate to find new territory. Birds had the highest overlap with 11.6 percent, attributed to their range from flying. Mammals and amphibians were 4.4 and 3.6 percent likely to encounter a hybridization event. Overall, about 6.4 percent of all species are expected to come into contact to even have the chance to hybridize with other compatible species. Meaning, the polar bear is not in danger of ‘dying out’ due to ‘miscegenation’.
What is missed in the article mentioned at the beginning is that polar bears and grizzly bears are even able to produce offspring at all. This is due to the two splitting around 350 kya to 6 million years ago. This article then says something vaguely familiar:
After beginning to branch off from brown bears, the polar bear’s ancestors under went a series of evolutionary changes in order to survive in the Arctic. The bears adapted to a life of hunting seals and surviving extreme cold. One of the most remarkable adaptations was the ability to thrive on a fat-rich diet withoutapparent heart damage. (sounds like the Inuit or other Eskimo tribes; emphasis theirs)
‘The bears’ could be switched to ‘the Eskimoes’ or ‘The Inuit’and make complete sense. The Inuit also live off a high-fat diet. The higher n-3 gives immunity and boosts in health to a slew of diseases as well.
The Inuit and their ancestors evolved special genetic mutations that allowed them to partly counteract the effect of a diet high in fat. Nearly 100 percent of the Inuit have these genes, while 2 percent of Europeans and 15 percent of Han Chinese do, which means that they synthesize n-3 differently than the Inuit. Over time eating a diet high in fats, the Inuit evolved these genetic adaptions to better adapt to their environment. The genes they have also lower LDL (bad) cholesterol and fasted insulin levels, which presumably has an effect on cardiovascular disease and diabetes. This used to be the case, but “exposure to a more Western lifestyle” has made Diabetes Mellitus in the Inuits comparable to that of the general population. Since growth is reliant on a person’s whole fatty acid profile, the Inuits are, as a result of these mutations, 1 inch shorter than they should be. The same mutations causing shorter height in the Inuit have also been found in Europeans. Researchers have found many genes responsible for height, but this was “one of the strongest effects ever found by geneticists”.
These genetic mutations are around 20,000 years old and originate with their Siberian ancestors. They think that the adaptation came about in the last Ice Age, but the selection is far stronger in the Inuit, due to them being one of the furthest populations away from the equator.The researchers have also found that the Inuits have another common mutation in their population that is involved in the differentiation of brown, subcutaneous fat cells and brite fat cells. Brite fat cells burn fat for more heat, showing another adaptation they had from their diet and direct environment. This helped them survive the harsh climate.
A strict Inuit diet shows evolution in action, that populations forced to subsist mostly on one type of food/macronutrient can and will adapt to their environment over time, proving that evolution exists. However, you cannot infer from the Inuits that the effect they gain from this diet will carry over to the general population.
The Science Daily article then goes on to say people have asked themselves whether they “Should be on a Stone Age diet”. My answer to that is a resounding “No” if you think the diet will do anything different from any other diet and weight training. As stated in the SD article, you cannot say that other populations, for instance, evolved to eat a certain way cannot be made as the Inuit have certain genetic mutations that no other populations have, in the frequency they do, for that matter.
The DS article, more interestingly, doesn’t bring up how two different species are interbreeding. Humans have a Fst distance of less than .5. The Fst for polar and grizzly bears is 0.2688. Two differing populations separated anywhere between 350 kya to 6 million years ago, can interbreed, and so can humans. Sewall Wright, the creator of the Fst concept, has said that if this differentiation was noticed in any other species, that they would be noted as distinct subgroups. When it comes to human genetics and science, science chooses to take the “egalitarian route” and deny the existence of race. However, when it comes to polar and grizzly bears, talking about how polar bears are a subspecies of grizzly bears and the polar bears adapted to the cold leading to physical and physiological differences, this is fine. Just like when Rushton proposed Differential-K Theory, which is the application of r/K selection theory to humans, it got shot down, despite E.O. Wilson who co-founded r/K selection theory stating “I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.” Rushton’s main thesis has also never been refuted. No other explanation can fully explain the variables Rushton describes in Race, Evolution, and Behavior like r/K selction theory does.
Polar bears are not going away, and if they were, it’d just be evolution in action as the point of life is to breed and carry on your lineage (however, fitness is increased for the grizzly bear as he is gaining more habitat, yet decreasing for the polar bear due to a warming planet). The strongest populations get selected for, while the weakest become absorbed/wiped out. Since the planet is warming, as well as the grizzly bears looking for more environment some, not all, are mating with polar bears. This does not mean that polar bears will go extinct due to inbreeding with grizzly bears. Inuits are proof of the existence of evolution with how they adapted to their high-fat diet and cold environment, but you cannot use this information on their diet and say that the benefits from a high fat diet would be the same in other populations.
Science Daily: Mom’s Exposure to BPA During Pregnancy Can Put Her Baby on Course to Obesity
1750 words
Science Daily came out with an article today that exposure to BPA invitro for babies is correlated with obesity at age 7. 94 percent of the women tested had detectable levels of BPA. BPA is also linked with early onset puberty, which I will also speak on later in this article as it has implications for one of my theories.
I briefly touched on BPA in my article What’s the Cause of the Cucking of Europe? where I said:
I advise all of you (women included, there are many deleterious effects of BPA on the mother as well as the baby prenatally), to discontinue use of plastics with BPA in them.
The above-linked study shows that preeclampsia is correlated with elevated levels of BPA in the blood levels in the pregnant mothers, fetal blood, and the placenta. BPA was found to be elevated in mother’s fetal tissue with preeclampsia in comparison to the mothers with lower levels of BPA in their fetal tissue. I will come back to the BPA link with preeclampsia later in the article as it has implications for ethnic groups in America.
The paper, which was just released on the 17th, called Bisphenol A and Adiposity in an Inner-City Birth Cohort, carried out tested BPA 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, they discovered that 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 researchers then conclude that BPA exposure invitro “may be an important underlying factor in the obesity epidemic” and that “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.”
If true, this has huge implications for the way we look at the obesity epidemic in this country. Who are the most likely to be obese? “Hispanics” and blacks (Ogden et al, 2014).
Returning to what I brought up earlier about early onset puberty: in my article on the hormone leptin being a cause for earlier menarche in black girls, I noted that since black girls were more likely to be heavier as well as mature faster than white girls, that differences in leptin were the cause of differences in menarche between the two groups. Elevated levels of serum leptin were correlated with body fat and differences in maturation between the two groups. Differences remained, but lessened, after controlling for differences in fat mass, maturation, age, and physical fitness.
Since BPA is correlated with adiposity in children and black girls have earlier menarche DUE to there being a higher chance of black girls being overweight in comparison to white girls, BPA is yet another piece to the puzzle of this phenomena, along with, of course, evolution. Ingestion of BPA is an environmental factor, however, with these changes in body chemistry in the children invitro due to increased BPA consumption by the pregnant mothers, it leads to one cause that can be prevented from further occurring due to our new knowledge.
The study was carried out on a cohort from NYC. In 2010 in NYC, the city was: 44 percent white, 25.5 percent black, 12.7 percent Asian with the rest being filled out by ‘Hispanics’ (not a racial category) and mixed-race people. Even after they matched for SES and other environmental factors, these differences persisted. However, this study was only carried out on those women who self-identified as either Dominican (basically African) and black. To quote the researchers:
Women were included if they self-identified as either African American or Dominican and had resided in Northern Manhattan or the South Bronx for at least 1 year before pregnancy. Exclusion criteria included mother’s report of: cigarette smoking or use of other tobacco products during pregnancy, illicit drug use, diabetes, hypertension, known HIV, or a first prenatal visit after the 20th week of gestation.
So, we have a full sample of Caribbean Africans and African Americans in this study. What else can we learn about those two populations and their consumption of things with BPA in them?
The above Figure (7) is taken from the U.S. Department of Agriculture and the Food Surveys Research Group study on differences in drinking tap and bottled water.in different populations in the country. As you can see in this figure (what is notable is the ages 12-19 and 20 to 60 in the table), whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. However, Mexican American girls, like black girls, are also entering puberty earlier. Since both populations have a substantial percentage of them overweight and obese (factor for serum leptin production which then causes early onset puberty), this again shows a strong correlation between body fat gain and early onset puberty. Moreover, this also shows that both Dominican and black populations consume more bottled water than do white populations, both populations are more likely to be obese or overweight (even after controlling for SES) which causes leptin production earlier causing periods to happen much sooner than in populations who drink less bottled water and use other products with BPA in them. .
Going back to preeclampsia, it is a condition that pregnant women develop that’s characterized by hypertension (high blood pressure) and protein in the urine. It’s known that black women suffer from it the most. More interestingly, over the past ten years, rates of preeclampsia have been increasing in the black female population. As the researchers note in the article, BPA is correlated with preeclampsia. Blacks have a higher rate and chance of being diagnosed with hypertension as well. All of these differing variables coalesce into our current obesity epidemic. With blacks and “Hispanics” being more likely to be overweight/obese drink more bottled water, have a higher risk for hypertension, higher risk for preeclampsia and having earlier menarche, these help explain, in part, racial/ethnic differences in obesity.
