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Myopia, IQ, and Race

1200 words

We’ve all heard of the nerd stereotype. One of the main ones is that nerds wear glasses. However, as most of my readers may know, stereotypes are based on fact more often than not. From the black criminal and sprinter, to the hyper-intelligent East Asian, to the intelligent and creative Europeans, we see that these so-called ‘stereotypes’ arise because stereotypes are actually average traits. Therefore, this ‘nerd stereotype’ that they always wear glasses is based on averages, so there must be a genetic component behind it. In this article I will talk about the genetics of myopia, reasons why researchers believe it arises, and racial differences in the prevalence of myopia.

Myopia, better known as nearsightedness, has a pleiotropic relationship with intelligence. Pleiotropy is the single gene or set of genes controlling multiple, possibly unrelated, phenotypic traits. So if the two traits are correlated, then there is a good chance that if one wears glasses they may have higher average intelligence.

Rosner and Belkin (1987) found that the prevalence of myopia was higher in more intelligent and educated groups. They found a strong association between the rate of myopia, years of schooling and intelligence level. Schooling and intelligence weigh equally with myopia, showing that those who are myopic tend to stay in school longer and are more intelligent than average.

Saw et al (2004) show that there may be similar genes associated with eye growth or size (myopia) and neocortical size (*possibly* correlated with IQ, we know it is). This is exactly what Cohn, Cohn, and Jensen found in 1987; that there was a pleiotropic relationship between IQ and myopia. One set of genes controls one or multiple phenotypic traits. They also say that nonverbal IQ is correlated with myopia in the Singaporean cohort independent of near work from the children (such as reading). Nonverbal IQ may be an independent risk factor of myopia independent of books read per week. They conclude that more research needs to be taken out to untangle the cause and effect of the myopia/intelligence/reading relationship.

Mirashi et al (2014) show in a sample of 4600 myopia-inflicted Germans between the ages of 35 and 74 that about 53 percent of the sample had graduated from college compared to 24 percent of the sample who didn’t go to school past high school. They, too, conclude that higher levels of myopia are associated with higher educational achievement and post-school professional achievement and that those who were myopic had higher levels of educational achievement than those in the sample who weren’t myopic.

More recently, Verma and Verma (2015) state that there is evidence that both genetic and environmental factors play a role in the prevalence of myopia. Moreover, Czepida, Lodykowska, and Czepita (2008) come to the same conclusion; that children with myopia have higher IQs and was verified in other countries (the USA, the Czech Republic, Denmark, Israel, New Zealand).

The correlation between myopia and IQ is between .2 and .25 (Jensen, 1998 b; 149). Jensen writes on page 150:

. . .the degree of myopia was measured as a continuous variable (refraction error) by means of optical techniques in a group of sixty adolescents selected only for high IQs (Raven matrices) and their less gifted full siblings, who averaged fourteen IQ points lower, a difference equivalent to 0.92o. The high-IQ subjects differed significantly from their lower-IQ siblings in myopia by an average of 0.39a on the measure of refraction error.1161 In other words, since there is a within-families correlation between myopia and IQ, the relationship is intrinsic. However, it is hard to think of any directly functional relationship between myopia and IQ. The data are most consistent with there being a pleiotropic relationship. The causal pathway through which the genetic factor that causes myopia also to some extent elevates g (or vice versa) is unknown. Because the within-family relationship of myopia and IQ was found with Raven’s matrices, which in factor analyses is found to have nearly all of its common factor variance on g ,n it leaves virtually no doubt that the IQ score in this case represents g almost exclusively. (emphasis his)

Therefore, as noted earlier, we would see a slight variation in the general population between those with high IQs and those who wear glasses and are myopic.

Jensen also talks about race and myopia. He says that Asians have the highest rates of myopia, while blacks have the lowest rate and whites have a rate slightly higher than blacks.

In a tribute to Arthur Jensen, edited by Helmuth Nyborg, it states that East Asians have the highest rates of myopia, with blacks having the lowest rate and whites being intermediate (Rushton’s Rule of Three).  Ashkenazi Jews have a rate of myopia two times higher than that of gentiles, on par with East Asians. These are yet other biological correlates with the g factor that also lend credence to the hereditarian hypothesis.

Glassescrafter.com also shows that East Asians have a higher rate of myopia with blacks having a lower rate:

Certain types of visual disturbances affect some races more frequently. Asian-Americans, for example, are more likely to be near-sighted than Caucasians or African-Americans. African-Americans have the lowest incidence of near-sightedness, but are more prone to cataracts and some other eye diseases. Eye problems, including the need to wear glasses, also can run in families.

Of course, if myopia is a pleiotropic trait (there is good evidence that there is), and wearing glasses runs in families as well as high intelligence, it can be safely hypothesized that the two indeed do have a relationship with each other. The biological correlates show enough that these traits, too, follow Rushton’s Rule.

Finally, Au, Tay and Kim (1993) present data that shows the prevalence and severity of myopia is associated with higher education. They also report on data that Rosner and Belkin reported the prevalence of myopia in males with and IQ of 80 or less was 8 percent while the rate increased up to 27.3 among those with an IQ of 128 or higher. Reported separately, it was concluded that the myopia rates in the cohort of 110,236 young Singaporean males correlated with race (Au, Tay, and Lim, 1993). The myopia rate for the Chinese was 48.5 (IQ 105), for Eurasians it was 34.7, for Indians it was 30.4 (IQ 82), and for Malays it was 24.5 (IQ 92). It’s worth noting that India’s IQ is depressed by disease and bad nutrition, and if this were to be ratified their IQ would be around 94. So this, again, shows the biological correlate with IQ and myopia as it’s showing on the Indians’ genotype.

