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Misconceptions on Calories In and Calories Out
2550 words
(To those from “myproana.com”, DO NOT misconstrue what I wrote here. What I wrote here is perfectly understandable. I am NOT saying that “you have no metabolism”. My point is, low kcal dieting CAN and WILL destroy your metabolism. The literature is vast on this subject and it’s waiting for you to read it. Any further confusions, please comment and I will answer your questions.)
“Eat Less and move more!!! That’s how you lose weight!” What people who don’t understand about human metabolism and homeostasis is that when caloric reduction occurs, the body drops the metabolism to match the amount of kilocalories (kcal) it is receiving. Thus, weight will plateau and you will need to further decrease caloric consumption to lose more weight. In this article, I will go through what a calorie is, common misconceptions of Calories In and Calories Out, the reasons for metabolic slow down, the process of thermodynamics that people who don’t understand this research cry out whenever it’s said, and finally starvation experiments that prove metabolic slow down occurs during a decrease in caloric intake and how this metabolic slow down persists after the diet is over.
A kilocalorie is the heat required to raise 1 kilogram of water 1 degree celsius. This definition is used whenever people say ‘Calorie’.
Misconceptions on kcal in/kcal out
- One of the biggest misconceptions people have on Calories In/Calories out is that these variables are independent of each other. However, they are extremely dependent variables. When you decrease Calories In, your body decreases Calories Out. Basically, a 20 percent reduction in kcal will result in a 20 percent reduction in metabolism which the end result ends up being minimal weight loss.
- The next big assumption people have about Calories In and Calories Out is the assumption that the Basal Metabolic Rate (BMR) remains stable. Of course, measuring the caloric intake is simple. However, measuring caloric outtake is a much more complicated process. When ever the Total Daily Energy Expidenture (TDEE) is spoken of, that involves the BMR, thermic effect of food, nonexercise activity thermogenesis (the energy expidenture of all activities sans sports), excess post-exercise consumption (EPOC, a measurably increased rate of oxygen intake following increased oxygen depletion), as well as exercise. the TDEE can increase or decrease by as much as 50 percent depending on caloric intake as well as the aforementioned variables.
- The third misconception people have is that we have conscious control over what we eat. We decide to eat when we are hungry (obviously). But numerous hormonal factors dictate the decision on when to eat or when to stop. We stop eating when we are full, which is hormonally mediated. Like breathing, the regulation of body fat is under automatic control. Just like we don’t have to remind ourselves to breath or remind our heart to beat, we don’t need to remind ourselves to eat. Thus, since hormones control both Calories In and Calories Out, obesity is a hormonal, not caloric disorder.
- The fourth misconception is that fat stores are essentially unregulated. However, every single system in the body is regulated. Height increases come from growth hormones; blood sugar is regulated by insulin, glucagon, and numerous other hormones; sexual maturation is regulated by testosterone and estrogen (as well as the hormone leptin which I will return to later); body temperature is mediated by a thyroid-stimulating hormone, among numerous other biologic factors. Though, we are told that the production of fat cells is unregulated. This is false. The best researched hormone on the storage of fat cells that we know of is the hormone leptin which was discovered in 1994. So if hormones dictate fat gain, obesity is a hormonal, not caloric disorder.
- And the final misconception is that a calorie is a calorie. This implies that the only important variable on weight gain is caloric intake and thus all foods can be reduced to how much caloric energy they have. But a calorie of potatoes doesn’t have the same effect on the body as a calorie of olive oil. The potatoes will increase the blood glucose level, provoking a response from the pancreas, which olive oil will not. Olive oil is immediately transported to the liver and has no chance to induce an insulin response and so there is no increase in insulin or glucose.
All five of these assumptions have been proven false.
[9/21/16 edit:]
Calories in/out implies that during extended caloric restriction no matter the type of kcal (fat, CHO, protein, alcohol, except when alcohol is ingested your body puts fat storage on hold until all alcohol is metabolized from the body. You can see how wiith chronic drinkers as they are obese a lot of the time, with there being a strong link between alcoholism and obesity as there are nunmerous pathways related with each other that lead to excessive eating as well as dependance on alcohol and other drugs) ingested, as long as caloric restriction is continued that weight (fat) loss will be achieved. CICO adherents say that “a calorie is a calorie”, but what’s funny with that statement is that is violates the Second Law of Thermodynamics. Naturally, to CICO adherents since “a calorie is a calorie”, kcal would be restricted from fat since it’s the most calorie dense macro (alcohol coming in second at 7 kcal per gram). By doing this, CHO will be increased, as is recommended by all of the ‘experts’. “Increase CHO, fat leads to CD!!!” This isn’t true, that’s another reason for cutting fat, the supposed ‘increased risk of heart disease”. However, when this occurs, insulin is spiked and when insulin is spiked the body doesn’t use the fat stores for energy it uses the glucose from the carbs.
Putting this all together, let’s say someone’s TDEE is 2000 kcal per day (for a 14k kcal per week average) and they reduce it to 1200 kcal and go on a LFHC diet like is commonly recommended. Insulin remains high and therefore fat cannot be tapped into. This is due to the CICO mantra (which violates the 2nd LoT) “a calorie is a calorie” that leads people to believe that all calories are ‘equal’ in terms of hormonal responses in the body. Let’s take a piece of bread and a teaspoon of olive oil. When you eat the piece of bread, insulin is spiked in response to the glucose from the carbohydrate. When you drink the olive oil, it’s immediately absorbed by the liver eliciting no insulin spike. Clearly, with a long term LFHC diet, this will consistently occur and the body will be continuously using CHO for energy and not the fat stores as insulin is continuously spiked in the body. Insulin either tells the body to store fat or not burn it for energy. Eventually, over time, this leads to insulin resistance (however, insulin resistance may precede obesity and diabetes) and more metabolic problems amongst a myriad of other variables.
As kcal is reduced to 1200 per day, the body is forced to match its metabolism to what your intaking as it can’t get energy from anywhere else since “a calorie is a calorie”. This happens during any calorie restricted diet and is why diets are doomed to fail. This same thing happened with The Biggest Loser contestants. Notice how The First Law of Thermodynamics isn’t broken? It’s irrelevant.
See how the mantra “a calorie is a calorie” violates the Second law of thermodynamics and fails because the CICO model doesn’t take insulin into the equation, which is a causal factor with obesity?
[End edit]
The correlation between weight gain and caloric consumption has recently been discovered. Ladabaum, et al (2014) examined trends in obesity from 1988 to 2010. The trends they observed were: obesity, abdominal obesity, physical activity and caloric consumption in US adults. They discovered that the obesity rate increased at .37 percent per year while caloric intake remained virtually the same.
The Law of Thermodynamics
The first law of thermodynamics states that energy can not be created nor destroyed in an isolated system (this is important). People often invoke the LoT to support the Calories In and Calories Out model. Dr. Jules Hirsch says in this NYT article:
There is an inflexible law of physics – energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content – reduce obesity – one must reduce calories taken in, or increase output by increasing activity, or both. This is true whether the calories come from pumpkins or peanuts or pâtés de foie gras.
To quote MD Jason Fung, author of The Obesity Code:
But thermodynamics, a law of physics, has minimal relevance to human biology for the simple reason that the human body is not an isolated system. Energy is constantly entering and leaving. In fact, the very act we are most concerned about-eating-puts energy into the system. Food energy is also excreted from the system in the form of stool Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight gain were mentioned even a single time. (Fung, 2016: 33)
We assume with the model of the calorie-balancing scale that fat gain or fat loss is unregulated, however, no system in the body is unregulated like that. Hormones tightly regulate all bodily functions. Body fat is no exception. The body actually has numerous ways in which to control body fat. Distribution of energy is the problem with fat accumulation. Too much energy is diverted to fat creation as opposed to body-heat production. Most of this is under automatic control, except exercise (which even then, there is a genetic basis for motivated exercise). We can’t decide whether or not to allocate calories to nail production or increase stroke volume. These metabolic processes are almost impossible to measure, and thus most assume that it’s relatively constant. Particularly, Calories In is not assumed to change in response to Calories Out. We assume these are independent variables. Reducing calories in only works if calories out remains constant. However what we find is that a sudden reduction of Calories In leads to a similar reduction of Calories Out and no weight is lost as the body balances its energy budget.
Starvation experiments
In 1919, a landmark study was carried out by Francis Benedict. The volunteers in the study agreed to a semi-starvation diet ranging from 1400 to 2100 kcal, approximately 30 percent of the subject’s bodyweight. The question was whether or not decreased caloric intake lead to a decrease in metabolism. The results were shocking.
The subjects experienced a 30 percent reduction in metabolism, with their initial caloric expidenture being 3000 kcal dropping to 1950 kcal. A 30 percent reduction in kcal resulted in a 30 percent decrease in metabolism. The First Law of Thermodynamics is not broken.
Towards the end of WWII, Dr. Ancel Keys wanted to improve understanding of starvation and better help Europe after the War. With an average height of 5 feet 10 inches and an average weight of 153 pounds, these were normal men, which Dr. Keys wanted to see the effects of a semi-starvation diet on those with a normal weight. For the first three months of the study, they were given slightly over 3000 kcal. Though over the next six months, they were given 1570 kcal. Eventually, some men were decreased to less than 1000 kcal a day. They were given a diet of foods high in carbs and low to no animal meat as that was the condition in Europe at the time. Moreover, they also had to walk 22 miles a week as exercise. Again, the results were shocking.
Dr. Keys showed that they had a 40 percent decrease in metabolic rate. The body decreased its metabolism to match the amount of calories consumed. They showed a 20 percent decrease in strength, a significant decrease in heart rate (55 to 35 beats per minute), stroke volume decreased by 20 percent, body temperature dropped to 95.8 degrees Fahrenheit (which makes sense since less caloric consumption means less energy for the body to convert into heat), physical endurance dropped by half, blood pressure dropped, they became tired and dizzy and finally their hair and nails grew extremely brittle. They couldn’t stop thinking about food. Some of them wrote cookbooks, others dreamed about food. They became obsessed with eating. All of these causes go directly back to decreased caloric consumption as the amount of heat produced by the body decreased due to an increase in caloric consumption. In sum, the body responds to a decrease in caloric intake by dropping metabolism.
Metabolic slow down
Recent data has come out on decreased energy expidenture due to dieting from contestants on the show The Biggest Loser. The contestants were followed for six years after the show ended. Fothergill, et al (2016) showed that after six years, most contestants gained back the original weight they lost, but their metabolism was still decreased by 600 kcal.
The mean metabolic adaptation had increased to 500 kcal per day, which explains why RMR remained 700 kcal per day below the baseline level despite a 90 lb body weight regain. The researchers even said that this large metabolic difference couldn’t be explained by the different calirometer used at the end of the six year period.
Substantial weight loss induces biological changes that promote weight gain.
Moreover, after a period of dieting, your brain panics and thinks it’s starving. During this time, the the production of the hunger hormone ghrelin increases. Levels of this hormone increase right before a meal and steadily decrease after. This is one of the many hormones that control when we’re hungry and this is one of the many reasons why diets fail and do not work long term.
Our bodies have homeostatic mechanisms that cause us to gain back or lose weight whenever caloric consumption is increased or decreased. The main cause is the body weight set-point which I will cover in a future article.