These differences can be attributed to consumption of bottled water, i.e., consuming things with made with and packaged in plastic as well as canned foods. From my experience with Dominican and black New Yorkers, they tend to have horrible lifestyles, tend to drink tons of bottled water and also tend to be overweight or obese at a higher rate in comparison to the general population. This leads to biologic factors changing (i.e., earlier menarche in younger girls) in these young girls, leading to devastating effects on their body chemistry.
This study, yet again, proves another underlying factor for obesity in certain populations in the country. And what do you know? It’s the populations that already have the highest rate of obesity in the country. When it becomes definitive that BPA consumption by pregnant mothers does lead to underlying factors in obesity. To quote the researchers: “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.” This will be HUGE for our understanding of underlying causes to obesity! Moreover, if (when) this is fully corroborated, it can then be said that by mothers exposing their children in the womb to excess levels of BPA, there is a chance that they are “giving their own choice to make their children have a higher chance of being obese, as they know the dangers of BPA consumption during pregnancy and all of the negative variables associated with it.”
This is an extremely interesting and important study for our understanding of obesity. Since BPA consumption invitro is correlated with higher fat mass index in girls at age 7, and since those girls who tend to be more overweight and obese than other populations, we can then say that BPA has a hand in obesity in children, which then causes serum leptin to be released, causing way menarche in these populations. An increase in sexual maturation has been linked to the obesity epidemic, which began around 60 years ago. The cause of this is due to the demonization of the fat macro and carbohydrates, all the while it was reversed. This destroyed insulin sensitivity for many Americans, leading to a huge majority of our health problems today.
In conclusion, underlying factors for obesity keep appearing. Due to racial/ethnic differences in bottled water consumption (one of the most common BPA products in households), which the effects of BPA may alter how fat cells are formed in early life, this accounts for, in part, excess adiposity in differing populations. These underlying factors could help show where some of these racial/ethnic differences in obesity come from. Since the two populations in the study (black American and Dominican) both have high levels of adiposity, both drink a lot of bottled water and both have earlier menarche than do whites (who drink LESS bottled water), this shows that some (a lot?) of the variation in obesity between ethnic/racial groupings can be explained by these underlying factors.
** I have one problem with this study. They assessed fat mass index with bioelectrical impedance.The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.
In Defense of Jason Richwine
3900 words
I came across two articles today, one from The Atlantic and the other from judgybitch.com. Both have attacked Jason Richwine’s dissertation in which he calls for a change to the US immigration policy to turn away low IQ immigrants and only accept high IQ ones. I agree fully with this (if it’s completely controlled, of course). This would drop crime as well as save us more money in welfare and other government programs that low IQ peoples take.
By 2050, 9 out of 10 people in the US will be obese or overweight and by 2020 80 percent of US men will be obese or overweight. This is due, in part, to an influx of those with lower IQs from South of the Border. Jason Richwine’s argument for testing immigrants will, in turn, lower obesity rates in America.
Dr. James Thompson noted how continued mass immigration from the South of the Border would decrease IQ, this is a real and pressing issue. A country is only as good as its majority population and by allowing all of these low IQ people into the country, our country will transform into theirs, which is ironic since that’s the exact thing they’re running away from. You cannot run away from genetics. The overall ‘Hispanic’-white gap is 10.2 points or .72 SDs. That will lower the average IQ of the country even more, and in turn, give us all a lowered quality of life. The average IQ of Mexico is 88 (Lynn and Vanhanen, 2002) so by allowing unfettered mass immigration without checking average IQs to see if they’ll be of any use to us as a country will lead to eventual irreversible effects if this isn’t stopped soon.
The first article I’ll look at is the one from The Atlantic:
Let’s start with the fact that there is no such thing as a direct test of general mental ability. What IQ tests measure directly is the test-taker’s display of particular cognitive skills: size of vocabulary, degree of reading comprehension, facility with analogies, and so on. Any conclusions about general mental ability are inferences drawn from the test-taker’s relative mastery of those various skills.
IQ tests test g or the general intelligence factor which encompasses all mental abilities. I guess the author of this piece has never heard of Raven’s Progressive Matrices. It’s a ‘culture free’ IQ test where the test is based on pattern recognition. No bias there.
Even then, if they don’t speak English and speak Spanish, they can get tests in their native language which are not biased. Gottfredson (1994) and 51 other eminent intelligence researchers signed a 25 point statement in which one of the statements was:
Intelligence tests are not culturally biased against American blacks or other native-born, English-speaking peoples in the U.S. Rather, IQ scores predict equally accurately for all such Americans, regardless of race and social class. Individuals who do not understand English well can be given either a nonverbal test or one in their native language.
They will be given the nonverbal test (RPM, see below) or one in their native language, which still test the same underlying concept of the general intelligence factor.
They found that being raised by high-SES (socioeconomic status) parents led to an IQ boost of between 12 and 16 points – a huge improvement that testifies to the powerful influence that upbringing can have.
False. See below.
A study of twins by psychologist Eric Turkheimer and colleagues that similarly tracked parents’ education, occupation, and income yielded especially striking results. Specifically, they found that the “heritability” of IQ – the degree to which IQ variations can be explained by genes – varies dramatically by socioeconomic class. Heritability among high-SES (socioeconomic status) kids was 0.72; in other words, genetic factors accounted for 72 percent of the variations in IQ, while shared environment accounted for only 15 percent. For low-SES kids, on the other hand, the relative influence of genes and environment was inverted: Estimated heritability was only 0.10, while shared environment explained 58 percent of IQ variations.
Turkheimer was right that he did find gene x environment interactions that made genetic influences weaker and shared environment stronger for those from poorer homes in comparison to those from more affluent homes. Though most studies show no interaction effects, or interactions vary significantly.
Other studies have shown that heritabilities are the same both within as well as between white and black samples. That led Jensen to label this the ‘default hypothesis’. Researchers analyzed full and half siblings from the NLSY on three Peabody Achievement Tests. 161 black full siblings, 106 pairs of black half siblings, 314 pairs of full white siblings and 53 pairs of white half-siblings. with measures in math and reading. The best fitting model for all of the data was by which the sources of the sources of the differences between those within race and the differences between races were the same, at 50 percent genetic and environmental. The combined model (50/50) best explains it, whereas the culture-only and genetics-only models are inadequate.
IQ tests are good measures of innate intelligence–if all other factors are held steady.
This is wrong. IQ tests are fine all around the world. RPM is one of the best out there and correlates with g between .8 and .9.
But if IQ tests are being used to compare individuals of wildly different backgrounds, then the variable of innate intelligence is not being tested in isolation. Instead, the scores will reflect some impossible-to-sort-out combination of ability and differences in opportunities and motivations. Let’s take a look at why that might be the case.
Intelligence – g – is the same across every population in the world.
Comparisons of IQ scores across ethnic groups, cultures, countries, or time periods founder on this basic problem: The cognitive skills that IQ tests assess are not used or valued to the same extent in all times and places
This is why they get re-standardized.
Indeed, the widespread usefulness of these skills is emphatically not the norm in human history. After all, IQ tests put great stress on reading ability and vocabulary, yet writing was invented only about 6,000 years ago – rather late in the day given that anatomically modern humans have been around for over 100,000 years. And as recently as two hundred years ago, only about 15 percent of people could read or write at all.
Doesn’t matter. See Raven’s Progressive Matrices above. The general intelligence factor is the same in all populations around the world. There are ways to give intelligence tests, such as RPM, to those who don’t read or write.
More generally, IQ tests reward the possession of abstract theoretical knowledge and a facility for formal analytical rigor.
Abstract thought is linked with intelligence. Those with higher IQs are more analytical than those with lower IQs.
To grasp how culturally contingent our current conception of intelligence is, just imagine how well you might do on an IQ test devised by Amazonian hunter-gatherers or medieval European peasants.
I touched on this in my refutation of Robert Sternberg. The concept of g does not change over time. The more intelligent you are, the better chance you’ll have to survive in those places.
Such skills are used more intensively in the most advanced economies than they are in the rest of the world. And within advanced societies, they are put to much greater use by the managers and professionals of the socioeconomic elite than by everybody else. As a result, American kids generally will have better opportunities to develop these skills than kids in, say, Mexico or Guatemala. And in America, the children of college-educated parents will have much better opportunities than working-class kids.
Those skills are used much more in advanced economies because of higher average innate intelligence. The children of college-educated parents have much better opportunities than working-class kids because intelligence is strongly linked to socioeconomics status.
Among the strongest evidence that IQ tests are testing not just innate ability, but the extent to which that innate ability has been put to work developing specific skills, is the remarkable “Flynn effect”: In the United States and many other countries, raw IQ scores have been rising about three points a decade. This rise is far too rapid to have a genetic cause. The best explanation for what’s going on is that increasing social complexity is expanding the use of the cognitive skills in question – and thus improving the opportunities for honing those skills.
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 effect”.
…
Thus the secular increase in test scores (the “Lynn±Flynn effect”) is not a “Jensen effect” nor is this the first time the discriminating power of the Jensen effect has been shown.
The Flynn effect is acutely embarrassing to those who leap from IQ score differences to claims of genetic differences in intelligence.
Not at all, since it’s easily explainable by better nutrition since the beginning of the industrial revolution. It’s also not even on g so why this gets discussed is beyond me.