The association between myopia and intelligence isn’t definite yet, however with more studies looking into the relationship between these variables I believe it will be concrete that those who are more myopic tend to have higher IQs due to the pleiotropic nature of IQ and myopia. Since reading is heritablethose with higher IQs as children tend to read more as adults, and the racial gradient is noticed in children, it’s pretty safe to say that myopia and IQ are linked pleiotropically and give more credence to the hereditarian hypothesis. Most studies find a statisically positive correlation between myopia and intelligence. Along with the racial disparities in myopia as well as intelligence, it’s pretty safe to say that the relationship is genetic and pleiotropic in nature since the races also differ in these variables.

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The Evolution of Violence: A Look at Infanticide and Rape

1700 words

The pioneer of criminology was a man named Cesare Lombroso, an Italian Jew (a leftover remnant from the Roman days), who had two central theories: 1) that criminal behavior originated in the brain and 2) criminals were an evolutionary throwback, a more primitive type of human. Lombroso felt strongly about the rehabilitation of criminals, at the same time believing in the death penalty for “born criminals”. Though, with new advances in criminology and new insights to the brain, it looks like Lombroso was right with his theory of born criminals.

Why are you 100 times more likely to be killed on your birthday? Why are children 50 times more likely to be murdered by their stepfather than biological one? Why do some parents kill their children? Finally, why do men rape not only strangers, but also rape their wives? All of these questions can be answered with evolutionary psychology.

Evolutionarily speaking, antisocial and violent behavior wasn’t a random occurrence. When these actions occurred tens of thousands of years ago, they were because resources were being acquired from these actions. Thus, we can see some modern criminal acts as resource competition. The more resources one has, the easier it is for him to pass his genes on to the next generation (a big driver for violence). In turn, women are more attracted to males who can provide resources and protection (those who were more antisocial and violent). This also explains these prison romances, in which women get into romances with murderous criminals since they are attracted to the violence (protection) and resources (theft).

The mugger who robs for a small amount of money is increasing his odds of resource acquisition. Drive-by shootings in violent neighborhoods increase the status of those who survive the shootout. What looks like a simple brawl over nothing may be one attempting to increase social dominance. All of these actions have evolutionary causes. What drive these actions are our ‘Selfish Genes’.

The more successful genes are more ruthlessly selfish in their struggle for survival, which then drives individual behavior. The individual behaviors that occur due to our selfish genes may be antisocial and violent in nature, which in our modern society is frowned upon. The name of the game is ‘fitness’. The amount of children you can have in your time allotted on Earth. This is all that matters to our genes. Even those accomplishments you think of, such as completing college or attaining mass amounts of capital all fall back to fitness. With that, increasing your fitness and ensuring your genetic lineage passes on to the next generation is greatly enhanced.

Biological fitness can be enhanced in one of two ways. You can have as many children as possible, giving little parental care to each, or you can have fewer children but show more attention and care to them. This is known as r/K Selection Theory. Rushton’s r/K Selection Theory compliments Dawkins Selfish Gene theory in that the r-strategist is maximizing his fitness by having as many children as possible, while the K-strategist increases his fitness by having fewer children in comparison to the r-strategist but showing more parental attention. There are, however, instances in which humans kill children, whether it’s a mother killing a newborn baby or a stepfather killing a child. What are the reasons for this?

Killing Kids

The risk of being a homicide victim in the first year of life is highest in the first year of life. Why? Canadian Psychologists Daly and Wilson demonstrated in inverse relationship between degree of genetic relatedness and being a victim of homicide. Daly and Wilson discovered that the offender and victim are genetically related in only 1.8 percent of all homicides. Therefore, 98 percent of all murders are killings of people who do not share the killer’s genes.

Many stories have been told about ‘wicked stepparents’ in numerous myths and fairytales. But, as we know, a lot of stories have some basis in reality. Children of stepparents are 40 times more likely to suffer abuse at the hands of a stepparent. People who are living together who are unrelated to one another are more likely to kill one another. Even adoptions are more successful when the adopting parents view the child as genetically similar to themselves.

In this study carried out by Maillart, et al, it was discovered that for mothers, the average age of offense for filicide was 29.5 years for the mother and 3.5 years for the babe. Bourget, Grace, and Whitehurst, 2007 showed that a risk factor for infanticide was a second child born to a mother under 20-years of age. The reasoning for this is simple: at a younger age the mother is more fertile, and thus, more attractive to potential mates. The older the woman is the more sense it makes to hold on to the genetic investment since it’s harder to make up for the genetic loss late in her reproductive life.

Genetic relatedness, fitness, and parental investment show, in part, why filicides and infanticides occur.

Raping Your Wife

There are evolutionary reasons for rape as well. The rape of a non-relative can be looked at as the ultimate form of ‘cheating’ in this selfish game of life. One who rapes doesn’t have to acquire resources in order to attract a mate, he can just go and ‘take what he wants’ and attempt to spread his genes to the next generation through non-consensual sex. It’s known that rape victims have a higher chance of getting pregnant, with 7.98 percent of rape victims becoming pregnant. (News article) One explanation for this is that the rapist may be able to possibly detect how fertile a woman is. Moreover, rapists are more likely to rape fertile women rather than infertile women.

One rapist that author of the book The Anatomy of Violence, Adrian Raine interviewed said that he specifically chose ugly women to rape (Raine, 2013: 28). He says that he’s giving ugly women ‘what they want’, which is sex. There is a belief that women actually enjoy sex, and even orgasm during the rape, even though they strongly resist and fight back during the attack. Reports of orgasm during rape are around 5 to 6 percent (Raine, 2013: 29), but the true number may be higher since most women are embarrassed to say that they orgasmed during a rape.

Men, as we all know, are more likely to engage in no-strings-attached sex more than women. This is due to the ‘burden’ of sex: children. Women are more likely to carefully select a partner who has numerous resources and the ability to protect the family. Men don’t have the burden of sticking around to raise the child.

Men are more likely to find a sexual relationship more upsetting in comparison to women who are more likely to find an emotional infidelity as more distressing. This data on Americans still held true for South Korea, Germany, Japan, and the Netherlands. Men are better than women at detecting infidelity, and are more likely to suspect cheating in their spouses (Raine, 2013: 32). Unconscious reason being, a man doesn’t want to raise a child who is not genetically similar to themselves.

