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Science Proves It: Fat-shaming Doesn’t Work
2250 words
Milo Yiannopoulos published an article yesterday saying that “fat-shaming works”. It’s clear that the few papers he cites he didn’t read correctly while disregarding the other studies stating the opposite saying “there is only one serious study”. There is a growing body of research that says otherwise.
He first claims that with the knowledge of what he is going to show will have you armed with the facts so that you can hurl all the insults you want at fat people and genuinely be helping them. This is objectively wrong.
In the study he’s citing, the researchers used a quantitative analysis using semi-structured interview data (which is used when subjects are seen only one time and are instructed by the researchers what the guidelines of the experiment will be in order to get the reliable, comparable, and quality data) on 40 adolescents who lost at least 10 pounds and maintained their weight loss for at least a year. This guideline came from Wing and Hill (2001) who say that maintaining a 10 percent weight loss for one year is successful maintenance. He claims that the abstract says that bullying by the peer group induces weight loss. Though, it’s clear that he didn’t read the abstract correctly because it says:
In contrast to existing literature, our findings suggest that primary motivating factors for adolescent weight loss may be intrinsic (e.g., desire for better health, desire to improve self-worth) rather than extrinsic. In addition, life transitions (e.g., transition to high school) were identified as substantial motivators for weight-related behavior change. Peer and parental encouragement and instrumental support were widely endorsed as central to success. The most commonly endorsed weight loss maintenance strategies included attending to dietary intake and physical activity levels, and making self-corrections when necessary.
Peer encouragement and instrumental support were two variables that are the keys to success in childhood weight loss maintenance, not fat-shaming as he claims.
The same study found that obese people were more likely to lose weight around “life transitions,” like starting high school. In other words, people start to worry about how others will see them, especially when they need to make a good first impression. Fear of social judgement is key. So keep judging them.
The study didn’t find that at all. In fact, it found the opposite.
According to a new study, while most teens’ weight loss attempts don’t work, the ones who do lose weight successfully, quite simply, do it for themselves, rather than to please their (bullying) peers or (over-pressuring) parents.
He then cites a paper from the UCLA stating that social pressure on the obese (fat-shaming) will lead to positive changes. Some of the pressures referenced are:
If you are overweight or obese, are you pleased with the way you look?
Are you happy that your added weight has made many ordinary activities, such as walking up a long flight of stairs, harder?
The average fat person would say no to the first two.
Are you pleased when your obese children are called “fatty” or otherwise teased at school?
Fair or not, do you know that many people look down upon those excessively overweight or obese, often in fact discriminating against them and making fun of them or calling them lazy and lacking in self-control?
Self-control has a genetic component.In a 30 year follow-up to the Marshmallow Experiment, those who lacked self-control during pre-school had a higher chance of becoming obese 30 years later. Analyzing self-reported heights and weights of those who participated in the follow-up (n=164, 57 percent women), the researchers found that the duration of the delay on the gratification task accounted for 4 percent of the variance in BMI between the subjects, which, according to the researchers, was responsible for a significant portion of the variation in the subjects. The researchers also found that each additional minute they delayed gratification that there was a .2 reduction in BMI.
Why? Because people change their health and dietary habits to mimic that of their friends and loved ones, especially if they spend lots of time around them. Peer pressure encourages people to look like the people they admire and whose company they enjoy. Unless there’s a more powerful source of social pressure (say, fat shaming) from the rest of society, of course.
Not even thinking of the genetic component. The increase in similarity relative to strangers is on the level of 4th cousins. Thus, since ‘dietary habits are mimicked by friends and family’, what’s really going on is genotypic matching and that, not socialization, is the cause for friends and family mimicking diets.
There is only one serious study, from University College London, that suggests fat-shaming doesn’t work, and it’s hopelessly flawed. Firstly, it’s based on survey data — relying on fat people to be honest about their weight and diets. Pardon the pun, but … fat chance!
Moreover, the study defines “weight discrimination” much like feminists define “misogyny,” extending it to a dubiously wide range of behaviours, including “being treated poorly in shops.” The study also takes survey answers from 50-year olds and tries to apply them to all adults. But in what world do 20-year-olds behave the same way as older people?
The paper he cites, Perceived Weight Discrimination and Changes in Weight, Waist Circumference, and Weight Status, does say what he claims. However, the researchers do say that due to having a sample of people aged 50 and older that it wasn’t applicable to younger populations (as well as other ethnicities, this sample being 97.9 percent white). (Which you can tell he did not read, and if he did he omitted this section.)
The researchers found that 5.1 percent of the participants reported being discriminated on the basis of their weight. They discovered that those who experienced weight discrimination were more likely to engage in behaviors that promoted weight gain, and were more likely to see an increase in weight and waist circumference. Also observed, was that weight discrimination was a factor in early onset obesity.
Present research indicates that in addition to poorer mental health outcomes, weight discrimination has implications for obesity. Rather than motivating people to lose weight, weight discrimination increases the risk for obesity. Sutin and Terraciano (2013) conclude that though fat shaming is thought to have a positive effect on weight loss and maintenance, it is, in reality, associated with maintenance of obesity. Also seen in this sample of over 6,000 people was that those who experienced weight discrimination were 2.5 times more likely to become obese in the next few years.Further, obese subjects were 3.2 times as likely to remain obese over the next few years.
Sutin et al (2014) also showed how weight discrimination can lead to “poor subjective health, greater disease burden, lower life satisfaction and greater loneliness at both assessments and with declines in health across the four years”.
Puhl and Heuer (2010) says that weight discrimination is not a tool for obesity prevention and that stigmatization of the obese leads to threatened health, the generation of health disparities and, most importantly, it interferes with effective treatments.
Tomiyama (2014) showed that any type of fat shaming leads to an increase in weight and caloric consumption.
Shvey, Puhl, and Brownell (2011) found in a sample of 73 overweight women, that those who watched a video in which weight discrimination occurred ate 3 times as many calories than those who did not see the video. The authors conclude that despite people claiming that weight discrimination works for weight loss, the results of the study showed that it leads to overeating, which directly challenges the (wrong) perception on weight discrimination being positive for weight loss.
Participants were from an older population, in which weight change and experiences of weight discrimination may differ relative to younger populations so findings cannot be assumed to generalize
Puhl and King (2013) show that weight discrimination and bullying during childhood can lead to “depression, anxiety, low self-esteem, body dissatisfaction, suicidal ideation, poor academic performance, lower physical activity, maladaptive eating behaviors, and avoidance of health care.”
I expect we’ll see more of these pseudo-studies, and not just because academics tend to be lefties. Like climate scientists before them, I suspect a substantial number of “fat researchers” will simply choose to follow the political winds, and the grant money that follows them, rather than seeking the truth.
He is denying the negative implications of fat-shaming, disregarding the ‘one study’ (or so he claims) that shows the opposite of what he cited (which he didn’t read fully). I also like how these studies are called ‘pseudo-studies’ when the conclusion that’s found is a conclusion he doesn’t like. Really objective journalism there.
The reverse is also true. Just being around attractive women raises a man’s testosterone.
The researchers say that talking with a beautiful woman for five minutes led to 14 percent increase in testosterone and a 48 percent increase in cortisol, the anti-stress hormone.
Of course, this has its grounds in evolution. When two people are attracted to each other, they begin to mimic each other’s movements and using the same body language unconsciously. The researchers he cited concluded that “women may release steroid hormones to facilitate courtship interactions with high-value men“. This, of course, has an evolutionary basis. Women seek the best mate that will be able to provide the most for them. Men and women who are more attractive are also more intelligent on average with the reverse holding true for fat people, who are uglier and less intelligent on average.
Though it would be to un-PC to conduct an experiment proving it, it stands to reason that looking at fat, ugly people depresses testosterone. This is certainly how any red-blooded man feels when looking at a hamplanet.
Depressed testosterone is associated with many negative health outcomes, and thus the mere presence of fat people is actively harming the population’s health — particularly men’s, since we’re more visual. We ban public smoking based on the minuscule effects of “passive” intake, so why aren’t the same lefty, public-health aware politicians clamouring for a ban on fat people being seen in public?
A study conducted on people’s hormonal response to the obese and overweight may indeed show a decrease in testosterone and cortisol. Though, these hormonal responses are temporary, which he doesn’t say.
Instead, the same lefties who want to stop us having fags or drinking too much in public (and even alcoholics and chain smokers are healthier than the obese) are the same ones urging the authorities to treat “fat-shaming” as a crime and investigate it. Insane!
There are, contrary to popular belief, obese people who are metabolically healthy. Blüher (2012) reviewed the data on obese patients and found that 30 percent of them were metabolically healthy with the obese patients having similar levels of insulin sensitivity similar to lean individuals.
Moreover, new research has found that having a BMI of 27 leads to a decrease in mortality. In a huge study of over 120,000 people, the researchers gathered people from Copenhagen, Denmark, recruiting people from 1976 to 2013. They were then separately compared to those who were recruited in the 70s, 90s, and 00s. Surprisingly, the BMI linked with the lowest risk of having died from any cause was 23.7 in the 70s, 24.6 in the 90s, and 27 from 2003-2013. Due to the results of this study, the researchers are arguing that BMI categories may need adjusting.
As shown in that 2014 study, young people in particular are concerned about what their peers think about them, especially when they start high school. That’s why it’s so critical to let them know that their instincts are correct, and that they can’t be “healthy at any size.”
If you can be unhealthy at any size, why can’t you be ‘healthy at any size’? As I’ve shown, those with a BMI of 27, on average, are metabolically similar to those with to those with lower BMIs. Since, in the study previously cited, BMI increased while mortality decreased, technological advancements in caring for diseases, such as Diabetes Mellitus, improved, this is one possible explanation for this.
Those with a BMI under 25 may still suffer from negative effects, the same as obese people. They may suffer from metabolic syndrome, high triglycerides, low HDL, small LDL particles, high blood sugar and high insulin. Those who are skinny fat need to worry more about their vital organs, as the fat deposits they carry are white fat which is wrapped around the vital organs in the body. These are some of the reasons why being skinny fat can be more dangerous than being obese or overweight: they think that because their BMI is in the ‘normal range’ that they’re fine and healthy. Clearly, sometimes even being ‘underlean’ can have serious consequences worse than obesity.
Then he brings up smoke shaming and bills being passed to stop smokers from smoking in certain public areas lead to a decrease in smoking, so fat shaming makes sense in that manner.
Except it doesn’t.
Humans need to eat, we don’t need to smoke. Moreover, since the rising rates in obesity coincide with the increase in height, it has been argued by some researchers that having an obese population is just a natural progression of first world societies.
Fat shaming doesn’t work. It, ironically, makes the problem worse. The physiological components involved with eating are a factor as well. It is known that the brain scans of the obese and those addicted to cocaine mirror each other. With this knowledge of food changing the brain, we can think of other avenues that do not involve shaming people for their weight, which increases the problem we all hate.