Specifically, it is based on the ahistorical and ethnocentric assumption of a fixed relationship between the development of certain cognitive skills and raw mental ability. In truth, the skills associated with intelligence have changed over time–and unevenly through social space–as society evolves.
The relationship exists and there is a strong correlation between cognitive skills and raw mental ability. More intelligent people have better functioning societies than less intelligent people. This is an objective fact.
But contrary to the counsel of despair from hereditarians like Richwine, those deficits aren’t hard-wired. Progress in reducing achievement gaps will certainly not be easy, but a full review of the IQ evidence shows that it is possible. And it will be aided by policies, like immigration reform, that encourage the full integration of Hispanics into the American economic and cultural mainstream.
Jason Richwine is correct. Progress in achievement gaps will not close, barring the continued dysgenesis that America is facing. Immigration reform will not change anything. They don’t want to assimilate; they want to come and leech off of our Welfare State. The denial of genetics and scholastic achievement won’t be able to be held for long. In this study in which Robert Plomin was one of the researchers, it was found that 60 percent of the difference between individual 16-year-old students in the UK could be attributed to genetic factors. We know that IQ is linked to academic achievement and since that’s heritable as well, we will soon see that race and ethnic differences in IQ and academic achievement are, without a shadow of a doubt, are real and do not exist because of any economic deprivation or some other kind of non-biologic factors.
For the second article, from judgybitch.com, in which she only says one correct thing in it and it’s:
Here’s a little pet theory of mine I’d like to throw out, just for the hell of it. I think humans prefer lighter skin and hair and eye colors because those tend to be the result of recessive genes. A man with darker tones who has a child with a woman of lighter tones will almost always see his genes expressed in the children. Dark tones tend to be dominant. The preference for lighter skin is a natural paternity test.
This is called sexual selection, which is natural selection which arises for selection of traits in the opposite sex. Selecting for certain traits which the opposite sex found appealing, for example, is how long hair got sexually selected for outside of Africa along with selection for hair, eye, and skin color. Selecting for these traits had them become more prevalent and they eventually stayed due to intense selection for them.
For example, Eurasian women got selected for beauty and Eurasian men who got selected for intelligence as men had to be more intelligent in order to hunt for food. Conversely, African women gathered and hunted for food and became slightly more intelligent than African men who became the more attractive sex (Fuerle, 2008).
But other than this she is wrong.
You know what IS linked very strongly to lower IQs?
Malnutrition.
http://www.sciencedaily.com/releases/2004/11/041117005027.htm
http://www.ncbi.nlm.nih.gov/pubmed/2628311
http://www.nature.com/pr/journal/v5/n11/abs/pr1971371a.html
The idea is not even the slightest bit controversial. Children who are starved, especially in the earliest years of life, perform very poorly on IQ tests compared to peers who received adequate nutrition. Like, really poorly. IQ’s down around 60 (100 is average).
Let’s look at this world hunger map, shall we?
http://www.geographictravels.com/2008/07/world-hunger-map.html
Oh well now, would you look at that. Looks like it’s mostly black and Hispanic folks who are starving. And all those white folks are living life to the hilt, with full bellies and bright futures.
Must be a coincidence.
It’s not a coincidence. There is no coincidence that if you superimpose an IQ map over the world hunger map, that a super majority of the low IQ countries would have bad nutrition and be starving, whereas those higher IQ populations would have better nutrition and, therefore, higher IQs and lack of malnutrition and starvation. There are environmental factors involved in this, which I have gone through in my article IQ, Nutrition, Disease and Parasitic Load. Yes, those environmental variables decrease IQ; but in the case of Africa, if their full genotypic IQ were expressed in their phenotype, they would have an average IQ of 80, 9 points away from the lowest average European country which is Serbia at 89. They would then be able to have better functioning societies and not have to rely on outside aid. Though, their low IQs are the cause of evolution, those factors only cause about 10 points of difference (depending which of the variables I mentioned exist in those areas).
Let’s look at this map of food insecurity in the United States:
http://www.nextgenerationfood.com/news/food-insecurity-in-the-us/
Highest rates of food insecurity:
Mississippi
Texas
Arkansas
Lowest rates of food insecurity:
North Dakota
Massachusetts
Virginia
Gosh, I wonder where all the black and Hispanic people are? North Dakota, right?
According to the USDA, in a report titled Household Food Security in the United States in 2011, black and Hispanic families are more than twice as likely to experience food insecurity as white families (p. 11).
White 11.4% of families food insecure
Black 25.1%
Hispanic 26.2%
Gosh, I wonder where black and ‘Hispanic’ people are? Mississippi, Texas, and Arkansas right? What is the cause of the food insecurity? Lower intelligence. What is lower intelligence highly correlated with? Obesity.
If you keep in mind the fact that obesity (especially as the result of heavily processed, nutrient deficient junk foods) is also a form of malnutrition, it seems to me that there is an entirely different explanation for why certain racial groups might tend to perform lower on IQ tests.
Sure it is. A big cause for obesity is lowered intelligence (Kanazawa 2007). 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. The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that 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 clearly shows that those obese individuals who score low on IQ tests, more often than not, are obese because of their intelligence. The lack of ability to delay gratification is also correlated with low IQ (Mischel and Metzner, 1982).
Becoming obese is largely in part related to environmental factors, but there are correlates with obesity and genetic factors, as well as racial and ethnic differences in obesity, which are due, in part, to environmental as well as genetic factors. All of these factors fall back to a) lower intelligence, b) differing physiology and c) differing nutritional habits. Lower IQ is the main reason, though, for these differences which manifest itself as differences in scores of cognitive ability. Those with lower scores than have higher chances of having negative effects in life, such as low SES, higher chance of becoming obese and so on.
Correlation is not causation.
This is the liberals word phrase they use when they cannot contest data and know it so use the same old boring phrase. When you get the same result over and over using the scientific method, then it’s safe to say that the same results and conclusions that get brought up time and time again are real and cannot be explained away by the correlation does not mean causation line.
And furthermore, I haven’t read Richwine’s dissertation, nor do I plan to, so I don’t know if he offered any tentative explanations for his findings.
Didn’t even read it and is giving a critique of it. How does that work?
It looks to me like Richwine is a gigantic racist asshole, because he is using his findings to try and limit the opportunities for Hispanic people to come to the United States, because dumb spics.
Lower IQ people commit more crimes than do higher IQ people. This phenomenon is well-noted that those with lower intelligence commit crime, as the average IQ of a criminal in America, is 85, whereas the average IQ for a juvenile is 92. The average juvenile IQ is higher because more often than not, those who are habitual offenders in childhood become habitual offenders in adulthood, and at adulthood IQ drops from childhood where the environment was able to artificially boost their IQs.
What if I’m right? What if IQ differences are traceable to malnutrition? That would indicate a whole different set of interventions and policies than just turn them away.
You are part right, but that won’t put any big dent in any genetic/phenotypic IQ differences and still, mass immigration from South of the Border still wouldn’t be OK in the first place.
In shutting down the conversation about race and IQ, Harvard students are explicitly saying they don’t WANT to find a reason behind low performance on IQ tests amongst certain racial groups. They don’t CARE why some groups are not reaching their full human potential. They don’t give ONE SINGLE FUCK about anyone other than themselves. It could be as simple as making certain children have access to proper food and nutrition.
I at least give her credit for acknowledging the biological reality of race and the reality of IQ. But she thinks that malnutrition plays too big a part in the ethnic IQ gap than it does in reality.
As I have covered here before, people will do anything they can to deny the validity of IQ tests. However, their explanations cut it.
People who attempt to deny biological differences in intelligence because they strongly predict positive life outcomes will do anything to deny their validity. But that doesn’t change how strong a predictor they are in regards to predicting both positive and negative successes in life.
Those who attempt to deny any differences between races, like Chanda Chisala (I know you can see this Chanda, still waiting for a response to the criticism of your horrible article that “redneck genes” are the cause for the black-white IQ gap), who are wrong in their premises on the cause as well as how to fix the gap. They will do anything to attempt to explain away a gap which is, at least, 50 percent genetic in origin.
The attack on Jason Richwine is because, of course, he’s right. They don’t want to admit he is right so they do whatever they can to discredit his argument, by calling him a ‘racist’. But that doesn’t negate his data, and as seen above, any arguments against Richwine’s dissertation are unfounded.
Germany is going to begin IQ testing their immigrants, why can’t we?
The Weston A. Price Foundation and Nutritional Myths
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There is a ‘foundation’ called the Weston A. Price Foundation. They push heavily questionable data, along with not updating their material when refuted or new studies come out. It was started in 1999 by Sally Fallon and nutritionist Mary Enig (Ph.D.). The Price Foundation advocates drinking raw milk, yet they have been criticized by the FDA for saying this.
Dr. Weston A. Price was a well-respected dentist from Cleveland. His son died from tooth decay which got him interested in the causes for tooth decay in modern populations. In 1939, he wrote Nutrition and Physical Degeneration. He and his wife traveled around the world and conducted various studies on modern populations living in isolated areas and compared them to those of the same country of origin in modern populations.