And a quote from Sandra Aamodt’s book “Why Diets Make Us Fat“:
“Leibel finds that metabolic suppression persists in dieters who have kept weight off for one to six years, so he scoffs at claims that the successful weight loss story disproves his ideas. “If you talk to people who’ve done it – not the studies, but people who actually manage to lose weight and keep it off – they’ll tell you what I’m telling you,” he says: that the only way to achieve this goal was to allow themselves to be hungry all the time while increasing their physical activity substantially. Indeed, his point is supported by data on the eating and exercise habits of people listed in the National Weight Control Registry, who have lost at least thirty pounds and kept it off for one year. A calorie calculator says that Dennis Asbury should have needed 2,100 calories to maintain his weight at 150 pounds, but instead he found that he needed to eat 400 to 500 calories less than that. Such metabolic suppression is the difference between being within the defended range and being below it. Many people blame others for eating too much or exercising too little, assuming incorrectly that both are under voluntary control, but it’s much harder to justify holding people responsible for diet-induced changes in the way the body burns energy.” (Aamodt, 2016, pg. 68)
Conclusion
The fact of the matter is, kcal in and out is completely misunderstood due to a non-understanding of human metabolism. As we decrease our caloric intake, our body adjusts its metabolism down to match the amount of kcal we are currently consuming. This is why Calories In and Calories Out does not tell the whole story. Our body constantly fights to maintain what is normal, its set-point. When thrown out of what the brain considers ‘normal’ the brain through the hypothalamus does whatever it can to get us back to its set-point. Thus, obesity is a hormonal, not a caloric disorder.
Nordicist Fantasies: The Myth of the Blonde-Haired, Blue-Eyed Aryans and the Origins of the Indo-Europeans
750 words
Nordicists say that the Aryans, the Indo-Europeans, had blonde hair and blue eyes. Though, recent genetic evidence shows that the origin of the Indo-European language is from the Russian steppe, originating from the Yamnaya people. The originators of the Indo-European languages weren’t blonde-haired and blue-eyed, but dark-haired and dark-eyed. Better known as the ‘Kurgan Hypothesis’, this is now the leading theory for the origin of Indo-European people.
Haak et al (2016) showed that at the beginning of the Neolithic period in Europe (approximately 7 to 8 kya) that a closely related group of farmers appeared in Germany, Hungary, and Spain. These ancient populations were different from the indigenous peoples from the Russian steppe, the Yamnaya, who showed high affinity with a 24000-year-old Siberian sample. Approximately 5 to 6 kya, farmers throughout Europe had more hunter-gatherer ancestry than their predecessors from the early Neolithic, but the Yamnaya from the Russian steppe were descended from the Eastern European hunter-gatherers, but also from a population with Near East ancestry (Ancient North Eurasians, ANE). Further, the migration of haplotypes R1b and R1a traveled into Europe 5000 years ago.
The Late Neolithic Corded Ware culture from Germany trace approximately 75 percent of their ancestry to the Yamnaya, which confirms a massive migration from Eastern Europe to the heartland of the continent 4500 years ago. This ancestry from the Yamnaya persisted in all of the Europeans sampled up until approximately 3000 years ago, and is common in all modern-day Europeans. The researchers then conclude that this provides evidence for a steppe origin for some of the Indo-European languages from Europe.
As mentioned above, Haber et al (2016) show how, as I alluded to above, that the Yamnaya people share distant ancestry with the Siberians, which is probably the source of one of the three ancient populations that contributed to the modern-day European gene pool (Ancient North Eurasians, West European hunter-gatherers, and Early European farmers from Western Asia with the fourth population being the Yamnaya people).
Olade et al (2015) show that since the Basque people speak a pre-Indo-European language that this indicates that the expansion of Indo-European languages is unlikely to have begun during the early Neolithic (7 to 8 kya). They, like Haak et al, conclude that it’s in agreement with the hypothesis of the Indo-European languages coming out of the East, the Russian steppe, around 4500 years ago which is associated with the spread of Indo-European languages into Western Europe.
Finally, it is known that the Yamnaya people had dark skin (relative to today’s Europeans), dark hair, and dark eyes. Knowing what is presented in this article, this directly goes against the Nordicist fantasy of the blue-eyed, blonde-haired Indo-Europeans. Nordicists also like to claim that the Indo-Europeans had blonde hair and blue eyes, when genetic evidence goes directly against this claim:
For rs12913832, a major determinant of blue versus brown eyes in humans, our results indicate the presence of blue eyes already in Mesolithic hunter-gatherers as previously described. We find it at intermediate frequency in Bronze Age Europeans, but it is notably absent from the Pontic-Caspian steppe populations, suggesting a high prevalence of brown eyes in these individuals.
Further, the Yamnaya were a tall population. Since the Yamnaya had a greater genotypic height, it stands to reason that Northern European populations have more Yamnaya ancestry.
The Yamnaya herded cattle and other animals, buried their dead in mounds called kurgans, and may have created some of the world’s first wheeled vehicles. They were a nomadic population that, some linguists say, had a word for wheel. The massive migration into Western Europe from the Russian steppe contributed large amounts of North Asian ancestry in today’s Europeans. The Yamnaya are also shown to be the fourth ancient population that is responsible for modern-day Europeans.
Modern-day genetic testing is shattering all of these myths that are told about the origins of Europeans and Proto-Indo-European peoples and languages. The ACTUAL basis for most PIE languages is from the Russian steppe, from a relatively (to modern Europe) dark-skinned, dark-haired, and dark-eyed people who then spread into Europe 4500 years ago.
The Nordicist fantasies of the Aryans, the originators of Proto-Indo-European languages has been put to rest. It was originally proposed based off of myths and stories, mostly from ancient Indo-European cultures who were situated thousands of miles away from the original Indo-Europeans (the Yamnaya).
The Kurgan Hypothesis is now the theory that’s largely accepted by the scientific community as being the homeland of the Proto-Indo-Europeans. The Yamnaya people now make a fourth founding population for Europeans, with the other three being West European hunter-gatherers, Ancient North Eurasians, and Early European Farmers.
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.
Obesity and Intelligence
1600 words
[Edit: My view here has changed, read my recent article Is Diet an IQ Test? It isn’t and it is, of course, much more nuanced than ‘IQ’ (which is a proxy for social class’ leading to obesity which would imply lack of funds and education on what and when to eat. Obesity is much more complex than ‘IQ’, numerous other variables come into play and since ‘IQ’ (which is just a proxy for general knowledge ‘is low then the individual in question won’t know what and when to eat and since this occurs in low income families more often than not who have low IQs then this effects them the most.]
The relationship between intelligence and obesity is often misinterpreted. Numerous studies have concluded that becoming obese leads to a drop in IQ. This mistake happens due to improper interpretation of cross-sectional studies. However, analyses of population-based, longitudinal data show that low intelligence from birth causes obesity. No credible evidence exists for obesity lowering intelligence. There are, however, mountains of evidence showing that low intelligence from childhood leads to obesity (Kanazawa, 2014).
Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ. Those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs to learn how to manage their weight. Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).
Less intelligent individuals are more likely to become obese than those who are more intelligent. With what we know about low IQ people and how there is a strong relationship between low intelligence and lack of ability to delay gratification, we can see how this lack of thought for future problems for their actions in the present can manifest itself in obesity.
This study claims that there is a link between morbid obesity and a drop in IQ. The researchers compared 24 children who weighed 150 percent of their bodyweight before age 4 with 19 children and adults with Prader Willi’s Syndrome, using 24 siblings as controls as “they share the same socioeconomic environment and genetics”. Prader Willi’s Syndrome (PWS) is a chromosomal disorder in which chromosome 15 is deleted. They have an almost insatiable desire to eat,which can cause one suffering from PWS to eat themselves to death. Those with PWS were found to have an IQ of 63, while those who became obese were found to have an IQ of 78 with the control siblings having an IQ of 106. The researchers were surprised to see such a difference in IQ between siblings. They then state that this could be one facet of obesity that could be irreversible. MRI scans of the cohort discovered white matter lesions on the subjects with PWS and early-onset obesity. The researcher says that these lesions could affect food seeking centers in the brain leading to a want to gorge on food. Seeing how those with PWS eat when unsupervised, this is an interesting hypothesis.
This study compared 49 teens with metabolic syndrome and 62 peers without the disorder, while controlling for socioeconomics status. They found significantly lower scores in arithmetic, attention and attention span, spelling, mental flexibility and regions of the brain with lower volumes of matter in the hippocampus and white matter integrity.
There are a few problems with these two studies. In a population-representative birth cohort study of 1037 children, it was found that cohort members who became obese had a low IQ, as expected. But, contrary to what your study said, cohort members didn’t exhibit a decline in IQ from becoming obese, they instead had a lower IQ since childhood. There is no evidence of obesity contributing to a decline in IQ, even in obese individuals and those on the verge of metabolic syndrome. Another problem is that they wrongly conclude that obesity leads to lowered intelligence, completely misinterpreting the extremely strong negative correlation between obesity and intelligence.
This study shows how obese mothers give birth to less intelligent children. In an observational study (already garbage), the researchers took 3412 participants and found a strong relationship with pre-pregnancy obesity and math and reading scores in children. For math, a 3 percent reduction was observed. There was a 3-point drop in reading scores with math scores showing a decline of 2 points. These differences are within the normal variation between tests, so it’s nothing to take note of. Also, this is an observational study. I have shown above that longitudinal studies are superior for this, as well as researchers misinterpreting the results found from their studies.
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.
Blacks Are Less Violent Than Whites?
1850 words
I’ve read a lot of crazy things in my life, though this must be the craziest. Someone really believes that “blacks are less violent than whites“. To believe such a claim, you would have to close your eyes to all of the relevant data. From naming outright falsities to obscuring data to fit his narritive, this article will show and refute a distorted reality, one that the Left wishes to show, to one simply looking for the truth to interracial crime.
Don’t be modest, Caucasians. The Holocaust
The Holocaust is really beyond the scope of this blog, but check out the CODOH Library for the truth on this matter.
This is not unique to Europeans. The Rwandan Genocide (which was due to ethnocentrism) and the ethnic cleansing currently occurring in Central Africa aren’t real? Fact of the matter is, is that every ethnicity has participated in ‘ethnic cleansing’, which is really just protecting genetic interests. This is a non-factor as this has gone on before European colonialism.
Colonialism was good for the native inhabitants of Africa. Speaking of the Caribbean, how well did it end for the Haitians after they defeated Napolean?
Oh? You mean how a majority of the slaveholders were Sephardic Jews? Or how there are reports from New Orleans from their 1860 census that showed 3000 freed blacks owned slaves, accounting for 28 percent of the city’s population? In 1860 Louisiana, at least 6 blacks owned more than 65 slaves, with the biggest number of slaves being 165 slaves who worked on a sugar plantation. How about the Jews’ role in American slavery? Moreover, at the height of slavery, a paltry 6 percent of Southern whites owned slaves, when combined with the North it was 1.4 percent. An estimated 3000 blacks had about 20000 slaves in 1860. But tall is only about the whites who did slavery, and not about the Arabs and how they started enslaving Africans FIRST, in 650 AD.
The Alternative Hypothesis just had a post the other day about the non-genocide of American Indians. Basically, their population was anywhere between 1.5 and 2 million people. Population reduction for the Native Americans was only 0.22 percent!! Doesn’t seem like such a ‘genocide’ to me. If so, that’s the slowest genocide I’ve ever heard of.
People segregate naturally. We’re more segregated now than we were 50 years ago! Must be those residual effects from Jim Crow huh?
But somehow in the media it’s the black man who is portrayed as the savage.
It’s just not fair. We white folks are so much better at race-based aggression than our darker complected brothers.
More intelligent than them, that’s why.
Just this Wednesday a white guy walked into a historic African American Church in South Carolina, was accepted as part of the service, stayed for about an hour before shouting a spiteful message and gunning down several parishioners!
Now that’s some hate right there!
