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When critics of the mainstream approach towards modern African-American grievance questions the agency of the population to improve their standards of living, they often cite either how minorities such as poor European immigrants of the Early 20th century assimilated better despite discrimination, or how Black immigrants from Africa occupy a higher mode of living.
While multiple factors contribute to the discrepancy, one caught my attention which struck me a paradoxical but soon started to make sense as I dug deeper. That trait being the lack of effective widespread “unity” among not just Black Americans but many other populations, especially those in Africa.
– The Situation
As for my titular use of “chaos” to describe it, I owe it to an Unz commenter who contrasted it from individualism or collectivism. For an intra-regional example, you have riots or protests regarding threats seen as pertaining to the racial mass, yet you have commonly cited the lack of the same regard for those killed by perpetrators of the same race.
From an inter-regional example I refer to the words of my father that, despite the beliefs of some, there is no “Black America” in which the interests or beliefs of blacks due to having comparatively looser connections than others based on a national level. This is noted by regional variance in ideology between blacks during the Progressive Era or better yet modern African conflicts, many of which can be classified as Christians versus Muslims on the larger scale yet can even be observed on a finer, pre-colonial level of identities (Osaghae and Suberu 2005).
“There are numerous examples of pre-colonial migration, usually stimulated by wars or natural disasters, which have continued to generate bitter conflicts today owing to continuing discrimination against the immigrants by the original settlers. These include the eighteenth century mass migration of Oyo Modakeke into Ife in search of a safe haven from the internecine wars of the Oyo empire; the movement of Urhobo and Ijaw into Warri, where the Itsekiri claim to have been the original settlers; the migration of the Jukun-Chamba from Cameroon to parts of the present Taraba state, originally settled by the Kuteb; and the sixteenth century settlement of Hausa merchants in Zangon Kataf within a territory occupied by the Kataf (Isumonah 2003; Mustapha 2000). “
I attribute three reasons why this would be.
One being geography, as these behaviors are most notable with African nations that often overlap in cultural spheres despite living on a huge continent, and also how Black Americans probably covering the largest area relative to other New World African descent populations thus making diversification more enabled.
The second being the process of slavery in New World populations giving various forms of cultural transmission amongst black slaves by region who as well came through different tribes, either producing the typical “Scot-Irish” Black culture or a “Creole” culture, like the Gullah people of the South East. The Third, the Basal reason, being the effects of Genetic interests at hand as put by RR and how African Diversity works.
Here Razib Khan explains that when Foreign Admixture is removed, African diversity is higher among individuals than for major geographical groups.In other words, while geographically diverse, the actual organization of the diversity in the context of cultural boundaries is more stratified due to the lack of breeding, be it outbreeding or replacement involved in nations.
This suggestion is strengthened by famous blogger Jayman attributing this to the lack of large states in Africa to the lack of especially large states in Africa. Granted, you did have relatively large ones in the Sahel but the didn’t last as long as those in Eurasia, falling mainly due to internal struggles.
In the presence of cultural homogeneity, reflecting of a shared lineage, you see improvements in places such as Botswana (Tswana-Sotho) or Ghana (Akan people) partially due to better cultural, and thus likely genetic, unity due to past nationhoods. Apparently, though for short duration, the Tswana formed a political body as large as France,
This is also consistent with the observations made by Sir Harry Hamilton Johnston, a famous colonialist researcher on African and US blacks, on African born blacks on the sea Islands of the South East, which he describes as of “Yoruba Stock” in semblance.
“Also they are when away from white influence inclined to sparsity of clothing-not nowadays a common trait in the United States negro. They are also pure negroes entirely without any infusion of white blood. Crime is very rare among them.” The Negro in the New World by Harry Hamilton Johnston p. 470
A good modern example would be the demographics of West Africa Immigrants, being principally Akan of Ghana and the Yoruba or Igbo of Nigeria, who each come from relatively well constructed precolonial formations. What is also of note is how their prominence seems to be correlated to the extent in which Cousin Marriage is practiced, possibly reflective of the precolonial patterns of cousin marriage
Application for the U.S population in kin networks, where it does not work.
PP, in which he discussed the ethnocentrism of different groups, said this regarding blacks and kin altruism.
“And yet eventually these extremely different tribes mixed, and so you would have parents raising kids who have genetic variants very alien to their own, and this probably contributed to the breakdown of the black family: it’s harder for kin altruism to get selected when the kids you are altruistic to, don’t resemble you that much genetically because their other parent is so unlike you that they don’t inherit your high degree of kin altruism or inherit it as a recessive unexpressed trait. And when kin altruism gets only weakly selected for, racial loyalty (which is probably just an outgrowth of kin loyalty) is probably weakly selected for too.”
Which would be incorrect. Yes, while crossing over does occur, a child would be overall close to their parent’s overall genetic background on the level of relatedness. Leaping from that neglected detail, he assumes from his evidence of “lack of racial loyalty” would that blacks have less ethnic nepotism and thus weaker kin altruism despite not taking into account of selection occurring within subgroups of various constructs like you see in Africa which would apply to families inside them.
If this theory was even supportable, one would expect the opposite that actually occurs with the percentage of Black children to return to relatives compared to White children.
“Of the 94,483 black children discharged from foster care, 12,860, or 13%, were discharged to a relative guardian. Of the 182,941 white children discharged from foster care in 2004, 20,453, or 11%, were discharged to a relative guardian.Of the 15,087 black children adopted from foster care, 4077, or 27%, were adopted by a relative. Of the 29,244 white children adopted from foster care, 5861, or 20%, were adopted by a relative. Of the 279,421 black kids living in foster care for some portion of the year, 69,888 or 25% were living with relatives. Of the 474,734 white children living in foster care for some portion of the year, 101,300, or 21%, were living with relatives.
So black children getting adopted from foster care are somewhat more likely to be adopted by relatives than white kids (27% vs. 20%), black kids exiting foster care are slightly more likely to be discharged to a relative guardian than white kids (13% to 11%), and black kids in foster care are slightly more likely to be living with relatives than white kids (25% vs. 21%). The differences support the hypothesis that blacks are more likely to utilize kinship care networks, but not by a lot, at least in regard to the foster care system.”
From Audacious Epigone, who also notes that despite the higher likelihood of such networks that doesn’t explain disproportion in foster care. Though evidence for IQ is at best moderate, interpersonal indicators were stronger (Azar, Stevenson, and Johnson 2012)).
“SIP problems were associated with direct measures of neglect (e.g., cognitive stimulation provided children, home hygiene, belief regarding causes of child injuries). Further, for the direct measures that were most closely linked to CPS Neglect Status, IQ did not add significant predictive capacity beyond SIP factors in preliminary model testing. Implications for intervention with PID discussed.”
This is possibly linked to EI scores found to differ between Whites and Blacks (Whitman, Kraus, and Rooy 2014)
“The present work examines applicant reactions to a test of emotional intelligence (EI) using an organizational sample of 334 job applicants. Results indicated that Blacks had higher face validity and opportunity to perform perceptions of EI than Whites, but that Whites performed significantly better than Blacks on the EI test. Although exploratory analyses revealed that test performance was positively related to test reactions, we also found that the magnitude of this relationship differed between Blacks and Whites for the opportunity to perform perceptions. We discuss our findings by offering practical advice for organizations considering or using a measure of EI for selection and assessment.”
Evidence for Kin networks is also supported by more data (Taylor 2013).
“Turning first to findings for family support networks, four significant differences were observed in this analysis. African Americans gave assistance to their family members more often than non-Hispanic Whites, were more likely to have daily contact with their extended family members than both non-Hispanic Whites and Black Caribbeans, and had more frequent interactions with their family than Black Caribbeans. Three general conclusions can be drawn from these findings for family assistance and interaction. First, these findings are consistent with prior work indicating that African Americans have similar or higher levels of involvement with kin than non-Hispanic Whites, but are inconsistent with reports that African Americans have lower levels of family support than Whites (e.g., Hogan et al., 1993). As noted in previous reviews of this literature (Sarkisian & Gertsel, 2004), comparisons across studies are problematic given important differences in the dependent variables used. The present study’s investigation of several dimensions of family support relationships (e.g., enacted support, emotional support, contact, negative interaction) in diverse groups of the population and using a common set of sociodemographic correlates clarifies the nature of race/ethnic differences in these relationships.”
It also found, however, weaker ties outside the family, which strengthen my suggestion of finer stratification of kin ties than just simply less selection.