The countries he conducted studies in include: isolated and modernized Swiss, isolated and modernized Gaelics, isolated and modernized Eskimos primitive and modernized North American Indians, isolated and modernized Melanesians isolated and modernized Polynesians, isolated and modernized African tribes, isolated and modernized Australian Aborigines, Isolated and modernized Torres Strait islanders, isolated and modernized New Zealand Maori, ancient civilizations of Peru, isolated and modernized Peruvian Indian. He found that despite having no forms of dental hygiene that they had better dental crests and a lower, almost non-existent case of cavities in their population. He states that primitive people lived longer, but, this is not the case.
In private, Dr. Price told his family to eat a vegetarian diet. That has its problems as well. Since the average American doesn’t know how to correctly supplement certain vitamins and minerals, this will lead to nutrient deficiencies and eventually, less ability to fight off disease.
Though, the type of ‘science’ that the Price Foundation pushes will lead you to sickness and even, maybe, eventual death. They tell people to consume raw milk (this site is affiliated with the Price Foundation). They recommend diets high in saturated fats and no fruits and vegetables for children. However, it’s been very well-established that lack of those aforementioned foods leads to an increase in cancer in adulthood.
The WAPF recommends people to eat high amounts of saturated fat, which is the type of fat found in animals. Using data taken from the Food and Agricultural Organization of the United Nations (FAO) study done in 38 countries from 1979-1981, Kestelhoot, Lessafire and Joossens (1991) discovered that per person supply of fat from dairy products and lard cancer mortality were significantly correlated with total, breast, prostate, colorectal and lung cancer. Their findings support the concept of the role of saturated fat in the elevation of cancer risk.
A prominent name for the WAPF is Dr. Joseph Mercola, doctor of osteopathic medicine. The FDA has issued an order to Dr. Mercola to stop his illegal claims. He’s a snake oil salesman, just like the rest of the WAPF and those affiliated with them. Back in 2009, Dr. Mercola made unsubstantiated scientific claims about the nature of the H1N1 (Swine Flu) virus. It’s clear that Mercola, though he does have actual information on his website, is just getting paid by the WAPF to be just a name and put forth false claims so people will believe him since he has the title of “Doctor”.
They even make claims with some serious implications for babies if parents follow their advice. They recommend that a baby be given a blend of cow’s milk with heavy cream and oil and another blend of cow’s liver, beef broth, whey protein and various other oils. However, this type of diet for a newborn infant is extremely dangerous. Infants deficient in iron can begin to have a whole slew of health problems including anemia and damage to intelligence, behavior and motor functioning. Putting a baby on this diet will lead to lifelong problems that will not reverse even with a correct amount of iron. Lack of iron is correlated with diminished intelligence in children, but in children aged 5 and up it is possible to reverse the effect with increased supplementation of iron. The cause for the irreversibility of intelligence in those younger than five years of age is due to that being one of the most critical time for brain development where the brain needs all of the right amount of vitamins and nutrients it can get.
The WAPF is about as unscientific as you can get. They push old and outdated studies which only conform to their agenda. However, they do have good intentions. What Dr. Price saw when he visited the isolated peoples was that they had good dental hygiene despite not taking care of their teeth. This then inspired the two women who then started the WAPF. The WAPF may have been started with good intentions based on Dr. Price’s data, but it’s archaic in comparison to the type of data we have today. The diet pushed by the WAPF will lead to health implications and eventual death due to heart attack, cancer or some other type of disease correlated with high saturated fat intake. Most people become blind and have tunnel vision with their beliefs. No matter how many times they’re shown that they’re wrong and here is why they still hold on to their beliefs. It leads to artery clogging, which then does not allow correct blood flow which leads to heart attack or stroke and eventual death. These claims need to be thrown in the trash as soon as they come out, because due to the lack of nutritional information on the average American, they will see the word “Organization” and “.org” and think it’s a reputable place for information, where if you listen to it you will suffer severe health consequences.
Most people become blind and have tunnel vision with their beliefs. No matter how many times they’re shown that they’re wrong and here is why they still hold on to their beliefs. People don’t like to hear that they are wrong. When people are presented with contrary information, they gather support for their beliefs with “paradoxical enthusiasm”.This is because people have become so invested in their worldview that when provided contradictory evidence they lack the self-esteem to admit they were wrong and change their view. There is also something called “the backfire effect“, in which correcting of a wrong perception actually increases misperceptions.
The tunnel vision that people with huge misconceptions have, in this case nutrition, leads to them attempting to find anything they can to substantiate their claims, even if they’re objectively false. To take nutritional advice from one who is not a registered dietician (like Andrew Anglin and his pushing for the Paleo Diet, even when refuted on the clear false pretenses he makes in regards to his ‘articles’ like Europeans not evolving to eat tropical fruits and is therefore not natural [citation needed]. This also goes hand-in-hand with his look at the table showing the X/A ratio between Europeans, Africans, the Pan Ancestor and Bonobos, which he took to say that the African genome is closer to that of bonobos which is clearly untrue). Don’t follow what these ‘health gurus’ say because they are not up to date on the newest information and push shoddy and outdated ‘nutritional information’ to the average American who doesn’t know any better about nutrition.
This organization is dangerous to the health of those who give heed to their claims which are not based in science. It is dangerous to young infants whose parents believe their scientific double-talk. It is dangerous to those who drink raw milk and eat an excess of saturated fat which increases cancer rates. They have legitimate doctors who write in favor of them, yet one of the better-known names has been given statements by the FDA to stop illegal claims. The WAPF is full of snake oil salesman who want nothing more than to make a profit off of the nutritional ignorance of the average American. Get nutritional information from a verified source, not a place that denies science like the WAPF.
Are There Genetic Causes for Obesity?
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We all know about the Healthy At Every Size Movement (HAES) and how they claim that genetics is the cause of them being overweight and or obese and that genetics is the cause that they cannot lose weight as well as other people. I’m not here today to defend that they are right and that’s why they can’t lose weight (because lets be honest, they have no idea what they’re talking about, nor can they reference any type of study that says it), nor am I here today to give any credence to the HAES movement. I’m here today to talk about genetic causes for obesity as well as causalities that people don’t talk about and believe that kcal in and kcal are the only factors in becoming obese (I have never, nor will I ever dispute that kcal in and out has been the biggest factor involving obesity, just there are underlying causes that people do not talk about, which is the a huge cause in keeping people obese). What people don’t understand is that there are underlying factors that no one talks about that lead to obesity.
When people say that there are no genetic underpinnings for obesity, they are speaking on a subject that they are extremely ignorant about. They always say “kcal in and out”. Right, which I have never disputed. Though, those same people cannot say a thing to the studies that I provide, because they cannot adapt to new information and just parrot the same things as if that disproves the studies that I link. Furthermore, obesity and diabetes (which there is a close relationship between the two), are both nowhere near close enough to being understood.
I have already covered here that ability to delay gratification has a genetic component, and that those with low ability to delay gratification, as noted in my post, had a higher chance of becoming obese than those with a better ability to delay gratification. Some people have said to me that the Marshmallow Experiment didn’t have anything to do with the ability to delay gratification, that it was something else entirely, but alas, the individual obviously said nothing more when I asked him to comment on the post so my readers can read the exchange.
You all know that I covered ethnicity and obesity, but I’m making this post to serve as a something to reference while in discussion with people, as well as educate people who don’t know about these studies.
As noted in my previous article on obesity, there are racial difference in obesity (that pretty much follow Rushton’s Rule). Of course there are socioeconomic factors that are involved there, but to say that there is no genetic component is intellectually dishonest. To believe that there are absolutely no genetic causes for obesity and that environmental factors means everything shows that that person has no idea what they are talking about.
According to a meta-study of twins and families, the heritability of BMI is between .75 and .82. This used mono and dizygotic twins, as well as having over 140 thousand participants. They observed 12 countries, all with differing racial/ethnic groups and the results were the same.
While in a discussion with someone, I got linked these studies: Obese toddlers have dramatically lowered IQ, Obese toddlers have dramatically lowered IQ 2 and Obesity lowers children’s IQ. This is hilarious. The causalities are completely reversed. I would love to hear the explanation for the physiological mechanism that has obesity lower IQ. Well, Satoshi Kanazawa tackled this in his study back in 2014, that low IQ leads to obesity, obesity doesn’t lead to low IQ.
A few of the highlights include:
- Cross-sectional studies conclude that obesity lowers IQ, whereas longitudinal studies conclude that those who become obese already have a low IQ since childhood
- Careful examination of longitudinal studies in Sweden, New Zealand and America clearly show that the casual direction goes from low IQ to obesity, not obesity to low IQ
- There is NO scientific evidence that shows that obesity leads to lowered IQ. There is, however, ample evidence, both in scientific theory as well as ample amounts of evidence that lower IQ people become obese
Individuals with IQs below 74 at 18 have BMI of 26.59 at 40, whereas those with IQs above 126 have BMI of 25.75 (P < 0.001). Similarly, there is a clear and monotonically negative association between intelligence at 18 and the BMI change from 18 to 40. Individuals with IQs below 74 gain 5.19 in BMI in 22 years, whereas those with IQs above 126 gain 3.73 (P < 0.001). Their conclusion remains identical even when they control for systolic and diastolic blood pressure, resting pulse rate, birth place, birth year, and education at conscription. Their results from a large population sample of Swedish men make it clear that it is adolescent intelligence that influences BMI in middle age, not the other way around
The fact of the matter is this: obesity does not lower IQ. Those with certain agendas would like you to believe that becoming obese drops IQ, whereas ample scientific data shows the opposite. Including this study which states that those in the cohort who became obese didn’t see a drop in IQ from childhood, instead, those individuals who became obese already had a lower IQ since childhood. You already know that I did not get a response to these studies. That’s because showing people that they’re wrong actually makes them believe their wrong beliefs more, especially if they have low self-confidence (how ironic).