But this begs another question: why would a man rape his wife? One reason is that when a man discovers his spouse has been unfaithful, he would want to inseminate her as quickly as possible.

There has never in the history of humankind been one example of women banding together to wage war on another society to gain territory, resources or power. Think about it. It is always men. There are about nine male murderers for every one female murderer. When it comes to same-sex homicides, data from twenty studies show that 97 percent of the perpetrators are male. Men are murderers. The simple evolutionary reason is that women are worth fighting for. (Raine, 2013: 32)

A feminist may look at this stat and say “MEN cause all of the violence, MEN hurt women” and attempt to use this data as ‘proof’ that men are violent. Yes, we men are violent, and there is an evolutionary basis for it. However, what feminists who push the ‘all sexes are equal’ card don’t know, is that when they say ‘men are more likely to be murderers’ (which is true), they are actively accepting biological differences between men and women. Most of these differences in crime come down to testosterone. I would also assume that men would be more likely to have the ‘warrior gene’, otherwise known as the MAOA-L gene, which ups the propensity for violence.

The sociobiological model suggests that poorer people kill due to lack of resources. And one reason that men are way more likely to be victims of homicide is because men are in competition with other men for resources.

Going back to the violence on stepchildren that I alluded to earlier, aggression towards stepchildren can be seen as a strategic way of motivating unwanted, genetically dissimilar others out of the home and not take up precious resources for the next generation bred by the stepfather (Raine, 2013: 34).

Women also have a way to increase their fitness, which a brunt of it is through sexual selection. Women are known to be ‘worriers’. That is, they rate dangerous and aggressive acts higher than men. Women are also more fearful of bodily injury and more likely to develop phobias of animals. In these situations, women are protecting themselves and their unborn (or born) children by maximizing their chances for survival by being more fearful of things. This can help explain why women are less physically violent than men and why those murder stats are so heavily skewed towards men: biology.

Women compete for their genetic interests with beauty and childbearing. The more beautiful the woman, the better resources a woman can acquire from a male and this will ensure a healthy life for the offspring.

Evolutionary psychology can help explain the differences in murder between men and women. It can also explain why young mothers kill their children and why stepparents are so abusive to, and are more likely to murder stepchildren. Of course, a social context is involved but we need to look at evolutionary causes for what we think we may be able to simply explain. Because it’s, more often than not, more complex than we could imagine. And that complexity is our Selfish Genes doing anything possible to reproduce more copies of itself through its vehicle: the human body.

The Evolution of Morality

Summary: Moral reasoning is just a post hoc search for reasons to justify the judgments people have already made. When people are asked why, for certain questions, they find things morally wrong, they say they cannot think of a reason but they still think it is wrong. This has been verified by numerous studies. Moral reasoning evolved as a skill to further social cohesiveness and to further our social agendas. Even in different cultures, those with matching socioeconomic levels have the same moral reasoning. Morality cannot be entirely constructed by children based on their own understanding of harm. Thus, cultural learning must play a bigger role than the rationalists had given it. Larger and more complex brains also show more cognitive sophistication in making choices and judgments, confirming a theory of mine that larger brains are the cause of making correct choices as well as making moral judgments.

The evolution of morality is a much-debated subject in the field of evolutionary psychology. Is it, as the nativists say, innate? Or is it as the empiricists say, learned? Empiricists, better known as Blank Slatists, believe that we are born with a ‘blank slate’ and thus acquire our behaviors through culture and experience. In 1987 when John Haidt was studying moral psychology (now known as evolutionary psychology), moral psychology was focused on the third answer: rationalism. Rationalism dictates that children learn morality through social learning and interacting with other children to learn right from wrong.

Developmental psychologist Jean Piaget focused on the type of mistakes that children would make when seeing water moved from different shape glasses. He would, for example, put water into the same size glasses and ask children which one had more water. They all said they held the same amount of water. He then poured water from one glass into a taller glass and then asked the children which glass held more water. Children aged 6 and 7 say that the water level changed since the water was now in a taller glass. The children don’t understand that just because the water was moved to a taller glass doesn’t mean that there is now more water in the glass. Even when parents attempt to explain to their children why there is the same amount of water in the glass, they don’t understand it because they are not ready cognitively. It’s only when they reach an age and cognitive stage that they are ready to understand that the water level doesn’t change, just by playing around with cups of water themselves.

Basically, the understanding of the conservation of volume isn’t innate, nor is it learned by parents. Children figure it out for themselves only when their minds are cognitively ready and they are given the right experiences.

Piaget then applied his rules from the water experiment with the development of children’s morality. He played a marble game with them where he would break the rules and play dumb. The children the responded to his mistakes, correcting him, showing that they had the ability to settle disputes and respect and change rules. The growing knowledge progressed as children’s cognitive abilities matured.

Thus, Piaget argued that like children’s understanding of water conservation is like children’s understanding of morality. He concludes that children’s reasoning is self-constructed. You can’t teach 3-year-old children the concept of fairness or water conservation, no matter how hard you try. They will figure it out on their own through dispute and do things themselves, better than any parent could teach them, Piaget argued.

Piaget’s insights were then expanded by Lawrence Kohlberg who revolutionized the field of moral psychology with two innovations: developing a set of moral dilemmas that were presented to children of various ages. One example given was that a man broke into a drug store to steal medication for his ill wife. Is that a morally wrong act? Kohlberg wasn’t interested in whether the children said yes or no, but rather, their reasoning they gave when explaining their answers.

Kohlberg found a six-stage progression in children’s reasoning of the social world that matched up with what Piaget observed in children’s reasoning about the physical world. Young children judged right and wrong, for instance, on whether or not a child was punished for their actions, since if they were punished for their actions by an adult then they must be wrong. Kohlberg then called the first two stages the “pre-conventional level of moral judgment”, which corresponded to Piaget’s stage at which children judge the physical world by superficial features.

