SMOKERS TEND TO BE DEPRESSED -- AND IT'S GENETIC

Popular summary below followed by abstract. Note that the genes predisposing to smoking also predispose to generally bad behaviour -- which helps to explain the long-known fact that smoking tends to be part of a syndrome of general social disadvantage: Smokers tend to be dumber, poorer etc. The present finding shows how broad that syndrome is

SMOKING and depression have a common genetic link, according to a new study in the journal Twin Research and Human Genetics. The study found that nicotine dependence and major depression are both associated with extreme rebellious behaviour during childhood and adolescence -- a condition known as "conduct disorder". In 1992, the research team conducted telephone interviews with 3360 pairs of male twins aged 35 to 53, who served in the military during the Vietnam War. Fifty-six per cent of the pairs were genetically identical twins, and 44 per cent were fraternal twins who shared half their genes. Answers from each twin were compared to estimate the genetic and environmental influences on nicotine addiction and major depression. Genes that increased a person's risk of developing nicotine addiction and major depression were also found in those with conduct disorder. The findings may also help to explain why smoking seems to run in some families, say the authors.

Source

Journal Abstract follows:

Common Genetic Risk of Major Depression and Nicotine Dependence: The Contribution of Antisocial Traits in a United States Veteran Male Twin Cohort

By Qiang Fu et al.

Many studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

Twin Research and Human Genetics. Volume: 10, Issue: 3, June 2007, 470-478





SOME HOPE FOR CROHN'S DISEASE

Popular summary followed by journal abstract. The benefit conferred by the drug seems rather weak, sadly. Only a net 8% of patients showed some benefit from the drug after 6 weeks, rising to 10% after 26 weeks. Still no real light at the end of the tunnel

CROHN'S disease -- an inflammatory disorder of the gastrointestinal tract -- affects an estimated 28,000 Australians and has no known medical cure. But a study in the New England Journal of Medicine this week has found that a new drug called certolizumab pegol is an effective treatment for adults with the disease. The drug acts by blocking a protein called tumour necrosis factor (TNF), which is a major cause of gut inflammation. The study involved 662 patients with moderate to severe Crohn's disease, who were randomly assigned to receive certolizumab pegol or a placebo. After six weeks, 35 per cent of patients who received the drug showed improvement in their symptoms, while improvement was seen in 27 per cent of patients who received the placebo. The only side effect of certolizumab pegol was a small increase in the risk for serious infection, including one case of pulmonary tuberculosis.

Source


Abstract:

Certolizumab Pegol for the Treatment of Crohn's Disease

By: William J. Sandborn et al.

Methods: In a randomized, double-blind, placebo-controlled trial, we evaluated the efficacy of certolizumab pegol in 662 adults with moderate-to-severe Crohn's disease. Patients were stratified according to baseline levels of C-reactive protein (CRP) and were randomly assigned to receive either 400 mg of certolizumab pegol or placebo subcutaneously at weeks 0, 2, and 4 and then every 4 weeks. Primary end points were the induction of a response at week 6 and a response at both weeks 6 and 26.

Results: Among patients with a baseline CRP level of at least 10 mg per liter, 37% of patients in the certolizumab group had a response at week 6, as compared with 26% in the placebo group (P=0.04). At both weeks 6 and 26, the corresponding values were 22% and 12%, respectively (P=0.05). In the overall population, response rates at week 6 were 35% in the certolizumab group and 27% in the placebo group (P=0.02); at both weeks 6 and 26, the response rates were 23% and 16%, respectively (P=0.02). At weeks 6 and 26, the rates of remission in the two groups did not differ significantly (P=0.17).

Serious adverse events were reported in 10% of patients in the certolizumab group and 7% of those in the placebo group; serious infections were reported in 2% and less than 1%, respectively. In the certolizumab group, antibodies to the drug developed in 8% of patients, and antinuclear antibodies developed in 2%.

Conclusions: In patients with moderate-to-severe Crohn's disease, induction and maintenance therapy with certolizumab pegol was associated with a modest improvement in response rates, as compared with placebo, but with no significant improvement in remission rates.

NEJM Volume 357:228-238; July, 2007

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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].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

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