One person does something and that means….what exactly? It shows one person is hateful! Look at averages, not singular events.
Whenever anyone brings up race and violence, the first thing people mention is crime.
Because they are linked to each other. Why wouldn’t the two things be mentioned in the same breath?
There is more black-on-black crime than white-on-black crime, they say. And they’re correct!
According to a 2013 FBI Uniform Crime Report, when it comes to murder, 90 percent of black victims were killed by black offenders.
However, what people fail to mention is that according to the very same report, 83 percent of white victims were killed by white offenders, too.
These numbers don’t show black people are more violent than white people. They show that BOTH white and black people would rather kill within their own race.
Yea they show that both would rather kill within race, however you miss something very important here: Interracial crime!
First, we find that during the 2012/2013 period, blacks committed an average of 560,600 violent crimes against whites, whereas whites committed only 99,403 such crimes against blacks. This means blacks were the attackers in 84.9 percent of the violent crimes involving blacks and whites. This figure is consistent with reports from 2008, the last year DOJ released similar statistics. Perhaps not coincidentally, that was the year Mr. Obama was elected president.
In terms of raw numbers, black people and white people actually commit about the same number of murders. But you wouldn’t know that from the media.
Not really. Per capita rates are more important than raw numbers, luckily we have data on that!
As of 2008, young black men kill at a rate of 7 times higher than white men.
Homicide Trends in the United States, 1980-2008 Annual Rates for 2009 and 2010 pg 11
Is that the same number of murders?? I’m looking at the same stat in a completely different way than you are.
The FBI is charged under the Hate Crime Statistics Act with compiling statistics on spite-based legal transgressions. In its most recent report, for 2013, hate crimes based on race are far more numerous than any other kind.
- The FBI is biased towards blacks and ‘hate crimes’. How about all of the countless times we here about blacks attacking whites using racial epithets during the attack? Too many to count. They are, however, not counted as hate crimes by the FBI because it doesn’t fit their narritive.
- I wonder how those numbers would look if actual hate crimes were included in this data (black on white included).
According to the FBI statistics, 54.5 percent of the reported single-bias hate crimes that were racially motivated in 2013 targeted blacks. Only 16.3% target whites.
Want to talk bias? The amount of black on white hate crimes that are NOT categorized as such. This skews the statistics considerably.
Would our economy really have been so robust without the free labor of all those slaves?
Yes. Whites could have done it, but getting blacks to do it was cheaper and more efficient. Using brains to get ahead is what life is all about. Whites build great societies anywhere. Our economy would have been as robust as it is now without America never having a history of slavery.
Heck! Would we even have a country at all if we hadn’t murdered all those indigenous peoples in the first place?
Is a population decline of 0.22 percent per year ‘murdering all those indigenous peoples’?
So let’s put it to rest. When it comes to hate crimes, white folks kill! But don’t feel too bad, black folks. There are things you’re good at, too. Like nonviolent resistance.
This guy is delusional. Just because MLK preached non-violence doesn’t mean that blacks as a whole are non-violent. Look at crime stats from anywhere in the world.
After all this time, black people have very rarely used violence as a means to achieve their ends, to try to secure the rights and freedoms white America guards so jealously.
Is this guy living in the same America as I am?
In just the past year or so, unarmed black folks have been assaulted or killed for holding toy guns
Go ahead and pick out the real one, then do it from a distance when you get a phone call that there is a kid walking around while waving a gun.
He died due to asthma, obesity, and heart disease, that’s why he couldn’t breathe; he was 350 pounds. He also did not comply with the officers’ orders, which is why he needed to be taken down in such a fashion.
listening to music at a gas station
Dunn did say that Davis said he was going to kill him with a shotgun and that’s when he grabbed his gun out of his glove box.
asking for help after a car accident
Freak accidents happen that get blown up? Damn, that proves whites are more violent huh!?!?
Yea, people still believe that Trayvon got killed for ‘wearing a hoody’. We have jurys for a reason. We have trials for a reason. We have laws like Stand Your Ground for a reason. Trayvon was killed because if Zimmerman hadn’t of protected his life, he would be dead. All of these people complaining about the verdict, if you were put into that same situation, would you allow yourself to be killed for fear of being called ‘racist’?
Listen to police when they tell you to do something. Especially during an investigation. This shouldn’t even need to be said.
1) The Baltimore Six are going to get off for it. They caused no harm. 2) He threw himself around in the back of the van causing his own death.
and now just going to church!
Right. They were killed just for going to Church. eyeroll
And the response from the black community has been pretty darn nonviolent. Yeah there’s been some shouting and looting, but very little beating or killing.
‘Pretty darn non-violent. Which is why immediately after, blacks began false flagging Church burnings in an attempt to pin them on whites. So ‘peaceful’, right?
White folks, can you imagine having to undergo such indignity on a daily basis and NOT responding in kind!?
Can’t tell if serious. Just recently, a beta Trump supporter was thrown down on the ground by a ‘young black male’ and did not retaliate.
No wonder a blonde white girl from a Christian fundamentalist home darkened her skin, curled her hair and tried to pass as black! Sometimes – often really – it’s darn embarrassing to be white! Black folks have the moral high ground.
Because Dolezal is a moron. Blacks have the moral high ground? Please show me where this occurs.
Somehow they live in an American society that heaps hatred on their every move and they respond with dignity and perseverance.
There’s no reason at all for this right? Just good old fashioned ‘racism’?
So why are black people so nonviolent?
They aren’t. See the whole of sub-Saharan Africa to see how ‘non-violent’ they are.
Damned if I know! But I wish us white folks would take a lesson from them.
Yes!! The white man has tons to learn from the criminal black man! Much to learn about taking welfare and not working!!
Blacks have 2.5 to 4.9 percent higher testosterone than whites, which is causes more violence and crime. Beaver (2014) states that blacks who have the MAOA-L 2 repeat allele have significantly highier chances of being shot, stabbed or reporting shootings and stabbings than other genotypes. Blacks also have the highest rate of the 3 repeat allele (53 percent compared to 37 percent for whites) and 2 repeat allele (5 percent compared to .1 percent for whites). Moreover, he didn’t speak about how black violent crime is genetic in nature. This is mirrored in the crime rate and how violent blacks really are.
This is the age of the Internet where we have amassed tons of human knowledge which is readily available with a few hits of a few buttons. If people still want to be ignorant spewing falsities, it’s on them. But the truth is out there for those who seek it.
Blacks are not ‘non-violent’. Go to the nearest ghetto and see how ‘non-violent’ blacks are.
Transvestic Disorder and Gender Dysphoria Identification and Prevention
2150 words
Abstract
Transvestic Disorder comes about in early childhood and manifests itself in sexually deviant actions. Men suffering from TD who aren’t homosexual, more likely than not, show attraction to themselves dressed in women’s clothing. The signs of TD are noticed at an early age when the individual begins to cross dress. TD is also correlated highly with numerous sexually deviant actions. Fluoxetine and serotonin reuptake blockers may be able to lessen TD since it is an impulsive disorder. With TD being co-morbid with OCD, by treating OCD we can better treat TD itself and give a better quality of life to the patient suffering from the disease. Since autogynephilia and transgenderism are related, measures taken to alleviate TD and autogynephilia could be taken to alleviate symptoms of gender dysphoria, since autogynephilia leads to transgenderism.
Transvestic Disorder and Gender Dysphoria Identification and Prevention
Transvestic disorder is a paraphilic disorder, classified by the American Psychological Association (2013), in which males dress up as women to gain sexual gratification. The individual suffering from TD suffers from compulsions to want to dress as a woman, which causes distress due to the individual not wanting their secret to come out. This then leads to the quality of life of the individual to decrease due to constantly being worried about his secret coming out. TD is diagnosed when a male has sexual feelings and gets sexual arousal from dressing in women’s clothing. It is only diagnosed when these activities are ongoing for at least six months. TD is also similar to another paraphilic disorder called ‘autogynephilia’ (Lawrence, 2011), in which the subject is aroused at the thought of himself being a female, so he, therefore, then begins to dress as a woman to fulfill his sexual desires. Blanchard (1989) proposed that most gender-dysphoric males who do not show sexual arousal to men, instead show sexual arousal to themselves dressed in the opposite sex’s clothing. He concludes that the hypothesis is supported that major types of those men who cross-dress are nonhomosexual, and do so because they become aroused at the thought of dressing as a woman. The DSM V says that autogynephilia is a specifier to transvestic disorder. This is because they are characterized by the same things (American Psychological Association, 2013).
The signs of TD are noticed at very early ages. Most notable are when children begin to cross-dress at or before puberty. This then continues into their adult lives where it begins to be a problem and cause dysfunction due to needing to keep their secret. Dr. Mark Griffiths (2012) states that all though children may engage in transvestic behavior, what differentiates it between an adult suffering from TD is that the child who cross-dresses does so for excitement and pleasure, not for sexual pleasure. Though some researchers say that the disorder is brought on through childhood trauma, i.e., accidental exposure to women’s clothing or exposure to a woman who is undressing. Numerous studies have also concluded that many men who suffer from TD have had to deal with parental separation during childhood.
The American Psychological Association (2013), reports that fewer than 3 percent of males are characterized as having transvestic disorder. TD is most always seen in males, though Moser (2009) noted that in his study using the Autogynephilia Scale for Women (ASW), that out of the 29 respondents that sent back questionnaires, 90 percent would be classified as having autogynephilia. Though, by using a more meticulous definition, only 28 percent were seen to be autogynephilic (Moser, 2009).
Langstrom and Zucker (2005) observed in a sample of 2,450 18 to 60-year-olds in Sweden that transvestic disorder was correlated significantly with being separated from their parents, homosexual relations, higher masturbatory frequency, being easily aroused sexually and pornography use. Also noticed, was a positive attitude in regards to sexual arousal from pain, exposing oneself to a stranger and voyeurism were all positively correlated with TD. Langstrom and Zucker observed how TD is co-morbid with many other paraphilic disorders as well as other deviant behavior. By attempting to treat what TD is correlated with, symptoms of TD can be lessened.
Men suffering from TD and autogynephilia are told that women are the standard of beauty. They then look at themselves in the mirror and see a male and not the standard of beauty they were told of growing up. They then turn to cross-dressing to finally see their “beauty standard” in the mirror but keep it a secret. This strong want to keep their disorder a secret then leads to dysfunction. Men suffering from TD will go to any lengths to hide their secret. This then causes extreme dysfunction in their lives, which leads to a lessened quality of life.
Less than three percent of males suffer from TD in the American population, as such, it is classified as a deviant lifestyle as it deviates from the norm of the population. It causes distress due to them not wanting their secret to be discovered. This, in turn, leads to dysfunction where the individual cannot live their daily lives to the fullest due to their abnormal disorder. It finally leads to danger due to their secret beginning to consume their lives so that they’re not discovered.
There are ways to treat TD. Usmani et al (2012) follow a case study in which a 17-year-old Indian male who had occurring desires to wear his mother’s clothes. He then would masturbate in his mother’s clothes to alleviate himself. This continued on for two years so he could pleasure himself. He was caught by his parents wearing his mother’s clothes and was beaten by them for it. He then said that it is a compulsive behavior and cannot be helped. This case also shows the obsessive compulsive side to TD. They have an urge so strong they cannot help but to do it compulsively to alleviate their sexual desires. He also said that the occurring thoughts then affected his schoolwork as he was so preoccupied with the thought of wearing women’s clothes. All of his brain scans were found to be normal, so what brought on this case in the individual in the case study? He was then diagnosed with TD and prescribed fluoxetine, an antidepressant SSRI. The dose was started at 20 mg and increased by 40 mg once a day for two weeks. In his six-month follow-up, he reported lessened desire to masturbate with women’s clothes (Usmani et al, 2012).