During elementary school, most children move on from the pre-conventional level and understand and manipulate rules and social conventions. Kids in this stage care more about social conformity, hardly ever questioning authority.

Kohlberg then discovered that after puberty, which is right when Piaget found that children had become capable of abstract thought, he found that some children begin to think for themselves about the nature of authority, the meaning of justice and the reasoning behind rules and laws. Kohlberg considered children “‘moral philosophers’ who are trying to work out coherent ethical systems for themselves”, which was the rationalist reasoning at the time behind morality. Kohlberg’s most influential finding was that the children who were more morally advanced frequently were those who had more opportunities for role-taking, putting themselves into another person’s shoes and attempting to feel how the other feels through their perspective.

We can see how Kohlberg and Piaget’s work can be used to support and egalitarian and leftist, individualistic worldview.

Kohlberg’s student, Elliot Turiel, then came along. He developed a technique to test for moral reasoning that doesn’t require verbal skill. His innovation was to tell children stories about children who break rules and then give them a series of yes or no questions. Turiel discovered that children as young as five normally say that the child was wrong to break the rule, but it would be fine if the teacher gave the child permission, or occurred in another school with no such rule.

But when children were asked about actions that harmed people, they were given a different set of responses. They were asked if a girl pushes a boy off of a swing because she wants to use it, is that OK? Nearly all of the children said that it was wrong, even when they were told that a teacher said it was fine; even if this occurred in a school with no such rule. Thus, Turiel concluded, children recognize that rules that prevent harm are moral rules related to “justice, rights, and welfare pertaining to how people ought to relate to one another” (Haidt, 2012, pg. 11). All though children can’t speak like moral philosophers, they were busy sorting information in a sophisticated way. Turiel realized that was the foundation of all moral development.

There are many rules and social conventions that have no moral reasoning behind them. For instance, the numerous laws of the Jews in the Old Testament in regards to eating or touching the swarming insects of the earth, to many Christians and Jews who believe that cleanliness is next to Godliness, to Westerners who believe that food and sex have a moral significance. If Piaget is right then why do so many Westerners moralize actions that don’t harm people?

Due to this, it is argued that there must be more to moral development than children constructing roles as they take the perspectives of others and feel their pain. There MUST be something beyond rationalism (Haidt, 2012, pg. 16).

Richard Shweder then came along and offered the idea that all societies must resolve a small set of questions about how to order society with the most important being how to balance the needs of the individual and group (Haidt, 2012, pg. 17).

Most societies choose a sociocentric, or collectivist model while individualistic societies choose a more individualist model. There is a direct relationship between consanguinity rates, IQ, and genetic similarity and whether or not a society is collectivist or individualistic.

Shweder thought that the concepts developed by Kohlberg and Turiel were made by and for those from individualistic societies. He doubted that the same results would occur in Orissa where morality was sociocentric and there was no line separating moral rules from social conventions. Shweder and two collaborators came up with 39 short stories in which someone does something that would violate a commonly held rule in the US or Orissa. They interviewed 180 children ranging from age 5 to 13 and 60 adults from Chicago and a matched sample of Brahmin children and adults from Orissa along with 120 people from lower Indian castes (Haidt, 2012, pg. 17).

In Chicago, Shweder found very little evidence for socially conventional thinking. Plenty of stories said that no harm or injustice occurred, and Americans said that those instances were fine. Basically, if something doesn’t protect an individual from harm, then it can’t be morally justified, which makes just a social convention.

Though Turiel wrote a long rebuttal essay to Shweder pointing out that most of the study that Shweder and his two collaborators proposed to the sample were trick questions. He brought up how, for instance, that in India eating fish is will stimulate a person’s sexual appetite and is thus forbidden to eat, with a widow eating hot foods she will be more likely to have sex, which would anger the spirit of her dead husband and prevent her from reincarnating on a higher plane. Turiel then argued that if you take into account the ‘informational assumptions’ about the way the world works, most of Shweder’s stories were really moral violations to the Indians, harming people in ways that Americans couldn’t see (Haidt, 2012, pg. 20).

Jonathan Haidt then traveled to Brazil to test which force was stronger: gut feelings about important cultural norms or reasoning about harmlessness. Haidt and one of his colleagues worked for two weeks to translate Haidt’s short stories to Portuguese, which he called ‘Harmless Taboo Violations’.

Haidt then returned to Philadelphia and trained his own team of interviewers and supervised the data collection for the four subjects in Philadelphia. He used three cities, using two levels of social class (high and low) and within each social class was two groups of children aged 10 to 12 and adults aged 18 to 28.

Haidt found that the harmless taboo stories could not be attributed to some way about the way he posed the questions or trained his interviewers, since he used two questions directly from Turiel’s experiment and found the same exact conclusions. Upper-class Brazilians looked like Americans on these stories (I would assume since Upper-class Brazilians have more European ancestry). Though in one example about breaking the dress-code of a school and wearing normal clothes, most middle-class children thought that it was morally wrong to do this. The pattern supported Shweder showing that the size of the moral-conventional distinction varied across cultural groups (Haidt, 2012, pg. 25).

The second thing that Haidt found was that people responded to harmless taboo stories just as Shweder predicted: upper-class Philadelphians judged them to be violations of social conventions while lower-class Brazilians judged them to be moral violations. Basically, well-educated people in all of the areas Haidt tested were more similar to each other in their response to harmless taboo stories than to their lower-class neighbors.

Haidt’s third finding was all differences stayed even when controlling for perceptions of harm. That is, he included a probe question at the end of each story asking: “Do you think anyone was harmed by what [the person in the story] did?” If Shweder’s findings were caused by perceptions of hidden victims, as was proposed by Turiel, then Haidt’s cross-cultural differences should have disappeared when he removed the subjects who said yes to the aforementioned question. But when he filtered out those who said yes, he found that the cultural differences got BIGGER, not smaller. This ended up being very strong evidence for Shweder’s claim that morality goes beyond harm. Most of Haidt’s subjects said that the taboos that were harmless were universally wrong, even though they harmed nobody.