There have been genes that have been found that are associated with binge eating. If a young adolescent has this particular variant on the FTO gene, they are 20 to 30 percent more likely to binge eat than those who don’t have the variant. This was observed in girls particularly, who were 30 percent more likely to binge eat if they had the variation.
Dr. Peter Atilla had a TED Talk on how obesity may be hiding an even more insidious problem. To quote from the transcript:
Yet when it came to a disease like diabetes that kills Americans eight times more frequently than melanoma, I never once questioned the conventional wisdom. I actually just assumed the pathologic sequence of events was settled science.
Three years later, I found out how wrong I was. But this time, I was the patient. Despite exercising three or four hours every single day, and following the food pyramid to the letter, I’d gained a lot of weight and developed something called metabolic syndrome. Some of you may have heard of this. I had become insulin-resistant.
Now, most researchers believe obesity is the cause of insulin resistance. Logically, then, if you want to treat insulin resistance, you get people to lose weight, right? You treat the obesity. But what if we have it backwards? What if obesity isn’t the cause of insulin resistance at all? In fact, what if it’s a symptom of a much deeper problem, the tip of a proverbial iceberg? I know it sounds crazy because we’re obviously in the midst of an obesity epidemic, but hear me out. What if obesity is a coping mechanism for a far more sinister problem going on underneath the cell? I’m not suggesting that obesity is benign, but what I am suggesting is it may be the lesser of two metabolic evils.
You can think of insulin resistance as the reduced capacity of our cells to partition fuel, as I alluded to a moment ago, taking those calories that we take in and burning some appropriately and storing some appropriately. When we become insulin-resistant, the homeostasis in that balance deviates from this state. So now, when insulin says to a cell, I want you to burn more energy than the cell considers safe, the cell, in effect, says, “No thanks, I’d actually rather store this energy.” And because fat cells are actually missing most of the complex cellular machinery found in other cells, it’s probably the safest place to store it. So for many of us, about 75 million Americans, the appropriate response to insulin resistance may actually be to store it as fat, not the reverse, getting insulin resistance in response to getting fat.
You can think of insulin as this master hormone that controls what our body does with the foods we eat,whether we burn it or store it. This is called fuel partitioning in the lingo. Now failure to produce enough insulin is incompatible with life. And insulin resistance, as its name suggests, is when your cells get increasingly resistant to the effect of insulin trying to do its job. Once you’re insulin-resistant, you’re on your way to getting diabetes, which is what happens when your pancreas can’t keep up with the resistance and make enough insulin.
But most important, I was left with these three burning questions that wouldn’t go away: How did this happen to me if I was supposedly doing everything right? If the conventional wisdom about nutrition had failed me, was it possible it was failing someone else? And underlying these questions, I became almost maniacally obsessed in trying to understand the real relationship between obesity and insulin resistance.
So what I’m suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance.Maybe we should be asking ourselves, is it possible that insulin resistance causes weight gain and the diseases associated with obesity, at least in most people? What if being obese is just a metabolic response to something much more threatening, an underlying epidemic, the one we ought to be worried about?
Let’s look at some suggestive facts. We know that 30 million obese Americans in the United States don’t have insulin resistance. And by the way, they don’t appear to be at any greater risk of disease than lean people. Conversely, we know that six million lean people in the United States are insulin-resistant, and by the way, they appear to be at even greater risk for those metabolic diseases I mentioned a moment ago than their obese counterparts. Now I don’t know why, but it might be because, in their case, their cells haven’t actually figured out the right thing to do with that excess energy. So if you can be obese and not have insulin resistance, and you can be lean and have it, ******this suggests that obesity may just be a proxy for what’s going on.******
So what if we’re fighting the wrong war, fighting obesity rather than insulin resistance? Even worse, what if blaming the obese means we’re blaming the victims? What if some of our fundamental ideas about obesity are just wrong?
Personally, I can’t afford the luxury of arrogance anymore, let alone the luxury of certainty. I have my own ideas about what could be at the heart of this, but I’m wide open to others. Now, my hypothesis, because everybody always asks me, is this. If you ask yourself, what’s a cell trying to protect itself from when it becomes insulin resistant, the answer probably isn’t too much food. It’s more likely too much glucose: blood sugar. Now, we know that refined grains and starches elevate your blood sugar in the short run,and there’s even reason to believe that sugar may lead to insulin resistance directly. So if you put these physiological processes to work, I’d hypothesize that it might be our increased intake of refined grains, sugars and starches that’s driving this epidemic of obesity and diabetes, but through insulin resistance,you see, and not necessarily through just overeating and under-exercising.
The fact of the matter is this: we need to look at any and all causes to do with obesity. To fully understand this disease is to look at any and all factors involving it. To discard theories and make new ones, or just disregard what was looked at. People who say that we shouldn’t look at these types of things really have no idea what they’re talking about. To fully understand a problem, we need to look at any and all causes that may be underlying.
I’m currently writing a research paper on Prader-Willi’s Syndrome (which I will post here when I’m done with it), and as I was watching the documentary, a few things jumped out at me:
- They are infantile
- They clearly have a lack of ability to delay gratification
- Prader-Willi’s people have an IQ, on average of 70
- Due to being infantile, they have a lack of ability to delay gratification, so along with that, they have lower IQs which is correlated with lack of abstract thought
To say that these people “can control themselves” and they “just need to eat less” is dishonest, to say the least. Those people with disorders such as these really have no say in the matter.
In a follow-up to the Marshmallow Experiment, studies were done on those individuals they could still find 40 years later. What was found that those who lacked the ability to delay gratification in pre-school ended up becoming obese. We need to identify those children with low ability to delay gratification because it’s clear that those with the lack of ability to delay gratification end up becoming obese in adulthood.
This is a favorite of mine. People may say “Fat shaming is good!!! It leads to people thinking about what they’re doing and, in turn, they will lose weight!!!” How wrong that is. Present research indicates that in addition to poorer mental health outcomes, weight discrimination has implications for obesity. ******Rather than motivating people to lose weight, weight discrimination increases the risk for obesity.****** Why people think that making fun of people will lead to weight loss is beyond me.
Interestingly, a slightly different pattern emerged when the analyses were based on measured BMI. When the sample with measured weight and height was limited to participants who were overweight at baseline, the risk of obesity was a little stronger but essentially the same (OR = 2.18, 95% CI = 1.04–4.45). In contrast, when this sample was limited to normal weight participants at baseline, there was not enough data for the analysis: of the 14 participants in the normal weight category who reported weight discrimination, none became obese
Similar to weight gain, weight discrimination was associated with remaining obese over the period between the two assessments (see Table 1). That is, those who experienced discrimination based on their weight were over three times more likely to remain obese at follow-up, rather than drop below the obesity threshold, than those who did not experience such discrimination.
The evidence is clear: weight discrimination actually increases the problem that people actually laugh at and make fun of people for. How ironic is that?
In conclusion (I will add to this post as new research comes out), to say that there are no underlying causes of obesity is intellectually dishonest. There are clear underlying causes to this obesity epidemic, which we need to look at any and all of these causes to fully understand obesity better (which we are nowhere close to understanding this problem).
How Did Man Evolve to Eat?
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How did we evolve to eat? I’ve been through Paleo Diet two times, and briefly touched on intermittent fasting in the second Paleo refutation. That is how man, no matter where he evolved in the world, ate. We didn’t know when we would get our next meal, therefore, evolutionary mechanisms evolved in us to have intermittent fasting be beneficial to us.
Intermittent fasting is halting the consumption of food for at least 14 hours for women and 16 hours for men. We evolved gathering and eating our food intermittently. Ability to function at a high level, physically and mentally, during extended periods without food, were crucial to human evolution. Your body performs best in a fasted state.
While you’re in a fasted state, the amount of catecholamines (adrenaline and noradrenaline) increase. That is your fight or flight mechanism. Catecholamines also increase fat burning, binding to fat cells putting them out of the cell to be burned off.
With increased catecholamine production from being in a fasted state which burns off body fat, you are also more alert as well. This is another evolutionary advantage. When Man was hunting for food he was in a fasted state, as he didn’t have access to food like we do today. Due to being in a fasted state with increased catecholamine production, this was a great advantage to being better prepared to be ready in case of a surprise attack by a predator or to always be on the ready to attack prey when seen. The scientific literature, though new and growing, supports this thesis with the amount of catecholamine production increased 24 hours after a fast.
Intermittent fasting leads to a dramatic increase in neural autophagy. Autophagy deals with the destruction of cells in the body, controlled digestion of damaged organelles in the cell. The conclusion of the study is, fasting is a simple, easy way to increase neural autophagy. It’s good for keeping the brain healthy, by destroying bad cells, letting the body rejuvenate them.