“Several significant differences in friendship networks were observed in this analysis. Non-Hispanic Whites interacted with their friends and gave support to their friends more frequently than African Americans. Additionally, non-Hispanic Whites received support from friends more frequently than both African Americans and Black Caribbeans. Many of the differences between African Americans and non-Hispanic Whites could reflect basic differences in their levels of involvement in friendship networks. For instance, 16.7% of African-Americans, 16.1 % of Black Caribbeans and 9.7% of non-Hispanic Whites report that they never receive help from friends. Similarly, African Americans (11%) were twice as likely as non-Hispanic Whites (4.7%) to indicate that they hardly ever or never interact with friends. Lower levels of involvement with friends among African Americans could be due to estrangement from friends, isolation from friends or exclusive involvement with kinship networks (Ajrouch et al., 2001). Collectively, these results, and previous research (Griffin et al., 2006; Waite & Harrison, 1992), indicate that non-Hispanic Whites are more likely than African Americans to interact with friendship networks and to identify friends as an important source of support.”
This lack of support was not seen, however, with fictive kin or congregational members. So perhaps wither the perception of relationship or differences in genetic similarity may answer some of these questions.
People talk a lot about intelligence and brain size. Something that’s most always brought up is how the human brain increased in size the past 4 million years. According to PP, the trend for bigger brains in hominins is proof that evolution is “progressive”. However, people never talk about a major event in human history that caused our brains to suddenly increase: the advent of fire. When our ancestors mastered fire, it was then possible for the brain to get important nutrients that influenced growth. People say that “Intelligence is the precursor to tools”, but what if fire itself is the main cause for the increase in brain size in hominins the past 4 million or so years? If this is the case, then fire is, in effect, the ultimate cause of everything that occurred after its use.
The human brain consumes 20-25 percent of our daily caloric intake. How could such a metabolically expensive organ have evolved? The first hominin to master fire was H. erectus. There is evidence of this occurring 1-1.5 mya. Not coincidentally, brain size began to tick upward after the advent of fire by H. erectus. Erectus was now able to consume more kcal, which in turn led to a bigger brain and the beginnings of a decrease in body size. The mastery and use of fire drove our evolution as a species, keeping us warm and allowing us to cook our food, which made eating and digestion easier. Erectus’s ability to use fire allowed for the biggest, in my opinion, most important event in human history: cooking.
With control of fire, Erectus could now cook its foods. Along with pulverizing plants, it was possible for erectus to get better nutrition by ‘pre-digesting’ the food outside of the body so it’s easier to digest. The advent of cooking allowed for a bigger brain and with it, more neurons to power the brain and the body. However, looking at other primates you see that they either have brains that are bigger than their bodies, or bodies that are bigger than their brains, why is this? One reason: there is a trade-off between brain size and body size and the type of diet the primate consumes. Thinking about this from an evolutionary perspective along with what differing primates eat and how they prepare (if they do) their food will show whether or not they have big brains or big bodies. How big an organism’s brain gets is directly correlated with the amount and quality of the energy consumed.
There is a metabolic limitation that results from the number of hours available to feed and the low caloric yield of raw foods which then impose a trade-off between the body size and number of neurons which explains why great apes have small brains in comparison to their bodies. Metabolically speaking, a body can only handle one or the other: a big brain or a big body. This metabolic disadvantage is why great apes did increase their brain size, because their raw-food diet is not enough, nutritionally speaking, to cause an increase in brain size (Azevedo and Herculano-Houzel, 2016). Can you imagine spending what amounts to one work day eating just to power the brain you currently have? I can’t.
Energy availability and quality dictates brain size. A brain can only reach maximum size if adequate kcal and nutrients are available for it.
Total brain metabolism scales linearly with the number of neurons (Herculano-Houzel, 2011). The absolute number of neurons, not brain size, dictates a “metabolic constraint on human evolution”, since people with more neurons need to sustain them, which calls for eating more kcal. Mammals with more neurons need to eat more kcal per day just to power those brains. For instance, the human brain needs 519 kcal to run, which comes out to 6 kcal per neuron. The brain is hugely metabolically expensive, and only the highest quality nutrients can sustain such an organ. The advent of fire and along with it cooking is one of, if not the most important reason why our brains are large (compared to our bodies) and why we have so many neurons compared to other species. It allowed us to power the neurons we have, 86 billion in all (with 16 billion in the cerebral cortex which is why we are more intelligent than other animals, number of neurons, of course being lower for our ancestors) which power human thought.
The Expensive Tissue Hypothesis (ETA) explains the metabolic trade-off between brain and gut, showing that the stomach is dependent on body size as well as the quality of the diet (Aiello, 1996). As noted above, there is good evidence that erectus began cooking, which coincides with the increase in brain size. As Man began to consume meat around 1.5 million years ago, this allowed for the gut to get smaller in response. If you think about it, it makes sense. A large stomach would be needed if you’re eating a plant-based diet, but as a species begins to eat meat, they don’t need to eat as much to get the adequate amount of kcal to fuel bodily functions. This lead to the stomach getting smaller, and along with it so did our jaws.
So brain tissue is metabolically expensive but there is no significant correlation between brain size and BMR in humans or any other encephalized mammal, the metabolic requirements of relatively large brains are offset by a corresponding gut reduction (Aiello and Wheeler, 1995). This is the cause for the low, insignificant correlation between BMR and our (relatively large brains, which correlates to the amount of neurons we have since our brains are just linearly scaled-up primate brains).
Evidence for the ETA can be seen in nature as well. Tsuboi et al (2015) tested the hypothesis in the cichlid fished of Lake Victoria. After they controlled for the effect of shared ancestry and other ecological variables, they noted that brain size was inversely correlated with gut size. Perhaps more interestingly, they also noticed that when the fish’s’ brain size increased, increased investment and paternal care occurred. Moreover, more evidence for the ETA was found by Liao et al (2015) who found a negative correlation between brain mass and the length of the digestive tract within 30 species of Anurans. They also found, just like Tsuboi et al (2015), that brain size increase accompanied an increase in female reproductive investment into egg size.
Moreover, another cause for the increase in brain size is our jaw size decreasing. This mutation occurred around 2.4 million years ago, right around the time frame that erectus discovered fire and began cooking. This is also consistent with, of course, the rapid increase in brain size which was occurring around that time. The room has to come from somewhere, and with the advent of cooking and meat eating, the jaw was, therefore, able to get smaller along with the stomach which increased brain size due to the trade-off between gut size and brain size. Morphological changes occurred exactly at the same time changes in brain size occurred which coincides with the advent of fire, cooking, and meat eating. Coincidence? I think the evidence strongly points that this is the case, the rapid increase in brain size was driven by fire, cooking, and meat eating.
The rise of bipedalism also coincided with the brain size increase and nutritional changes. Bipedalism freed the hands so tools could be made and used which eventually led to the control of fire. Lending more credence to the hypothesis of bipedalism/tools/brain size is the fact that there is evidence that the first signs of bipedalism occurred in Lucy, our Australopithecine ancestor who had pelvic architecture that showed she was clearly on the way to bipedalism. There is more evidence for bipedalism in fossilized footprints of australopithecines around 3 mya, coinciding with Lucy, tool use and eventually the advent and use of fire as a tool to cook and ward off predators. Ancient hominids could then better protect their kin, have higher quality food to eat and use the fire to scare off predators with.
The nutritional aspect of evolution and how it co-evolved with us driving our evolution in brain size which eventually led to us is extremely interesting. Without proper nutrients, it’s not metabolically viable to have such a large brain, as whatever kcal you do eat will need to go towards other bodily functions. Moreover, diet quality is highly correlated with brain size. Great apes can never get to the brain size that we humans have, and their diet is the main cause. The discovery and control of fire, the advent of cooking and then meat eating was what mainly drove the rapid increase of brain size starting 4 mya.
In a way, you can think of the passing down of the skill of fire-making to kin as one of the first acts of cultural transference to kin. It’s one of the first means of Lamarckian cultural transference in our history. Useful skills for survival will get passed down to the next generation, and fire is arguably the most useful skill we’ve ever come across since it’s had so many future implications for our evolution. The ability to create and control fire is one of the most important skills as it can ward off predators, cook meat, be used to keep warm, etc. When you think about how much time was freed up upon the advent of cooking, you can see the huge effect the control of fire first had for our species. Then think about how we could only control fire if our hands were freed. Then human evolution begins to make a lot more sense when put into this point of view.