Paraphilias and other related disorders have been thought of as sexual addictions. Though it has been argued that they are not sexual addictions, but are sexual compulsions (Stein et al, S 1992). The researchers reviewed 13 patients who showed signs of TD and were administered serotonin reuptake blockers. The symptoms of those individuals were then divided into paraphilias, non-paraphilic sexual addictions, and sexual addictions. Stein et al discovered that paraphilias had the least improvement with the reuptake blockers whereas sexual compulsions showed the best improvement. They end up concluding that paraphilias and other related disorders are on the impulsive end of the spectrum compared to the compulsive end. These impulsions, then, have those men suffering from TD have the urge to dress in women’s clothes to fulfill their sexual impulsion.
TD is co-morbid with obsessive compulsive disorder (Abdo, Hounie, de Tubino Scanavino, and Miguel, 2001). They used longitudinal case studies in which they assessed two individuals who had OCD as well as TD. They conclude that some cases of TD may be OCD related and not always be caused by gender dysphoria. Since OCD and TD are co-morbid, by treating symptoms of OCD, the want to cross-dress will lessen, which will then lessen the symptoms of TD. Treatments could include SSRI and fluoxetine, as previously stated in the paper. Other treatment for TD should be looked at, such as treatment for OCD due to the co-morbidity between the two. By doing so, feelings of wanting to cross-dress may lessen due to one of the underlying causes (OCD) of TD being treated.
Autogynephlia could also explain transgenderism.Transvestism can be called both a paraphila and a sexual orientation. Lawrence (2004) says that it can explain mid-life MtF transitions, progression from transvestism to transgenderism, the prevalence of other paraphilias among MtF transsexuals and the late development of male intrest in MtF transsexuals. However, when Lawrence says that “Hormone therapy and sex reassignment surgery can be effective treatments in autogynephilic transsexualism”, that is incorrect. The prevalence of suicide attempts among transgenders is 41 percent according to the Williams Institute, UCLA School of Law, in comparison to 4.6 percent for the average population. That’s almost ten times higher than the national average. Clearly, surgery doesn’t do anything to alleviate the feelings of gender dysphoria, and as shown in this paper, therapy and drugs like Prozac can better help to alleviate feelings of gender dysphora in transsexuals due to them being extremely similar to eachother. These two disorders greatly mirror each other. Since Lawrence (2004) observed that there is a progression from transvestism to transgenderism, using similar techniques that work on those with TD may also work on those with gender dysphoria.
Discussion
TD can be helped with the correct therapy as well as right medication. With those, impulsions to wear women’s clothes, as well as impulsions to commit abnormal acts will be greatly lessened and quality of life will be restored to a somewhat normal level. Due to co-morbidity between TD and OCD, treating OCD will, in turn, better help the patient suffering from TD. When more studies are carried out on those suffering from TD, we can see whether or not SSRI drugs and fluoxetine will have the desired effect in alleviation of the symptoms of TD. The individual in the Usmani study reported lessened symptoms and impulsions of cross-dressing, so by identifying which parts of the brain are and were activated during the fluoxetine therapy, we can then better give better care and treatment to those suffering from TD. We can also use some data from TD cases for transgenders, as TD and transgenders have a lot of things in common. With therapy as well as, maybe even fluoxetine (which is just Prozac), and high doses of testosterone/estrogen, this could possibly help to alleviate ‘gender dysphoria’. It could also lower the suicide rate as it’s completely possible that these interventions could fix them mentally.
Conclusion
There is little current literature in treating TD, due to it being a shameful disorder and many men not speaking about what they suffer from. One major way in which to help those with TD is to administer SSRI drugs, in which compulsion to cross-dress, and other attitudes associated with TD lessened. Blanchard (1989) proposed the autogynephilia theory for those transgenders who are not attracted to men. With the obseration by Lawrence (2004) on how autogynephilia and transgenderism are related, this can better help those with transgenderism, as they can get correct help and the right hormones they need, instead of the opposite hormones. SSRI therapy is a good candidate in treating TD, as drastic changes in deviant behavior are seen while the patient is taking the SSRI drug. Seeing as most cases of TD begin in childhood before puberty, by better identifying warning signs of these disorder, we can better treat those children who are at risk of developing these disorders before they become a big problem later in life. As more men come out and say that they suffer from these disorders, more studies can be carried out that corroborate the findings in the studies laid out here. It is extremely promising that these disorders can be treated with common drugs already on the market. In those individuals suffering from TD as well as OCD, by treating the OCD first (which may be an underlying cause) the symptoms of TD may be lessened and the individual may eventually have the ability to lead a life without TD. In using these measures on those with transgenderism, this could possibly alleviate suicide rates and other negative variables associated with these paraphilic disorders and sexual orientations.
References
Abdo, C.H.N., Hounie, A., de Tubino Scanavino, M., & Miguel, E.C. (2001). OCD and transvestism: Is there a relationship?. ACTA Psychiatrica Scandinavica, 103(6
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.
Blanchard, R. (1989). The Concept of Autogynephilia and the Typology of Male Gender Dysphoria. The Journal of Nervous and Mental Disease, 177(10), 616-623. doi:10.1097/00005053-198910000-00004
Griffiths, M. (2012, February 28) Dressed to thrill? A brief overview of transvestic fetishism. Retrieved from https://drmarkgriffiths.wordpress.com/2012/02/28/dressed-to-thrill-a-brief-overview-of-transvestic-fetishism/
Lawrence AA . Autogynephilia: An Underappreciated Paraphilia . In: Balon R, Hrsg . Sexual Dysfunction: Beyond the Brain-Body Connection. Adv Psychosom Med 2011 ; 135 – 148
Långström, N., & Zucker, K. J. (2005). Transvestic fetishism in the general population: Prevalence and correlates. Journal of Sex and Marital Therapy, 31, 87–95
Moser, C. (2009). Autogynephilia in Women. Journal of Homosexuality, 56(5), 539-547. doi:10.1080/00918360903005212
Stein DJ, Hollander E, Anthony DT, Schneier FR, Fallon BA, Liebowitz MR, Klein DF: Serotonergic medications for sexual obsessions, sexual addictions, and paraphilias. J Clin Psychiatry 1992; 53:267–271
Usmani et al, (2012) Treatment of Transvestic Fetishism With Fluoxetine: A Case Report. Iran J Psychiatry Behav Sci. 2012 Autumn-Winter; 6(2): 100–101
Polar Bears, Inuits, Evolution and Fst
1150 words
The Daily Stormer published an article today that claimed that “Polar bears are miscegenating with grizzly bears“. When polar bears and grizzly bears mate, they produce a “pizzly bear“. Due to this, the polar bear population is shrinking and the grizzly bear population is growing.
Scientists say this doesn’t look good for the polar bears; though these hybridizations are not due to ‘climate change’, as is suggested. Using a computer model, the researchers generated a prediction of the Earth’s climate from 2071 to 2100. The model analyzed how different species of birds, mammals and amphibians would need to migrate to find new territory. Birds had the highest overlap with 11.6 percent, attributed to their range from flying. Mammals and amphibians were 4.4 and 3.6 percent likely to encounter a hybridization event. Overall, about 6.4 percent of all species are expected to come into contact to even have the chance to hybridize with other compatible species. Meaning, the polar bear is not in danger of ‘dying out’ due to ‘miscegenation’.
What is missed in the article mentioned at the beginning is that polar bears and grizzly bears are even able to produce offspring at all. This is due to the two splitting around 350 kya to 6 million years ago. This article then says something vaguely familiar:
After beginning to branch off from brown bears, the polar bear’s ancestors under went a series of evolutionary changes in order to survive in the Arctic. The bears adapted to a life of hunting seals and surviving extreme cold. One of the most remarkable adaptations was the ability to thrive on a fat-rich diet withoutapparent heart damage. (sounds like the Inuit or other Eskimo tribes; emphasis theirs)
‘The bears’ could be switched to ‘the Eskimoes’ or ‘The Inuit’and make complete sense. The Inuit also live off a high-fat diet. The higher n-3 gives immunity and boosts in health to a slew of diseases as well.
The Inuit and their ancestors evolved special genetic mutations that allowed them to partly counteract the effect of a diet high in fat. Nearly 100 percent of the Inuit have these genes, while 2 percent of Europeans and 15 percent of Han Chinese do, which means that they synthesize n-3 differently than the Inuit. Over time eating a diet high in fats, the Inuit evolved these genetic adaptions to better adapt to their environment. The genes they have also lower LDL (bad) cholesterol and fasted insulin levels, which presumably has an effect on cardiovascular disease and diabetes. This used to be the case, but “exposure to a more Western lifestyle” has made Diabetes Mellitus in the Inuits comparable to that of the general population. Since growth is reliant on a person’s whole fatty acid profile, the Inuits are, as a result of these mutations, 1 inch shorter than they should be. The same mutations causing shorter height in the Inuit have also been found in Europeans. Researchers have found many genes responsible for height, but this was “one of the strongest effects ever found by geneticists”.
These genetic mutations are around 20,000 years old and originate with their Siberian ancestors. They think that the adaptation came about in the last Ice Age, but the selection is far stronger in the Inuit, due to them being one of the furthest populations away from the equator.The researchers have also found that the Inuits have another common mutation in their population that is involved in the differentiation of brown, subcutaneous fat cells and brite fat cells. Brite fat cells burn fat for more heat, showing another adaptation they had from their diet and direct environment. This helped them survive the harsh climate.
A strict Inuit diet shows evolution in action, that populations forced to subsist mostly on one type of food/macronutrient can and will adapt to their environment over time, proving that evolution exists. However, you cannot infer from the Inuits that the effect they gain from this diet will carry over to the general population.
The Science Daily article then goes on to say people have asked themselves whether they “Should be on a Stone Age diet”. My answer to that is a resounding “No” if you think the diet will do anything different from any other diet and weight training. As stated in the SD article, you cannot say that other populations, for instance, evolved to eat a certain way cannot be made as the Inuit have certain genetic mutations that no other populations have, in the frequency they do, for that matter.
The DS article, more interestingly, doesn’t bring up how two different species are interbreeding. Humans have a Fst distance of less than .5. The Fst for polar and grizzly bears is 0.2688. Two differing populations separated anywhere between 350 kya to 6 million years ago, can interbreed, and so can humans. Sewall Wright, the creator of the Fst concept, has said that if this differentiation was noticed in any other species, that they would be noted as distinct subgroups. When it comes to human genetics and science, science chooses to take the “egalitarian route” and deny the existence of race. However, when it comes to polar and grizzly bears, talking about how polar bears are a subspecies of grizzly bears and the polar bears adapted to the cold leading to physical and physiological differences, this is fine. Just like when Rushton proposed Differential-K Theory, which is the application of r/K selection theory to humans, it got shot down, despite E.O. Wilson who co-founded r/K selection theory stating “I think Phil is an honest and capable researcher. The basic reasoning by Rushton is solid evolutionary reasoning; that is, it is logically sound. If he had seen some apparent geographic variation for a non-human species – a species of sparrow or sparrow hawk, for example – no one would have batted an eye. … when it comes to [human] racial differences, especially in the inflamed situation in this country, special safeguards and conventions need to be developed.” Rushton’s main thesis has also never been refuted. No other explanation can fully explain the variables Rushton describes in Race, Evolution, and Behavior like r/K selction theory does.