Dysgenic Fertility and America’s Obesity Crisis
1050 words
The dysgenic trend currently occurring in America has implications for obesity as well. Since intelligence is negatively correlated with obesity, as America’s average IQ decreases, the rates of obesity in our country will increase. This is due to the high correlation between intelligence and obesity. As we continue to allow unfettered immigration into America, the average IQ of the country will decrease, while the amount of people that are overweight and obese will increase.
The ethnic differences in obesity rates lead more credence to what I am saying. As the demographics shift, more people will be overweight or obese due to having a lower IQ. Whites, too, are experiencing this dysgenic effect, as intelligent people of all ethnicities are not reproducing. As more and more genetically less fit individuals continue to have a higher rate of reproduction in comparison to intelligent individuals, this crisis will continue to persist.
Those with lower intelligence have less of an ability to delay gratification, which has a strong genetic component. As more people breed who cannot delay their gratification, the rates of obesity will increase in the country. Of course, the lack of ability to delay gratification comes with a lowered IQ. This is what we see in regards to sex. Those with higher IQs lose their virginities at a later age in comparison to those with lower IQs. Along with the data from Kanazawa that shows that more intelligent people have a lower BMI than those with lower intelligence, this study gives more credence to the theory that those with higher levels of intelligence can better delay their gratification.
JayMan says that there is evidence for an increased genetic load for those with lower IQs, which we can then reason that this also leads to a higher prevalence for obesity in low IQ populations. JayMan then says that many of the genes found to influence obesity seem to operate in the brain and that they have a pleiotropic effect, meaning that multiple genes affect one or more traits. With the increased genetic load comes with an increased chance to have a lower IQ and become obese, as these two things correlate with the lack of ability to delay gratification.
Of course, these problems persist due to modern medicine. With the advent of better medicine, it allowed us to beat diseases that formerly would have been devastating to the population at large. This led to an increase of alleles with negative effects in the population that continue to pass down through the generations. Along with these advances in medical technology, welfare and other government-funded programs also enable those that are less genetically fit. Since intelligence is correlated with ability to care for offspring, as well as r- and K-selected traits, those with lower intelligence exhibit more r-selected traits. This is why America is facing a dysgenic fertility crisis. Welfare props up those with less intelligence, giving them more incentives to breed. They then breed more low IQ children who then will live off of the government. This vicious cycle then continues unfettered due to how America’s dysgenic welfare structure is implemented.
Before the advent of modern technology, those who were less genetically fit didn’t survive to pass on their genes. But, in the modern day with all of our superior technology, this allows the less intelligent to breed when in the past they would have been selected out of the gene pool due to being less biologically fit.
Another variable that is involved with the dysgenic fertility of America is Mexican immigration. With the influx of illegal (and legal) peoples from the South of the Border, this is having both dysgenic effect on both the average intelligence of our country along with the average BMI. The average BMI for the average American male is 28.6. In the 1950s, 10 percent of American adults were obese compared to 35 percent of American adults today. Now, this has to do with ability to access food, as well as the effect of the media on children has a huge effect on obesity, due in part to not getting a full nights sleep, as that is correlated with obesity. However, an increase in genetic load, which also comes with a decrease in intelligence, has a lot to do with this as well. The increase in the BMI of the average American has to do with immigration as well. The rates of obesity for different ethnicities in America are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for ‘Hispanics’. So of course, with more immigration from the South of the Border, the average IQ for America is decreasing while obesity rates are increasing, due mostly to this illegal immigration.
Height and intelligence are both correlated. Ever since the advent of the industrial revolution, we have had an excess surplus of food. As Gina Kolata says in her book Rethinking Thin, an increase in obesity is inevitable. She says this since the increase in genetic height and IQ has occurred, so the increase in obesity follows with it. We need to influence those with higher IQs to have more children. Further, we also need to restrict immigration to only high-skilled immigrants (only when necessary) to reverse this trend that has been occurring since the 1960s. Though, with higher levels of intelligence one can forgo their urges and live a healthier lifestyle due to having higher cognition which leads to a better ability to delay gratification than one with lower intelligence.
Those with higher IQs make better choices on what to eat than those with lower IQs. This is shown in the BMIs of the intelligent and non-intelligent population. As more and more people with lower genotypic IQ come into the country, the quality of life will decrease as will the average intelligence of the country. In turn, the BMI of the average American will increase along with the decrease of our country’s average intelligence. To ameliorate this, we need to have extremely stringent criteria on who we allow into the country. An IQ test, to start, would be a good idea. As those with higher intelligence have less of a genetic load and have less of a chance of becoming obese than one with a lower IQ, the current dysgenic effect that this unfettered immigration is having on America can be lessened.
Obesity and Intelligence
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[Edit: My view here has changed, read my recent article Is Diet an IQ Test? It isn’t and it is, of course, much more nuanced than ‘IQ’ (which is a proxy for social class’ leading to obesity which would imply lack of funds and education on what and when to eat. Obesity is much more complex than ‘IQ’, numerous other variables come into play and since ‘IQ’ (which is just a proxy for general knowledge ‘is low then the individual in question won’t know what and when to eat and since this occurs in low income families more often than not who have low IQs then this effects them the most.]
The relationship between intelligence and obesity is often misinterpreted. Numerous studies have concluded that becoming obese leads to a drop in IQ. This mistake happens due to improper interpretation of cross-sectional studies. However, analyses of population-based, longitudinal data show that low intelligence from birth causes obesity. No credible evidence exists for obesity lowering intelligence. There are, however, mountains of evidence showing that low intelligence from childhood leads to obesity (Kanazawa, 2014).
Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ. Those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs to learn how to manage their weight. Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).
Less intelligent individuals are more likely to become obese than those who are more intelligent. With what we know about low IQ people and how there is a strong relationship between low intelligence and lack of ability to delay gratification, we can see how this lack of thought for future problems for their actions in the present can manifest itself in obesity.
This study claims that there is a link between morbid obesity and a drop in IQ. The researchers compared 24 children who weighed 150 percent of their bodyweight before age 4 with 19 children and adults with Prader Willi’s Syndrome, using 24 siblings as controls as “they share the same socioeconomic environment and genetics”. Prader Willi’s Syndrome (PWS) is a chromosomal disorder in which chromosome 15 is deleted. They have an almost insatiable desire to eat,which can cause one suffering from PWS to eat themselves to death. Those with PWS were found to have an IQ of 63, while those who became obese were found to have an IQ of 78 with the control siblings having an IQ of 106. The researchers were surprised to see such a difference in IQ between siblings. They then state that this could be one facet of obesity that could be irreversible. MRI scans of the cohort discovered white matter lesions on the subjects with PWS and early-onset obesity. The researcher says that these lesions could affect food seeking centers in the brain leading to a want to gorge on food. Seeing how those with PWS eat when unsupervised, this is an interesting hypothesis.
This study compared 49 teens with metabolic syndrome and 62 peers without the disorder, while controlling for socioeconomics status. They found significantly lower scores in arithmetic, attention and attention span, spelling, mental flexibility and regions of the brain with lower volumes of matter in the hippocampus and white matter integrity.
There are a few problems with these two studies. In a population-representative birth cohort study of 1037 children, it was found that cohort members who became obese had a low IQ, as expected. But, contrary to what your study said, cohort members didn’t exhibit a decline in IQ from becoming obese, they instead had a lower IQ since childhood. There is no evidence of obesity contributing to a decline in IQ, even in obese individuals and those on the verge of metabolic syndrome. Another problem is that they wrongly conclude that obesity leads to lowered intelligence, completely misinterpreting the extremely strong negative correlation between obesity and intelligence.
This study shows how obese mothers give birth to less intelligent children. In an observational study (already garbage), the researchers took 3412 participants and found a strong relationship with pre-pregnancy obesity and math and reading scores in children. For math, a 3 percent reduction was observed. There was a 3-point drop in reading scores with math scores showing a decline of 2 points. These differences are within the normal variation between tests, so it’s nothing to take note of. Also, this is an observational study. I have shown above that longitudinal studies are superior for this, as well as researchers misinterpreting the results found from their studies.
So because of those factors involving the mother and child, that is what accounts for it. Not the environmental factors brought up.
This study claims that overweight parents are more likely to fail. This is all due to the fact that low IQ people are more likely to be obese or overweight, with heritability of BMI being .8, you can see how low IQ is the cause of both of those variables.
This shows that binge eating is linked to memory loss. I heard about a study a few months ago actually like this. Rats were fed high fat diets and they noticed that the brain microglia actually started to eat neuronal pathways actually leading to a decrease in cognitive ability. But they said that returning to a new diet will stop its effects. Researchers say the negative cognitive effects are reversible, but I already gave the citstion about obesity not being linked to decreased IQ. I should also note that this study was carried out on rats and while this may be a factor for humans as well, a few studies need to be done.
Binge eating, however, actually has a genetic component. Though this was only observed in girls. One reason I can think of for this is that women need higher body fat for a leptin release so puberty can begin so they can bear children.
This article purports to show 5 ways obesity affects the brain. Obesity does cause food addiction, however, those who lack the ability to delay gratification are more likely to not be able to control their impulse to overeat. I always link to the MRI scan showing the control, obese and cocaine user’s brain. Interesting to see that sugar is just as addictive as cocaine. Obesity doesn’t make us more impulsive. Check out the Marshmallow Experiment, as well as its follow-up studies. Those who are more impulsive are more likely to be obese, as well as have lower SAT scores.
Satoshi Kanazawa also noted that childhood IQ predicted whether or not one would become obese at the age of 51. General intelligence in childhood has a direct effect on weight gain, BMI, and obesity, net of parents education and SES, parents BMI, the child’s social class, and sex. More intelligent children grew up to make healthier choices, and therefore stayed leaner than those children who were less bright. The link between childhood obesity and intelligence also shows that the effect between childhood g is unmediated by education of income. Meaning, those with lower IQs in a higher socioeconomic bracket STILL have the same chance of becoming obese as those in the lower socioeconomic bracket. Finally, parental BMI itself is a consequence of parental general intelligence, which the parents pass on to their children. This shows the extremely high heritability of obesity as well as showing how intelligence plays a factor in the causes of obesity.
The known differences in ethnic obesity rates generally mirror the intelligence of those populations. All populations are showing a sharp dysgenic decline, which coincides with a more obese population as well. Sociologists and the like may say that those who are poor cannot afford the same types of food that those who have more wealth can. However, this is a false statement. Whole foods are not more expensive. The conclusion that was (obviously) reached is that there is expensive and non-expensive junk food as well as whole foods. Natural diets will not cost more, all things being equal. If you know how to eat and how to buy food, you will avoid spending too much money. This goes back to intelligence. One with a higher IQ will be able to think of what his present actions will lead to in the future while those with a lower IQ live in the now without a care for the future, which then manifests itself in their obesity.
There are numerous articles showing that the causality for low intelligence is not becoming obese, but that those who become obese have a lower IQ since childhood. Longitudinal studies show the relationship, while observational studies show that obesity drops intelligence. Clearly, observational studies are inferior for seeing the relationship between IQ and obesity. This then leads to researchers misinterpreting the data and drawing wrong conclusions.