When thinking about brain size evolution as well as the rapid expansion of brain size evolution, nutrition should be right up there with it. People may talk about things like the cold winter hypothesis and intelligence ad nauseam (which I don’t doubt plays a part, but I believe other factors are more important), but meat-eating along with a low waist-to-hip ratio, which bipedalism is needed for all are much more interesting when talking about the evolution of brain size than cold winters. All of this wouldn’t be possible without bipedalism, without it, we’d still be monkey-like eating plant-based diets. We’d have bigger bodies but smaller brains due to the metabolic cost of the plant-based diet since we wouldn’t have fire to cook and tools to use as we would have still been quadrupeds. The evolution of hominin intelligence is much more interesting from a musculoskeletal, physiological and nutritional point of view than any simplistic cold winter theory.
What caused human brain size to increase is simple: bipedalism, tools, fire, cooking, meat eating which then led to big brains. The first sign of big brains were noticed right around the time erectus had control of fire. This is no coincidence.
Bipedalism, cooking, and food drove the evolution of the human brain. Climate only has an effect on it insofar as certain foods will be available at certain latitudes. These three events in human history were the most important for the evolution of our brains. When thinking about what was happening physiologically and nutritionally around that time, the rebuttal to the statement of “Intelligence requires tools” is tools require bipedalism and further tools require bigger brains as human brains may have evolved to increase expertise capacity and not IQ (more on that in the future), which coincides with the three events outlined here. Whatever the case may be, the evolution of human intelligence is extremely interesting and is most definitely multifaceted.
In my first article on this matter, I showed how Richard Lynn claims the average IQ in Italy is around “89-92” for Sicily and the South and around 103 for the North. I showed how he was wrong and what data he overlooked to fit his hypothesis. Lynn’s 2011 article IQs in Italy are higher in the north: A reply to Felice and Giugliano was a reply to Myth and reality: A response to Lynn on the determinants of Italy’s North–South imbalances. Felice and Giugliano brought up Lynn’s four main theses: a) the South’s “economic backwardness” in terms of economics ‘throughout history’; b) the evidence provided by Lynn wasn’t enough to ‘prove’ a cause of lower IQ for S. Italians; c) the evidence provided by Lynn wasn’t enough to show that S. Italians score lower than N. Italians; and d) the supposed ‘high rates of MENA admixture’ in S. Italians. I blew up all of these claims in the beginning of the year, more specifically I blew up up the claims about MENA admixture back in January. I’ll be going through Lynn’s 2010b article correcting any discrepancies. It’s worth noting that he still pushes the so-called ‘MENA admixture’ as being a substantial CAUSAL factor when there is NO evidence for this big of a ‘gap’ between the North and the South. The Lynn quotes will be from his 2010 paper linked above. I had also thought that ‘migrants’ from MENA countries could have contributed to the gap between the North and South, but since this isn’t the case for France then it shouldn’t be so for Italy. However, since Italy is a hub for these people when they first illegally enter Europe, they may stay and get counted as citizens and the children of these immigrants grow up and get accounted in the data. This is plausible, since a lot of ‘migrants’ may stay where they first get which is Southern Europe, mainly Sicily and Southern Italy.
We now present new data showing that IQs are higher in the north of Italy than in the south. In the previous study, data were presented for 12 Italian regions from the PISA (Program for International Student Assessment) 2006 study of the reading comprehension, mathematics and science performance of 15 year olds, regarded as measures of intelligence. We are now able to give similar data on the reading comprehension, mathematics and science performance of 15 year olds in 20 Italian regions obtained in the 2009 PISA study (OECD, 2010). These are given in Table 1. This shows, reading from left to right, the latitude of the Italian regions, the mean PISA scores for 12 regions for 2006 given in Lynn (2010a), the mean scores of 15 year olds on reading comprehension, mathematics and science understanding for the 20 Italian regions obtained in the 2009 PISA study, and the averages of the three 2009 PISA scores given because it provides a convenient summary of the scores on the three tests.
I already went through this in my previous article, but for clarity, I’ll go through this again.
Cornoldi, Giofrè, and Martini (2013) showed how there are problems inferring Italian IQ from the very PISA data that Lynn cites. There was a relevant decrease between the North and South. If the PISA test showed genetic proclivities between the North and South, why was there a relevant decrease in the three-year period? Because it is not an intelligence test, but a test of educational achievement. D’Amico et al (2011) conclude:
Our examination of intelligence test score differences between the north and south of Italy led to results that are very different from those reached by Lynn (2010a). Our results demonstrate that by using intelligence tests to assess differences in ability rather than using achievement scores as a proxy for intelligence, children from the south of Italy did not earn lower scores than those from the north of Italy. Rather, they were even higher in Raven’s CPM. However, we see no advantage in claiming that children in the south are “more intelligent” than children in the north, because these groups are different on a number of variables (e.g., environmental factors, educational influences, composition of the samples) that influence differences in test scores.
Either no difference or Southern Italians scored higher. When using purer measures of intelligence (Raven’s Progressive Matrices) so-called “differences” in “intelligence” disappear.
It will be noted that the regional differences in both language and math ability increase with age. For example, in language ability the regional differences in the youngest children (P2) range between 1.6 and −3.8, a difference of 5.4, while the differences in the oldest children (2S) range between 3.6 and −4.4, a difference of 8.0. Similarly, in math ability the regional differences in the youngest children (P2) range between 0.8 and −1.0, a difference of 1.8, while the differences in the oldest children (2S) range between 4.3 and −5.4, a difference of 9.7. These age differences would be predicted from the thesis that the regional differences have a genetic basis, because the heritability of intelligence increases during childhood (Plomin, DeFries, & McClearn, 1980, p. 334).
On other measures of achievement, such as the INVALSI examinations, Southern Italians do not score lower, and in some cases may even score higher (Robinson, Saggino, and Tommasi (2011). Moreover, the N/S differences in ‘cognitive ability’ don’t exist at age 7, the IQ/income relationship didn’t exist in the past, and the MENA admixture in Southern Italians is minute (Daniel and Malanima, 2011). The so-called MENA admixture that Nordicists and Lynn like to say is the subject of my next point.
Further data for the proportion of North African ancestry in the Italian regions are available in the frequency of the haplogroup E1b1b allele. This is a marker for North African ancestry, where it reaches frequencies above 50% and peaks at around 82% in Tunisia (Zalloua et al., 2008). The frequencies of the haplogroup xR1 and the E1b1b alleles are taken from Capelli et al. (2006), Capelli et al. (2007), Di Giacomo et al. (2003), Balaresque et al. (2010), Scozzari et al. (2001), and Semino et al. (2000). These data are given in columns 11 and 12 of Table 1 and the correlations between these and the other variables are given in Table 2.
As said and cited above, the so-called admixture from MENA populations in Southern Italians accounts for an extremely small fraction of the overall Southern Italian genome. The cause for lower achievement (“IQ” according to Lynn) in Southern Italians rests on this very pertinent point. And it’s wrong. Furthermore, and this is for Sicilians, the contribution of their genome by the Greeks is 37 percent, with the North African contribution being 6 percent. Daniel and Malanima (2011) ask ” Can the Greek heritage to the Western culture really be associated to a lower IQ?” The answer is, clearly, no. Moreover, a Central Italian province has the highest amount of MENA admixture, yet they have higher scores than Southern Italy. What does that tell you?
Richard Lynn’s Italian IQ data is garbage. Purer measures of intelligence such as Raven’s Colored Progressive Matrices show a decrease in the “intelligence gap” and in some cases, Southern Italians score higher than Northern Italians. When using measures of “IQ” from PISA data, these so-called differences disappear. Lynn’s data he cites in his 2010a paper don’t control for socio-cultural differences and school quality. There is numerous data that suggests the school quality in Southern Italy is worse than that of the North; this difference in school quality then affects educational achievement. Since PISA is a test of educational achievement and not intelligence (D’Amico et al, 2011), what accounts for these differences in achievement in the various studies may (and in my opinion, does) account for the differences in educational achievement between Northern and Southern Italians. The measurements in various studies may be influenced by the larger between-schools variability that is present in the South (Cornoldi et al, 2010; Daniel and Malanima 2011).
Finally, some people may point to the GDP differences between North and South Italy as proof of genetic/intelligence differences between them. However, the Mafia accounts for around a 20 percent drop in GDP in Southern Italy. To say that any differences in GDP can be accounted for without first controlling for things like this is dishonest. The presence of Mafia in areas shows lower growth and a sharper increase in murders. Each time homicides rise, GDP falls between 16-20 percent (Pinolli 2012). The presence of the Mafia had a devastating effect on the economies in that area between the 70s and 00s.