Polar bears are not going away, and if they were, it’d just be evolution in action as the point of life is to breed and carry on your lineage (however, fitness is increased for the grizzly bear as he is gaining more habitat, yet decreasing for the polar bear due to a warming planet). The strongest populations get selected for, while the weakest become absorbed/wiped out. Since the planet is warming, as well as the grizzly bears looking for more environment some, not all, are mating with polar bears. This does not mean that polar bears will go extinct due to inbreeding with grizzly bears. Inuits are proof of the existence of evolution with how they adapted to their high-fat diet and cold environment, but you cannot use this information on their diet and say that the benefits from a high fat diet would be the same in other populations.
“Philosophers of Science” and Race/IQ
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“Philosophers of Science” attempt to stick their heads into the race/IQ debate to give their field more credence than it should get with the hard sciences. They use bad arguments like saying that “gene-environment interactions are widespread and hard to entangle” (Block, 1995), not knowing that identical twins reared apart grow up to be so similar (Rushton and Jensen, 2005, p. 279). The only time they should stick their heads in this debate is when they’re affirming that the methodology used to test IQ as well as racial differences in IQ are sound; otherwise, they do not have the training to assess this. Most “Philosophers of Science” defend claims that disintegrate when presented with the relevant scientific evidence (Sesarardic, 2000). I will be referencing this paper for the length of this article.
Half of the paper analyzes Lewontin’s argument to Jensen in which he uses his now famous “seed argument” in which he says you can take two seeds from the same heterogeneous population and plant them in rich and poor soil and “. . . as a result, the phenotypic differences within each of the two groups of plants will be 100 percent heritable, but the difference between the two groups will be entirely due to differences in two environments (zero heritability).” The fact of the matter is, this argument is parroted by “Philosophers of Science” when Jensen never made that argument.
Jensen then systemically dismantled every environmental argument with empirical evidence that they don’t hold up.
Other researchers then made accusations of “racism” the reason for Jensen’s overlooking of this. James Flynn, a big opponent of the hereditarian hypothesis and Rushton and Jensen in general, say that Jensen is not a “racist”. There is also something called the “X-Factor”, which is when phenotypic differences between two groups can be explained by an environmental factor that has no within-group variation at all, a 0 heritability. Racism, however, is a poor excuse for the “X-Factor”. Both Flynn and Jensen rule out discrimination as being the cause for the “X-Factor” as well.
Simply put, Jensen doesn’t make inferences that the black-white IQ gap is genetically based on one or a few variables on their own, but everything put together, that’s where the remaining evidence put. “Philosophers of Science” don’t understand heritability coefficients to be saying what they do; they wouldn’t be saying that if they knew how they worked.
Sesardic brings up how Block (1995) only mentions three pieces of empirical evidence: The “Flynn Effect”, “data about caste-like minorities”, and the small amount of genetic variation between races.
- The Flynn Effect happens uniformly in all populations at a rate of 3 points per decade but has slowed considerably. This increase began starting around 1880, coinciding with the industrial revolution. Better nutrition increased brain size in all populations, which lead to an increase in IQ. The Flynn Effect is not on g, so to make any claims that the differences in IQ between blacks and whites, or global differences in IQ for that matter, can be changed with more favoring towards environmentalist positions are not consistent with the scientific literature. In 1945, the average white IQ in America was 85, the same as the average American black IQ today. Since the differences in IQ have stayed consistent despite better nutrition in all groups, this proves that the gap is genetic in origin. 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. Since the Flynn Effect does not occur on g, it should be a non-factor.
- Minorities are only “caste-like” because differences in IQ are heritable, leading to racial disparities in social class differences. We can see when we match blacks, whites, and “Hispanics” for IQ (100), that some differences disappear, other differences decrease dramatically, and even blacks and “Hispanics” beat out whites in a couple of variables. Through multiple IQ tests averaged over time as well as seeing that test differences between races stay mostly the same, we can then make the inference, with all of the other evidence, that racial and ethnic differences in IQ are mostly genetic in origin with the environment having very little effect. To say that “racism” or “stereotype threat” has any bearing on these racial differences in IQ is laughable because 1) stereotype threat is only replicable in the lab and 2) racism as a variable does not exist in IQ testing.
- The small amount of genetic variation between races as an argument for the non-existence of race is meaningless. There are around 3 billion base pairs in the human genome. The human races differ on around .1 percent of the genome, or around 3 million base pairs. This is more than enough genetic difference to show phenotypic differences (obviously) as well as genotypic differences (again, obviously). Richard Dawkins in the Ancestor’s Tale writes: “What is not correct is the inferene that race is therefore a meaningless concept.” Race is a perfectly valid concept, anyone who denies it has doesn’t know of all of the studies that show the existence of race and how it’s a scientifically taxonomic concept.
Sesardic then brings up how “Philosophers of Science” continuously cite The Mismeasure of Man and Steven Jay Gould in an attempt to denigrate scientists long dead. A few “glowing reviews” from two “Philosophers of Science”:
No one has done as much as Stephen J. Gould to expose race and intelligence studies for the garbage that they often are. (Brown 1998, 5)
Stephen Jay Gould has lucidly analyzed how filling the skulls with lead shot, and comparing the weights of the lead, could easily be infected with unconscious biases. (Kitcher 1997, 171)
The garbage that they often are? Steven Jay Gould is a long discredited ideologue who put his politics before actual science, ironically giving HIM the same bias he falsely accused Samuel Morton of having. James Flynn even says that Gould’s book evades all of Jensen’s best arguments (as most always happens with this debate) with his false belief that g is “reified” therefore leading to the study of race and IQ being meaningless since he has “rebutted the g factor”. I proved the existence of Spearman’s hypothesis the other day using Jensen’s writings that he empirically verified that Spearman’s hypothesis exists in 25 independent samples of blacks and whites along with the study by Dragt (2010) who used the method of correlated vectors to empirically prove the existence of Spearman’s hypothesis. In meta-analyses of Spearman’s hypothesis, he found that differences in intelligence between groups are largely based on cognitive complexity and any so-called “biases in mental testing” cannot account for these racial differences in cognitive ability.
In the definitive refutation of Steven Jay Gould’s “reanalysis” of Morton’s skulls, Lewis, et al definitively prove by remeasuring 308 of the 670 skulls that he had no implicit biases. They also found that if Morton’s biases were true, then there would be considerable overestimates of white skulls while there would be considerable underestiamates of non-white skulls. Ironincally enough, he considered his Egyptian skulls “Negroid” and overmeasured by 12 percent. He overmeasured three of those skulls, along with Seminole (by 8 percent) and native African Nergro (by 7 percent), falsifying the claim that Morton had a bias in measuring his skulls!! As I have brought up here numerous times, as Rushton has refuted him (and defended Morton’s results) as well as Jensen giving Gould a definitive rebuttal to his book. Gould should not be being cited seriously anymore. He should only be brought up as an example of extreme bias in the context of race as well as racial differences and a whole slew of other things that are politically motivated.
He finally rounds up the paper by bringing up how TJ Bouchard, showing that the Big Five Personality Traits have a high heritabilty, gets told that they are traits that carry a social judgment. However, we now know that 40-60 percent of the variation the Big Five is heritable, so this is a meaningless claim.
Sesardic ends the paper as follows:
Why is this small segment of contemporary philosophy of science in such a sorry state? On reflection, I prefer to leave this question as an exercise for the reader. My aim in this paper is to criticize a deviant philosophical trend, not to explain how it came about or why it spread.
My answer to this question is that most philosophers seem to be leftists. We can see with the vehement race denial that they want to believe so strongly that racial differences, as well as race as whole, does not exist. The fact that they attempt to say that these things are not a reality and based on faulty methodologies shows that they do not know what they are talking about. They show large misconceptions about heritability, and continuously cite Steven Jay Gould, even when Gould has been refuted numerous times as well it being shown that they don’t correctly understand heritability. They show large misconceptions of what is understood in the field of psychometrics and heritabilities and make faulty claims about the hereditarian hypothesis.
If the hereditarian hypothesis is to be refuted (it won’t), it will be from science and not philosophy or “Philosophers of Science”.
More g Denialism and more Gould Refuting
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It seems like every day something new comes out that attempts to discredit the reality of g (This paper came out in 2012.). Steven Jay Gould (in)famously wrote in The Mismeasure of Man:
The argument begins with one of the fallacies—reification, or our tendency to convert abstract concepts into entities (from the Latin res, or thing). We recognize the importance of mentality in our lives and wish to characterize it, in part so that we can make the divisions and distinctions among people that our cultural and political systems dictate. We therefore give the word “intelligence” to this wondrously complex and multifaceted set of human capabilities. (emphasis mine)
Which is the same thing that the researchers of the paper Fractioning Human Intelligence said to The Independent:
“The results disprove once and for all the idea that a single measure of intelligence, such as IQ, is enough to capture all of the differences in cognitive ability that we see between people,”
“Instead, several different circuits contribute to intelligence, each with its own unique capacity. A person may well be good in one of these areas, but they are just as likely to be bad in the other two,”
Just like The Mismeasure of Man is “the definitive refutation to the argument of The Bell Curve”, right?
In the above paper, they cite Gould twice writing:
It remains unclear, however, whether population differences in intelligence test scores are driven by heritable factors or by other correlated demographic variables such as socioeconomic status, education level, and motivation (Gould, 1981; . . .
They have been shown over numerous studies that population differences in intelligence are driven by heritable factors (Rushton and Jensen, 2005; Lynn and Vanhanen, 2006; Winick, Meyer, and Harris, 1975; Frydman and Lynn, 1988; Rushton, 2005)
More relevantly, it is questionable whether they relate to a unitary intelligence factor, as opposed to a bias in testing paradigms toward particular components of a more complex intelligence construct (Gould, 1981;
I will prove the existence of g in this article. There is also an empirical basis for the g factor.
It’s getting old now that researchers still think that they can “disprove g”, as a multitude of studies have already corroborated Spearman’s hypothesis as an empirical fact. That is, applying the scientific method, using the same hypothesis over a multitude of different studies and testing those predictions by experiment or further observation and modify the hypothesis when new information comes to light. Then, repeat the aforementioned steps until there are no discrepancies between the theory and experiment/observations.Then when consistency is obtained it then becomes a theory that provides a coherent set of premises that explain a class of events.
How many times has the Hampshire et al hypothesis been corroborated? I doubt it has been corroborated as many times as Spearman’s hypothesis has.
As I said the other day, Jensen tested Spearman’s hypothesis on 25 large independent samples, with each sample confirming Spearman’s hypothesis. Even matching blacks and whites for SES didn’t diminish the effect. Jensen then concludes that the overall chance for Spearman’s hypothesis being wrong is over 1 in a billion. Pretty high odds.
Even then, if this study were to be replicated the amount of times that Spearman’s hypothesis has, it still wouldn’t disprove g.
On page 558-559 of the Afterword to The Bell Curve, Charles Murray responds to many of Gould’s criticisms of the book. He writes:
He (Gould) continues: “The fact that Herrnstein and Murray barely mention the factor-analytic argument forms a central indictment around The Bell Curve and is an illustration of its vacuousness.” Where, Gould asks, is the evidence that g “captures a real property in the head?
Murray states that they “barely brought up the factor-analytical argument” because it was out of date; Gould was using statistics on g that were 50 + years old. Also, a reviewer of his book for the journal Nature said that Gould’s “discussion of the theory of intelligence stops at the stage it was more than a quarter of a century ago.” Gould was using old arguments, and, as Arthur Jensen states in his response to Gould:
Of all the book’s references, a full 27 percent precede 1900. Another 44 percent fall between 1900 and 1950 (60 percent of those are before 1925); and only 29 percent are more recent than 1950.