In conjunction with the evolutionary advantages of intermittent fasting, along with Genetic Similarity Theory, which has those care for others more because they share more alleles in common, and are therefore more closely related, the two evolved hand in hand to better make sure humans survive extended periods of time without food.
Which brings me to ‘starvation mode’. When people bring up starvation mode, they completely misrepresent the Minnesota Starvation Experiment. When they say that metabolic slowdown occurs when food is not consumed for a certain amount of time, they are correct, but they’re only half right. It’s a process called adaptive thermogenesis. Adaptive thermogenesis is the regulated production of heat in response to environmental changes in temperature and diet, which lead to metabolic inefficiency. When they talk about ‘starvation mode’, they talk about not having consumed food within the past, say 2 or 3 hours. That is a completely ignorant statement, as there are no deleterious effects of no food consumption until around 24 hours of fasting. ‘Metabolic slow down’ is not significant enough to prevent weight loss.
Now you may be thinking “What about breakfast, isn’t that the most important meal of the day?” Yes, “breakfast” is the most important meal of the day, but it doesn’t need to be had in the morning, immediately upon waking. The average person sleeps for about 8 hours, during that time, the body enters the fasted state. The “breakfast is the most important meal of the day myth” was originally pushed by Kellog’s in the 50s. The problem with any of these studies in regards to weight loss and or any other conclusions is that they are observational studies. The actual cause cannot be quantified. The slogan was created to obviously give Kellog’s more business, which was based on observational studies. The main hormone behind post-breakfast hunger is cortisol. The term ‘breakfast’ means “break your fast”, therefor “breakfast” can be had anytime AFTER your body goes into the fasted state.
Cortisol is secreted in response to a stressor, in order to help you cope with that stressor efficiently. Exercise (hunting for our ancestors), disrupts homeostasis because of the stressors that are put on the body. The stressors then require an adaptive response, which is cortisol. Most anything our ancestors did disrupted homeostasis, causing cortisol to be secreted. Because of increased cortisol levels during times of need, you can push through certain things than if you didn’t have that cortisol increase due to the stressor that made your body secrete the extra cortisol.
The stressors that our ancestors had to survive in the past, though, had a clear-cut line in beginning and end. Therefore, the fight or flight mechanism (catecholamine production) was easily secreted to elicit the needed response in order to survive, get food, and ultimately what evolution is about, making sure your shared genes pass on to the next generation. All of these responses in regards to intermittent fasting increase Man’s success on the planet, as well as evolutionary fitness. The strong selection pressures then select for those traits which are more advantageous, which pass down through the generations, getting better or becoming obsolete through non-use, e.g. migrating to a new area where those selection pressures that had certain traits arise weren’t in the new area.
To talk about another hormone, there is a hormone called ghrelin, which is secreted by the stomach in anticipation for a meal. It decreases after meal consumption and also stimulates the release of the growth hormone.
An evolutionary advantage for ghrelin is that it let Man know when the last time he ate was, as our bodies are pretty much like clocks and tell us certain things when it needs them, e.g. releasing ghrelin when it needs nutrients and sustenance, so they can then go and hunt for food, ensuring that their genetic lineage survives.
The drive for food, the drive to make sure genes pass on to the next generation, intermittent fasting and evolution of man, all intertwine with each other to tell the story of how we got to where we are today. There are way more health benefits to restricting periods of being in a fed state, and the evolution of those adaptive processes in our bodies from thousands of years of eating intermittently which our bodies had to evolve the traits that had us succeed in order to pass our genes on to the next generation. Everything we do in life is, at the most basic level, driven by our biology and the release of certain chemicals/hormones that make us seek out or want certain things.
In summary, the release of catecholamines in response to lack of food after a certain amount of time is one such example that shows that those evolutionary processes evolved to better protect us from extended periods of time without food, as well as giving us great benefits due to how our bodies evolved in response to those adaptations. This also leads to increased altruism for those with close genetic similarity, e.g. more alleles in common than with other peoples. The increased catecholamine production leads one to be more alert of their surroundings, which is an evolutionary advantage due to the release of ghrelin making man hungry, which in turn led to searching for food. That then led to an increase in the catecholamines to increase those adrenaline hormones to make man better prepared for any attack by a predator, and to be ready for any perspective prey he saw. Intermittent fasting, including all hormonal advantages involved with it, evolved closely together with altruism for one’s own people. This led to an increase in genetic fitness, as well as having a better chance to pass your genes on to the next generation.
North/South Differences in Italian IQ: Is Richard Lynn Right?
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Richard Lynn has stated that there are differences in Northern and Southern Italian IQ scores. Is he correct?
Lynn claims Italian IQ is 100 in the North and 90 in the South, with the lowest being IQ 89 in the Southern most part of Sicily.
Richard Lynn is of course, extremely controversial in his research areas of interest, mainly with his views on IQ and how it relates to the wealth of nations.
In his paper which talks about the North/South differences in IQ which predict differences in education, infant mortality, stature, and literacy.
Lynn’s methods were to take samples of the Program for International Student Assesment (PISA) which administers tests gauging the abilities of students in math, reading comprehension and science understanding. IQs were calculated by averaging science understanding, reading comprehension and mathematical ability, which the averages are expressed in SD unit deviations from the British PISA mean (n=502, SD 99). Figures are then converted to conventional IQs by multiplying them by 15. So the regional Italian IQs are expressed in comparison to the British IQ and SD (100 and 15 respectively).
His 10 data points are as follows:
First, the IQ in the northern regions of Italy measured by the PISA data is approximately 100 and therefore about the same as in Britain and other countries of northern and central Europe given in Lynn and Vanhanen (2002, 2006). This confirms the results of the standardization of the Colored Progressive Matrices in northern Italy reported by Prunetti (1985) and shows that IQs measured by the PISA data and by the Colored Progressive Matrices data are consistent. Regional IQs in Italy decline steadily through the central regions and into the south and reach a low of 89 in the most southerly region of Sicily. The first hypothesis of this study that there may be a north–south gradient of IQs in Italy is supported and quantified by the correlation of 0.963 between regional IQs and latitude.
First, the PISA data from 2013 shows Southern Italians scoring higher, and Northern Italians scoring around the same. Is that an increase in intelligence that happened in only 3 years? Did the genetics of Southern Italy change in 3 years? No.
The table above shows the changes in PISA scores for Southern Italy in only 3 years for all 3 subjects tested in PISA. Southern Italy increased by 26 points in reading, and Southern Italy and islands increased by 30 points. For math, 25 for the South and 34 for South and the islands. For science, 18 for the South and 22 for the South and the islands. The presence of non-native students may also be a factor in these score differences. You can see the differences from 3 years, and how even in 3 years, there was a slight decrease in scores in Northern Italy. Migrants, after coming in from the South of the country, then continue to go into the Northern part of the country. This could also explain a huge part of the differences, seeing as they may be counted as Italian citizens, yet aren’t native to the country.
The above table shows mean PISA scores for 2006 and 2009, showing a huge increase in scores from Southern Italy, and hardly any increase in Northern Italy. Any genetic changes in 3 years to show that big of an increase?
Source: Problems in deriving Italian regional differences in intelligence from 2009 PISA data
Two, the second hypothesis of this study is that the north–south gradient of IQs in Italy may explain much of the difference in economic development between the north and south of Italy
Wrong again. Southern Italy has a huge underground economy, that isn’t noted on the books. The GDP in Southern Italy is far from accurate and employment figures do not match reality.
These raw figures require a closer look, because one economist’s analysis of Calabria found low pay, high unemployment, and a very high level of consumer spending. In 1994, the government insurance agency placed the number of business enterprises in Calabria at 23,758, while Istat, carrying out the 1996 census, found about 90,000 businesses in the same region.The economist Domenico Marino concluded, on the basis of 4,000 interviews in Calabria, that 75 percent of the Calabrian work force would refuse a fairly low-paying job, despite a very high official level of unemployment. In Calabria, with its dire employment figures, 84 percent of the families own their own home. What such anomalies must mean is that real income in Calabria is far higher than what is “on the books.” Many among the vast numbers of officially unemployed are, in fact, partly or fully employed. They are earning no social benefits, but they are earning the daily lire that keep their families afloat.
This massive sector skews all the statistics. It means that the GDP for the Italian South (and for Italy as a whole) is far from accurate. And the unemployment figures do not reflect reality.
LOOKING TO 2007: ITALY TIMES TWO
Three, the third hypothesis we set out to examine is that regional IQ differences in Italy are also manifest in variables that can be regarded as correlates or effects of IQs, including stature, infant mortality, literacy, and years of education
When historical data on those variables are used, a different picture emerges. Correlations are insignificant and in the case of infant mortality, do not the supposed link of regional differences in intelligence and socioeconomic development.
Four, per capita incomes are also highly negatively correlated with rates of infant mortality in 1954–57 (r= −0.652), and 1999–2002 (r=−0.823).
When the years 1911, 1891 and 1871 are averaged in, there is no difference.
Lynn didn’t consider the data from the 1860s to average it in with the rest of his data.
Five, the ability of populations with high IQs to give their children better nutrition makes them healthier, more resistant to disease and reduces the risk of mortality, and also improves their children’s stature
Right. But there is no mortality difference, as seen above.