Shweder had won the debate. Turiel’s findings had been replicated by Haidt using Turiel’s methods showing that the methods worked on people like himself, educated Westerners who grew up in an individualistic culture. He showed that morality varied across cultures and that for most people, morality extended beyond the issues of harm and fairness.

It was hard, Haidt argued, for  a rationalist to explain these findings. How could children self-construct moral knowledge from disgust and disrespect from their private analyses of harmlessness (Haidt, 2012, pg. 26)? There must be other sources of moral knowledge, such as cultural learning, or innate moral intuitions about disgust and disrespect which Haidt argued years later.

Yet, surprises were found in the data. Haidt had written the stories carefully to remove all conceivable harm to other people. But, in 38 percent of the 1620 times people heard the harmless offensive story, they said that somebody was harmed.

Haidt found that it was obvious in his sample of Philadelphians that it was obvious that the subjects had invented post hoc fabrications. People normally condemned the action very quickly, but didn’t need a long time to decide what they thought, as well as taking a long time to think up a victim in the story.

He also taught his interviewers to correct people when they made claims that contradicted the story. Even when the subjects realized that the victim they constructed in their head was fake, they still refused to say that the act was fine. They, instead, continued to search for other victims. They just could not think of a reason why it was wrong, even though they intuitively knew it was wrong (Haidt, 2012, pg. 29).

The subjects were reasoning, but they weren’t reasoning in search for moral truth. They were reasoning in support of their emotional reactions. Haidt had found evidence for philosopher David Hume’s claim that moral reasoning was often a servant of moral emotions. Hume wrote in 1739: “reason is, and ought to be only the slave of the passions, and can never pretend to any other office than to serve and obey them.”

Judgment and justification are separate processes. Moral reasoning is just a post hoc search for reasons to justify the judgments people have already made.

The two most common answers of where morality came from are that it’s innate (nativists) or comes from childhood learning (empiricists), also known as “social learning theory”. Though the empiricist position is incorrect.

  • The moral domain varies by culture. It is unusually narrow in western education and individualistic cultures. Sociocentric cultures broaden moral domain to encompass and regulate more aspects of life.
  • People sometimes have gut feelings – particularly about disgust – that can drive their reasoning. Moral reasoning is sometimes a post hoc fabrication.
  • Morality can’t be entirely self-constructed by children based on their understanding of harm. Cultural learning (social learning theory, Rushton, 1981) not guidance must play a larger role than rationalist had given it.

(Haidt, 2012, pg 30 to 31)

If morality doesn’t come primarily from reasoning, then that leaves a combination of innateness and social learning. Basically, intuitions come first, strategic reasoning second.

If you think that moral reasoning is something we do to figure out truth, you’ll be constantly frustrated by how foolish, biased, and illogical people become when they disagree with you. But if you think about moral reasoning as a skill we humans evolved to further our social agendas – to justify our own actions and to defend the teams we belong to – then things will make a lot more sense. Keep your eye on the intuitions, and don’t take people’s moral arguments at face value. They’re mostly post hoc constructions made up on the fly crafted to advance one or more strategic objectives (Haidt, 2012, pg XX to XXI).

Haidt also writes on page 50:

As brains get larger and more complex, animals begin to show more cognitive sophistication – choices (such as where to forage today, or when to fly south) and judgments (such as whether a subordinate chimpanzee showed proper differential behavior). But in all cases, the basic psychology is pattern matching.

It’s the sort of rapid, automatic and effortless processing that drives our perceptions in the Muller-Lyer Illusion. You can’t choose whether or not to see the illusion, you’re just “seeing that” one line is longer than the other. Margolis also called this kind of thinking “intuitive”.

This shows that moral reasoning came about due to a bigger brain and that the choices and judgments we make  evolved because they better ensured our fitness, not due to ethics.

Moral reasoning evolved for us to increase our fitness on this earth. The field of ethics justifies what benefits group and kin selection with minimal harm to the individual. That is, the explanations people make through moral reasoning are just post hoc searches for people to justify their gut feelings, which they cannot think of a reason why they have them.

Source: The Righteous Mind: Why Good People Are Divided By Politics and Religion

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.

Dr. Fred Pescatore says:

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 Statusdoes 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.

 

Individual and Racial Differences in IQ and Allele Frequencies

1300 words

In the past 100 years since the inception of the IQ test there have been racial differences in test scores. What causes these score differences? Genetics? Environment? Both? Recently it has come out that populations do differ in allele frequencies that affect intelligence. David Piffer’s “forbidden paper on population genetics and IQ” was rejected by the new editor of the journal Intelligence. In the paper, he shows how IQ alleles vary in frequency by population. One reviewer even said it should not be put up for review, which Piffer believes there was a hidden agenda or a closed minded attitude. He even puts reviewers comments and responds to them. He says science should be transparent, which is why he’s showing the researchers’ comments on his paper.

His December, 2015 paper titled: A review of intelligence GWAS hits: Their relationship to country IQ and the issue of spatial autocorrelation shows that there are differing allele frequencies in which IQ between populations that affect IQ which are then correlated highly with average IQ by country (r=.92, factor analysis showed a correlation of .86). There was also a “positive and significant correlation between the 9 SNPs metagene and IQ”(pg. 45). However, Piffer does conclude that since the 9 alleles are present within all populations (Africans, Latin Americans, Europeans, South Asians, and East Asians) that the intelligence polymorphisms don’t appear to be race-specific, but were already present in Homo Sapiens before the migration out of Africa. He then goes on to say that it’s extremely likely that the vast majority of alleles were subject do differential selection pressure which lead increases in cognitive abilities at different rates rates in different geographical areas (pg. 49). It’s of course known that differing populations faced differing selection pressures which then lead to genotypic changes which then affected the phenotype. It’s not surprising that genes that correlate strongly with intelligence have differing frequencies in different geographical populations; it’s to be expected with what we know about evolution and natural selection. Below is the scatter plot showing the relationship between polygenic score GWAS (Genome Wide Association Studies) hits and IQ:

Scatter plot IQ-polygenic score

The fact that these differences exist should not come as a shock to those who want to seek the truth, but as seen with how David Piffer didn’t even get consideration for a revision, this shows the bias in science to studies such as this that show racial differences in intelligence exist.

