Talking to blondes makes you dumb?

According to the study reported below, men know less after talking to a blonde woman. Those of us who have been married to a blonde lady sure must have had a tough time in life! I am not going to question the findings at this stage as the article had not yet appeared in the online version of the journal at the time of writing, but if it is like most articles in the journal, it is not based on a representative sample of any known population so has no known generalizability. The people studied appear to have been French but it may not even apply to all Frenchmen.

What I DO want to do, however, is highlight the fallacy of the explanation given. The explanation in terms of stereotypes accepts the old view that stereotypes are in some way imprisoning. Studies of stereotyping have however long ago shown just the opposite: that stereotypes are highly flexible and responsive to new information. See here and here.

That some psychologists still believe the old myths about stereotyping is true to form, however. Psychologists tend to live in an eternal present with very little awareness of the research literature on the subjects they discuss. See here.

A more plausible explanation would be that brown-haired people are very often blonde in childhood so blonde is a signal of childhood and we have evolved to interact differently with children. But the best explanation should I think be obvious: For whatever reason, blondes are seen as more sexually attractive and sexual arousal is notorious for addling the brain -- particularly among Frenchmen, perhaps?

When men meet fair-haired women they really do have a "blonde moment". Scientists have found that their mental performance drops, apparently because they believe they are dealing with someone less intelligent. Researchers discovered what might be called the "bimbo delusion" by studying men's ability to complete general knowledge tests after exposure to different women. The academics found that men's scores fell after they were shown pictures of blondes.

Further analysis convinced the team that, rather than simply being distracted by the flaxen hair, those who performed poorly had been unconsciously driven by social stereotypes to "think blonde". "This proves that people confronted with stereotypes generally behave in line with them," said Thierry Meyer, joint author of the study and professor of social psychology at the University of Paris X-Nanterre. "In this case blondes have the potential to make people act in a dumber way, because they mimic the unconscious stereotype of the dumb blonde." The research adds to a body of evidence that people's behaviour is powerfully influenced by stereotypes. Previously scientists have found that people walk and talk more slowly in front of the elderly, while other studies have revealed that unconscious racial assumptions and prejudices emerge in written tests.

Researchers believe that blondes have been particularly vulnerable to stereotyping over the past century. The image of the dizzy blonde came to prominence in the 1925 Anita Loos novel Gentlemen Prefer Blondes. Film stars including Marilyn Monroe, Suzanne Somers and Goldie Hawn further popularised the "dumb blonde". The persona has more recently been boosted by celebrities such as Paris Hilton, the member of the hotel family nicknamed the "heirhead", and Jessica Simpson, the singer.

Others believe its origins go far deeper. According to researchers at St Andrews University, north European women evolved blonde hair and blue eyes at the end of the Ice Age to make them stand out from their rivals at a time of fierce competition for scarce males.

Psychologists have suggested that because white babies are often born blond, there is a primal association between blondness and childhood, encouraging people to admire and fawn over the pale-haired.

The new peer-reviewed study, published in the Journal of Experimental Psychology, was based on two trials. In all cases those participants exposed to images of blondes recorded the lowest scores.

Source





FAT GENE DISCVERED

A gene that contributes to obesity has been identified for the first time, promising to explain why some people easily put on weight while others with similar lifestyles stay slim. People who inherit one version of the FTO gene rather than another are 70 per cent more likely to be obese, British scientists have discovered. One in six people have the most vulnerable genetic makeup and weigh an average of 3kg more than those with the lowest risk. They also have 15 per cent more body fat.

The findings provide the first robust link between any common gene and obesity, and could eventually lead to new ways of tackling one of the most significant causes of ill health in developed countries such as the UK. One in four British adults is now classified as obese, and half of men and a third of women are overweight. Obesity is a major cause of heart disease, cancer and type-2 diabetes, and an adviser to the Government's health spending watchdog described it recently as a bigger national hazard than smoking, alcohol or poverty. If the biological function of the FTO gene can now be understood, it could become possible to design drugs that manipulate it to help people to control their weight.

"Even though we have yet to fully understand the role played by the FTO gene in obesity, our findings are a source of great excitement," said Professor Mark McCarthy of the University of Oxford, who led the research. "By identifying this genetic link, it should be possible to improve our understanding of why some people are more obese, with all the associated implications such as increased risk of diabetes and heart disease. New scientific insights will hopefully pave the way for us to explore novel ways of treating this condition."

While it has long been understood from family studies that obesity is heavily influenced by genetics, scientists have struggled to pin down individual genes that are involved. A handful of serious genetic mutations that cause rare obesity disorders such as Prader-Willi syndrome have been found, but the search for common genes that affect ordinary people's risk of becoming obese or overweight has remained elusive.

