Wednesday, December 19, 2007

Anorexia `cannot be picked up by looking at photographs of super-thin models'

I have long said that anorexia is just another obsessive compulsive disorder -- an inherited brain dysfunction or "psychosis". In layman's language, anorexics are "mad". The study below, however, is too small to be conclusive.

Anorexia may be caused by inherited differences in the way a sufferer's brain operates, leading to obsessive behaviour, according to research. Rather than being triggered by images of super-thin models and celebrities, the eating disorder could be brought on by the in-built way in which the brain responds to pleasure and reward. It has been argued that images of unhealthily thin stars in the media have encouraged anorexic behaviour in impressionable young women. But a study published in The American Journal of Psychiatry suggests that the brains of anorexia sufferers behave differently to those of the rest of the population and that certain people are born with a susceptibility to develop the condition.

A team of psychiatrists, led by Walter Kaye, of the University of Pittsburgh, tested the emotional responses of 13 former anorexics compared with those of 13 nonsufferers. The women were asked to play a computer game where correct guesses were rewarded financially. During the test, the team used functional MRI scans to monitor the participants' brain activity by measuring blood levels in certain areas.

Among the nonsufferers, the brain region connected to emotional responses - the anterior ventral striatum - showed strong differences between winning and losing the game. Among the women with a history of anorexia, however, there was little difference in activity between winning and losing. Professor Kaye said: "In anorexia, this might impact on food enjoyment. For anorexics, then, perhaps it is difficult to appreciate immediate pleasure if it does not feel much different from a negative experience."

Another brain area, the caudate, involved in linking actions to outcome and planning, was far more active in the recovering anorexics than in the control group. The former tended to have exaggerated worries about the consequences of their behaviours, looked for rules where there were none and were overly concerned about making mistakes.

"There are some positive aspects to this kind of temperament. Paying attention to detail and making sure things are done as correctly as possible are constructive traits in careers such as medicine or engineering," Professor Kaye said. "But carried to extremes, such obsessive thinking can be harmful, which is what happens in anorexia. This piece of research points to the fact that the brains of people with anorexia are wired differently. "This means they react and think in different ways to the ordinary person and that they are more likely to go on to develop anorexia regardless of whether they have been exposed to images of super-thin models."

Professor Kaye said that his study showed that even former anorexics still had difficulty enjoying simple pleasures. "What this points to is that anorexics have something different going on in their brains, which marks them out as having either different structures in the brain or different pathways for processing thought that stay with them for life. We may be able, with a lot of hard work, to get them back to eating, but deep down in their brain there appear to be biological differences that don't go away."

Ian Frampton, a psychologist at Exeter University, has been working with anorexics using the same MRI technology. He said: "Professor Kaye's research supports a growing feeling that anorexia is a biological condition caused by the brains of some people being structured in a different way. We are still conducting our research, but we are seeing similar things. "We are not totally sure what is happening in these youngsters but we think that some of this might be inherited or some might be due to a fault in the developing brain either in the womb or during early childhood."

Dr Frampton said that while all adolescent girls have issues about body image, for most it is a passing phase: "We need to move away from this idea that supermodels are to blame. It is probably not good for them to look as they do. But for anorexics, the desire not to eat and to be thin seems to be already in them and not something they can pick up by looking at a magazine. "There were, after all, anorexics before super-thin models."


Cholesterol mysteries

More proof that nobody really understands what goes on with cholesterol or the drugs used to treat it. See here for a summary of the "mysteries" concerned

Pfizer stunned heart doctors a year ago when it announced that its experimental good-cholesterol boosting drug had killed patients in final-stage trials. Now Merck says it plans to begin final-stage trials of a similar good-cholesterol boosting drug next year. Both the Merck compound and the ill-fated Pfizer compound raise HDL, or so-called good cholesterol, by blocking a key protein called CETP. The hope is that this, when combined with existing cholesterol drugs, will prevent more heart attacks. Pfizer's compound, torectrapib, was touted as the next big thing in cardiology--until large-scale human trials found a much higher death rate in patients that took it vs. Lipitor.

The terrible results from torcetrapib have thrown the field of boosting good cholesterol into turmoil. One theory is that the increased deaths were due to torcetrapib's tendency to raise blood pressure and boost aldosterone. But another theory is the entire mechanism is flawed, and the blocking CETP produces dysfunctional HDL that just worsens the problem. Confusing matters further, the big torcetrapib trial found not only more heart deaths but also more deaths from infection and cancer in those who took Lipitor alone.

Merck's drug anacetrapib doesn't raise blood pressure or aldosterone like the Pfizer compound. No increased heart side effects have been seen in trials so far. But whether it produces the right kind of HDL particles is unknown. "The simple answer is that it still is a puzzle" about what went wrong with torcetrapib, Merck research chief Peter Kim said at an analyst meeting Dec 11. The quality of HDL produced by CETP blockers "is a key question in the scientific community" currently. "We have to run clinical studies and evaluate whether this is a good mechanism."

Kim said Merck plans to move step-by-step into large-scale trails of its CETP drug next year by first doing more extensive trials next year to evaluate blood parameters over longer periods of time. In 2009, if these show no signs of problems, it plans to begin a a large-scale "outcomes" study to determine whether the drug prevents heart attacks. Exactly what form this trial would take has yet to be determined, Kim says, as "there are many things that are being argued about . we are still doing a lot of work in the labs."

Merck takes some confidence that blocking CETP can work from the fact that most animal studies show that CETP-blockers reduce artery gunk. Also, the HDL produced by anacetrapib appears to be functional in test tube experiments.

In another risky gambit, Merck says that it plans to file for regulatory approval for its obesity drug taranabant next year. The drug is the same class as Sanofi-Aventis' rimonabant (Acomplia), which was once heralded as a miracle pill but was roundly rejected by a U.S. Food and Drug Administration advisory panel last summer because of concerns over psychiatric side effects.

Kim says the company observed "dose-dependent psychiatric adverse events" in its trials of taranabant. He said that he thought the psychiatric effects were directly related to the drug's mechanism.

To minimize problems, the company is only studying the lower two of four doses used in the second-stage tests. It is also including people with controlled depression in its final-stage studies. It hasn't made a final decision as to what indications it will file for, although it will likely include obesity.

Merck says it has seven drugs in final-stage trials, including an osteoporosis drug that works by a new mechanism, a new cancer drug for treating sarcoma in collaboration with Ariad Pharmaceuticals, and a new hepatitis B vaccine.



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 conditions 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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