** This is a great one. In a meta-analysis of twin and family studies, including mono and dizygotic twin studies, with a sample of 140,525 people, heritability of BMI was found to be between .75 and .82. Both extremely high correlations. Since the heritability of intelligence as well as height (another good predictor of intelligence), there is good evidence for the claim that becoming obese is due to lower childhood IQ, which is genetic in nature.
Black American Men with More African Ancestry Less Likely to Be Obese
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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.
How to Use Current Knowledge to Effectively Treat the Symptoms of PWS Patients
2550 words
Abstract
Researchers have tried to manage those with Prader-Willi’s Syndrome for multiple decades. Though they have greatly curbed some of the implications of the disease, there are still numerous ways in which we can better use our knowledge of how the disease manifests in order to better help those suffering from PWS. Looking at research into how the extra chromosome 15 is linked to low IQ; IQ and its relationship to obesity; how the ability to delay gratification leads to obesity; growth hormone treatment to better treat low muscle mass and higher body fat; and finally using reinforcement theory to punish a response, where doing so will greatly diminish the probability of that response occurring again in the future; all of these factors can be used in conjunction to better mitigate problems from the disease. By examining all of these variables and thinking of better ways to handle them, we can then think of other, better ways to manage those with PWS. In doing so, we can better increase the quality of life of those suffering from PWS, as well as have less of a strain on healthcare workers who care for them. With new advances in technology with CRISPR Cas9, we can then edit the genomes and chromosomes of those suffering from this disease.
How to Use Current Knowledge to Effectively Treat and Manage the Symptoms of PWS Patients
How can we use the research on chromosomal differences, research on their IQ differences and their lack of ability to delay gratification that, in turn, would help those individuals with the disease? Seventy percent of PWS cases are attributed to the deletion of chromosome 15 (Ledbetter et al, 1981). Maternal uniparental disomy, which involves receiving an extra chromosome 15 from the mother, is yet another cause of PWS (Wang, 2004).
Whittington, Holland and Webb (2009) found that there was variation between families in deletion of chromosome 15. They found that the PWS and sibling IQ correlation was .3, a modest correlation. What was also noticed was that there were subtype differences which manifested itself in the familial differences in IQ. As they expected, the correlation with normal siblings and those with PWS was .5 in those who suffered from PWS due to unilateral disomy. But in the second subset (the chromosomal deletion subset), the correlation was negative at -0.07. Their research shows great promise in the role of chromosome 15 and IQ. They end up concluding that there needs to be an explanation for the small genetic differences between them. How can we use these differences in IQ to help people with PWS and what does this suggest for other symptoms of their disease?
Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ. The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs who also suffer from PWS to better maintain their good health. Since we can better identify those PWS individuals who have lower IQs based on how they got the disease, we can then show them more attention in an effort to have them manage their gratification better. Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).
Schlam et al. (2013) observed in a follow-up study to the Marshmallow Experiment that found in a longitudinal study of individuals they found forty years later from the original Marshmallow Experiment, due to inability to delay gratification forty years previously, that was one cause of becoming obese forty years later. Due to PWS sufferers having lower average IQs, and, therefore, a lack of ability to delay their gratification, this is direct evidence that those PWS sufferers with low IQs need more stringent measures to be taken on them, which would then be helpful to those individuals who have a hard time delaying their gratification, which is partially caused by the drop in IQ due to the additional chromosome 15. We can see how those with PWS act; they want their gratification now and do not want to wait for it. This is why, when unsupervised, that those with PWS gorge on the food they understand they should not have, but do so, nevertheless, since their low IQ is correlated with lack of ability to delay gratification, which manifests itself in their obesity. We clearly need to find better methods in which to help those with low ability to delay gratification, which would strongly help those suffering from PWS.
Dykens et al (1997) note that those with PWS have hyperphagia, which correlates with their insatiable want for food. They state that the lack of fullness is due to an altered function of the hypothalamus, which is the part of the brain that is in control of feelings of satiety. Certain States gave restrictions to homes that take care of those with PWS and have come under fire because of this, mainly due to human rights violations. We must ask, then, should we limit their access to food if it will prolong their lives? Will doing so inhibit their freedom to do as they choose? PWS sufferers also have coronary heart problems; one could argue that given their free ability to choose what they want to do unfettered will lead to premature death due to obesity-related complications. Does their disease truly not allow them to learn the consequences of their behavior? Do they have the intellect to really understand the consequences of their actions of consuming too much food? There is no established or known way to control those with insatiable eating habits due to hyperphagia. So would the best course of action to take with those with PWS actually be to constantly monitor them and to lock access to easily attainable food? My answer is yes, however, there is a clear fine line in whether restricting access to food and constantly monitoring those with PWS infringes on their human rights, or that doing so actually will help them live better, healthier lives since they would have the constant supervision around them to better control their out of control eating habits. When negative actions occur, one idea that can be shown to them is constant positive reinforcement so that they may be better able to understand that what they are doing is harmful to their bodies. We can then use positive reinforcement when they do reach a healthy weight, so, in turn, they will have a higher chance of keeping a healthy weight. They may reap the benefits of positive reinforcement, and stick more closely to their program, and therefore, stay healthy.
The hormone ghrelin is secreted from the hypothalamus. With an altered hypothalamus, this would cause ghrelin levels to overload; then the individual suffering from PWS would feel the need to insatiably gorge on food due to this chemical imbalance in the brain. Ghrelin increased feeding in rats and ghrelin is the physiological mediator of feeding and probably has a function in growth regulation by stimulating feeding and release of growth hormone (Nakazato et al, 2001). There is a correlation between want of food, ghrelin release and growth hormone production. By attempting to mediate these variables, those who suffer from PWS will be able to better control their eating habits through positive reinforcement and better, more sustainable habits. Since whenever we eat we get a release of ghrelin that makes us hungry, people pretty much set their own eating times by eating multiple times a day. This affects PWS patients the same way. They can’t stop eating, due in part to constantly eating which constantly releases ghrelin in their body.
PWS sufferers have low muscle tone and, conversely, more body fat. Growth hormones may be a valid way of alleviating that problem, which in turn will give them a slightly higher resting metabolic rate so that they may burn slightly more calories, in an effort to stay healthier. Growth hormone therapy is great for those with PWS though they are largely inactive and lead a sedentary lifestyle, the growth hormone will allow them to have less body fat and more muscle mass. As noted earlier in my paper, those suffering from PWS have altered function in their hypothalamus, which is also where growth hormone is secreted. Aycan and Bas (2014) state that treatment with growth hormones should be strongly considered for those with PWS.
PWS sufferers are also quick to anger, which can be correlated with their sub-average IQ. They may, for instance, become irate at the fact that they do not have constant access to food, and may turn to emotional, angry and infantile outbursts in an attempt to receive what they want. This is one way that it’s tricky to treat those with the disease. How do you tell an individual with PWS who wants something “No”? Measures should be taken to show those with the disease what they are doing to their bodies in the simplest way possible as to better get the point across to them. We can help those sufferers of PWS who are quick to anger with by allowing them to discern between right and wrong ways to handle times when they don’t get what they want with positive reinforcement.
Since those who suffer from PWS have behavioral problems, there are better measures we can take to assure that they don’t have their violent outbursts. When positive reinforcement is consistently shown to an individual who has PWS, he will have more success with his program. When they do something wrong, they can then be shown positive reinforcement, and through being shown positive things with reinforcement theory, they can better learn that certain actions they take are dangerous and shouldn’t be done again, as Rushton (1980) states: “If one rewards a response, it will increase the probability of the future occurrence of that response. If one punishes a response, it will decrease the future probability of the occurrence of that response.” (p. 90).
Discussion
In this paper, I have presented causes for PWS as well as effective ways to manage the disease. To look at how IQ affects individuals in regards to obesity and because it is highly correlated with other measures as well, we can then better help those with the disease. By seeing which individuals have the parental disomy version of PWS, we can then monitor them and give them better care because of their lowered IQ and make sure they stay at a healthy weight. One of the best measures to take is to heavily restrict food, i.e., make sure ability to access food at all hours of the day is restricted along with constant supervision. Though, there are rights groups fighting for them saying that their human rights are being infringed on. In allowing them to have free reign over what, how and when they eat, they will gorge themselves to obesity, as well as lead themselves to horrible complications that come along with increased food consumption. When one is caught consuming food he or she shouldn’t be consuming, punishing them and letting them understand that the behavior they took was wrong will lead to better choices and outcomes from those choices, due in part to the main facet of reinforcement theory, that punishing a response will lead to a reduced outcome in that response that was punished happening in the future. Also, with the advent of CRISPR Cas9, we will be able to edit genomes, and therefore, eventually, put an end to PWS. It will enable us to fix the chromosomal deletion and uniparental disomy, which will eradicate this disease.
Conclusion
There are better, more helpful ways in which to help those suffering from PWS. By identifying and attempting to correct these abnormalities, those who suffer from the disease can, therefore, have a better quality of life due in part to the extra measures taken. By understanding that their lower average IQs lead to a lot of the problems associated with the disease, we can better structure methods for them to keep on a healthy track and reinforce positive behavior through reinforcement theory. Since obesity is correlated highly with low IQ, we can, therefore, use this information to better help those who suffer from PWS that have low IQs. Locking up food instead of providing free access, as well as understanding they do not have the ability to delay gratification, would be a big start to find better ways to treat sufferers of PWS. Treating negative actions with positive reinforcement through reinforcement theory will lead to better and increased prosocial behavior. It’s been shown that if you punish a response, then it will decrease the future probability of that response occurring. The advent of CRISPR Cas9 will then allow us to edit the chromosomes of those with this disease in the future. Should we use genome editing on individuals with this disease, as well as several other chromosomal/genetic diseases? I believe we should, in doing so, we will greatly increase the quality of life of those with the disease.
References
Aycan, Z., & Baş, V. N. (2014). Prader-Willi Syndrome and Growth Hormone Deficiency. Journal of Clinical Research in Pediatric Endocrinology Jcrpe, 62-67.
Butler, M. G., Lee, P. D., & Whitman, B. Y. (2006). Management of Prader-Willi syndrome (3rd ed.). New York: Springer-Verlag.
Dykens, E. M., Goff, B. J., Hodapp, R. M., Davis, L., Devanzo P., Moss, F. . . King, B. (1997). Eating Themselves to Death: Have “Personal Rights” Gone Too Far in Treating People With Prader-Willi Syndrome? Mental Retardation, 35(4), 312-314.
Kanazawa, S. (2014). Intelligence and obesity. Current Opinion in Endocrinology & Diabetes and Obesity, 21(5), 339-344.
Ledbetter, D. H., Riccardi, V. M., Airhart, S. D., Strobel, R. J., Keenan, B. S., & Crawford, J. D. (1981). Deletions of Chromosome 15 as a Cause of the Prader–Willi Syndrome. New England Journal of Medicine N Engl J Med, 304(6), 325-329.