More than half of Gould’s references in The Mismeasure of Man are outdated by more than 50 years. Clearly, he was attempting to denigrate the old studies of intelligence, i.e., phrenology, even though this recent paper in the journal Nature recently said:
The genomic regions identified include several novel loci, some of which have been associated with intracranial volume
So, we have several loci that are associated with intracranial volume; this shows that those skull studies of yesteryear weren’t crazy. Moreover, the fact that Rushton and Ankney (1996) “reviewed 32 studies correlating measures of external head size with IQ scores or with measures of educational and occupational achievement, and they found a mean r .20 for people of all ages, both sexes, and various ethnic backgrounds, including African Americans” shows that there is a correlation of .20, albeit not too high but there, with external head size and IQ. This shows that Gould’s argument on phrenology is bunk, as modern studies confirm that there is a slight correlation between head size and IQ, and therefore g.
The fact that researchers are still bringing up Gould’s arguments on g show that there really is no good argument to discount it. Basically, any and all arguments that attempt to discredit g are bunk as Spearman’s hypothesis has been empirically verified:
Conclusion: Mean group differences in scores on cognitive-loaded instruments are well documented over time and around the world. A meta-analytic test of Spearman’s hypothesis was carried out. Mean differences in intelligence between groups can be largely explained by cognitive complexity and the present study shows clearly that there is simply no support for cultural bias as an explanation of these group differences. Comparing groups, whether in the US or in Europe, produced highly similar outcomes.
Along with Jensen’s 25 large independent studies that showed that the probability that Spearman’s hypothesis is false is 1 in a billion, this proves that Spearman’s hypothesis is an empirical scientific fact.
Newman and Just, (2005) state in verbal and spatial conditions that the frontal cortex revealed greater activation for high-g in comparison to low-g, supporting the idea that g reflects functions of the frontal lobe. The “seat” of general intelligence is the prefrontal cortex (Cole, et al, 2011, Roth, 2011). This can also be verified with MRI scans that show that those who have higher g have bigger prefrontal cortexes than those with lower g.
Moreover, the fact that Colom, et al (2006) show that in their sample that neuroanatomic areas underlying the g factor could be found across the entire brain including the frontal, parietal, temporal and occipital lobes, shows that this factor is present throughout the brain and all are correlated with g and work together in concert to manifest intellectual ability.
Other researchers have also used the method of correlated vectors on functional Magnetic Resonance Imaging (fMRI), which measures brain activity by detecting changes associated with blood flow. This technique is proven useful due to the fact that cerebral blood flow and neuronal action are correlated. Lee, et al write:
In conclusion, we suggest that higher order cognitive functions, such as general intelligence, may be processed by the coordinated ability may be attributable to the functional facilitation rather than the structural peculiarity of the neural network for g. In addition, our results demonstrated that the posterior parietal regions including bilateral SPL and right IPS could be the neural correlates for superior general intelligence. These findings would be the early step toward the development of biological measures of g which leads to new perspectives for behavior interventions improving general cognitive ability.
They also used the MCV to find that the frontal and parietal lobes are associated with g. Even these studies show that g shows up throughout the brain and not in one solitary spot (though, the PFC is still the seat of intelligence), this shows yet another biological basis for g.
Hampshire, et al write:
Thus, these results provide strong evidence that human intelligence is a construct that emerges from the functioning of anatomically dissociable brain networks.
However, with the above studies confirming that the seat of intelligence is the prefrontal cortex, along with great g ability possibly be attributable to the functional facilitation rather than the structural peculiarity of the neural network for g, this shows, along with the study proving Spearman’s hypothesis, that g is a real and measurable thing. g’s seat is the prefrontal cortex, and exceptional g may possibly be attributed to the functional facilitation of the neural network for g . What all of these studies show is that all though the Hampshire paper showed how they “demonstrate that different components of intelligence have their analogs in distinct brain networks.” that a) higher order cognitive functions may be processed by the coordinated activation of widely distributed brain areas (disproving the above quote), b) the seat of g is the prefrontal cortex, c) those with more g have bigger prefrontal cortexes and therefore bigger brains since the prefrontal cortex is the ‘seat’ of intelligence and d) Spearman’s hypothesis has been corroborated numerous times by many different researchers not named Arthur Jensen.
Highfield (one of the researchers in the study) ends the article as follows:
“We already know that, from a scientific point of view, the notion of race is meaningless. Genetic differences do not map on to traditional measurements of skin colour, hair type, body proportions and skull measurements.
This is something that never ends; it always comes up no matter how many times it’s been said. People can say “race is a social construct” all they want, it doesn’t make it true as there is a biological reality to race.
Now we have shown that IQ is meaningless too,” Dr Highfield said.
IQ is not biased, nor is it “meaningless“.
When will people learn not to cite men who have smeared their legacy in an attempt to defame men who they disagreed with ideologically? Citing Steven Jay Gould in 2016 shows a bias to want to discredit g as a main factor for many things in life including SES, educational attainment, wealth attainment and so forth. The g factor is a measurable thing, with the seat of the factor being the prefrontal cortex. No amount of attempting to dispute this factor can be done, as it’s been empirically verified numerous times.
Ethnic Genetic Interests and Group Selection Does Exist: A Reply to JayMan
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JayMan has said that ““Ethnic Genetic Interests” Do Not Exist (Neither Does Group Selection)“. It’s clear from what he says towards the end that he has some sort of bias to attempt to disprove Ethnic Genetic Interests and Group Selection. This will be a definitive refutation of JayMan’s belief of the non-existence of GST and GS. Along with Dr. Swaggins from the CoonU Blog, both of us today will prove that EGI and GS do in fact exist and that JayMan has an implicit bias in the denial of EGI and GS. I will also address JayMan’s comment to me in that same article that I never responded to save it for this article.
I first wrote an article, Genetic Similarity Theory, in reply to his denial of EGI. It was short, but I got my point across with the Price Equation. JayMan then comments:
Ethnic altruism can’t evolve through genetic similarity because the coefficient of relationship between co-ethnics (who aren’t close family) is pretty small. Even kin selection itself is pretty weak in general. How much time do you spend with your second and third cousins?
In-group favoritism likely evolved through individual selection for reciprocal altruism. Overall similarity simply allowed individuals to recognize likely partners for trading favors (shared language and customs may help). This may have even co-opted systems designed to act towards close kin – misfiring kin altruism, if you will.
Rebutting Jayman’s denial of the ethnic kinship coefficient requires an explanation of the concept of relatedness as a whole. How, for example, can I be 50% identical to my father if I’m 99.8% identical to all living humans? The answer is that I am not 50% identical to my father; rather, I am 50% identical to my father by comparison to the baseline level of relatedness of all living humans. If all living humans are 99.8% genetically identical then I’m 99.9% identical to my father. Jayman’s argument that two random co-ethnics aren’t related fails to factor this into account: a calculation of relation needs a baseline level of relatedness for comparison. So he’s correct in stating that two co-ethnics are not similar to one another- but only by comparison to the baseline level of relatedness of their entire population.
Since the ethnic kinship coefficient has been worked out to the equivalent of half siblings, it may be useful to frame the issue in those terms. If I am 25% identical to my half sibling by comparison to any other co-ethnic, it is because there is a quarter of my genome that I share with my half sibling due to our common descent. Specifically, our mutual descent from our mutual parent gives us a specific combination of genes that nobody else is likely to have. 25% of my genome is 100% identical to his alleles of the same genes and the other 75% is as similar to his as it is to any other co-ethnic, but taken as an average across my entire genome, any given allele is 25% more likely to be shared with him than it is everyone else in our race.
The ethnic kinship coefficient works in an uncannily similar way. Instead of inheriting those 25% identical genes from recent common ancestors, the two co-ethnics inherit the same genes due to the fact that people of their race usually have those genes (think melanin, keratin, microcephalin, EDAR, HERC2, or any other gene for which the frequency of alleles differs overpopulation). In spite of that difference in the origin of ethnic vs familial similarity, the mathematics are shockingly similar: according to Henry Harpending in his review paper Kinship and Population Subdivision, “Many studies agree that Fst [genetic distance between populations] in world samples of human populations is between ten and fifteen percent,” with “a conservative general figure” being 12.5%. What’s more, Fst “is computed for each allele at each locus, then averaged over all loci.” In other words, 1/8th of human genetic diversity is at the between-group level.
To put things into perspective, a 1/8th reduction in diversity within a family occurs when two half siblings (25% identical) have a child. There is a 1/16th chance that the common parent will pass a given allele to both children and that both children will pass that allele to their child, and a 1/16th chance for the same to occur for the other allele of the same gene; when computed allele for allele, “diversity” (odds of heterozygosity) goes down by 1/8th among a population that is 25% identical by descent.
One such calculation finds, for example, that a Frenchman is 24% identical to another Frenchman if your baseline for comparison is the genetic similarity between the French and Japanese.
This is the inevitable implication of the central tenet of HBD: that the various races of the world are genetically different from one another. It is also the inevitable implication of Lewontin’s famous finding that 15% of all human genetic variation is racial; if it were 100% then all co-ethnics would be identical and it were 0% then race wouldn’t exist at all. If it were 15%, though, then that 15% would be composed of genes whose alleles vary in frequency across populations; these are genes you share with co-ethnics much more often than you share with anyone else. If you’re more likely to share a lot of genes with co-ethnics than you are with anyone else, then you’re more genetically similar to co-ethnics than you are anyone else. When they sequence the genes of people of different races and compute the odds of similarity locus for locus, you’re much more likely to share some genes (ABCC11, MC1R, etc) with co-ethnics than you are others, but taken as an average across both copies of the entire genome, it’s about 25%. Apply those odds to the 20,000 or so genes in the human genome and the result will be consistent with the data that members of a given race are about 25% identical by comparison to members of other races.
We are not the first people to predict that these genetic differences would result in kin selection expressed as altruism towards co-ethnics and discrimination towards others; to quote an article by the late Henry Harpending posted in March 2012, “In the new diverse community the average person can find someone related as f~0.06, corresponding roughly to a great-grandchild at f=1/16. Suddenly there is a fitness payoff to discrimination.” (In this hypothetical population, an individual is 1/8th more related to a co-ethnic than to the average and 1/8th less related to some of a different race than to the average.) In an ethnically homogeneous population, discrimination of this kind will not occur because the fitness payoff of benefiting one co-ethnic or the other is the same, but in a heterogeneous population, you suddenly have people in whom you have comparatively more or less genetic interest. In December 2012, Harpending and Salter published “JP Rushton’s Theory of Ethnic Nepotism,” a paper predicting that the Fst data would support Rushton’s theory of ethnic genetic interest, by providing evidence for kin selection. Towards the end of this article, I will provide evidence for human altruistic behavior fitting the patterns predicted by kin selection, and I will present a likely animal model for subspecies competition over resources. In the meantime, however, there are more misconceptions to clear up.
JayMan says:
I suppose a key misunderstanding in the matter is the failure to realize that each individual gene contributes to fitness independently. Each gene is “out for itself”, so to speak. It just so happens that in any given organism, genes achieve success by working together (most of the time). As sucheach individual gene’s “aim” is to make more copies of itself. What’s going on in the rest of the genome is tangential to this. ((—>Each gene would be just as happy to mix with any other gene, so long as its own fitness is increased in the process.<—)) (Additions in last sentence for emphasis are mine)
Individual genes don’t always contribute to fitness independent of one another; the venerable Nicholas Wade has pointed out that there is at least one gene which confers different levels of selective disadvantage depending on the other genes they’re mixed up with: an allele that slightly increased risk of heart problems in Europeans causes big problems whenever it introgresses into Africans. Naturally, the population which has had this allele for longer has more genes elsewhere in the genome compensating for its negative effects, meaning that said allele will cause fitness problems after it introgresses into another population. Introgression is just a fancy word for race mixing, though, and there are other problems with it, as follows:
In a study of 100,000 mixed-race adolescent school children, those who identified themselves as such had higher health and behavior instances than those of one race. The effect was still observed even when SES and other factors were controlled for. A problem with an obvious genetic component.