Five, the ability of populations with high IQs to give their children better nutrition makes them healthier, more resistant to disease and reduces the risk of mortality, and also improves their children’s stature
There is a 1.7-inch difference between Northern and Southern Italian height. Which is explained by differences in nutrition between the regions, with the South having a more grain-based diet. Those effects are explained by a grain-based diet, and those Italians from America (which a huge majority are from the South of the country), actually show better educational attainment as well as more monetary success than their Northern counterparts.
Six, regional IQs in 2006 are highly correlated with the years of education of adults in 1951 (r=0.929), 1971 (r=0.871) and 2001 (r=0.886)
At the regional level, average IQs and current per capita GDP are highly related: for the year 2012, the correlation is 0.86. The link between IQ and regional development is, instead, much weaker when data for the years 1871, 1891 and 1911 are considered. Regional IQs and infant mortality rates in 1863–66 are positively correlated, contrarily to that which would be expected based on Lynn’s assumptions;
Two Italies? Genes, intelligence and the Italian North–South economic divide
This is explained simply. When Italy became unified in 1861, there were literacy differences in the country. 87 percent of the Southern population was illiterate in comparison to 67 percent of the Northern population.
The likely explanation for this high correlation is that the percentages of the population that were literate in 1880 was a function of IQs and therefore that the regional differences in IQs were present in 1880 and have been stable over the period 1880 to 2006.
Literacy and average years of schooling are better predictors of income levels than regional IQs.
The above table shows this.
Eight, it is an interesting question whether the differences in Italian regional IQs were present in earlier historical periods. Some useful data bearing on this question have been assembled by Murray (2003, pp. 303–5) who has compiled the numbers of “significant figures” (i.e. those who have made significant contributions to science, literature, music and art) and their places of birth for the whole of Europe from the year 1400 to 1950. His figures for the north, center and south of Italy are shown in Table 3.
Pretty damning right? Wrong.
More than half of the country is put into the ‘North’ section of what he is talking about, and how he did the dividing, it looks like this.
Murray also said that achievement happened in a few places in Italy, with Southern Italy being one of the many areas in Europe with ‘low achievement’, which includes a big part of Northern Italy as well. The achievements in Italy were mainly found in Tuscany, which the literacy rate wasn’t too high in 1880. Again, refuting Lynn on his thesis.
Nine, Putnam (1993, p. 159) and Tabellini (2007) have proposed that “civic trust” is a determinant of regional differences in economic development in Italy and in western Europe.
There are hardly any regional differences in economic development, as seen above.
A possible explanation for the northern regions having had higher IQs than the southern regions at least from 1880 and possibly from 1400 to 1600 is that the populations of the north and south are genetically different and these genetic differences are related to differences in intelligence.
Not at all. I touched on this in my Refuting Afrocentrism: Are Italians Black? article.
They write of the population genetics of Italy that “northern Italy shows similarities with countries of central Europe, whereas central and southern Italy are more similar to Greece and other Mediterranean countries.
See above. They are genetically the same:
Comparison with Germany and Italy, Germans are spread out farther on the graph than are Italians, are there huge genetic differences with Germans as well?
They write of the population genetics of Italy that “northern Italy shows similarities with countries of central Europe, whereas central and southern Italy are more similar to Greece and other Mediterranean countries. This corresponds to the well-known differences in physical type (especially pigmentation and size) between the northern and north-central Italians on the one side and southern Italians on the other”.
Pigmentation is explained by getting the same UV rays as Northern Africa:
Size differences explained by slight differences in nutrition.
Subsequent studies have confirmed the genetic impact of immigration from the Near East and North Africa into southern Italy. For instance, the Taql, p1 2f2-8-kb allele has a high frequency in the Near East and North Africa (Morocco, 81.8; Lebanon, 43.7; Tunisia, 34.1). The allele is also present but at a lower frequency (26.4) in southern Italy, including Sicily.
Using a single, or small number of loci will lead to you finding the same loci in different populations? Who knew!!
The diffusion of genes from the Near East and North Africa may explain why the populations of southern Italy have IQs in the range of 89–92, intermediate between those of northern Italy and central and northern Europe (about 100) and those of the Near East and North Africa (in the range of 80–84) (these IQs are given in Lynn, 2006). This also explains the north–south gradient of IQ in Italy in which the regional IQs do not show a clear dichotomy between north and south but rather a gradient in which IQs decline steadily with more southerly latitude.
Nope. I’ve covered this in my ‘Black Italians’ article:
Combined data from two large mtDNA studies provides an estimate of non-Caucasoid maternal ancestry in Italians. The first study sampled 411 Italians from all over the country and found five South Asian M and East Asian D sequences (1.2%) and eight sub-Saharan African L sequences (1.9%). The second study sampled 465 Sicilians and detected ten M sequences (2.2%) and three L sequences (0.65%).This makes a total of 3% non-white maternal admixture (1.3% Asian and 1.7% African), which is very low and typical for European populations, since Pliss et al. 2005, e.g., observed 1.8% Asian admixture in Poles and 1.2% African admixture in Germans. (Plaza et al. 2003; Romano et al. 2003)
Similar data from the Y-chromosome reveals Italians’ even lower non-Caucasoid paternal admixture. Both studies obtained samples from all over the mainland and islands. No Asian DNA was detected anywhere, but a single sub-Saharan African E(xE3b) sequence was found in the first study’s sample of 416 (0.2%), and six were observed in the second study’s sample of 746 (0.8%). The total is therefore a minuscule 0.6%, which decreases to 0.4% if only Southern Italians are considered and 0% if only Sicilians are considered.Again, these are normal levels of admixture for European populations (e.g. Austrians were found to have 0.8% E(xE3b) by Brion et al. 2004). (Semino et al. 2004; Cruciani et al. 2004)
An analysis of 10 autosomal allele frequencies in Southern Europeans (including Italians, Sicilians and Sardinians) and various Middle Eastern/North African populations revealed a “line of sharp genetic change [that] runs from Gibraltar to Lebanon,” which has divided the Mediterranean into distinct northern and southern clusters since at least the Neolithic period. The authors conclude that “gene flow [across the sea] was more the exception than the rule,” attributing this result to “a joint product of initial geographic isolation and successive cultural divergence, leading to the origin of cultural barriers to population admixture.” (Simoni et al. 1999)
One of the most important citations is the Simoni et al. 1999 cite. Which says that gene flow across the sea was more the exception than the rule. Those 3 studies above refute any ‘racial differences’ between Northern and Southern Italians.
There are problems deriving Italian IQ from PISA test scores. You cannot take PISA data and infer a group’s IQ from it!! Moreover, on purer measures of intelligence, such as Raven’s Progressive Matrices, there is no significant difference between North and South children. These are differences in achievement, not intelligence. None of the studies cited by Lynn were aimed at comparing Italian IQ across regions and none of them used the same age groups!! This is why his data on Italian IQ is wrong.
To conclude, we don’t know the true IQs of all of the regions of Italy. Lynn used faulty measures to make his theory (which doesn’t need fluff) of north/south disparities in IQ more palatable. He’s been refuted multiple times on this matter. I may do another in the future.
Italianthro source: Refuting Richard Lynn’s IQ Study
HBD and Diet Advice: Anglin Paleo Refutation Part 2
2300 words
A lot of people seem to have wrong views on nutrition. It’s not really taught in school, people think that it doesn’t matter so they do no independent research of their own and they believe anything and everything that comes out in the MSM as gospel. The thing is, the average person doesn’t read studies, or anything nutrition related for that matter, and believes most everything they read and hear in the MSM. I have talked about nutrition a bit here. I refuted Andrew Anglin’s atrocious writing and arguments for the Paleo Diet here and wrote on obesity and ethnicity including genetic and environmental causes. I also wrote on how nutrition is important prenatally as well as postnatally in developing children. I will also touch on comments in that Dailystormer article that jump out to me that need refuting.
Today I will talk about HBD and diet advice.
Steve Sailer wrote an article on HBD and Diet Advice back in September. He claims a few things that need to be disproven.
It’s common for nutrition scientists to give advice to white Americans based on studies done of what is good for nonwhites to eat. For example, in the 1980s, one of the most fashionable studies was of Japanese in Hawaii. The first generation ate mostly rice with little fat, and they had relatively few heart attacks. The next generation ate cheeseburgers and had higher rates of coronary disease than their parents.
I have covered this in the Dailystormer refutation.
Noted in this study are:
- High interpersonal variability in post-meal glucose observed in 800-person cohort
- Using personal and microbiome features enable accurate glucose response prediction
- Prediction is accurate and superior to common practice in an independent cohort
- Short-term personalized dietary interventions successfully lower post-meal glucose
You can see from the above bullet points that there is high interpersonal variability in post-meal glucose. What that means is, that between each individual in the cohort, there were different glucose spikes in each person.
They can accurately predict glucose response with certain tools. They devised a machine-learning algorithm that uses blood parameters, dietary habits, anthropometrics, physical activity, and gut microbiota measured in the cohort and showed that it accurately predicted personalized postprandial (post-meal) glycemic response to real-life meals.
They validated the prediction using a 100 person cohort.
Personalized dietary interventions showed interventions successfully lowered post-meal glucose. (Emphasis mine). This shows that each person should be on an individual diet and not on a one-size-fits-all diet.