Mischel, W., Ebbesen, E. B., & Zeiss, A. R. (1972). Cognitive and attentional mechanisms in delay of gratification. Journal of Personality and Social Psychology, 21(2), 204-218.
Nakazato, M., Murakami, N., Date, Y, et al (2001). A role for ghrelin in the central regulation of feeding Nature 409, 194-198
Rushton, J. P. (1980). Altruism, socialization, and society. Englewood Cliffs, NJ: Prentice-Hall.
Schlam, T. R., Wilson, N. L., Shoda, Y., Mischel, W., & Ayduk, O. (2013). Preschoolers’ Delay of Gratification Predicts their Body Mass 30 Years Later. The Journal of Pediatrics, 162(1), 90-93.
Whittington, J., Holland, A., & Webb, T. (2009). Relationship between the IQ of people with Prader-Willi syndrome and that of their siblings: Evidence for imprinted gene effects. Journal of Intellectual Disability Research, 53(5), 411-418.
YM Wang, L Chuang, BT Wang, et al. Maternal uniparental disomy in a patient with Prader-Willi syndrome with an additional small inv dup(15) chromosome. J Formos Med Assoc, 103 (2004), pp. 943–947
Science Daily: Mom’s Exposure to BPA During Pregnancy Can Put Her Baby on Course to Obesity
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Science Daily came out with an article today that exposure to BPA invitro for babies is correlated with obesity at age 7. 94 percent of the women tested had detectable levels of BPA. BPA is also linked with early onset puberty, which I will also speak on later in this article as it has implications for one of my theories.
I briefly touched on BPA in my article What’s the Cause of the Cucking of Europe? where I said:
I advise all of you (women included, there are many deleterious effects of BPA on the mother as well as the baby prenatally), to discontinue use of plastics with BPA in them.
The above-linked study shows that preeclampsia is correlated with elevated levels of BPA in the blood levels in the pregnant mothers, fetal blood, and the placenta. BPA was found to be elevated in mother’s fetal tissue with preeclampsia in comparison to the mothers with lower levels of BPA in their fetal tissue. I will come back to the BPA link with preeclampsia later in the article as it has implications for ethnic groups in America.
The paper, which was just released on the 17th, called Bisphenol A and Adiposity in an Inner-City Birth Cohort, carried out tested BPA in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.** Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors, they discovered that there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period.
The researchers then conclude that BPA exposure invitro “may be an important underlying factor in the obesity epidemic” and that “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.”
If true, this has huge implications for the way we look at the obesity epidemic in this country. Who are the most likely to be obese? “Hispanics” and blacks (Ogden et al, 2014).
Returning to what I brought up earlier about early onset puberty: in my article on the hormone leptin being a cause for earlier menarche in black girls, I noted that since black girls were more likely to be heavier as well as mature faster than white girls, that differences in leptin were the cause of differences in menarche between the two groups. Elevated levels of serum leptin were correlated with body fat and differences in maturation between the two groups. Differences remained, but lessened, after controlling for differences in fat mass, maturation, age, and physical fitness.
Since BPA is correlated with adiposity in children and black girls have earlier menarche DUE to there being a higher chance of black girls being overweight in comparison to white girls, BPA is yet another piece to the puzzle of this phenomena, along with, of course, evolution. Ingestion of BPA is an environmental factor, however, with these changes in body chemistry in the children invitro due to increased BPA consumption by the pregnant mothers, it leads to one cause that can be prevented from further occurring due to our new knowledge.
The study was carried out on a cohort from NYC. In 2010 in NYC, the city was: 44 percent white, 25.5 percent black, 12.7 percent Asian with the rest being filled out by ‘Hispanics’ (not a racial category) and mixed-race people. Even after they matched for SES and other environmental factors, these differences persisted. However, this study was only carried out on those women who self-identified as either Dominican (basically African) and black. To quote the researchers:
Women were included if they self-identified as either African American or Dominican and had resided in Northern Manhattan or the South Bronx for at least 1 year before pregnancy. Exclusion criteria included mother’s report of: cigarette smoking or use of other tobacco products during pregnancy, illicit drug use, diabetes, hypertension, known HIV, or a first prenatal visit after the 20th week of gestation.
So, we have a full sample of Caribbean Africans and African Americans in this study. What else can we learn about those two populations and their consumption of things with BPA in them?
The above Figure (7) is taken from the U.S. Department of Agriculture and the Food Surveys Research Group study on differences in drinking tap and bottled water.in different populations in the country. As you can see in this figure (what is notable is the ages 12-19 and 20 to 60 in the table), whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. However, Mexican American girls, like black girls, are also entering puberty earlier. Since both populations have a substantial percentage of them overweight and obese (factor for serum leptin production which then causes early onset puberty), this again shows a strong correlation between body fat gain and early onset puberty. Moreover, this also shows that both Dominican and black populations consume more bottled water than do white populations, both populations are more likely to be obese or overweight (even after controlling for SES) which causes leptin production earlier causing periods to happen much sooner than in populations who drink less bottled water and use other products with BPA in them. .
Going back to preeclampsia, it is a condition that pregnant women develop that’s characterized by hypertension (high blood pressure) and protein in the urine. It’s known that black women suffer from it the most. More interestingly, over the past ten years, rates of preeclampsia have been increasing in the black female population. As the researchers note in the article, BPA is correlated with preeclampsia. Blacks have a higher rate and chance of being diagnosed with hypertension as well. All of these differing variables coalesce into our current obesity epidemic. With blacks and “Hispanics” being more likely to be overweight/obese drink more bottled water, have a higher risk for hypertension, higher risk for preeclampsia and having earlier menarche, these help explain, in part, racial/ethnic differences in obesity.
These differences can be attributed to consumption of bottled water, i.e., consuming things with made with and packaged in plastic as well as canned foods. From my experience with Dominican and black New Yorkers, they tend to have horrible lifestyles, tend to drink tons of bottled water and also tend to be overweight or obese at a higher rate in comparison to the general population. This leads to biologic factors changing (i.e., earlier menarche in younger girls) in these young girls, leading to devastating effects on their body chemistry.
This study, yet again, proves another underlying factor for obesity in certain populations in the country. And what do you know? It’s the populations that already have the highest rate of obesity in the country. When it becomes definitive that BPA consumption by pregnant mothers does lead to underlying factors in obesity. To quote the researchers: “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.” This will be HUGE for our understanding of underlying causes to obesity! Moreover, if (when) this is fully corroborated, it can then be said that by mothers exposing their children in the womb to excess levels of BPA, there is a chance that they are “giving their own choice to make their children have a higher chance of being obese, as they know the dangers of BPA consumption during pregnancy and all of the negative variables associated with it.”
This is an extremely interesting and important study for our understanding of obesity. Since BPA consumption invitro is correlated with higher fat mass index in girls at age 7, and since those girls who tend to be more overweight and obese than other populations, we can then say that BPA has a hand in obesity in children, which then causes serum leptin to be released, causing way menarche in these populations. An increase in sexual maturation has been linked to the obesity epidemic, which began around 60 years ago. The cause of this is due to the demonization of the fat macro and carbohydrates, all the while it was reversed. This destroyed insulin sensitivity for many Americans, leading to a huge majority of our health problems today.
In conclusion, underlying factors for obesity keep appearing. Due to racial/ethnic differences in bottled water consumption (one of the most common BPA products in households), which the effects of BPA may alter how fat cells are formed in early life, this accounts for, in part, excess adiposity in differing populations. These underlying factors could help show where some of these racial/ethnic differences in obesity come from. Since the two populations in the study (black American and Dominican) both have high levels of adiposity, both drink a lot of bottled water and both have earlier menarche than do whites (who drink LESS bottled water), this shows that some (a lot?) of the variation in obesity between ethnic/racial groupings can be explained by these underlying factors.
** I have one problem with this study. They assessed fat mass index with bioelectrical impedance.The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.
In Defense of Jason Richwine
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I came across two articles today, one from The Atlantic and the other from judgybitch.com. Both have attacked Jason Richwine’s dissertation in which he calls for a change to the US immigration policy to turn away low IQ immigrants and only accept high IQ ones. I agree fully with this (if it’s completely controlled, of course). This would drop crime as well as save us more money in welfare and other government programs that low IQ peoples take.
By 2050, 9 out of 10 people in the US will be obese or overweight and by 2020 80 percent of US men will be obese or overweight. This is due, in part, to an influx of those with lower IQs from South of the Border. Jason Richwine’s argument for testing immigrants will, in turn, lower obesity rates in America.
Dr. James Thompson noted how continued mass immigration from the South of the Border would decrease IQ, this is a real and pressing issue. A country is only as good as its majority population and by allowing all of these low IQ people into the country, our country will transform into theirs, which is ironic since that’s the exact thing they’re running away from. You cannot run away from genetics. The overall ‘Hispanic’-white gap is 10.2 points or .72 SDs. That will lower the average IQ of the country even more, and in turn, give us all a lowered quality of life. The average IQ of Mexico is 88 (Lynn and Vanhanen, 2002) so by allowing unfettered mass immigration without checking average IQs to see if they’ll be of any use to us as a country will lead to eventual irreversible effects if this isn’t stopped soon.
The first article I’ll look at is the one from The Atlantic:
Let’s start with the fact that there is no such thing as a direct test of general mental ability. What IQ tests measure directly is the test-taker’s display of particular cognitive skills: size of vocabulary, degree of reading comprehension, facility with analogies, and so on. Any conclusions about general mental ability are inferences drawn from the test-taker’s relative mastery of those various skills.
IQ tests test g or the general intelligence factor which encompasses all mental abilities. I guess the author of this piece has never heard of Raven’s Progressive Matrices. It’s a ‘culture free’ IQ test where the test is based on pattern recognition. No bias there.
Even then, if they don’t speak English and speak Spanish, they can get tests in their native language which are not biased. Gottfredson (1994) and 51 other eminent intelligence researchers signed a 25 point statement in which one of the statements was:
Intelligence tests are not culturally biased against American blacks or other native-born, English-speaking peoples in the U.S. Rather, IQ scores predict equally accurately for all such Americans, regardless of race and social class. Individuals who do not understand English well can be given either a nonverbal test or one in their native language.
They will be given the nonverbal test (RPM, see below) or one in their native language, which still test the same underlying concept of the general intelligence factor.
They found that being raised by high-SES (socioeconomic status) parents led to an IQ boost of between 12 and 16 points – a huge improvement that testifies to the powerful influence that upbringing can have.
False. See below.
A study of twins by psychologist Eric Turkheimer and colleagues that similarly tracked parents’ education, occupation, and income yielded especially striking results. Specifically, they found that the “heritability” of IQ – the degree to which IQ variations can be explained by genes – varies dramatically by socioeconomic class. Heritability among high-SES (socioeconomic status) kids was 0.72; in other words, genetic factors accounted for 72 percent of the variations in IQ, while shared environment accounted for only 15 percent. For low-SES kids, on the other hand, the relative influence of genes and environment was inverted: Estimated heritability was only 0.10, while shared environment explained 58 percent of IQ variations.