Piffer’s data also corroborates Lynn and Meisenberg’s (2010) finding of a correlation of .907 with measured and estimated IQ. This shows that the differing allele frequencies affect IQ, which then affect a countries GDP, GNP, and over all quality of life.

With a sample with a huge n (over 100,000 subjects) cognitive abilities tests were performed on verbal-numerical reasoning, memory and reaction time (a huge correlate for IQ itself, see Rushton and Jensen, 2005). Davies et al (2016) discovered that there were significant genome-wide SNP based associations in 20 genomic regions, with significant gene-based regions on 46 loci!! Once we find definitive proof that intelligence differences vary between individuals, as well as the loci and genomic regions responsible, we can then move on to difference in allele frequency in depth (which Piffer 2015 was one of the starts to this project).

Moreover, genes that influence intelligence determine how well axons are encased in myelin, which is the fatty insulation that coats our axons, allowing for fast signaling to the brain. Thicker myelin also means faster nerve impulses. The researchers used HARDI to measure water diffusion in the brain. If the water diffuses rapidly in one direction, that shows the brain has very fast connections. Whereas a more broad diffusion would indicate slower signaling, thus lower intelligence. It basically gives us a picture of an individuals mental speed. Thinking of reaction time tests where Asians beat whites who beat blacks, this could possibly show how differing process times between populations manifest itself in reaction time. Since myelin is correlated with fast connections, we can make the inference that Asians have more than whites who have more than blacks, on average. The researchers also say that it’s a long time from now, but we may be able to increase intelligence by manipulating the genes responsible for myelin. This leads me to believe that there must be racial differences in myelin as well, following Rushton’s Rule of Three.

Since the mother’s IQ is the best predictor of the child’s IQ, this should really end the debate on its own. Sure on average, intelligent black mothers would birth intelligent children, but due to regression to the mean, the children would be less intelligent than the mother. JP Rushton also says that regression works in the opposite way. Both blacks and whites who fall below their racial means will have children who regress to the means of 85 and 100 respectively, showing the reality of the genetic mean in IQ between the races.

Why would differing allele frequencies lead to the same cognitive processes in the brain in genetically isolated populations? I’ve shown that brain circuits vary by IQ genes, and populations do differ in this aspect, like all other differing genotypic/phenotypic traits.

East Asians have bigger brains, as shown by MRI studies. Rushton and Rushton (2001) showed that the three races differ in IQ, brain size, and 37 different musculoskeletal traits. We know that West Africans and West African-descended people have genes for fast twitch muscle fibers (Type II) (Nielson and Christenson, 2001). Europeans and East Asians have slow twitch muscle fibers (Type I) for strength and endurance. (East Africans have this as well, which allows for ability to run for distance, which fast twitch fibers do not allow for. The same is true for slow twitch fibers and sprinting events.) Bengt Saltin showed that European distance runners have up to 90 percent slow twitch fibers (see Entine, 2000)! So are genetic IQ differentials really that hard to believe? With all of these differing variables in regards to intelligence that all point to a strong genetic cause for individual differences in other genes that lead to stark phenotypic differences between the races, is it really not plausible that populations differ in intelligence, which is largely inherited?

Is it really plausible that differing populations would be the same cognitvely? That they would have the same capacity for intelligence? Even when evolution occurred  in differing climates?  The races/ethnicities differ on so many different variables with differing genes being responsible for it. Would IQ genes really be out of the question? Evolution didn’t stop from the neck up. Different populations faced different selection pressures, so different human traits then evolved for better adaption in that environment. Different traits clearly developed in genetically isolated populations that had no gene flow with each other for tens of thousands of years. These differing evolutionary environments for the races put different pressures on them, selecting some for high IQ alleles and others for low IQ alleles.

We are coming to a time where intelligence differences between populations will become an irrefutable fact. With better technology to see how differing genes or sets of genes affect our mind as well as physiology, we will see that most all human differences will come down to differing allele frequencies along with differing gene expression. Following Rushton’s simple rule based on over 60 variables, East Asians will have the most high IQ alleles followed by Europeans and then blacks. The whole battery of different cognitive abilities tests that have been conducted over the past 100 years show us that there are differences, yet we haven’t been able to fully explain it by GWAS and other similar techniques. Charles Murray says within the next 5 to 10 years we will have definitive proof that IQ genes exist. After that, it’s only a matter of time before it comes out that racial differences in IQ are due to differing allele frequency as well as gene expression.

How to Use Current Knowledge to Effectively Treat the Symptoms of PWS Patients

2550 words

Abstract

Researchers have tried to manage those with Prader-Willi’s Syndrome for multiple decades. Though they have greatly curbed some of the implications of the disease, there are still numerous ways in which we can better use our knowledge of how the disease manifests in order to better help those suffering from PWS. Looking at research into how the extra chromosome 15 is linked to low IQ; IQ and its relationship to obesity; how the ability to delay gratification leads to obesity; growth hormone treatment to better treat low muscle mass and higher body fat; and finally using reinforcement theory to punish a response, where doing so will greatly diminish the probability of that response occurring again in the future; all of these factors can be used in conjunction to better mitigate problems from the disease. By examining all of these variables and thinking of better ways to handle them, we can then think of other, better ways to manage those with PWS. In doing so, we can better increase the quality of life of those suffering from PWS, as well as have less of a strain on healthcare workers who care for them. With new advances in technology with CRISPR Cas9, we can then edit the genomes and chromosomes of those suffering from this disease.