In sum, PISA is garbage to infer intelligence from as they are tests of achievement and not intelligence. Other tests of achievement show a decrease in the gap and/or Southern Italians scoring higher. Moreover, no substantial genetic differences exist between the North and the South, falsifying Lynn’s thesis for the causality of the differences between the North and the South. The oft-cited GDP difference between Northern and Southern Italy can be accounted for by the presence of the Mafia. Whenever the murder rate rises (due to Mafia activity), the GDP decreases. None of these factors have been taken into account and they explain the difference between the North and the South. It is environmental in nature–not genetic. Lynn’s Italian IQ data is garbage and should not be cited. It’s just a Nordicist fantasy that Southern Italians score lower than Nothern Italians.
Ethnic differences in the prevalence of obesity occur, majorly in part due to differences in the rates of metabolic syndrome (which is actually a few variables including high blood pressure, high blood sugar which leads to insulin resistance, excess visceral fat around the waist which is the ‘skinny fat‘ phenomenon, and abnormal blood pressure levels) and obesity. Ethnic differences in these variables do, in part, show how the three ethnies differ in rates of obesity. I will discuss the differences between each ethny in regards to metabolic syndrome and sleep and how it leads to the differences in ethnic obesity rates.
There is a ‘missing hour of sleep‘ when comparing blacks and whites. On average, blacks get 6.05 hours of sleep while whites get 6.85 hours of sleep. Of course, the same old racism argument comes up, which, if one ‘percieves’ discrimination, I wouldn’t doubt that it would have an effect on sleep due to a rise in cortisol, which affects sleep due to the raised levels making you restless and not able to fall asleep. Insulin levels then rise due to the rise in cortisol, which is the cause of obesity.
Some studies may try to say that racism and other forms of discrimination are a factor, without even thinking of genetic factors. Another study that Frost cites says that duration of deep sleep and duration of stage 2 (light sleep) is correlated correlated in African Americans with perceived discrimination. The authors defined ‘perceived discrimination’ as the extent to which one believes that their ethnic group have been discriminated against by society. Still even when controlling for discrimination, there were still marked differences between blacks and whites and how long they slept.
Frost then talks about how sleep patterns are heritable and cites studies done on Africans in Africa. One study found that there was an hour sleep difference between Ghanaians and Norwegians on the week days and between a quarter to half hour less on weekends. He shows another study showing that Nigerian college students sleep 6.2 hours a day while getting 70-minute naps in the afternoon.
Frost concludes that the African sleep patterns is normal on Africa. Africans are more active during the cooler times of the day and sleep during the bitter periods. Frost says those who evolved in more northerly climes are particularly adapted to a certain sleep pattern with the same holding true for Africans.
However, these sleep patterns in first world countries have negative effects on metabolism and rates of obesity.
Here are some more studies showing that blacks sleep less than whites:
The sleep of African Americans: a comparative review: The researchers found that blacks take longer to fall asleep than whites, report poorer sleep quality, have more light and less deep sleep, and nap more often and longer. This is a huge recipe for risk factors for obesity, and it shows in their demographics.
Unfair Treatment is associated with Poor Sleep in African American and Caucasian Adults: Pittsburgh SleepSCORE Project: This is one of the studies spoken about above that show that discrimination leads to less sleep. Though, it holds for both black and white adults. The researchers conclude:
Taken together, the confluence of perceived unfair treatment as a chronic stressor and poor sleep and the interplay between the two may have critical roles in long-term health problems.
African Genetic Ancestry is Associated with Sleep Depth in Older African Americans: The researchers hypothesized that “racial differences in sleep phenotypes would show an association with objectively measured individual genetic ancestry in AAs.” They conclude that the slow wave sleep may have genetic underpinnings.
Mexican Americans sleep less than do Mexican immigrants. US-born Mexicans are 40 percent more likely to be short sleepers. This is attenuated by environmental factors such as smoking and stress, which shorten the duration of sleep (smoking decreases the Body Set Weight, whereas cortisol along with insulin in tandem increase it).
Also, in this study by Roane et al (2014) looked at the link between sleep disturbances and stress in Mexican Americans (average age 55) and non-‘Hispanic’ whites (average age 66). Mexicans reported higher levels of sleep disturbance (25 percent) compared to whites (17 percent). They conclude that disturbed sleep was positively correlated with depression.
So both blacks and Mexicans sleep less than whites. These differences in sleep between these three ethnies also affect the prevalence of obesity in these populations.
Obesity and Sleep
It’s long been known that poor sleep habits make people fat. This is due to the effects of insulin and cortisol. Increased insulin comes before increased cortisol–increased insulin is the cause for obesity. Sleeping less is linked to obesity. Since, as described above, the three ethnies differ in sleep patterns, the same also holds true for obesity rates (Ogden at al, 2014). The trends are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for Hispanics. Though, sleep is only one factor involved with obesity.
Getting adequate sleep is extremely important. Not doing so can lead to a myriad of negative health implications:
Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity.
So a lack of sleep leads to an increase in ghrelin levels, decreased levels of leptin (the same effects as caloric restriction over time), increased appetite and hunger, increased evening cortisol (which insulin spikes then follow), decreased insulin sensitivity (the cortisol brings it back up and most people are insulin resistant independent of diet), decreased glucose tolerance, etc. We can see that these ethnic differences in sleep, which are partly genetic in nature, can and would have great effects on metabolism, contributing to the ethnic differences in obesity rates.
And from Harvard:
For example, in the Nurses’ Health Study, researchers followed roughly 60,000 women for 16 years, asking them about their weight, sleep habits, diet, and other aspects of their lifestyle. (2) At the start of the study, all of the women were healthy, and none were obese; 16 years later,women who slept 5 hours or less per night had a 15 percent higher risk of becoming obese, compared to women who slept 7 hours per night. Short sleepers also had 30 percent higher risk of gaining 30 pounds over the course of the study, compared to women who got 7 hours of sleep per night.
Damn!! This, pretty much, mirrors the black-white difference. I’d love to see a racial breakdown of this cohort and will keep an eye out for one, but in the meantime, those who were short sleepers had a 30 percent higher risk of gaining 30 pounds over the course of the study in comparison to women who got 7 hours of sleep per night. Blacks are the most likely group to be overweight and obese in the US, and this data from the Nurses Health Study (which tons of data can be drawn from this study) shows one reason why, however the driver is cortisol > insulin > processed carbs > increased insulin > insulin resistance > increased insulin > vicious cycle > obesity. These differences in sleep almost perfectly mirror the ethnic differences in obesity.
There are several possible ways that sleep deprivation could increase the chances of becoming obese. (1) Sleep-deprived people may be too tired to exercise, decreasing the “calories burned” side of the weight-change equation. Or people who don’t get enough sleep may take in more calories than those who do, simply because they are awake longer and have more opportunities to eat; lack of sleep also disrupts the balance of key hormones that control appetite, so sleep-deprived people may be hungrier than those who get enough rest each night.
Ah the old ‘exercise to increase the Calories Out part of the equation’. however, Calories Out does not stay constant. This also rebuts the ‘Eat Less and Move More’ CICO (Calories In/Calories Out) model of obesity, showing that because it doesn’t take insulin into account, it’s doomed to fail.
Speaking of insulin, it’s about time I focused on metabolic syndrome.
As I discussed in a previous post, Race, Obesity, Poverty, and IQ, metabolic differences exist between race/ethnicity. ‘Hispanics’ metabolize carbohydrates differently, blacks have a lower fiber intake (increased fiber protects against obesity, another correlate) while whites have a more high fat diet. Contrary to popular belief, dietary fat doesn’t make you fat as it’s the macro that spikes your insulin the least.
Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake. Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.
In ‘Hispanics’, several loci were discovered that play a role in hepatic (relating to the liver) fat content. Along with showing that ‘Hispanics’ have lower insulin (which due to low insulin, blood glucose builds up in the blood stream leading to diabetes) and showing that they metabolize glucose in the liver differently due to differing loci leading to more cases of fatty liver, this shows how and why ‘Hispanics’ have higher rates of Type II Diabetes Mellitus (TIIDM).
Since TIIDM affects Mexican Americans more, better measures to address their differences in carbohydrate metabolism need to be taken. Racial and ethnic differences in TIIDM are as follows:
7.6% of non-Hispanic whites
9.0% of Asian Americans
12.8% of Hispanics
13.2% of non-Hispanic blacks
15.9% of American Indians/Alaskan Natives
Whites eat a higher fat diet, which means a decrease in carbs. Asians eat white rice which spikes blood glucose eliciting a high insulin response leading to TIIDM, ‘Hispanics’, non-‘Hispanic’ blacks, and Indians and Alaskan Natives (I wish they separated Indians and Alaskan Natives as I’m almost positive that Alaskan natives have a lower rate) all eat high carb, low fat, low protein diets. Carbohydrates are a main staple, and since they spike insulin the most, they are the cause for obesity and TIIDM rates in these populations.