Turkheimer was right that he did find gene x environment interactions that made genetic influences weaker and shared environment stronger for those from poorer homes in comparison to those from more affluent homes. Though most studies show no interaction effects, or interactions vary significantly.
Other studies have shown that heritabilities are the same both within as well as between white and black samples. That led Jensen to label this the ‘default hypothesis’. Researchers analyzed full and half siblings from the NLSY on three Peabody Achievement Tests. 161 black full siblings, 106 pairs of black half siblings, 314 pairs of full white siblings and 53 pairs of white half-siblings. with measures in math and reading. The best fitting model for all of the data was by which the sources of the sources of the differences between those within race and the differences between races were the same, at 50 percent genetic and environmental. The combined model (50/50) best explains it, whereas the culture-only and genetics-only models are inadequate.
IQ tests are good measures of innate intelligence–if all other factors are held steady.
This is wrong. IQ tests are fine all around the world. RPM is one of the best out there and correlates with g between .8 and .9.
But if IQ tests are being used to compare individuals of wildly different backgrounds, then the variable of innate intelligence is not being tested in isolation. Instead, the scores will reflect some impossible-to-sort-out combination of ability and differences in opportunities and motivations. Let’s take a look at why that might be the case.
Intelligence – g – is the same across every population in the world.
Comparisons of IQ scores across ethnic groups, cultures, countries, or time periods founder on this basic problem: The cognitive skills that IQ tests assess are not used or valued to the same extent in all times and places
This is why they get re-standardized.
Indeed, the widespread usefulness of these skills is emphatically not the norm in human history. After all, IQ tests put great stress on reading ability and vocabulary, yet writing was invented only about 6,000 years ago – rather late in the day given that anatomically modern humans have been around for over 100,000 years. And as recently as two hundred years ago, only about 15 percent of people could read or write at all.
Doesn’t matter. See Raven’s Progressive Matrices above. The general intelligence factor is the same in all populations around the world. There are ways to give intelligence tests, such as RPM, to those who don’t read or write.
More generally, IQ tests reward the possession of abstract theoretical knowledge and a facility for formal analytical rigor.
Abstract thought is linked with intelligence. Those with higher IQs are more analytical than those with lower IQs.
To grasp how culturally contingent our current conception of intelligence is, just imagine how well you might do on an IQ test devised by Amazonian hunter-gatherers or medieval European peasants.
I touched on this in my refutation of Robert Sternberg. The concept of g does not change over time. The more intelligent you are, the better chance you’ll have to survive in those places.
Such skills are used more intensively in the most advanced economies than they are in the rest of the world. And within advanced societies, they are put to much greater use by the managers and professionals of the socioeconomic elite than by everybody else. As a result, American kids generally will have better opportunities to develop these skills than kids in, say, Mexico or Guatemala. And in America, the children of college-educated parents will have much better opportunities than working-class kids.
Those skills are used much more in advanced economies because of higher average innate intelligence. The children of college-educated parents have much better opportunities than working-class kids because intelligence is strongly linked to socioeconomics status.
Among the strongest evidence that IQ tests are testing not just innate ability, but the extent to which that innate ability has been put to work developing specific skills, is the remarkable “Flynn effect”: In the United States and many other countries, raw IQ scores have been rising about three points a decade. This rise is far too rapid to have a genetic cause. The best explanation for what’s going on is that increasing social complexity is expanding the use of the cognitive skills in question – and thus improving the opportunities for honing those skills.
Let’s say Flynn is right. The average black now is as intelligent as the average white in 1945. That’s supposed to show that the race difference in IQ is environmentally caused because there hasn’t been that much genetic change in the white population and the IQ has allegedly gone up 15 points. So, you can have a 15 point difference created by just an environmental change, no one knows why. Some think better nutrition or malnourished brain, etc. That’s also a fallacy. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. The Flynn Effect make’s that highly unlikely and here’s why.
The Flynn Effect, assuming it’s real, has been acting completely uniformly in every population. Any country you ask, the rate of increase is 3 per decade. That means it’s an environmental factor that affects whites and blacks the same way as well as the whole world. And as a result of this uniform environmental factor, you have a difference in IQ that’s being preserved. That would suggest that the response on the parts of blacks and whites is due to some non-environment factors, a genetic factor, which is making the difference in IQ remain constant as the Flynn Effect goes into effect.
What makes it even more unlikely, in the last 60 years, their environments have become very similar since segregation. These differences don’t exist now, they go to the same schools by court order, same TV shows, same movies, basically same environment for both, and yet, that increasing similarity in the environment, the Flynn Effect, the IQ gap has remained intact. Which means whatever counts for the gap is genetic and not environmental. The more and more similar the environment, the less and less of the difference can be due to the environment and the more and more it must be due to genes. So this 15 point gap surviving these changes in the environment, seems more and more likely to be genetic in origin.
So because this ‘Effect’ is the same across all populations and the gap didn’t close, that means it’s genetic. If the gap persisted even when IQs were rising 3 points per year, the B-W gap has still persisted, proving that it’s genetic.
That is why the Flynn Effect is irrelevant. This “Effect”, has been a slight upward trend in IQ, around 3 points per decade, which, in my opinion, has to do with the advent of better nutrition and an industrialized society. The rise in IQ started around 1880, almost perfectly coinciding with the industrial revolution in America. Along with a more industrialized society, it’s possible to give most citizens in the country good enough nutrition to where they are not iodine deficient (adding iodine to our salt boosted Americans IQs), as well as being deficient in zinc, iron, protein and certain B vitamins which the effects of not getting enough leads to the brain not growing to its full potential, which in turn leads to a lower IQ.
One more point on the Flynn Effect. The Flynn Effect does not occur on g, as it is not a Jensen Effect. Rushton defines Jensen Effect as follows:
Significant correlations occurring between g-factor loadings and other variables have been dubbed “The Jensen effect”.
…
Thus the secular increase in test scores (the “Lynn±Flynn effect”) is not a “Jensen effect” nor is this the first time the discriminating power of the Jensen effect has been shown.
The Flynn effect is acutely embarrassing to those who leap from IQ score differences to claims of genetic differences in intelligence.
Not at all, since it’s easily explainable by better nutrition since the beginning of the industrial revolution. It’s also not even on g so why this gets discussed is beyond me.
Specifically, it is based on the ahistorical and ethnocentric assumption of a fixed relationship between the development of certain cognitive skills and raw mental ability. In truth, the skills associated with intelligence have changed over time–and unevenly through social space–as society evolves.
The relationship exists and there is a strong correlation between cognitive skills and raw mental ability. More intelligent people have better functioning societies than less intelligent people. This is an objective fact.
But contrary to the counsel of despair from hereditarians like Richwine, those deficits aren’t hard-wired. Progress in reducing achievement gaps will certainly not be easy, but a full review of the IQ evidence shows that it is possible. And it will be aided by policies, like immigration reform, that encourage the full integration of Hispanics into the American economic and cultural mainstream.
Jason Richwine is correct. Progress in achievement gaps will not close, barring the continued dysgenesis that America is facing. Immigration reform will not change anything. They don’t want to assimilate; they want to come and leech off of our Welfare State. The denial of genetics and scholastic achievement won’t be able to be held for long. In this study in which Robert Plomin was one of the researchers, it was found that 60 percent of the difference between individual 16-year-old students in the UK could be attributed to genetic factors. We know that IQ is linked to academic achievement and since that’s heritable as well, we will soon see that race and ethnic differences in IQ and academic achievement are, without a shadow of a doubt, are real and do not exist because of any economic deprivation or some other kind of non-biologic factors.
For the second article, from judgybitch.com, in which she only says one correct thing in it and it’s:
Here’s a little pet theory of mine I’d like to throw out, just for the hell of it. I think humans prefer lighter skin and hair and eye colors because those tend to be the result of recessive genes. A man with darker tones who has a child with a woman of lighter tones will almost always see his genes expressed in the children. Dark tones tend to be dominant. The preference for lighter skin is a natural paternity test.
This is called sexual selection, which is natural selection which arises for selection of traits in the opposite sex. Selecting for certain traits which the opposite sex found appealing, for example, is how long hair got sexually selected for outside of Africa along with selection for hair, eye, and skin color. Selecting for these traits had them become more prevalent and they eventually stayed due to intense selection for them.
For example, Eurasian women got selected for beauty and Eurasian men who got selected for intelligence as men had to be more intelligent in order to hunt for food. Conversely, African women gathered and hunted for food and became slightly more intelligent than African men who became the more attractive sex (Fuerle, 2008).
But other than this she is wrong.
You know what IS linked very strongly to lower IQs?
Malnutrition.
http://www.sciencedaily.com/releases/2004/11/041117005027.htm
http://www.ncbi.nlm.nih.gov/pubmed/2628311
http://www.nature.com/pr/journal/v5/n11/abs/pr1971371a.html
The idea is not even the slightest bit controversial. Children who are starved, especially in the earliest years of life, perform very poorly on IQ tests compared to peers who received adequate nutrition. Like, really poorly. IQ’s down around 60 (100 is average).
Let’s look at this world hunger map, shall we?
http://www.geographictravels.com/2008/07/world-hunger-map.html
Oh well now, would you look at that. Looks like it’s mostly black and Hispanic folks who are starving. And all those white folks are living life to the hilt, with full bellies and bright futures.
Must be a coincidence.
It’s not a coincidence. There is no coincidence that if you superimpose an IQ map over the world hunger map, that a super majority of the low IQ countries would have bad nutrition and be starving, whereas those higher IQ populations would have better nutrition and, therefore, higher IQs and lack of malnutrition and starvation. There are environmental factors involved in this, which I have gone through in my article IQ, Nutrition, Disease and Parasitic Load. Yes, those environmental variables decrease IQ; but in the case of Africa, if their full genotypic IQ were expressed in their phenotype, they would have an average IQ of 80, 9 points away from the lowest average European country which is Serbia at 89. They would then be able to have better functioning societies and not have to rely on outside aid. Though, their low IQs are the cause of evolution, those factors only cause about 10 points of difference (depending which of the variables I mentioned exist in those areas).
Let’s look at this map of food insecurity in the United States:
http://www.nextgenerationfood.com/news/food-insecurity-in-the-us/
Highest rates of food insecurity:
Mississippi
Texas
Arkansas
Lowest rates of food insecurity:
North Dakota
Massachusetts
Virginia
Gosh, I wonder where all the black and Hispanic people are? North Dakota, right?
According to the USDA, in a report titled Household Food Security in the United States in 2011, black and Hispanic families are more than twice as likely to experience food insecurity as white families (p. 11).