 

How to Use Current Knowledge to Effectively Treat and Manage the Symptoms of PWS Patients

How can we use the research on chromosomal differences, research on their IQ differences and their lack of ability to delay gratification that, in turn, would help those individuals with the disease?  Seventy percent of PWS cases are attributed to the deletion of chromosome 15 (Ledbetter et al, 1981). Maternal uniparental disomy, which involves receiving an extra chromosome 15 from the mother, is yet another cause of PWS (Wang, 2004).

Whittington, Holland and Webb (2009) found that there was variation between families in deletion of chromosome 15. They found that the PWS and sibling IQ correlation was .3, a modest correlation.  What was also noticed was that there were subtype differences which manifested itself in the familial differences in IQ. As they expected, the correlation with normal siblings and those with PWS was .5 in those who suffered from PWS due to unilateral disomy. But in the second subset (the chromosomal deletion subset), the correlation was negative at -0.07. Their research shows great promise in the role of chromosome 15 and IQ. They end up concluding that there needs to be an explanation for the small genetic differences between them. How can we use these differences in IQ to help people with PWS and what does this suggest for other symptoms of their disease?

Kanazawa (2014), reviewed the data on the research between obesity and IQ. What he found was that those studies that concluded that obesity causes lowered intelligence only observed cross-sectional studies. Longitudinal studies that looked into the link between obesity and intelligence found that those who had low IQs since childhood then became obese later in life and that obesity does not lead to low IQ.  The average IQ for an individual suffering from PWS is 65 (Butler, Lee and Whitman 2006, p. 13), so that is one reason they have a tendency to be obese. He states that those with IQs below 74 gained 5.19 BMI points, whereas those with IQs over above 126 gained 3.73 BMI points in 22 years, which is a statistically significant difference. Also noted, was that those at age 7 who had IQs above 125 had a 13.5 percent chance of being obese at age 51, whereas those with IQs below 74 at age 7 had a 31.9 percent chance of being obese. This data makes it clear: low IQ is correlated with obesity, so we, therefore, need to find sufficient measures to help those with lower IQs who also suffer from PWS to better maintain their good health. Since we can better identify those PWS individuals who have lower IQs based on how they got the disease, we can then show them more attention in an effort to have them manage their gratification better. Moreover, the lack of ability to delay gratification is also correlated with low IQ (Mischel, Ebbeson, and Zeiss, 1972).

Schlam et al. (2013) observed in a follow-up study to the Marshmallow Experiment that found in a longitudinal study of individuals they found forty years later from the original Marshmallow Experiment, due to inability to delay gratification forty years previously, that was one cause of becoming obese forty years later. Due to PWS sufferers having lower average IQs, and, therefore, a lack of ability to delay their gratification, this is direct evidence that those PWS sufferers with low IQs need more stringent measures to be taken on them, which would then be helpful to those individuals who have a hard time delaying their gratification, which is partially caused by the drop in IQ due to the additional chromosome 15. We can see how those with PWS act; they want their gratification now and do not want to wait for it. This is why, when unsupervised, that those with PWS gorge on the food they understand they should not have, but do so, nevertheless, since their low IQ is correlated with lack of ability to delay gratification, which manifests itself in their obesity. We clearly need to find better methods in which to help those with low ability to delay gratification, which would strongly help those suffering from PWS.

Dykens et al (1997) note that those with PWS have hyperphagia, which correlates with their insatiable want for food. They state that the lack of fullness is due to an altered function of the hypothalamus, which is the part of the brain that is in control of feelings of satiety. Certain States gave restrictions to homes that take care of those with PWS and have come under fire because of this, mainly due to human rights violations. We must ask, then, should we limit their access to food if it will prolong their lives? Will doing so inhibit their freedom to do as they choose? PWS sufferers also have coronary heart problems; one could argue that given their free ability to choose what they want to do unfettered will lead to premature death due to obesity-related complications. Does their disease truly not allow them to learn the consequences of their behavior? Do they have the intellect to really understand the consequences of their actions of consuming too much food? There is no established or known way to control those with insatiable eating habits due to hyperphagia. So would the best course of action to take with those with PWS actually be to constantly monitor them and to lock access to easily attainable food? My answer is yes, however, there is a clear fine line in whether restricting access to food and constantly monitoring those with PWS infringes on their human rights, or that doing so actually will help them live better, healthier lives since they would have the constant supervision around them to better control their out of control eating habits. When negative actions occur, one idea that can be shown to them is constant positive reinforcement so that they may be better able to understand that what they are doing is harmful to their bodies. We can then use positive reinforcement when they do reach a healthy weight, so, in turn, they will have a higher chance of keeping a healthy weight. They may reap the benefits of positive reinforcement, and stick more closely to their program, and therefore, stay healthy.

The hormone ghrelin is secreted from the hypothalamus. With an altered hypothalamus, this would cause ghrelin levels to overload; then the individual suffering from PWS would feel the need to insatiably gorge on food due to this chemical imbalance in the brain. Ghrelin increased feeding in rats and ghrelin is the physiological mediator of feeding and probably has a function in growth regulation by stimulating feeding and release of growth hormone (Nakazato et al, 2001). There is a correlation between want of food, ghrelin release and growth hormone production. By attempting to mediate these variables, those who suffer from PWS will be able to better control their eating habits through positive reinforcement and better, more sustainable habits. Since whenever we eat we get a release of ghrelin that makes us hungry, people pretty much set their own eating times by eating multiple times a day. This affects PWS patients the same way. They can’t stop eating, due in part to constantly eating which constantly releases ghrelin in their body.

PWS sufferers have low muscle tone and, conversely, more body fat. Growth hormones may be a valid way of alleviating that problem, which in turn will give them a slightly higher resting metabolic rate so that they may burn slightly more calories, in an effort to stay healthier. Growth hormone therapy is great for those with PWS though they are largely inactive and lead a sedentary lifestyle, the growth hormone will allow them to have less body fat and more muscle mass. As noted earlier in my paper, those suffering from PWS have altered function in their hypothalamus, which is also where growth hormone is secreted. Aycan and Bas (2014) state that treatment with growth hormones should be strongly considered for those with PWS.