Yet another study done on white-Asian mixes notes that they have a two times higher rate to be diagnosed with psychological problems such as anxiety, depression and substance abuse.
It was found, in agreement that black-white mixes engaged in more risky behavior than did monoracial children. They also observe that mixed-race adolescents are stark outliers in comparison to whites and blacks, which still holds true despite being raised in similar environments to monoracial children.
Fitness doesn’t look increased in that process, seeing how mulatto children show more health problems and negative behavior than monoracial children. And given the data relating to the allele mentioned above, we can’t rule out the possibility that health problems in biracial children arise because their parents’ genes don’t necessarily work together.
There is no impact on one’s fitness from the race of one’s mate (or an offspring’s mate) so long as close relatives are off the table as mates (aside from the fitness impact of the particular genes such mates were bringing in the environment in question). The fitness impact to a White man’s genes if his daughter marries a Black man is the same as if she married an unrelated White man (again, fitness from gene function notwithstanding).
Do you really believe that? As shown above, mixed-race children show more health and behavior problems than do monoracial children. Africans were not selected for resistance to the negative effects of certain European genes as Europeans were, and we have no reason to believe that any race is selected to compensate for the negative effects of genes they don’t even have.
Just the same, the inclusive fitness impact to a White American is the same whether he focuses his altruistic act on an unrelated White American or on a Namibian; it is zero in both cases. If you adopt children rather than have your own, the fitness hit to you is the same whether your adopted children are White, Black, Chinese, or Venezuelan.
Again, this assumes that there are no genetic differences between populations, but there are, so your fitness is probably higher if you adopt a co-ethnic than if you adopt someone else.
Hence, there is no human ethnic group that exhibits ethnic nepotism. This includes Ashkenazi Jews. But these have nothing to do with ethnic nepotism, didn’t arise via kin selection, and don’t depend on genetic relatedness per se. This includes Ashkenazi Jews.
Ashkenazi Jews evolved their nepotism through thousands of years of getting driven out of countries. Along with being barred from certain jobs, this led to them being only able to do banking jobs and those jobs that took more intellect, which they then evolved their higher IQ as well as more group favoritism to help them in societies where they are the minority. This is clearly evident today with Jewish overrepresentation at elite universities; their average IQ of 110 suggests that they shouldn’t be that much of the student body since they’re six times as likely to be geniuses but many more times likely to make it into the top institutions. Odds are pretty good that that’s ethnic nepotism in action. We’re talking about a group of people 38% likely to consider themselves religious but 70% likely to believe the old mythos that the omnipotent, omniscient creator of everything that ever existed prefers them to literally everyone else, and judge whether someone is worthy of this inconceivably lofty status purely on the basis of their genetics; before they had handy-dandy PCR machines and enzymes, Jews determined someone to be Jewish by matrilineal descent, not cultural custom. If the Ashkenazim lacked any ingroup preferences of any kind during their time in Europe, they would’ve literally copulated themselves to death by marrying Gentiles until their population was totally absorbed by ours. What would you call it then, JayMan, if not EGI? They’re one of the best examples FOR the existence of EGI. See, the thing is, if someone is an Ashkenazi Jew, more often than not, they will be more related to each other than some other random person from another population.
This particular fact – that co-ethnics share genes – is why they have a genetic interest in one another.
The Ethnic Kinship Coefficient has been corroborated literally every time anybody calculated Fst values between different human races, and by JayMan’s understanding of kin selection it disproves his assertion that ethnic genetic interests do not exist:
This [relatedness] is the probability that a given relative of an individual possesses a copy of an allele the individual possesses.
Co-ethnics are about 25% more likely to share the statistically average allele than people of different races are, so the Hamiltonian drive to confer benefit on co-ethnics is comparable to the drive to confer benefit on secondary relations (half siblings, grandchildren, etc). In other words, it doesn’t matter that the frequency of altruistic alleles is unaffected by the presence of outsiders, because people have a genetic imperative to assist the genes they share with their co-ethnics either way (and are therefore selected for altruism/ethnic nepotism either way); since they are related to their co-ethnics regardless of context, they are selected for the desire to confer benefit on co-ethnics regardless of context, and they only have a genetic interest in derogating an outgroup if doing so will increase the fitness of the ingroup. This is why Harpending and Salter observe, in the paper linked above, that racial solidarity “strengthens in response to attacks perceived to be aimed at group identity, especially invasion of the homeland and physical harm done to co-ethnics.” Observe Donald Trump or Marine Le Pen excoriating the bureaucrats they deem responsible for an alleged invasion, or Black Lives Matter being more enraged about a Hispanic killing a black than by thousands of blacks killing thousands of other blacks. A supposed shift in altruistic allele frequencies was never the point, and to argue against it is to battle with strawmen.
If altruism is the result of kin selection, then an organism will confer benefit on the criterion of relatedness. If a European man saves a daycare with 8 Asian babies in it from some freak accident, then he saves as much of his own genes as were shared by those babies. If he saves a daycare with 8 European babies in it, he just saved a collection of his own copies of HERC2 or ABCC11 or EDAR or some other such gene which he previously failed to save as well. If he saves 8 of his co-ethnic first cousins, the proportion again goes up, this time by 12.5%. By the same mathematical model we use to explain kin selection (Hamilton’s Rule), we predict and observe that altruism will be expressed to various degrees depending on the degree of relatedness.
The adaptation to this would have nothing to do with magical altruism genes which change in frequency when Japanese people arrive in France. Rather, the selection pressures predicted by the kin selection model would select for organisms that exhibited compassion and cooperation in proportion to relatedness.
The fact that co-ethnics share so many genes means that they do have a genetic interest in one another, if kin selection is real. I personally believe that kin selection is a clearer and more likely explanation for altruism than group selection in most cases, but due to the difficulty of determining causality in processes that occurred thousands if not millions of years ago (namely the original evolution of altruistic behavior), I doubt that the scientific community can put this one to bed yet. For the purposes of this issue, however, JayMan has already professed his belief that group selection has never occurred, meaning that one of a few different things must be true.
- Humans are not altruistic at all. Untrue.
- Humans are altruistic, but not due to kin selection or group selection. Unlikely; we can talk about mutual back-scratching all we want but the fact that people take bullets and jump on grenades for one another means that mutual benefit cannot be our only reason to confer benefit upon others.
- Humans are altruistic due to kin selection. This explanation is consistent with genetics and evolutionary theory; evolution holds that survival is a matter of passing on genes and genetics show that related organisms have many of the same genes. It also has pretty good predictive power (it predicts familial love, racism, and other real phenomena). For these reasons, I’m going to be arguing from the assumption that kin selection is a primary reason for human altruism, and that it, therefore, must exist in humans.
Due to the genetic similarity between co-ethnics, there is a genetic interest between them. Each has a Darwinian interest in the other comparable to roughly 25% of their own survival. Operating from the assumption that kin selection is the reason for human altruism, one would predict one of the following possibilities:
- Humans will prefer to confer benefit to their co-ethnics over others due to the fitness advantage gained by doing so,
- That humans cannot perceive genetic similarity and have therefore been selected to benefit one another regardless of genetic similarity in hopes that they hit the mark by accident,
- Humans do prefer those who are genetically similar but are incapable of perceiving the genetic differences between the various human subspecies, or
- Humans understand the genetic differences between themselves and others but for whatever reason will not take the 25% fitness advantage. I’m going to go ahead and throw this one out.
We know that humans prefer others on the basis of genetic similarity, and we know that nearly all human cultures have considered those of different ethnicities to be “the other,” or at least different in some significant way. We know that people can determine someone’s biological race based on their appearance, in any case, and in his 1996 book Race in the Making: Cognition, culture, and the child’s construction of human kinds, Lawrence Hirschfeld found that even children could do so. All of which means that humans can get a rough idea of genomic similarity (or difference) using phenotype and family history as a proxy, and that race is among the types of genetic difference that humans are capable of perceiving. If humans prefer one another based on the criterion of genetic similarity (they do), and race is a genetic difference that humans can perceive (it is), then we expect humans to generally prefer those of their own race (they do).
Even in studies of bereavement, Littlefield and Rushton (1986) put forth ten hypotheses (I will only bring the ones up that prove the case for EGI) to make the case for Genetic Similarity Theory:
- A mother will grieve more than the father: this is due to the mother having finite number of ova, have a more limited reproductive potential than do men and also bear the burden of bearing children, this shows that each offspring of a mother is more important to the overall success to her genes than the are to the father’s.
- Male children will be grieved for more intensely than female children. This is due to a male having a higher chance to have more children and spread his genes to more progeny.
- Similar children will be grieved for more intensely than dissimilar children. GST explains the phenomenon of assortative mating, the phenomenon that spouses will be genetically similar on those traits more influenced by genetics. One consequence of assortative mating is that one parent may be more similar to the child than the other. This can be illustrated as follows: Rushton and Littlefield: “If a father gives his child 50% of his genes, 10% of which are shared with the mother, and the mother gives the child 50% of her genes, 20% of which are shared with the father, the child would be 60% similar to the mother and 70% similar to the father (Rushton et al., 1984)”. So we can see that depending on the amount of genes a child gets from his parent will infer whether or not they are genetically similar to which parent, and in the case of a possible surprise death, the parent who believes the child looks (shares more alleles in common with) like their selves, will grieve longer and more intensely due to having a greater fitness hit due to the increased GST.
This study shows good evidence that the more genetically similar the child is to the grieving parent, the more strong and intense the grieving process will be. How mothers and fathers will risk their lives for their children, their genetic endowment, shows another truth to this phenomenon: altruism. Altruism for those who are genetically similar to yourself. We can then take this and show that since co-ethnics are closer to each other than they are to distant populations, and that since they are more genetically similar to themselves, the same kind of derogation and suspicion that parents give strangers who come around their children, co-ethnics will give to non-co-ethnics when they appear in their homeland. Robert Putnam’s research corroborates this.
Altruism/nepotism does increase when out-groups come to the land. When this occurs, the native population of the country will, in theory, become more altruistic to co-ethnics since their genetic interests are at stake. This is currently occurring in Eastern and Southern Europe in countries like Hungary, Poland, Spain, and Italy.
The model has pretty good predictive power since it predicts racism and other phenomena, which I’ll dive into now. Applying the kin selection model to humanity we expect that altruism will not only be doled out proportionally with respect to genetic similarity, but also to the number of babies the recipient is likely to have. I wouldn’t do as much for my DNA by saving the residents of a retirement home as I would by saving a daycare. And saving women is smarter than saving men. Hence, when the Titanic sinks, the rallying cry of the day is literally “save the women and children!” (Because the people who didn’t do that throughout our biological history had less of an impact on our gene pool than the ones who did.)
So you’re going to see innumerable charities for the benefit of children, and comparatively, nobody trying to solve the conundrum of how terrible life is in nursing homes for the elderly. On the Forbes list of top US charities, numbers 1-4 all frequently work with children (as do many others) and numbers 5, 6, 12, and 14 are specifically for children. None of them are specifically for the elderly; making sure that Grandpa isn’t miserable and alone registers nowhere in the top 50 items of our society’s to-do list.