White 11.4% of families food insecure
Black 25.1%
Hispanic 26.2%
Gosh, I wonder where black and ‘Hispanic’ people are? Mississippi, Texas, and Arkansas right? What is the cause of the food insecurity? Lower intelligence. What is lower intelligence highly correlated with? Obesity.
If you keep in mind the fact that obesity (especially as the result of heavily processed, nutrient deficient junk foods) is also a form of malnutrition, it seems to me that there is an entirely different explanation for why certain racial groups might tend to perform lower on IQ tests.
Sure it is. A big cause for obesity is lowered intelligence (Kanazawa 2007). What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ. The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This clearly shows that those obese individuals who score low on IQ tests, more often than not, are obese because of their intelligence. The lack of ability to delay gratification is also correlated with low IQ (Mischel and Metzner, 1982).
Becoming obese is largely in part related to environmental factors, but there are correlates with obesity and genetic factors, as well as racial and ethnic differences in obesity, which are due, in part, to environmental as well as genetic factors. All of these factors fall back to a) lower intelligence, b) differing physiology and c) differing nutritional habits. Lower IQ is the main reason, though, for these differences which manifest itself as differences in scores of cognitive ability. Those with lower scores than have higher chances of having negative effects in life, such as low SES, higher chance of becoming obese and so on.
Correlation is not causation.
This is the liberals word phrase they use when they cannot contest data and know it so use the same old boring phrase. When you get the same result over and over using the scientific method, then it’s safe to say that the same results and conclusions that get brought up time and time again are real and cannot be explained away by the correlation does not mean causation line.
And furthermore, I haven’t read Richwine’s dissertation, nor do I plan to, so I don’t know if he offered any tentative explanations for his findings.
Didn’t even read it and is giving a critique of it. How does that work?
It looks to me like Richwine is a gigantic racist asshole, because he is using his findings to try and limit the opportunities for Hispanic people to come to the United States, because dumb spics.
Lower IQ people commit more crimes than do higher IQ people. This phenomenon is well-noted that those with lower intelligence commit crime, as the average IQ of a criminal in America, is 85, whereas the average IQ for a juvenile is 92. The average juvenile IQ is higher because more often than not, those who are habitual offenders in childhood become habitual offenders in adulthood, and at adulthood IQ drops from childhood where the environment was able to artificially boost their IQs.
What if I’m right? What if IQ differences are traceable to malnutrition? That would indicate a whole different set of interventions and policies than just turn them away.
You are part right, but that won’t put any big dent in any genetic/phenotypic IQ differences and still, mass immigration from South of the Border still wouldn’t be OK in the first place.
In shutting down the conversation about race and IQ, Harvard students are explicitly saying they don’t WANT to find a reason behind low performance on IQ tests amongst certain racial groups. They don’t CARE why some groups are not reaching their full human potential. They don’t give ONE SINGLE FUCK about anyone other than themselves. It could be as simple as making certain children have access to proper food and nutrition.
I at least give her credit for acknowledging the biological reality of race and the reality of IQ. But she thinks that malnutrition plays too big a part in the ethnic IQ gap than it does in reality.
As I have covered here before, people will do anything they can to deny the validity of IQ tests. However, their explanations cut it.
People who attempt to deny biological differences in intelligence because they strongly predict positive life outcomes will do anything to deny their validity. But that doesn’t change how strong a predictor they are in regards to predicting both positive and negative successes in life.
Those who attempt to deny any differences between races, like Chanda Chisala (I know you can see this Chanda, still waiting for a response to the criticism of your horrible article that “redneck genes” are the cause for the black-white IQ gap), who are wrong in their premises on the cause as well as how to fix the gap. They will do anything to attempt to explain away a gap which is, at least, 50 percent genetic in origin.
The attack on Jason Richwine is because, of course, he’s right. They don’t want to admit he is right so they do whatever they can to discredit his argument, by calling him a ‘racist’. But that doesn’t negate his data, and as seen above, any arguments against Richwine’s dissertation are unfounded.
Germany is going to begin IQ testing their immigrants, why can’t we?
Leptin and its Role in the Sexual Maturity of Black Girls
1200 words
There are differences between the races in regards to sexual maturity. I’ve recently discovered that leptin plays a role in black female teenagers and how they reach puberty earlier than that of white women. This is one out of many variables that prove Rushton’s three-way rule; that the races all differ on certain variables, on average.
Buried in the middle of this article on black and white differences in body composition, it is observed that the mean concentration of leptin was significantly greater in black girls than that of white girls. The authors conclude that leptin may play an important role in the accelerated growth and sexual maturation of black girls:
In one study, the mean leptin concentration was significantly (P < 0.01) higher in 57 black girls (15.0 ± 10.1 μg/L) than in 79 white girls (8.4 ± 11.1 μg/L) aged 8–17 y (58). The authors concluded that this difference might play an important role in the accelerated growth and sexual maturation of black girls. Likewise, Nicklas et al (57) reported a strong correlation between leptin and %BF for both black (r = 0.71, P < 0.0001) and white (r = 0.61, P < 0.001) obese postmenopausal women, but a significant racial difference in leptin concentration (36.0 ± 4.8 compared with 45.8 ± 3.5 μg/L; P < 0.05), respectively. Additionally, leptin correlated with resting energy expenditure in black women (r = 0.58, P < 0.001) but not in white women (r = 0.08).
Also noticed, was that leptin correlated with REE (resting energy expenditure) in black women but not in white women.
Wong et al (1998), state that because African-American girls tend to be heavier and mature faster than white girls, then there must be a leptin difference between the 2 groups. He measured serum leptin concentrations in 12 hour fasted blood samples of 57 black and 79 white girls. Body comp was measured by x-ray absorptiometry, sexual maturity by doctor examination and physical fitness by treadmill testing. What was found was the serum leptin levels were positively correlated with body fat, maturation and insulin were higher in the black girls after controlling for age. Differences remained, but lessened, after controlling for differences in fat mass, maturation, and physical fitness. This is more proof that leptin is a cause for the role in earlier sexual maturity in black girls.
Kaplowitz (2008) observed in his paper Link Between Body Fat and the Timing of Puberty that several studies have shown that the increase in earlier sexual maturation may indeed be linked to the obesity epidemic which started to rise around 50 to 60 years ago when fat was demonized as “being the cause for fat gain”, all the while carbs were championed as a better macro over fat. Of course, we now know that’s not true, but the implications of this lie that we’ve been told are now coming out in the light 50 years later.
Kaplowitz states that the evidence currently out points to obesity being a cause for earlier puberty in girls, rather than earlier puberty causing an increase in body fat (hmmm.. where have I heard confusing one cause for another before? Oh yeah, the IQ/obesity cause).Many studies have come out that show, in both rats and humans, that leptin may be the critical link between body fat and earlier puberty. Both mice and humans who were deficient in leptin both failed to reach puberty unless leptin was administered. Though he says that leptin may end up playing a permissive, rather than a critical metabolic signal that initiates puberty. But with the data of black girls having higher leptin levels, leptin being correlated highly with body fat, and both being highly correlated with increased sexual maturation show the reason why black girls are a) more sexually active at a younger age and b) why black girls mature faster than white girls. He finally concludes that it makes evolutionary sense that body fat and reproduction in girls evolved as a mechanism to ensure that pregnancy won’t occur unless adequate levels of body fat are had.
This is yet more biological evidence for physiological differences between the races.
When fat mass increases, so do leptin levels. When leptin levels increase, puberty happens earlier. Black girls have higher rates of leptin, which correlates highly with body fat and sexual maturity, so it’s no surprise that we see these factors here.
What are evolutionary causes for this? Well, seeing Africa’s life expectancy, the rate of parasitic load as well as disease in Africa, and Rushton’s r/K Life History Theory, which states that those more r selected will have more children and show less care for them whereas those more k selected will have less progeny, but show more care, we can easily see how such a mechanism evolved. With IQ being highly correlated with life expectancy (at .95), we can see part of the reason why, for instance, black women evolved to have higher rates of 2 egg twinning in comparison to whites (16 per 1000 for blacks, 8 per 1000 for whites and 4 per 1000 for Orientals). To quote Rushton from Race, Evolution, and Behavior:
Black women, compared to white women, average a shorter period of ovulation and produce more eggs per ovulation in addition to all the other characteristics in Table 1.1. As mentioned, the rate of dizygotic twinning, a direct index of egg production, is less than 4 per 1,000 births among Mongoloids, 8 per 1,000 among Caucasoids, and 16 or greater per 1,000 among Negroids. (pg. 6)
This is a clear evolutionary strategy. Have more children where it’s less hospitable and there is a higher mortality rate, especially for young children and have fewer children where it is more stable and less environmental dangers are around.
Even more evidence to bolster my claim is how 82 percent of black women are overweight or obese (Ogden et al, 2014). Genes related to obesity have also been found in African-Americans, as well as European-Americans, which also bolster the claim seeing as the genes were found to do the same things in both populations. To quote myself from the above article:
In a study published back in 2013, researchers were looking for obesity genes in African Americans. The study, which involved more than 70,000 men and women of African descent, they were able to identify 3 SNPs that were associated with obesity and BMI in the sample population. What was also found, was that those same genetic sequences also heighten rates of obesity in peoples with no African ancestry, all of the genetic variants associated with obesity were also found in European populations. The same genes found in African populations did the same in European populations, and vice versa.
To quote the paper:
We provide evidence for a shared genetic influence on BMI across populations, as we found directionally consistent associations with the majority of known BMI risk variants. This observation suggests that bioloically functional alleles are ancient and probably arose before migrations out of Africa. In addition, we were able to refine the window of association of some of the previously established BMI loci, which may eventually help identify the biologically functional variant(s).
BMI is also between .75 and .82 heritable. These factors show yet another cause for black women’s high obesity rates, of course with eating garbage food all of the time, but I’m talking about evolutionary reasons.
There are reasons why black girls mature faster than white girls, it’s because of leptin, which precedes an increase in body fat to prepare for eventual menstruation and higher body fat helps to protect the baby in vitro. R/K Life History Theory then shows the evolutionary reasons why earlier sexual maturity happens for black girls over white girls: lower life expectancy.
Are There Genetic Causes for Obesity?
2500 words
We all know about the Healthy At Every Size Movement (HAES) and how they claim that genetics is the cause of them being overweight and or obese and that genetics is the cause that they cannot lose weight as well as other people. I’m not here today to defend that they are right and that’s why they can’t lose weight (because lets be honest, they have no idea what they’re talking about, nor can they reference any type of study that says it), nor am I here today to give any credence to the HAES movement. I’m here today to talk about genetic causes for obesity as well as causalities that people don’t talk about and believe that kcal in and kcal are the only factors in becoming obese (I have never, nor will I ever dispute that kcal in and out has been the biggest factor involving obesity, just there are underlying causes that people do not talk about, which is the a huge cause in keeping people obese). What people don’t understand is that there are underlying factors that no one talks about that lead to obesity.