PWS sufferers are also quick to anger, which can be correlated with their sub-average IQ. They may, for instance, become irate at the fact that they do not have constant access to food, and may turn to emotional, angry and infantile outbursts in an attempt to receive what they want. This is one way that it’s tricky to treat those with the disease. How do you tell an individual with PWS who wants something “No”? Measures should be taken to show those with the disease what they are doing to their bodies in the simplest way possible as to better get the point across to them. We can help those sufferers of PWS who are quick to anger with by allowing them to discern between right and wrong ways to handle times when they don’t get what they want with positive reinforcement.

Since those who suffer from PWS have behavioral problems, there are better measures we can take to assure that they don’t have their violent outbursts. When positive reinforcement is consistently shown to an individual who has PWS, he will have more success with his program. When they do something wrong, they can then be shown positive reinforcement, and through being shown positive things with reinforcement theory, they can better learn that certain actions they take are dangerous and shouldn’t be done again, as Rushton (1980) states: “If one rewards a response, it will increase the probability of the future occurrence of that response. If one punishes a response, it will decrease the future probability of the occurrence of that response.” (p. 90).

Discussion

In this paper, I have presented causes for PWS as well as effective ways to manage the disease. To look at how IQ affects individuals in regards to obesity and because it is highly correlated with other measures as well, we can then better help those with the disease. By seeing which individuals have the parental disomy version of PWS, we can then monitor them and give them better care because of their lowered IQ and make sure they stay at a healthy weight. One of the best measures to take is to heavily restrict food, i.e., make sure ability to access food at all hours of the day is restricted along with constant supervision. Though, there are rights groups fighting for them saying that their human rights are being infringed on. In allowing them to have free reign over what, how and when they eat, they will gorge themselves to obesity, as well as lead themselves to horrible complications that come along with increased food consumption. When one is caught consuming food he or she shouldn’t be consuming, punishing them and letting them understand that the behavior they took was wrong will lead to better choices and outcomes from those choices, due in part to the main facet of reinforcement theory, that punishing a response will lead to a reduced outcome in that response that was punished happening in the future. Also, with the advent of CRISPR Cas9, we will be able to edit genomes, and therefore, eventually, put an end to PWS. It will enable us to fix the chromosomal deletion and uniparental disomy, which will eradicate this disease.

Conclusion

There are better, more helpful ways in which to help those suffering from PWS. By identifying and attempting to correct these abnormalities, those who suffer from the disease can, therefore, have a better quality of life due in part to the extra measures taken. By understanding that their lower average IQs lead to a lot of the problems associated with the disease, we can better structure methods for them to keep on a healthy track and reinforce positive behavior through reinforcement theory. Since obesity is correlated highly with low IQ, we can, therefore, use this information to better help those who suffer from PWS that have low IQs. Locking up food instead of providing free access, as well as understanding they do not have the ability to delay gratification, would be a big start to find better ways to treat sufferers of PWS. Treating negative actions with positive reinforcement through reinforcement theory will lead to better and increased prosocial behavior. It’s been shown that if you punish a response, then it will decrease the future probability of that response occurring. The advent of CRISPR Cas9 will then allow us to edit the chromosomes of those with this disease in the future. Should we use genome editing on individuals with this disease, as well as several other chromosomal/genetic diseases? I believe we should, in doing so, we will greatly increase the quality of life of those with the disease.

 

References

Aycan, Z., & Baş, V. N. (2014). Prader-Willi Syndrome and Growth Hormone Deficiency. Journal of Clinical Research in Pediatric Endocrinology Jcrpe, 62-67.

Butler, M. G., Lee, P. D., & Whitman, B. Y. (2006). Management of Prader-Willi syndrome (3rd ed.). New York: Springer-Verlag.

Dykens, E. M., Goff, B. J., Hodapp, R. M., Davis, L., Devanzo P., Moss, F. . . King, B. (1997). Eating Themselves to Death: Have “Personal Rights” Gone Too Far in Treating People With Prader-Willi Syndrome? Mental Retardation, 35(4), 312-314.

Kanazawa, S. (2014). Intelligence and obesity. Current Opinion in Endocrinology & Diabetes and Obesity, 21(5), 339-344.

Ledbetter, D. H., Riccardi, V. M., Airhart, S. D., Strobel, R. J., Keenan, B. S., & Crawford, J. D. (1981). Deletions of Chromosome 15 as a Cause of the Prader–Willi Syndrome. New England Journal of Medicine N Engl J Med, 304(6), 325-329.

Mischel, W., Ebbesen, E. B., & Zeiss, A. R. (1972). Cognitive and attentional mechanisms in delay of gratification. Journal of Personality and Social Psychology, 21(2), 204-218.

Nakazato, M., Murakami, N., Date, Y, et al (2001). A role for ghrelin in the central regulation of feeding Nature 409, 194-198

Rushton, J. P. (1980). Altruism, socialization, and society. Englewood Cliffs, NJ: Prentice-Hall.

Schlam, T. R., Wilson, N. L., Shoda, Y., Mischel, W., & Ayduk, O. (2013). Preschoolers’ Delay of Gratification Predicts their Body Mass 30 Years Later. The Journal of Pediatrics, 162(1), 90-93.

Whittington, J., Holland, A., & Webb, T. (2009). Relationship between the IQ of people with Prader-Willi syndrome and that of their siblings: Evidence for imprinted gene effects. Journal of Intellectual Disability Research, 53(5), 411-418.

YM Wang, L Chuang, BT Wang, et al. Maternal uniparental disomy in a patient with Prader-Willi syndrome with an additional small inv dup(15) chromosome. J Formos Med Assoc, 103 (2004), pp. 943–947

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