The effect of FTO emerged from a major study of the genetic origins of disease funded by the Wellcome Trust known as the Case Control Consortium, in which 2,000 people with type-2 diabetes had their genomes compared to 3,000 healthy controls. Scientists from Oxford and the University of Exeter first found that certain versions of the FTO gene were more common among people with type-2 diabetes, but that the effect disappeared when the data were adjusted for obesity. This led them to wonder whether FTO actually influenced obesity instead, and they followed up their theory in a further 37,000 people.

FTO comes in two varieties or "alleles", and everyone inherits two copies of the gene, one from each parent. The team found that people who inherit two copies of one variant - 16 per cent of white Europeans - were 70 per cent more likely to be obese than those who inherited two copies of the other allele. The 50 per cent of subjects who inherited one copy of each FTO variant had a 30 per cent higher risk of obesity. Those in the highest risk group weighed an average of 3kg more and those at medium risk were an average of 1.2kg heavier. In each case, the extra weight was entirely accounted for by more body fat, not greater muscle or extra height. The results, which are published in the journal Science apply to both men and women, and to children as young as seven.

FTO will not be the only gene that influences obesity, and inheriting a particular variant will not necessarily make anyone fat. "There are going to be lots of slim people with two copies of the bad allele, and if people who have the more favourable version overeat or don't exercise they are still going to become obese," Professor McCarthy said. "This is not a gene for obesity, it is a gene that contributes to risk." The biological function of FTO remains unknown, and the scientists now plan to study this by creating genetically modified mice in which the gene is knocked out.

Professor McCarthy said the gene is highly active in the hypothalamus, a part of the brain involved in appetite control, suggesting that one potential way it might have its effect. The gene could also influence how readily fat cells are laid down.

The research involved too many people to control for exercise and diet, so it is not yet known whether FTO affects how much people eat or how active they are. Andrew Hattersley, who headed the Exeter group, said it might nevertheless explain how people with apparently similar lifestyles differ in their propensity to put on weight. "Our findings suggest a possible answer to someone who might ask: `I eat the same and do as much exercise as my friend next door, so why am I fatter?'" he said. "There is clearly a component to obesity that is genetic."

Professor McCarthy played down the idea of screening people for FTO, so they can change their diet or exercise habits if they are found to be at higher risk. "We are not pushing genetic testing here. A 3kg increase is significant, but it is not 30kg, and there are always going to be other genes and environmental factors involved. The best way of predicting who is becoming obese is to weigh them."

Independent obesity experts said the discovery was highly significant. Susan Jebb of the MRC Human Nutrition Unit said: "This research provides clear evidence of a biological mechanism which makes some people more susceptible to gaining weight in a world where food is plentiful and sedentary lifestyles the norm. By studying the action of this gene we may learn more about the detailed causes of obesity."

Professor Steve O'Rahilly of Cambridge said: "It is unlikely to be the only such genetic variant, but it is the first to be discovered. Unfortunately we have no idea what this gene actually does to alter our degree of fatness. It is made in every cell in the body and doesn't look like any genes whose functions we understand so we have very few clues as to how it might affect a person's risk of obesity. This is a very exciting first step but there is much work still to do."

Source

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Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

9). And how odd it is that we never hear of the huge American study which showed that women who eat lots of veggies have an INCREASED risk of stomach cancer? So the official recommendation to eat five lots of veggies every day might just be creating lots of cancer for the future! It's as plausible (i.e. not very) as all the other dietary "wisdom" we read about fat etc.

10). And will "this generation of Western children be the first in history to lead shorter lives than their parents did"? This is another anti-fat scare that emanates from a much-cited editorial in a prominent medical journal that said so. Yet this editorial offered no statistical basis for its opinion -- an opinion that flies directly in the face of the available evidence.

Even statistical correlations far stronger than anything found in medical research may disappear if more data is used. A remarkable example from Sociology:

"The modern literature on hate crimes began with a remarkable 1933 book by Arthur Raper titled The Tragedy of Lynching. Raper assembled data on the number of lynchings each year in the South and on the price of an acre's yield of cotton. He calculated the correla-tion coefficient between the two series at -0.532. In other words, when the economy was doing well, the number of lynchings was lower.... In 2001, Donald Green, Laurence McFalls, and Jennifer Smith published a paper that demolished the alleged connection between economic condi-tions and lynchings in Raper's data. Raper had the misfortune of stopping his anal-ysis in 1929. After the Great Depression hit, the price of cotton plummeted and economic condi-tions deteriorated, yet lynchings continued to fall. The correlation disappeared altogether when more years of data were added."

So we must be sure to base our conclusions on ALL the data. But in medical research, data selectivity and the "overlooking" of discordant research findings is epidemic.

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