Turning my attention over to metabolic syndrome and blacks and whites, we can see that black women with PCOS have an increased risk for cardiovascular disease and metabolic syndrome in comparison to white women with PCOS. The researchers say that after controlling for age and body mass index (BMI) “black women with PCOS had a significantly increased prevalence of low high-density lipoprotein and high glucose. The general CVD risk was significantly increased in black adults with PCOS.” Though, a longitudinal study needs to be carried out to assess the independent impact of race and PCOS with CVD (Cardiovascular Disease).
Blacks have a higher chance to be diagnosed with metabolic syndrome since they are also at increased risk to have elevated blood pressure (hypertension), become obese, and be diabetic. This is due to their diet, which is due to their low IQ (obesity is correlated with intelligence), and different metabolism in comparison to whites.
There are also metabolic differences between race and sex. Fat oxidation is lower in black than white men and in African American men/women and white men/women, they have a lower metabolic rate!!! 24-hour energy expenditure is lower in black women in comparison to white women, whereas physical activity energy expenditure (PAEE) is the same as whites. Contrasted with women, black men had higher PAEE than white men. The authors conclude:
In conclusion, this comparative study of 24-h energy metabolism in African Americans and whites with use of a respiratory chamber not only confirms the previous findings from ventilated-hood studies of a lower resting metabolic rate, but also suggests a lower 24EE in African American women than in white women. Although only marginal ethnic differences in metabolic rate were found in men, African American men seem to have a lower rate of fat oxidation than do white men. The underlying mechanisms for these sex differences and the significance of these findings with respect to the development and maintenance of obesity remains to be investigated in longitudinal studies.
Metabolic Syndrome and Obesity
Black American men are the least likely male ethnic group to be overweight or obese in America (69.2 percent) compared to ‘Hispanic’ men (78.6 percent) and white men (71.4 percent) (Ogden et al, 2014). As a result of being less likely to be obese, black men as a whole suffer from diabetes and other diseases that are correlated with higher body fat. Conversely, for women the rate for white women is 63.2 percent, 77.2 percent for ‘Hispanic’ women and 82.4 percent for black women. Why do black men have lower rates of obesity and chronic health diseases?
Klimentidis et al (2016) set out to find why black men have lower rates of obesity than black women despite having the same socioeconomic and environmental factors. Using 2814 self-identified African Americans from the Atherosclerosis Risk in Communities study, they estimated each individual’s degree of African ancestry using 3,314 genetic markers. They then tested whether sex modifies the association of West African genetic ancestry and body mass index, waist circumference, and waist to hip ratio. Also, they adjusted for income and education as well as examined associations of ancestry with the phenotypes of males and females separately. They recreated their results with the Multi-Ethnic Study of Atherosclerosis (n= 1611 AA).
They discovered that West African ancestry is negatively correlated with obesity as well as central obesity, which is obesity around the midsection, among black men but not black women. Also noted, was that black men with more African ancestry had a lower waist to hip ratio and less central adiposity than black men with less African ancestry. They conclude that their results suggest that a combination of male gender and West African ancestry is correlated with protection against central obesity and suggests that a portion of the difference in obesity (13.2 percent difference) may be due, in part to genetic factors. The study also suggests that there are specific genetic and physiologic differences in African and European Americans.
This study confirms two things. 1) Black women are more likely to be obese than black men as well as the general population. 2) Black men have less of a chance of becoming obese or overweight as well as less of a chance of incurring the risks that come along with being obese or overweight. The degree of African ancestry is the cause in both black men and black women for these differences in the rate of overweight and obese individuals in both populations. One of my theories also got confirmed. Since obesity is partly genetic in African Americans, and black girls have an earlier menarche (period) than white girls due to higher body fat which activates the hormone leptin, which precedes an increase in body fat to prepare for eventual menstruation, I theorize that black girls have earlier menarche than white girls due to r/K Selection Theory. It’s an evolutionary advantage to be able to have children earlier, as the population dies younger.
Evolutionarily speaking, black men needed to be more fit in order to protect the clan from predators. This is also why blacks evolved narrower hips (Rushton, 1995). Higher body fat allows for more protection for a baby in vitro, which is why an increase in leptin precedes an increase in body fat, which then causes black girls to have an earlier puberty.
One of the questions I would like answered is whether it’s the actual degree of African ancestry that is the cause of black men being less likely to be obese or it’s the cause of higher degree of European ancestry. European American men do have a slightly higher risk of being overweight or obese than African American men, so there is some credence to this hypothesis. Three SNPs were found to be correlated with obesity in African American populations as well as European American populations; this could be one cause.
Wagner and Heyward (2000) discovered biological differences exist between blacks and whites. They reviewed the literature on the differences between blacks and whites in fat-free body mass (water, mineral, and protein) fat patterning and body dimensions and proportions. Blacks, in general, have greater bone mineral density and body protein content than do whites, resulting in lower fat-free bone density. They also note racial differences in the differences of subcutaneous body fat, which is the body fat that’s just below the skin, as opposed to visceral body fat which is found in the peritoneal cavity, which can be measured with calipers to give a rough estimate of total body fat adiposity. The conclusion reached in the study was that differences in FFB (fat-free body) was statistically significant between blacks and whites. They also have a greater BMC (bone mineral content) and BMD (bone mineral density) than do whites. They also argue that for a given BMI (body mass index), blacks might have less adiposity because they tend to be more mesomorphic. Researchers push for the development of racial-specific equations to better see differences in FFB.
With the above study noting that there is a substantial difference between blacks and whites in FFB, there may be some truth to a negative effect of European ancestry on blacks in terms of obesity acquisition. However, lower FFB in black men is one reason why black men can’t swim as well as whites.
One of the causes for both racial and gender discrepancies in obesity is genetic in origin. The difference between black men and black women is 13.2 percent whereas for white men and white women the difference is 8.2 percent. There is a clear genetic difference between races that is the cause for this discrepancy. Black men and black women have the same socioeconomics status and live in the same environment, so some of the differences in obesity noticed in this population must be genetic in origin.
Freedman et al (2004) observed that, as expected, black men were more likely to choose heavier figures as an ideal body for women than white men. Also expected was that both groups would choose figures with a low waist to hip ratio, but black men would choose a lower waist to hip ratio as ideal. They also show weight to be a more important cue than waist to hip ratio in mate selection as well as supporting the theory that black men’s preferences may serve as a protective factor against eating and body image pathology in black women.
To give an example of the above study in action, we can look at Mauritania. They force feed their women up to 16,000 kcal a day in an effort to make them obese, as that’s what is seen as attractive in their society. Mauritanian love songs also describe the ideal woman as fat. Obesity is so celebrated in their society that parents beam at the fact that their daughters look obese, as they have a better chance of getting partners.
The higher the degree of West African ancestry in black men, the lower the chance they have for obesity. I do wonder, though, if it’s because they have less European ancestry or because they have more African ancestry. Black men with more African ancestry are less likely to be obese than black men with less African ancestry, so there is a correlation there that I would like to see explored in the future. Differences in fat-free body mass have been noticed between blacks and whites, but this is one of the first studies to my knowledge that shows that genetic differences between black men and black women may be part of the cause for obesity differences in that population. Cultural differences in perception of beauty, of course, come into play in regards to differences between black and white men, however, the cause of black women having higher rates of obesity is due in part to genetic factors, which then leads to black men liking that as their beauty standard.
A lot of people seem to confuse causes between ‘Islam’ and behavior that’s just ‘low IQ’. Whenever these attacks like shootings, sexual assaults and rapes happen, that’s due to their low IQ; not religion. I wrote about this in IQ, Inbreeding and Clannishness. All of the behavior you see is due to low IQ. 1) being in an area with a hot climate and 2) cousin marriage has been going on there ever since Jews from the Levant introduced it to them around 200 BC. To quote myself:
Those innate behaviors which result in the favoring in all areas of life, themselves and their family, is a result of genetic similarity because of the closely related genes they share (the father’s brother’s daughter type is the most common in the Muslim world). Also, first and second cousin marriages are more common, which also result in increased altruism for their own family because of the close genetic similarity, but also those in their own group, which is mediated by the brain hormone oxytocin.
In a paper on the mean IQ of Muslims and non-Muslim countries, Donald Templer states that the Muslim world, which used to be have great intellectual achievements from the 7th to 12th centuries, has seen an underrepresentation in highly creative contributions in science journals. This is because of the inbreeding effect (2.5 to 10 point drop in IQ) of close cousin marriage. He ends up saying that genetic factors are more important than social/cultural/religious values (back to the inbreeding, causing defects and lowering IQ) in regards to IQ.