And you’re going to see things like this, in spite of the fact that men are equally likely if not a hair more likely to get lung cancer and it’s a big killer in both sexes because people care more about “women” than they do about “people.” And I’m not joking or cherry-picking: Lung Force’s blog is seemingly more about women’s feelings than about lung cancer, no doubt because these people are aware that breast cancer research receives way more funding than prostate cancer research does in spite of similar death rates . In other words, it’s a well-known fact among people whose jobs are to stir up altruism that people will give more resources for the well-being of women than for the well-being of men.
All of which is just another case of altruism that “just so happens” to confer group and/or kin benefit, and does so proportionally to the expected increase in fitness, precisely as kin selection would predict. I would expect people to donate more to co-ethnics as well, were it not for the facts that:
a) It’s fashionable in our society to virtue signal niceness to swarthier folks, and
b-z) Haitian children literally eat dirt for breakfast.
In any case, you can look at where rich nonwhites send their donation dollars, be it the fitness benefit gained by JayZ when he donates to clean water causes in Africa, or by George Lopez in his “contributions to the Latino community“. This isn’t a cherry-picked trend of statistically irrelevant anecdotes: Blacks donate to other Blacks, “Identity-based giving is gaining momentum in the Latino, Asian American, Arab American, and Native American communities,” and “Latino’s motivation to give is embedded in a sense of responsibility and desire to give back to their community.” Much of the work of such people may end up benefiting Whites who happen to be there when a catastrophe hits a bunch of the donor’s co-ethnics (observe a Black donating to Hurricane Katrina; New Orleans is majority black, but not devoid of Whites), or occasionally they’ll donate to other nonwhites. But I’m not holding my breath for the day they raise awareness for the White squatter camps in South Africa.
Basically, any time that a person does a nice thing for another person, it will be proportional to any combination of three factors: genetic similarity, assumed number of offspring, and/or how bad the recipient needs help. All three of these are predicted by kin selection since all three are factors which predict the fitness gained by engaging in an altruistic act.
Importantly, virtually every culture on Earth preferred co-ethnics to others prior to the Communist subversion of the West, at which point accusations of racism became something of a social death sentence. (You don’t believe me on the Communist subversion thing- think it’s a conspiracy? Google up where all of this “social construct” ideology we keep encountering ultimately came from, and look up who’s promoting it today.) One could claim that whether a culture is “racist” or not depends on “culture” rather than biology, and point to the modern West as an example of an “anti-racist” culture, but in that case, it’s one hell of a coincidence that every race on Earth generally preferred themselves to everyone else, and did so for 10,000 years or more if you count prehistory. Considerably more likely is that populations with no ingroup preference are subsumed by other populations who gain a fitness advantage by doing so (they mounted no defense because they didn’t understand the need to do so) and that the majority of modern humans are therefore descended mostly from passionate racists.
Co-ethnics have a real genetic interest in one another due to large amounts of shared DNA, meaning that ethnic genetic interest is real. Humans do act on genetic interests in general, as the family studies show, and they are capable of perceiving racial genetic differences, as the ethnicity studies show; it is, therefore, likely that they will act on these ethnic genetic interests as they do with other genetic interests, because racism is caused by the innate preference for genetically similar people. In other words, racism is a biological phenomenon instead of a cultural one.
That, or nearly every culture ever in the history of forever was racist by pure coincidence.
To put subspecies competition into perspective, I will point out that wolves and coyotes have a Fst value between 0.056 and 0.121 and can interbreed. We can call subspecies and other taxonomic classification a social construct if we like; technically we’d be correct in the case of canids, to whom the words “species” and “subspecies” are doled out in a pretty arbitrary fashion. We can say that the admixture is proof that the wolf and coyote DNA doesn’t care about which other genes it’s combined with, if we like. But everything we say about it does absolutely nothing to change the fact that the biological fitness of coyotes massively drops when they share territory with wolves.
Understatement of the week: the implications of having to compete for the same resources is probably why canids fight for territory. Wolf packs, being direct family, would no doubt have a high Fst with other wolf packs, no different from how I’m more similar to my grandpa than I am my housemates. They fight for territory on a familial level because of genetic interest, and they have been observed fighting for territory on the level of subspecies as well, with a clear genetic interest in doing so. The only difference between them and us in this respect is that our method of acquiring resources relies on commerce rather than hunting, and so we weren’t selected for the propensity to wander around a given territory fighting off other families who intrude. That’s not good for business; in fact, I’d be willing to bet that warfare usually occurs in humans when the profit incentive for conquest is greater than the profit incentive for trade. Humans who don’t engage in a lot of commerce and belong to inbred populations, though, have fewer incentives towards peace and higher Fst values relative to others- and they aren’t above killing the guys from the next tribe over. What a surprise that these village’s conflicts had to do with territory and breeding, both of which have to do with fitness. In any case, humans from populations selected for agriculture and commerce engaging in this sort of behavior is the exception that proves the rule, because the only reason anybody knows about the interfamilial warfare of the Hatfields and McCoys is that it falls under the “man bites dog” rule.
I have this radical view that biological rules still apply to humans, and that we are therefore self-replicating bags of meat smart enough to understand that we are self-replicating bags of meat. I see little difference between wolves reclaiming their old hunting grounds and the Reconquista movement. Coyotes had taken over when the wolves kept getting killed by men; Spaniards took over when a storm of viruses killed off most of the Natives. Even after the Spanish admixture, the Fst values between Whites and the now-mestizos likely falls within the range of coyote-wolf Fst values. Wolves feed their kind with elk and we feed ours ultimately with money; the distribution of elk meat to wolves isn’t good for coyotes and I’m willing to bet that the distribution of money and jobs to other nations and their peoples explains much of our abysmal birth rates in the West (with birth control technologies being another primary factor). We had lots of kids back when there were blue collar jobs you could get fresh out of high school which instantaneously elevated you to the middle class. We could afford to have them, no different from the fact that European nobles had more kids on average than us commoners. If current economic, cultural, and political trends continue, though, then ethnic Europeans might go out roughly 50x faster than the Neanderthals did.
Biological organisms show preference of those who are similar at the level of self (me), family (the Kennedys), tribe or nation (Papuan tribes or Mexico), race or subspecies (Native Americans), and species (I eat pork and kill spiders more often than I eat aboriginal Australians and kill Sentinelese people). All are the same phenomenon (attempts to increase the odds of self-replication at the genetic level), all are predicted with Fst values and Hamilton’s Rule, all are observed in animals to whom “culture” doesn’t apply, and all are observed in mankind.
Now, the question is this: how would GST be detected? Numerous ways. Location, for one. Since up until around 50 years ago, most countries were monoracial, those in your general proximity will, more often than not, be more genetically similar to you than a group that’s 50 miles away. Culture, which is an expression of genetics, is yet another way that GST can be detected. Since culture is an expression of genetics, when that culture is expressed, this shows other genetically similar co-ethnics that this individual shares more genes in common than those who don’t share their culture. There is also matching by phenotype, which goes along with the location aspect. But, as I stated in my article Genetic Similarity Theory as a Cause for Ethnocentrism:
It’s clear that we are more altruistic to people who look more phenotypically similar to ourselves, to pass on and benefit copies of our genes. This evolved in spite of the negative impact on behalf of the altruist. The altruist is helping copies of his shared genes survive so that they may be copied into the next generation of progeny. The tendency to favor co-ethnics is the tendency to attempt to help pass on shared genes, as if the phenotype is similar, more often than not, the genotype is as well. This is the basis for ethnocentrism.
There is also what is called the “Grandmother’s hypothesis” in which the researchers theorize that women live past menopause to help take care of their grandchildren. In doing so, they can then make sure their grandchildren are well-fed and nourished. The researchers state that by using Hamilton’s relation coefficients (what we have been using in this article), that a grandmother should share 25 percent of genes with her grandchildren. Ted Sallis says:
Therefore (and this is the important point), a paternal grandmother, all else being equal, is genetically less related to a grandson than to a granddaughter, and less related to a grandson than is a maternal grandmother. Conversely, a paternal grandmother likely is more genetically related to a granddaughter than is a maternal grandmother, given the certainty that the granddaughter possesses an X chromosome from the paternal grandmother.
The researchers hypothesized that the grandmother’s investment in grandchildren will be directly mirrored by how genetically similar they are to each other. The authors conclude that women live past menopause to help care for their children’s offspring. Since they share 25 percent of their genes with their grandchildren, they too, have a genetic investment in making sure they get adequate nutrition and are well cared for. They found that in 7 previously studied populations that “separating grandchild survivorship rates by sex reveals that X-chromosome relatedness correlates with grandchild survival in the presences of MGMs and PGMs. In all seven populations, boys survive better in the presence of their MGM than PGM. In all bar one population, the PGM has a more beneficial effect on girls than on boys. Our X-linked grandmother hypothesis demonstrates how the effects of grandmothers could be sex-specific because of the unusual inheritance pattern of the X-chromosome.”
This is what this whole debate is about: ability to detect genetic similarity in co-ethnics. Matching by phenotype, culture, and general proximity will, with good chance, bring you together with someone who shares more alleles in common with you and someone who you would feel more altruistic towards since you have a genetic interest in ensuring that some of your genes survive to the next generation.
Mixed-race relationships don’t discredit the existence of EGI/GST, in fact, it helps to strengthen it. Americans of mixed ancestry made up for ethnic dissimilarity by matching up on the more heritable traits, whereas the correlation is lower for those traits that are more influenced by the environment. Since the correlation is higher for heritable traits, i.e., BMI, personality, alcoholism, aggressiveness, criminality, psychiatric disorders and so on. Since the correlations are higher than in the environmentally mediated traits and since mixed-race couples match on more heritable traits than on the traits more influenced by the environment, this shows us that even though they are marrying outside of their race/ethnicity, they still match up on the more heritable traits and not the traits more influenced by the environment.
JayMan brings up the concept of reciprocal altruism as if it negates the effect of racial/ethnic altruism as a whole. It does not. Reciprocal altruism and Genetic Similarity Theory go hand-in-hand as genetic similarity eliminates the need for the reciprocation to occur again. Since two related individuals share more genes in common with each other than two unrelated individuals, this then caused reciprocation and GST to evolve hand-in-hand with each other. To quote Rushton:
Thiessen and Gregg (1980) make the same point. Thiessen and Gregg state that “cooperation among `nonrelatives’ (`reciprocal altruism’) may be based in large part on genetic and phenotypic similarity” (p. 133).
Another reason that GST and reciprocal altruism go hand in hand is that genetic similarity at certain important loci can predict the efficacy of a reciprocal altruistic relationship; Fowler & Christakis find that close friends are as similar as 4th cousins, and Guo et al find the same for spouses. Selecting for phenotypic compatibility means selecting for genetic similarity at the loci which determine the relevant phenotypes (height, IQ, personality and so on). For example, different races of the world differ in Big Five personality traits, and the reason for these differences is likely genetic. If a statistically normal, introverted East Asian prefers to associate with fellow introverts, what are his odds of becoming best friends with a comparatively gregarious Black man? A gregarious Asian or an introverted Black may become fast friends with those of other races, but most of their kinsmen are more stereotypical.
Ultimately, however, what it comes down to is this: if a gene can better ensure its own survival by bringing about the reproduction of family members with whom it shares copies with, then it can also do so by bringing about the reproduction of any organism that it shares genes with. Meaning altruistic self-sacrifice. But, if there is a fitness gain for the altruist, then how is it altruism? Simple. The altruist is just protecting genetic interests. The altruist is just being driven by his genes to save copies of itself. This is basically what we humans are: organisms that only attempt to bring about those with similar genetics to ourselves.
NotPoliticallyCorrect 