When people say that there are no genetic underpinnings for obesity, they are speaking on a subject that they are extremely ignorant about. They always say “kcal in and out”. Right, which I have never disputed. Though, those same people cannot say a thing to the studies that I provide, because they cannot adapt to new information and just parrot the same things as if that disproves the studies that I link. Furthermore, obesity and diabetes (which there is a close relationship between the two), are both nowhere near close enough to being understood.
I have already covered here that ability to delay gratification has a genetic component, and that those with low ability to delay gratification, as noted in my post, had a higher chance of becoming obese than those with a better ability to delay gratification. Some people have said to me that the Marshmallow Experiment didn’t have anything to do with the ability to delay gratification, that it was something else entirely, but alas, the individual obviously said nothing more when I asked him to comment on the post so my readers can read the exchange.
You all know that I covered ethnicity and obesity, but I’m making this post to serve as a something to reference while in discussion with people, as well as educate people who don’t know about these studies.
As noted in my previous article on obesity, there are racial difference in obesity (that pretty much follow Rushton’s Rule). Of course there are socioeconomic factors that are involved there, but to say that there is no genetic component is intellectually dishonest. To believe that there are absolutely no genetic causes for obesity and that environmental factors means everything shows that that person has no idea what they are talking about.
According to a meta-study of twins and families, the heritability of BMI is between .75 and .82. This used mono and dizygotic twins, as well as having over 140 thousand participants. They observed 12 countries, all with differing racial/ethnic groups and the results were the same.
While in a discussion with someone, I got linked these studies: Obese toddlers have dramatically lowered IQ, Obese toddlers have dramatically lowered IQ 2 and Obesity lowers children’s IQ. This is hilarious. The causalities are completely reversed. I would love to hear the explanation for the physiological mechanism that has obesity lower IQ. Well, Satoshi Kanazawa tackled this in his study back in 2014, that low IQ leads to obesity, obesity doesn’t lead to low IQ.
A few of the highlights include:
- Cross-sectional studies conclude that obesity lowers IQ, whereas longitudinal studies conclude that those who become obese already have a low IQ since childhood
- Careful examination of longitudinal studies in Sweden, New Zealand and America clearly show that the casual direction goes from low IQ to obesity, not obesity to low IQ
- There is NO scientific evidence that shows that obesity leads to lowered IQ. There is, however, ample evidence, both in scientific theory as well as ample amounts of evidence that lower IQ people become obese
Individuals with IQs below 74 at 18 have BMI of 26.59 at 40, whereas those with IQs above 126 have BMI of 25.75 (P < 0.001). Similarly, there is a clear and monotonically negative association between intelligence at 18 and the BMI change from 18 to 40. Individuals with IQs below 74 gain 5.19 in BMI in 22 years, whereas those with IQs above 126 gain 3.73 (P < 0.001). Their conclusion remains identical even when they control for systolic and diastolic blood pressure, resting pulse rate, birth place, birth year, and education at conscription. Their results from a large population sample of Swedish men make it clear that it is adolescent intelligence that influences BMI in middle age, not the other way around
The fact of the matter is this: obesity does not lower IQ. Those with certain agendas would like you to believe that becoming obese drops IQ, whereas ample scientific data shows the opposite. Including this study which states that those in the cohort who became obese didn’t see a drop in IQ from childhood, instead, those individuals who became obese already had a lower IQ since childhood. You already know that I did not get a response to these studies. That’s because showing people that they’re wrong actually makes them believe their wrong beliefs more, especially if they have low self-confidence (how ironic).
There have been genes that have been found that are associated with binge eating. If a young adolescent has this particular variant on the FTO gene, they are 20 to 30 percent more likely to binge eat than those who don’t have the variant. This was observed in girls particularly, who were 30 percent more likely to binge eat if they had the variation.
Dr. Peter Atilla had a TED Talk on how obesity may be hiding an even more insidious problem. To quote from the transcript:
Yet when it came to a disease like diabetes that kills Americans eight times more frequently than melanoma, I never once questioned the conventional wisdom. I actually just assumed the pathologic sequence of events was settled science.
Three years later, I found out how wrong I was. But this time, I was the patient. Despite exercising three or four hours every single day, and following the food pyramid to the letter, I’d gained a lot of weight and developed something called metabolic syndrome. Some of you may have heard of this. I had become insulin-resistant.
Now, most researchers believe obesity is the cause of insulin resistance. Logically, then, if you want to treat insulin resistance, you get people to lose weight, right? You treat the obesity. But what if we have it backwards? What if obesity isn’t the cause of insulin resistance at all? In fact, what if it’s a symptom of a much deeper problem, the tip of a proverbial iceberg? I know it sounds crazy because we’re obviously in the midst of an obesity epidemic, but hear me out. What if obesity is a coping mechanism for a far more sinister problem going on underneath the cell? I’m not suggesting that obesity is benign, but what I am suggesting is it may be the lesser of two metabolic evils.
You can think of insulin resistance as the reduced capacity of our cells to partition fuel, as I alluded to a moment ago, taking those calories that we take in and burning some appropriately and storing some appropriately. When we become insulin-resistant, the homeostasis in that balance deviates from this state. So now, when insulin says to a cell, I want you to burn more energy than the cell considers safe, the cell, in effect, says, “No thanks, I’d actually rather store this energy.” And because fat cells are actually missing most of the complex cellular machinery found in other cells, it’s probably the safest place to store it. So for many of us, about 75 million Americans, the appropriate response to insulin resistance may actually be to store it as fat, not the reverse, getting insulin resistance in response to getting fat.
You can think of insulin as this master hormone that controls what our body does with the foods we eat,whether we burn it or store it. This is called fuel partitioning in the lingo. Now failure to produce enough insulin is incompatible with life. And insulin resistance, as its name suggests, is when your cells get increasingly resistant to the effect of insulin trying to do its job. Once you’re insulin-resistant, you’re on your way to getting diabetes, which is what happens when your pancreas can’t keep up with the resistance and make enough insulin.
But most important, I was left with these three burning questions that wouldn’t go away: How did this happen to me if I was supposedly doing everything right? If the conventional wisdom about nutrition had failed me, was it possible it was failing someone else? And underlying these questions, I became almost maniacally obsessed in trying to understand the real relationship between obesity and insulin resistance.
So what I’m suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance.Maybe we should be asking ourselves, is it possible that insulin resistance causes weight gain and the diseases associated with obesity, at least in most people? What if being obese is just a metabolic response to something much more threatening, an underlying epidemic, the one we ought to be worried about?
Let’s look at some suggestive facts. We know that 30 million obese Americans in the United States don’t have insulin resistance. And by the way, they don’t appear to be at any greater risk of disease than lean people. Conversely, we know that six million lean people in the United States are insulin-resistant, and by the way, they appear to be at even greater risk for those metabolic diseases I mentioned a moment ago than their obese counterparts. Now I don’t know why, but it might be because, in their case, their cells haven’t actually figured out the right thing to do with that excess energy. So if you can be obese and not have insulin resistance, and you can be lean and have it, ******this suggests that obesity may just be a proxy for what’s going on.******
So what if we’re fighting the wrong war, fighting obesity rather than insulin resistance? Even worse, what if blaming the obese means we’re blaming the victims? What if some of our fundamental ideas about obesity are just wrong?
Personally, I can’t afford the luxury of arrogance anymore, let alone the luxury of certainty. I have my own ideas about what could be at the heart of this, but I’m wide open to others. Now, my hypothesis, because everybody always asks me, is this. If you ask yourself, what’s a cell trying to protect itself from when it becomes insulin resistant, the answer probably isn’t too much food. It’s more likely too much glucose: blood sugar. Now, we know that refined grains and starches elevate your blood sugar in the short run,and there’s even reason to believe that sugar may lead to insulin resistance directly. So if you put these physiological processes to work, I’d hypothesize that it might be our increased intake of refined grains, sugars and starches that’s driving this epidemic of obesity and diabetes, but through insulin resistance,you see, and not necessarily through just overeating and under-exercising.
The fact of the matter is this: we need to look at any and all causes to do with obesity. To fully understand this disease is to look at any and all factors involving it. To discard theories and make new ones, or just disregard what was looked at. People who say that we shouldn’t look at these types of things really have no idea what they’re talking about. To fully understand a problem, we need to look at any and all causes that may be underlying.
I’m currently writing a research paper on Prader-Willi’s Syndrome (which I will post here when I’m done with it), and as I was watching the documentary, a few things jumped out at me:
- They are infantile
- They clearly have a lack of ability to delay gratification
- Prader-Willi’s people have an IQ, on average of 70
- Due to being infantile, they have a lack of ability to delay gratification, so along with that, they have lower IQs which is correlated with lack of abstract thought
To say that these people “can control themselves” and they “just need to eat less” is dishonest, to say the least. Those people with disorders such as these really have no say in the matter.
In a follow-up to the Marshmallow Experiment, studies were done on those individuals they could still find 40 years later. What was found that those who lacked the ability to delay gratification in pre-school ended up becoming obese. We need to identify those children with low ability to delay gratification because it’s clear that those with the lack of ability to delay gratification end up becoming obese in adulthood.
This is a favorite of mine. People may say “Fat shaming is good!!! It leads to people thinking about what they’re doing and, in turn, they will lose weight!!!” How wrong that is. Present research indicates that in addition to poorer mental health outcomes, weight discrimination has implications for obesity. ******Rather than motivating people to lose weight, weight discrimination increases the risk for obesity.****** Why people think that making fun of people will lead to weight loss is beyond me.
Interestingly, a slightly different pattern emerged when the analyses were based on measured BMI. When the sample with measured weight and height was limited to participants who were overweight at baseline, the risk of obesity was a little stronger but essentially the same (OR = 2.18, 95% CI = 1.04–4.45). In contrast, when this sample was limited to normal weight participants at baseline, there was not enough data for the analysis: of the 14 participants in the normal weight category who reported weight discrimination, none became obese
Similar to weight gain, weight discrimination was associated with remaining obese over the period between the two assessments (see Table 1). That is, those who experienced discrimination based on their weight were over three times more likely to remain obese at follow-up, rather than drop below the obesity threshold, than those who did not experience such discrimination.
The evidence is clear: weight discrimination actually increases the problem that people actually laugh at and make fun of people for. How ironic is that?
In conclusion (I will add to this post as new research comes out), to say that there are no underlying causes of obesity is intellectually dishonest. There are clear underlying causes to this obesity epidemic, which we need to look at any and all of these causes to fully understand obesity better (which we are nowhere close to understanding this problem).
HBD and Diet Advice: Anglin Paleo Refutation Part 2
2300 words
A lot of people seem to have wrong views on nutrition. It’s not really taught in school, people think that it doesn’t matter so they do no independent research of their own and they believe anything and everything that comes out in the MSM as gospel. The thing is, the average person doesn’t read studies, or anything nutrition related for that matter, and believes most everything they read and hear in the MSM. I have talked about nutrition a bit here. I refuted Andrew Anglin’s atrocious writing and arguments for the Paleo Diet here and wrote on obesity and ethnicity including genetic and environmental causes. I also wrote on how nutrition is important prenatally as well as postnatally in developing children. I will also touch on comments in that Dailystormer article that jump out to me that need refuting.