I also put a map of individualism and collectivism in Europe here. You can see that the collectivist countries are fighting back more. The countries/regions where it’s more red roughly matches up to the situation. You can see how in Central, Northern and Northwestern Europe they’re more individualistic, as well as more atheist, than those collectivist countries. So that leads to what we see with this ‘welcome refugees’ signs, as well as, I would assume, more oxytocin in the brain for Europeans, which leads to more altruism towards other peoples. Of course, 1000 years ago, the high altruism was fine due to being a mostly homogeneous society. But when others move in who are not from the area, and who do not have the same biology as you due to certain selection pressures, that’s when the ‘clash of cultures’ commences. Which it’s not really a clash of culture, more like a clash of biology, because 2 groups who shouldn’t live together are being forced to live together.
This also brings me to people who confuse the causality between Islam and blacks. As I said, it’s a low IQ religion (which I have provided enough evidence for my case). So blacks who become Muslim do so because of low IQ. Anything after that doesn’t mean that being a Muslim had them do it. Lets say that Islam never popped up and the same peoples were still there, continuing such close inbreeding, would that be Islam doing it? No. It’s their biology. **
Using environmental factors (Islam, culture) is what leftists do. In my post on behavior not equaling genes plus environment, I showed how people create their own environments based on their own genetics. The environment we put ourselves in is based on our genetics. We can clearly see that Islam is bringing their culture (genetics) to Europe and are incompatible with Europe as well as all Western societies around the world. Due to this, we can see that wherever any population goes, it will be the same from the original place they emigrated from if migration in large enough numbers occurs. A country is only as good as its majority population.
In Non-Western People are Abnormal to Our Societies, I showed how due to differing cultures (genetics), these third-world immigrants coming into our countries cannot readily assimilate due to differing average IQs and other hormones that lead to crime differentials with the native population. Though Arabs are Caucasian, evolving closer to the equator lead to higher levels of testosterone as more exposure to the sun increases vitamin D levels, which is not a vitamin but actually a steroid hormone. These differences in testosterone then lead to more sex attacks with high testosterone combined with low IQ. Lower IQ people are less likely to be virgins than higher IQ people. This shows that higher IQ people have less testosterone and can also hold back urges more than lower IQ people. This then translates over to an increase of sexual assaults by ‘migrants’ to European women. These ‘abnormalities’, though, would be abnormal anywhere. Putting differing cultures (genetics) in a place with a completely different culture will lead to strife due to genetic distance between the two populations.
I wrote in Evolutionary Reasons for Suicide Bombings that Muslims who suicide bomb do so to increase inclusive fitness. The increase in inclusive fitness comes about due to the suicide bomber having no prospects as well as no kids, so he/she is just taking up resources. By committing suicide, they are freeing resources for others who have a better chance to spread their genes. Many suicide bombers come from middle-class backgrounds, which further proves the case for genetic interests being the cause for this. The majority of Al-Qaeda members come from educated, middle-class backgrounds. Even for Palestinian suicide bombers, none of them were poor, uneducated, simple minded nor depressed.
The average IQ for a criminal is 85 adult offenders, 92 for juvenile offenders. What’s the average IQ in the Middle East? 81, around 1.3 SD lower than average, and 4 points lower for chronic adult offenders in America. The lower IQ comes from being more inbred, which then manifests itself in the crime rate. The strife in the middle east can also be traced back to IQ and consanguinity rates in those populations. How inbred a population is predicts IQ as well as how much strife occurs in those populations.
Germany has said they will begin IQ testing their ‘migrants’. If it works well (I highly doubt it will, and if it is, it won’t be implemented well) this could curb some attacks that happen. Since IQ differences between populations are one of the biggest causes for crime differentials (lower IQ is also correlated with higher testosterone) between them, screening for and only allowing high IQ ‘migrants’ in would curb some violent crime and sex attacks if implemented on a wide enough scale. IQ differences between populations are one of the biggest reasons for differences between any population you can think of.
For a comparison, we can use Christian Arabs. Christian Arabs are less inbred than Muslim Arabs, which shows in the amount of terror attacks committed by Christian Arabs, which I can’t find any data for. If anyone has found any, leave a comment. hbdchick then says this about consanguinity between Christian Arabs and Muslim Arabs:
so, the rate of cousin-marriage amongst lebanese christians was 16.5% while the rate for muslims approached double that at 29.6%.
christians married cousins more distant than first cousins at a slightly higher rate than they did first cousins: 8.6% (>1C) versus 7.9% (1C). muslims, on the other hand, favored first cousin marriage: 17.3% (1C) versus 12.3% (>1C). this is a similar pattern found elsewhere in the middle east/arab world. in egypt, for instance, copts tend to marry second cousins while muslims tend to marry first cousins (no, i can’t find the reference!).
there was also more fbd marriage amongst muslims (6.4%) versus christians (3%).
This is directly mirrored in how often we hear about Christian Arab attacks and crime (I haven’t heard of this), showing that consanguinity rates can predict crime rates. Due to this extreme inbreeding, they are more genetically similar, which leads to higher amounts of altruism for their own group, in turn leading to derogation of the out-group. Europeans are, on average, less inbred than Muslims. This is why it’s said that Muslims are incompatible with our societies. They are more clannish and altruistic for their own. Like JP Rushton said, groups will proliferate ideas that are good for their genetic interests.
Even more evidence can be shown with Chechen inbreeding. I can’t find any data on Chechen IQ, so lets use the closest country to Chechnya, which is Georgia with an average of 94. Since inbreeding can depress IQ 2.5 to 10 points, Chechnya’s average IQ should be somewhere around the mid-80s. This shows similarity with the consanguinity rate. hbdchick then concludes:
it’s no wonder, then, that they still engage in blood feuds (just like the albanians). you’d half expect them to build tower houses for protection during clan disputes like the albanians or the maniots.
Muslim (Arab) populations are incompatible to Western societies due to how inbred they are. Their own societies are built on their genetics, which they then bring to the West and attempt to bring what they’re running from to their new host country.
In conclusion, whenever people say “it’s Islam doing it”, it’s low IQ behavior. Those with lower IQ are more likely to be drawn to Islam. Islam developed after 1300 years after the start of Arab inbreeding. We can draw, from IQ from American criminals, that 85 is the sweet spot for criminality, and since criminality is correlated with low IQ more so than any other variable you can think of. A good example of this is a low IQ person coaxed into committing a crime. It’s an obvious biological difference, the sociopolitical garbage is just that, garbage. The biology drives the politics. Consanguinity rates are one of the biggest factors. You should be concerned with the biology aspect.
Note: When I say “Muslim” I mean Arab. I am also not attempting to “apologize” for terror attacks. I’m simply looking at it through the lens of evolutionary psychology. Most people who read this blog know why Africans act the way they act, and African “migrants” are no different.
Towards the end of last year, it was said that “male and female brains don’t differ“. Male and female brains differ from the number of neurons to differences in g that affect intelligence, to differences in temperament and differences in the hormones testosterone and estrogen. Other than accounting for differences in physical appearance between the sexes, the differences between the sexes in the two hormones accounts for brain differences as well. This is yet another blank slate argument, years after cognitive neuroscience affirmed that behavior is rooted in the brain and that we are not in fact “blank slates”, these same old and outdated arguments keep being pushed, of course, in part due to the growing number of “transgenders” and an influx of non-western people who are abnormal to our societies. This attempt to have the general public to believe that we have minds of Silly Puddy (to borrow a phrase from Steven Pinker) is an attempt to have us accept all of the things that get pushed on us through the media.
You may have read that having a male brain will earn you more money.
Men do make more money than women, and this isn’t the cause of the imaginary gender pay gap. Even Thomas Sowell, the liberal icon has refuted this myth. Men make more money than women due to, which I will get to below, higher intelligence.
Or maybe that female brains are better at multitasking.
Anecdotal evidence suggests it. Evolutionary evidence suggests it. Studies suggest it. But ever since the Jewish feminist push in the 20th century, this strive for egalitarianism between the sexes became mainstream, which helps to still keep the notion of “blank slatism” alive.
The idea that people have either a “female” or “male” brain is an old one, says Daphna Joel at Tel Aviv University in Israel. “The theory goes that once a fetus develops testicles, they secrete testosterone which masculinises the brain,” she says. “If that were true, there would be two types of brain.”
Anyone else surprised that someone from Tel Aviv University is making these claims? Are we supposed to believe that testosterone doesn’t affect the brain? Are we supposed to believe that higher testosterone, higher estrogen and other biologic differences in brain structure don’t account for behavioral differences between the sexes?