Of course the next generation had higher rates of coronary disease than their parents. High carb, high fat diets lead to coronary blockage, leading to heart attacks and other coronary implications.
That is due to the demonization of fat starting in the 70s. We were told that fat is bad and carbs were fine. That turned out not to be the case. That’s what led to the obesity explosion. People think that eating fat “makes you fat”. Well if that’s the case, eating protein leads to kidney failure and eating carbs leads to Diabetes Mellitus. It’s stupid to think of it that way. Anything in excess is bad for you.
The RDA (Recommended Daily Values) for women is as follows:
69 grams of fat, which comes out to 585 kcal, 300 grams CHO which comes out to 1200 kcal and 53 grams of protein which comes out to 215 kcal. For men, it’s 80 grams of fat which comes out to 720 kcal, 375 grams CHO which comes out to 1500 kcal and 70 grams of protein which comes out to 280 kcal. This is data from the FDA on dietary recommendations for the average America.
Protein is nowhere near high enough. Protein is the main macronutrient you want to eat if you want to stay fuller longer as it has a higher TEF (Thermic Effect of Food). In the linked study, they come to the conclusion that TEF contributed to the satiating power of foods. Protein has the highest TEF of all of the macros, and because of this, some researchers have lobbied to have protein count as 3.2 kcal instead of 4 kcal. So if you want to stay fuller, eat more protein, fewer carbs and more fat. Carbs spike your insulin leading to insulin spikes, which lead to you feeling hungry sooner, as most people ingest fast digesting carbohydrates.
Sailer then cites this NYT article that says:
Today, at least 10 percent of Americans regularly take fish oil supplements. But recent trials have failed to confirm that the pills prevent heart attacks or stroke. And now the story has an intriguing new twist.
Wrong. So, so wrong. Controlled studies clearly show that omega-3 consumption had a positive influence on n-3 (fatty acid) intake. N-3 has also been recognized as a modulator of inflammation as well as the fact that omega-3 fatty acids down-regulate genes involved in chronic inflammation, which show that n-3 is may be good for atherosclerosis.
Studies have shown an increase in omega-3 consumption leads to decreased damage from heart attacks.
Omega-3 may also reduce damage after a stroke.
Dietary epidemiology has also shown a link between n-3 and mental disorders such as Alzheimers and depression. N-3 intake is also linked to intelligence, vision and mood. Infants who don’t get enough n-3 prenatally are at risk for developing vision and nerve problems. Other studies have shown n-3’s effects on tumors, in particular, breast, colon and prostate cancer.
Omega-3’s are also great for muscle growth. Omega-3 intake in obese individuals along with exercise show a speed up in fat-loss for that individual.
Where do these people get their information from? Not only are omega-3’s good for damage reduction after a stroke and a heart attack, they’re also good for muscle growth, breast, colon and prostate tumor reduction, infants deficient in omega-3 prenatally are at risk for developing nerve and vision problems. Increase in omega-3 consumption is also linked to increases in cognition, reduces chronic inflammation and is linked to lower instances of depression.
Omega-3’s are fine. As I said with the Anglin refutation, do not listen to those with no background in nutrition as they most likely have no idea what they are talking about.
Rasmus Nielsen, a geneticist at the University of California, Berkeley, and an author of the new study, said that the discovery raised questions about whether omega-3 fats really were protective for everyone, despite decades of health advice. “The same diet may have different effects on different people,” he said.
See above links on omega-3 intake and all of the positive/negative factors.
In the future, maybe you’ll be able to get your DNA analyzed and be given a list of diets in rank order of their likelihood that they will work for you. But, right now, you can still try different diets. In particular, ask your relatives about what has worked and not worked for them.
That doesn’t matter, as diets should be tailored to the individual, as seen in the Cell study.
Oh, wow. I just found that Anglin wrote a refutation to those who deny the Paleo Diet. Let’s see what that’s about.
And maybe these people have scientific research and/or personal experience to back up what they’re saying. I’m not insulting them for disagreeing with me on diet, that is clearly their right.
The evolutionary argument for Paleo does not line up with your statements. As I noted in my previous article, if you want to eat Paleo because it works with what you like to eat, good for you. But doing it for any magic benefits is stupid, as there are none.
I know for a fact that at least 9 out of 10 people who dare to take this challenge will report back positively if they follow it properly for a month, and this means a whole lot more than someone’s opinion about what it might or might not do, theoretically.
Want to know why people will report back positively? Any time you begin a new diet, especially one on a kcal restriction, your body will drop weight quickly. That’s what piranha personal trainers use on unknowing people. Telling them that they’re doing a “great job”, when in actuality, that happens to everyone who begins a new diet.
Instead, they are arguing theoretically, making highly debatable statements like “White people have evolved to be able to consume dairy products.”
The above map shows lactose intolerance for countries around the world. Ancient Europeans began dairying around 7500 ya and were lactose intolerant when starting to drink milk. But along with faster evolution, which includes no gene flow from other parts of the world, that led to Europeans evolving to, on average, have lower rates of lactose intolerance.
People should really learn what they’re talking about before they say it.
The way to know whether or not they are beneficial is to quit them for a period and see how you feel.
Placebo effect.
Currently, because the scientific literature on these topics is so convoluted and debated on, there is no other conceivable way to prove it one way or another than through our own testing.
The science is pretty solid on this. Anecdotes don’t mean anything to studies.
Many have referred to paleo as a “fad diet.” And it may be a diet that is a fad, but it is also a diet with a thousands upon thousands of years long precedent. One might even suggest that it is the consumption of grains and dairy that are the “fad,” as it is a relatively new trend, in the scope of things.
It IS A FAD DIET ; with NO basis in science that Europeans should eat that way.
If you feel as if you are at peak physical health eating grains and dairy, and have no desire to spend time trying to improve on this, than by all means skip the challenge.
Is he implying that the Paleo Diet is the only diet that doesn’t allow grains and dairy? Not true at all. The Slow Carb Diet is the same, as well as any other high fat, high protein low-carb diet.
We should also note that the definitions of vegetarianism were different then, and Hitler did eat eggs and probably wasn’t completely meat-free.
That’s vegetarianism. Veganism is the more extreme one you’re thinking of where absolutely no animal products are consumed at all.
Vegetarian diets are shown to lead to vitamin inadequacies such as zinc, calcium, iron, manganese, selenium, and copper. Vegetarianism works, it just has to be well-planned. You need to make sure you get the right amount of essential as well as non-essential amino acids, high amounts of protein and make sure you’re not nutrient deficient.
Last time I wrote that White rice and potatoes are good carbs, but I want to be clear that they are not necessary unless you are both already at 5% body weight and you are highly active.
They are not ‘good carbs’. They are white carbs, which are bad for us if we don’t go to the gym to utilize the CHO being ingested. Five percent body-fat? That’s for competition bodybuilders and marathon and distance runners. The average person will never cut down to the level of body-fat. CHO is extremely useful if you’re highly active and go to the gym.
Even if you are not active, you need to consume a decent amount of carbs once a week in order to keep your metabolism from slowing down too much. However, it is probably preferable to use fruits for this purpose, as they contain more micronutrients.
Correct. If you eat a low-carb diet, you need a CHO refeed once a week to keep metabolism high. Though, using fruits is stupid. I know the Paleo thing, but there are many reasons why fructose (the sugar found in fruit) is bad for you. Sugar is just as addictive as cocaine. So telling the average person to ‘use fruits for this purpose’ is stupid, as the average person doesn’t know when to stop eating.
Yes, this diet will technically cost more than a processed foods and grain-based diet, all things being equal. The only reason anyone ever ate grains in the first place is because they were cheap, and processed foods were invented for the same reason. Any natural and healthy diet is going to cost more, all things being equal. However, things don’t have to be equal.
Wrong. 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. I personally spend 70 dollars a week on food for myself, with all of my meals planned out. 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.
I tried to answer most of the questions people had in the last thread, but it was so filled up with denialism I could have missed something. So ask here.
I hope you answer this, as well as my other refutation of your horrible nutrition article. I doubt it though.
How did we really evolve to eat?
The most common form of eating, 3 meals a day, is abnormal from an evolutionary perspective. We didn’t evolve eating 3 times a day. We evolved eating intermittently. The study says that intermittent energy restriction periods of up to 16 hours are fine. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Again, another huge benefit for intermittent fasting. As the data comes out on human cohorts, we will be able to see all of the great effects that IF has for us, because that’s how any human population, no matter where they evolved, evolved eating.
There are beneficial effects to IF including reduced oxidative damage and increased cellular stress resistance. Rats put on an IF diet show heightened life-spans. IF is also extremely useful to keep a youthful brain as you age.
There are a mountain of studies that show how beneficial IF is to us and is the TRUE way humans evolved to eat, not any specialized diets. We evolved eating intermittently, and with our hedonistic society we live in now, along with low ability to delay gratification, as well as other factors I have covered in my previous nutrition articles, have led to the effects we see in America, and around the world today.
In conclusion, don’t listen to people who have no background in nutrition. They tell clearly wrong information, and those who aren’t privy to new information in the nutrition world, won’t know that they are being lied to and or manipulated into believing things based on shoddy evidence.
IQ, Nutrition, Disease and Parasitic Load
1600 words
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.
NotPoliticallyCorrect 