Today I will talk about HBD and diet advice.
Steve Sailer wrote an article on HBD and Diet Advice back in September. He claims a few things that need to be disproven.
It’s common for nutrition scientists to give advice to white Americans based on studies done of what is good for nonwhites to eat. For example, in the 1980s, one of the most fashionable studies was of Japanese in Hawaii. The first generation ate mostly rice with little fat, and they had relatively few heart attacks. The next generation ate cheeseburgers and had higher rates of coronary disease than their parents.
I have covered this in the Dailystormer refutation.
Noted in this study are:
- High interpersonal variability in post-meal glucose observed in 800-person cohort
- Using personal and microbiome features enable accurate glucose response prediction
- Prediction is accurate and superior to common practice in an independent cohort
- Short-term personalized dietary interventions successfully lower post-meal glucose
You can see from the above bullet points that there is high interpersonal variability in post-meal glucose. What that means is, that between each individual in the cohort, there were different glucose spikes in each person.
They can accurately predict glucose response with certain tools. They devised a machine-learning algorithm that uses blood parameters, dietary habits, anthropometrics, physical activity, and gut microbiota measured in the cohort and showed that it accurately predicted personalized postprandial (post-meal) glycemic response to real-life meals.
They validated the prediction using a 100 person cohort.
Personalized dietary interventions showed interventions successfully lowered post-meal glucose. (Emphasis mine). This shows that each person should be on an individual diet and not on a one-size-fits-all diet.
Of course the next generation had higher rates of coronary disease than their parents. High carb, high fat diets lead to coronary blockage, leading to heart attacks and other coronary implications.
That is due to the demonization of fat starting in the 70s. We were told that fat is bad and carbs were fine. That turned out not to be the case. That’s what led to the obesity explosion. People think that eating fat “makes you fat”. Well if that’s the case, eating protein leads to kidney failure and eating carbs leads to Diabetes Mellitus. It’s stupid to think of it that way. Anything in excess is bad for you.
The RDA (Recommended Daily Values) for women is as follows:
69 grams of fat, which comes out to 585 kcal, 300 grams CHO which comes out to 1200 kcal and 53 grams of protein which comes out to 215 kcal. For men, it’s 80 grams of fat which comes out to 720 kcal, 375 grams CHO which comes out to 1500 kcal and 70 grams of protein which comes out to 280 kcal. This is data from the FDA on dietary recommendations for the average America.
Protein is nowhere near high enough. Protein is the main macronutrient you want to eat if you want to stay fuller longer as it has a higher TEF (Thermic Effect of Food). In the linked study, they come to the conclusion that TEF contributed to the satiating power of foods. Protein has the highest TEF of all of the macros, and because of this, some researchers have lobbied to have protein count as 3.2 kcal instead of 4 kcal. So if you want to stay fuller, eat more protein, fewer carbs and more fat. Carbs spike your insulin leading to insulin spikes, which lead to you feeling hungry sooner, as most people ingest fast digesting carbohydrates.
Sailer then cites this NYT article that says:
Today, at least 10 percent of Americans regularly take fish oil supplements. But recent trials have failed to confirm that the pills prevent heart attacks or stroke. And now the story has an intriguing new twist.
Wrong. So, so wrong. Controlled studies clearly show that omega-3 consumption had a positive influence on n-3 (fatty acid) intake. N-3 has also been recognized as a modulator of inflammation as well as the fact that omega-3 fatty acids down-regulate genes involved in chronic inflammation, which show that n-3 is may be good for atherosclerosis.
Studies have shown an increase in omega-3 consumption leads to decreased damage from heart attacks.
Omega-3 may also reduce damage after a stroke.
Dietary epidemiology has also shown a link between n-3 and mental disorders such as Alzheimers and depression. N-3 intake is also linked to intelligence, vision and mood. Infants who don’t get enough n-3 prenatally are at risk for developing vision and nerve problems. Other studies have shown n-3’s effects on tumors, in particular, breast, colon and prostate cancer.
Omega-3’s are also great for muscle growth. Omega-3 intake in obese individuals along with exercise show a speed up in fat-loss for that individual.
Where do these people get their information from? Not only are omega-3’s good for damage reduction after a stroke and a heart attack, they’re also good for muscle growth, breast, colon and prostate tumor reduction, infants deficient in omega-3 prenatally are at risk for developing nerve and vision problems. Increase in omega-3 consumption is also linked to increases in cognition, reduces chronic inflammation and is linked to lower instances of depression.
Omega-3’s are fine. As I said with the Anglin refutation, do not listen to those with no background in nutrition as they most likely have no idea what they are talking about.
Rasmus Nielsen, a geneticist at the University of California, Berkeley, and an author of the new study, said that the discovery raised questions about whether omega-3 fats really were protective for everyone, despite decades of health advice. “The same diet may have different effects on different people,” he said.
See above links on omega-3 intake and all of the positive/negative factors.
In the future, maybe you’ll be able to get your DNA analyzed and be given a list of diets in rank order of their likelihood that they will work for you. But, right now, you can still try different diets. In particular, ask your relatives about what has worked and not worked for them.
That doesn’t matter, as diets should be tailored to the individual, as seen in the Cell study.
Oh, wow. I just found that Anglin wrote a refutation to those who deny the Paleo Diet. Let’s see what that’s about.
And maybe these people have scientific research and/or personal experience to back up what they’re saying. I’m not insulting them for disagreeing with me on diet, that is clearly their right.
The evolutionary argument for Paleo does not line up with your statements. As I noted in my previous article, if you want to eat Paleo because it works with what you like to eat, good for you. But doing it for any magic benefits is stupid, as there are none.
I know for a fact that at least 9 out of 10 people who dare to take this challenge will report back positively if they follow it properly for a month, and this means a whole lot more than someone’s opinion about what it might or might not do, theoretically.
Want to know why people will report back positively? Any time you begin a new diet, especially one on a kcal restriction, your body will drop weight quickly. That’s what piranha personal trainers use on unknowing people. Telling them that they’re doing a “great job”, when in actuality, that happens to everyone who begins a new diet.
Instead, they are arguing theoretically, making highly debatable statements like “White people have evolved to be able to consume dairy products.”
The above map shows lactose intolerance for countries around the world. Ancient Europeans began dairying around 7500 ya and were lactose intolerant when starting to drink milk. But along with faster evolution, which includes no gene flow from other parts of the world, that led to Europeans evolving to, on average, have lower rates of lactose intolerance.
People should really learn what they’re talking about before they say it.
The way to know whether or not they are beneficial is to quit them for a period and see how you feel.
Placebo effect.
Currently, because the scientific literature on these topics is so convoluted and debated on, there is no other conceivable way to prove it one way or another than through our own testing.
The science is pretty solid on this. Anecdotes don’t mean anything to studies.
Many have referred to paleo as a “fad diet.” And it may be a diet that is a fad, but it is also a diet with a thousands upon thousands of years long precedent. One might even suggest that it is the consumption of grains and dairy that are the “fad,” as it is a relatively new trend, in the scope of things.
It IS A FAD DIET ; with NO basis in science that Europeans should eat that way.
If you feel as if you are at peak physical health eating grains and dairy, and have no desire to spend time trying to improve on this, than by all means skip the challenge.
Is he implying that the Paleo Diet is the only diet that doesn’t allow grains and dairy? Not true at all. The Slow Carb Diet is the same, as well as any other high fat, high protein low-carb diet.
We should also note that the definitions of vegetarianism were different then, and Hitler did eat eggs and probably wasn’t completely meat-free.
That’s vegetarianism. Veganism is the more extreme one you’re thinking of where absolutely no animal products are consumed at all.
Vegetarian diets are shown to lead to vitamin inadequacies such as zinc, calcium, iron, manganese, selenium, and copper. Vegetarianism works, it just has to be well-planned. You need to make sure you get the right amount of essential as well as non-essential amino acids, high amounts of protein and make sure you’re not nutrient deficient.
Last time I wrote that White rice and potatoes are good carbs, but I want to be clear that they are not necessary unless you are both already at 5% body weight and you are highly active.
They are not ‘good carbs’. They are white carbs, which are bad for us if we don’t go to the gym to utilize the CHO being ingested. Five percent body-fat? That’s for competition bodybuilders and marathon and distance runners. The average person will never cut down to the level of body-fat. CHO is extremely useful if you’re highly active and go to the gym.
Even if you are not active, you need to consume a decent amount of carbs once a week in order to keep your metabolism from slowing down too much. However, it is probably preferable to use fruits for this purpose, as they contain more micronutrients.
Correct. If you eat a low-carb diet, you need a CHO refeed once a week to keep metabolism high. Though, using fruits is stupid. I know the Paleo thing, but there are many reasons why fructose (the sugar found in fruit) is bad for you. Sugar is just as addictive as cocaine. So telling the average person to ‘use fruits for this purpose’ is stupid, as the average person doesn’t know when to stop eating.
Yes, this diet will technically cost more than a processed foods and grain-based diet, all things being equal. The only reason anyone ever ate grains in the first place is because they were cheap, and processed foods were invented for the same reason. Any natural and healthy diet is going to cost more, all things being equal. However, things don’t have to be equal.
Wrong. Whole foods are not more expensive. The conclusion that was (obviously) reached is that there is expensive and non-expensive junk food as well as whole foods. I personally spend 70 dollars a week on food for myself, with all of my meals planned out. Natural diets will not cost more, all things being equal. If you know how to eat and how to buy food, you will avoid spending too much money.
I tried to answer most of the questions people had in the last thread, but it was so filled up with denialism I could have missed something. So ask here.
I hope you answer this, as well as my other refutation of your horrible nutrition article. I doubt it though.
How did we really evolve to eat?
The most common form of eating, 3 meals a day, is abnormal from an evolutionary perspective. We didn’t evolve eating 3 times a day. We evolved eating intermittently. The study says that intermittent energy restriction periods of up to 16 hours are fine. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Again, another huge benefit for intermittent fasting. As the data comes out on human cohorts, we will be able to see all of the great effects that IF has for us, because that’s how any human population, no matter where they evolved, evolved eating.
There are beneficial effects to IF including reduced oxidative damage and increased cellular stress resistance. Rats put on an IF diet show heightened life-spans. IF is also extremely useful to keep a youthful brain as you age.
There are a mountain of studies that show how beneficial IF is to us and is the TRUE way humans evolved to eat, not any specialized diets. We evolved eating intermittently, and with our hedonistic society we live in now, along with low ability to delay gratification, as well as other factors I have covered in my previous nutrition articles, have led to the effects we see in America, and around the world today.
In conclusion, don’t listen to people who have no background in nutrition. They tell clearly wrong information, and those who aren’t privy to new information in the nutrition world, won’t know that they are being lied to and or manipulated into believing things based on shoddy evidence.
NotPoliticallyCorrect 