We have data that this is the case, though:
Sex steroid hormones exert a profound influence on the sexual differentiation and function of the neural circuits that mediate dimorphic behaviors. Both estrogen and testosterone are essential for male typical behaviors in many species. Recent studies with genetically modified mice provide important new insights into the logic whereby these two hormones coordinate the display of sexually dimorphic behaviors: estrogen sets up the masculine repertoire of sexual and territorial behaviors, and testosterone controls the extent of these male displays.
To believe that testosterone doesn’t cause masculinization of the brain will have to have one deny all of the literature out there. Why people believe that sex differences, as well as racial/ethnic differences, are rooted in experience and not biology is truly mind boggling.
“There are not two types of brain”
And below this, they basically say that the “gender fluid” phenomenon is ‘ok’. Differences between individual boys and girls and individual men and women are extremely evident just by casual observation, so to attempt to say that individual brains cannot be shown to have full-on male or female characteristics is insincere. The fact that, as shown above, testosterone mediates the masculinization of the brain, we can see that these differences in brain structure do exist, and are accounted for by exposure to testosterone invitro, which then cause the differences in the brains of men and women.
Although the team only looked at brain structure, and not function, their findings suggest that we all lie along a continuum of what are traditionally viewed as male and female characteristics. “The study is very helpful in providing biological support for something that we’ve known for some time – that gender isn’t binary,” says Meg John Barker, a psychologist at the Open University in Milton Keynes, UK.
Gender is binary. Female and male characteristics do exist. Males and females differ in certain structures of the brain as seen in a study reviewing over 20 years of the study of sex differences in the brain.
“Across all kinds of spatial skills, we find very, very few that are sensitive to sex,” says Hausmann. “We have also identified spatial problems where women outperform men – the black-and-white idea of a male or female brain is clearly too simple.”
The sex differences on spatial skills tests are rooted in brain structure. Researchers measured a 10 percent difference between men and women in overall amount of parietal lobe surface area. Since how we process information is obviously a result of cognitive processes in the mind, differences between the sexes in brain structure show how men and women can differ in certain cognitive tasks. Of course, some spatial problems can be women can outperform men on some spatial tasks, no one disputes that. However, what the average battery of tests shows is that men have higher visio-spatial intelligence than men.
Alexandra Kautzky-Willer, head of the Gender Medicine Unit at the Medical University of Vienna in Austria, agrees that things aren’t so simple. “There are differences between men and women when you look in large groups, and these are important for diagnosis and treatment,” she says. “But there are always more differences within genders. We always need to look at culture, environment, education and a person’s role in society,” she says.
Just like there “is more difference within race than between them”, right? Culture is a product of genetics and IQ, we put ourselves into certain environments based on our genes, education is largely heritable, a person’s worth to society is based on IQ and the Big Five personality traits, which are at least 50 percent heritable, all of which are rooted in brain processes.. Those factors don’t prove that there are no differences between the brains of the sexes because all of them can be explained, in part due to genetic factors.
These findings, they claim, say that it’s impossible to say what features a person’s brain will have based on the known sex of the brain. With differences in gray matter, brain size and other regions in the brain, we can definitively say whether or not the brain is male or female. Sure some outliers will occur, but the overall bulk, we would see that the sex would be guessed with a super majority being correct.
Joel envisions a future in which individuals are not so routinely classified based on gender alone. “We separate girls and boys, men and women all the time,” she says. “It’s wrong, not just politically, but scientifically – everyone is different.”
Here we are with the point of this article: to attempt to normalize this trend of degenerate behavior that the media pushes which begins to permeate our society. Chromosomal differences between men and women show the sex differences. X means woman, Y means man. Some may point to some anomalies, but anomalies occur in nature all the time and are not a representative of the population.
This also shows with differences in brain size, that causes a difference in IQ between men and women. The study found that men had brains that were, on average, 8 to 13 percent larger than women’s. Since we know that the IQ/brain size correlation is .35, more often than not, men will have higher IQs than women due to having slightly larger brains. And the data is consistent with the finding that men and women have slightly differing IQ scores, which shows in the difference in average brain volume between men and women.
In JP Rushton’s refutation to Steven Jay Gould’s revised edition of The Mismeasure of Man, he states that Gould claims that when accounting for body size and age that the difference in brain size drops from 182 grams to 113 grams, then invokes unspecified age and body size parameters and that accounting for these differences then the sex difference in brain size will vanish. Ankney (1992) reexamined the autopsy data of Ho et al (1980) and found that uncorrected for body size, the difference between men and women’s brains was 140 grams; After correcting for body size, the difference between men and women was 100 grams. This shows that around 30 percent of the difference between men and women in brain size is attributed to body size.
In this review, Rushton did state that men and women had the same scores on tests of intelligence and that this provided a paradox due to the differences in brain size between men and women and similar IQ scores. However, Rushton and Jackson (2006) showed that men and women differ by 3.63 IQ points on average, among a multitude of other strong correlates with the difference in IQ scores.
Men have 23 billion neocortical neurons, women with 19 percent less, at 19 billion (Pakkerson and Gunderson, 1997). Seeing as cortical neuron activity moderates perception in the brain, the differences in neocortical neurons affect other processes and mental faculties in the brain as well.
All of these brain differences then manifest themselves in cultural achievement between men and women.
Charles Murray (2003), in his book Human Accomplishment shows differing societies’ human accomplishments and how these differences in human accomplishment have shaped our society today. He gathered data on women Nobel Prize winners from 1901-2000 and found this:
Murray states on p. 273, 274 and 275 that women have an underrepresentation in the sciences. You would figure, if this so-called “white cis male patriarchy” was out to have women be underrepresented, they wouldn’t have allowed the feminist movement to come full-swing in the early 1900s. Well, the numbers on women Nobel Prize winners from 1901-1950 is: 2 percent sciences total, 4 percent chemistry,2 percent medicine, 2 percent physics and 11 percent literature with a 4 percent representation in total. From 1951-2000, it was 2 percent sciences total, 1 percent chemistry, 4 percent medicine, 1 percent in physics and 8 percent in literature for a total of 3 percent.
Now, this does show women’s high verbal ability at play with regards to the number of literary Nobel Prizes’ they have, but this shows that after the Feminist Movement, that when they got ‘equality’, they failed to produce the same as men. This data corroborates what I noted earlier: that there is a significant amount of cortical neuronal difference between men and women, there is a 3.63 IQ point difference between men and women on average, and finally the data on Nobel Prizes corroborates this information.
The Defense Ministers of Sweden, Norway, the Netherlands, and Germany embody what is going on at the moment in these countries with the ‘migrant’ crisis. We can see with Russia’s aversion to the scenario currently happening in Europe, that with their Defense Minister, these things that are currently happening in those aforementioned countries won’t happen in Russia.
This is shown in how men and women’s overall leadership capabilities, ability to lead meetings and differing managing strategies. All of these differences, of course, are due to brain differences between men and women.
Women are more emotional than men due to biology, so in times of war with a woman Defense Minister, since men and women differ in inductive and deductive reasoning traits, women won’t be deductive, which is a logical process in which a conclusion is drawn from multiple premises that are assumed to be true, which men excel at. Women, however, excel at inductive reasoning, which is making broad generalizations from specific observations. It seems that in war time, deductive reasoning would be better, seeing as the conclusion is drawn from things that are assumed to be true. Men make better leaders than women because, since, on average, men don’t think with their emotions while women do.
Men and women’s brains differ on the individual level, of course, like all things between groups, sexes, and individuals. The push to deny human nature, and in turn, invoke a blank slate argument even in the face of science is shown in the way that our society is headed. Between differences in brain size, scholastic achievement, IQ, brain weight, Nobel Prizes, neocortical neurons and other gender-specific differences, these innate differences in brain structure manifest themselves in society and the types of jobs women want and acquire. Women cannot lead as well as men and while they ‘lead differently’, the best type of leader to have is a man as men think with logic and facts whereas women think with emotion, on average.
Many people in the alt-right say that “the Ashkenazi Jews are Khazar”. This is not true. This is based on an autobiography by a Jew who thought that if Europeans thought the Jews were European, they wouldn’t want to kill them. This is also based on one study, where all the rest of the literature says they derive from the Levant and the Middle East. I will go through the myth and then tell the truth of the origins of the Ashkenazi Jews.
In this research paper by Eran Elhaik, he says that the rise of European Jewry is explained by the rise of Judeo-Khazars. Though contribution of Khazar genetics can only be estimated by empirically, but the absence of genome-wide data precluded the Khazar hypothesis. The findings by Elhaik, he says, support the Khazarian hypothesis and it represents the European Jewish genome as an amalgamation of Caucasus, European and Semitic ancestry.
Razib Khan has this to say about it:
In general I have to say that the historical framework of the paper is very skeletal, verging on incoherent (at least to me).
Setting aside the historical fuzziness of the paper, the major issue I have is that though the methods are totally kosher, so to speak, the data you put into them strongly shape your outcomes. Dienekes and Maju both anticipated my own key concern. The “Middle Eastern” aspect of Ashkenazi Jewish ancestry might in fact be most well represented by populations in the zone of the northern Fertile Crescent and Eastern Anatolia; rather near or overlapping with the homelands of several of the Caucasian populations used in the above study as a proxy for Khazars. Additionally, modern Palestinians (the HGDP data set) are used as a reference to the Middle Eastern ancestors of Jews. I now believe that the Arabian contribution to the ancestry of Levantine and Iraqi Muslim population which dates to after the 7th century, and differentiates Muslim Arabs from their local non-Muslim Arab* co-ethnics, is significant. Perhaps on the same order of Germanic ancestry in modern England which dates to the 6th century and later. In plainer language the Caucasian component that is being detected in this paper may simply be a indigenous Middle Eastern ancestral element which has now been somewhat displaced northward in its modal frequency due to the expansion of the Arabs, and later the admixture of some Sub-Saharan admixture among Muslim Arabs.
Finally, despite the fact that I praise the author’s utilization of a wide array of contemporary statistical genetic methods, one can’t just do away with a thick and sturdy historical framework and reasonable questions derived from this superstructure.
The new findings were seen as support for the idea that there was significant admixture with non-Jews in Greco-Roman times. This is based on the clustering of the European/Syrian Jews and the fact that these groups have been separated since ancient times. The authors argue that the data are consistent with historical accounts of proselytism and large-scale conversions to Judaism in ancient times. When I reviewed the historical data in A People That Shall Dwell Alone (Ch. 4, pp. 62-78), I ended up rejecting this theory, coming down on the side of historians who doubted how important conversion really was. One thing that convinced me was that there was a lot of evidence for biases against converts. For example, once they converted they were regarded as very undesirable marriage partners and that a pure Jewish genealogy was a very big asset in the marriage market. Families keep their genealogies for generations, and there is a lot of evidence for hostility toward converts. Contrary to Atzmon et al., conversion is not required to explain the large numbers of Jews in the ancient world.
Though, this theory, before this one singular study came out, was first put forth by Arthur Koestler in his book The Thirteenth Tribe. He became interested in the founding of the Hungarian empire, and how the Khazars were at the center of that. He then makes a huge jump in logic to say that all of European Jewry are descended from those from Khazaria who then converted to Judaism.
This theory was quickly latched on to by the alt-right when it first was published and used as ammunition to say that the Jews weren’t the rightful bearers of Canaan (modern-day Israel/Palestine). However, we know that Jewish populations are more closely related to each other than to outside populations:
Livshits, Sokal and Kobylianskyt investigated the genetic affinities of Jewish populations. They concluded that Jewish populations are more like one another than they are to non-Jews and that pairs of Jewish populations from different locations are more alike than pairs of non-Jewish populations. They maintained that the most economical explanation of their findings is that the modern Jewish population throughout the world was derived from a common original gene pool which underwent few changes during the dispersion of the Jewish people. They also reported that it was highly likely that the common origin of the Jewish populations was more recent than that of the non-Jews.
Which, if Ashkenazi Jew were Khazar, we wouldn’t see this coming up in genetic testing.
Even the world’s foremost researchers on the Jews like Dr. Kevin Macdonald and Dr. David Duke say that the Khazar Hypothesis is long refuted.
In Ted Sallis’ article on the Occidental Observer, More Jewish Genetics: The “Weak Khazar Hypothesis” he cites a study which says that there may be a minute component in the Ashkenazi Jewish genome which is Khazar, which that part is from a North Caucaus population. Though, that might just be showing genetic similarity and not that some of the Ashkenazi Jewish genome derives from those populations.
David Duke even accepted the Khazar theory as true for years as he admits, however, he says that it wasn’t until he thought of the hypothesis both scientifically and logically that his doubts on the theory became aroused.
He says that Koestler, who he didn’t know was a communist Jew, bragged in a Jewish magazine that he made the hypothesis to fight anti-semitism. He believed, and cited the Gospels as evidence, that if he could get Europeans to believe they are related by blood to Jews, that anti-semitism would be lessened. Dr. Duke then goes through many studies which show that, in fact, the Khazar hypothesis is long discredited.
In my own articles on this website, I have written about the origins of Ashkenazi Jews.
A few thousand years ago, male Jews migrated from the Middle East and mated with beautiful Roman women who then converted to Judaism. The four major founders of the Ashkenazi Jew population have ancestry in prehistoric Europe, and not the Caucus or the Near East. The four minor founders share a deep European ancestry. So with genetic testing, we can see that the majority of the Ashkenazi population didn’t have its origins in the Caucus or Levant, but through assimilation of Roman women who converted to Judaism.
Male Jews migrated from the Levant to Rome during Greco-Roman times, which mass conversions led to 6 million Roman women who then began to practice Judaism. The genetic proximity of Ashkenazi Jews and Syrian Jews to Northern Italians, Sardinians and French populations suggest that there is non-Semitic ancestry in Ashkenazi Jews. The findings also say that any theories of Ashkenazi Jews having ancestry in Khazaria or from Slavs are incompatible with genetic studies. The close genetic similarity of Ashkenazi Jews and Southern Europeans has been noted in many studies.
So we have male Jews from the Levant who trekked to Rome around Greco-Roman times. They took beautiful Roman women as wives, who then converted to Judaism.
These two new studies from within the past few years again corrobarate that Ashkenazi Jews are not Khazarian, but derive from the same four founder populations; ancient European women and are not descended from Turkish populations.
Blogger Diversity is Chaos believes so. He says:
Persian Jews converted Turks to Judaism to create the rump of what would become today’s Jewish population, DNA research has revealed. The fascinating insight, which shows that most Ashkenazi Jews descend from Turkey, was made possible by state-of-the-art computer modelling and genetic techniques. The project, led by Israeli-born Dr Eran Elhaik, even pinpointed Iskenaz, Eskenaz and Ashanaz – three Turkish villages an ancient Silk Road route which still exist today – as part of the original Ashkenazi homeland.
As shown above, this is wrong. No idea why he wrote this article the other day, seeing as this debate has been put to rest for years.
He said that the word Ashkenaz likely derives from Ashguza, the ancient Assyrian and Babylonian term for Iron Age Eurasian steppeland people known as Scythians.
No. It is Biblical:
from modern Hebrew, from Ashkenaz, son of Japheth, one of the sons of Noah (Gen. 10:3).
Concurrent analysis of Yiddish suggests that it was originally a Slavic languagewhich the researchers think was developed by Jewish tradesmen travelling along the Silk Roads linking China and Europe 1,200 years ago.
The prevalent view claims Yiddish has a German origin, whereas the opposing view suggests a Slavic origin with strong Iranian and weak Turkic substrata,” they say. “One of the major difficulties in deciding was the unknown geographical origin of Yiddish speaking Ashkenazic Jews,” they say, but their analysis “demonstrates that Greeks, Romans, Iranians, and Turks exhibit the highest genetic similarity with Ashkenazic Jews”.
They show genetic similarity to those populations due to population migration. I have touched on and already linked to the origins of the Roman component in the Ashkenazi Jewish genome, and the same applies for those other populations. Genetic similarity does not mean that those populations were a founder population, or even that there is ancestry from those peoples.
Yiddish and modern German are both derived from the same source, which is Middle High German. Why, if they were Khazar, would it be derived from Middle High German? Why would the Ashkenazic travelers speak Old French, Hebrew and Aramaic? Yiddish is an amalgamation of languages with an extremely heavy German component. As the Jews traveled, they picked up new languages and began to integrate them into their language and eventually Yiddish formed.
To conclude, those who still believe and push the Khazar hypothesis are ideologically blinded. They let their bias cloud their judgement to the facts. Just because one singular study came out that says the Jews are Khazar is meaningless…. Since all other studies have shown that Jews, all Jews no matter where they live in the world, show affinities with the Middle East. Even the world’s foremost scholars on the Jewish people say that the Khazar hypothesis is wrong. One study on this doesn’t show that “all Jews descend from Khazars”, as we have to take a look at all studies as a whole and see where they point. All studies do not point to an origin like this, so it’s safe to say that this one study be thrown in the trash where it belongs. It’s intellectually dishonest to believe the Khazar hypothesis when it has been discredited time and time again by the newest genomic studies.
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 . 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.