Thursday, February 22, 2007


There has been a lot of very weak research purporting to show adverse effects of "secondhand" tobacco smoke -- i.e. smoke inhaled by a nonsmoker as a byproduct of being in the presence of a smoker. The research below would seem to bypass the usual criticisms -- though it should be noted that it provides no data on longevity effects. Given the known reduced longevity of smokers, however, the findings must be considered as very suggestive. Journal abstract follows:

Exposure to Secondhand Smoke and Biomarkers of Cardiovascular Disease Risk in Never-Smoking Adults

By Andrea Venn & John Britton

Background--Exposure to secondhand smoke has been associated with a disproportionately high risk of coronary heart disease, thought to be mediated through inflammation, platelet aggregation, and/or endothelial dysfunction. The epidemiological association between objectively measured exposure to secondhand smoke and biomarkers of heart disease risk has not been investigated, however.

Methods and Results--We have investigated the cross-sectional relation between secondhand smoke exposure, measured objectively as cotinine, and recognized biomarkers of heart disease risk, namely C-reactive protein, homocysteine, fibrinogen, and white blood cell count, in 7599 never-smoking adults from the Third National Health and Nutrition Examination Survey. Compared with subjects with no detectable cotinine, those with detectable but low-level cotinine (range, 0.05 to 0.215 ng/mL) had significantly higher levels of both fibrinogen (adjusted mean difference, 8.9 mg/dL; 95% CI, 0.9 to 17.0; P=0.03) and homocysteine (0.8 æmol/L; 95% CI, 0.4 to 1.1; P<0.001) but not C-reactive protein or white blood cell count. Effect estimates of similar magnitude and significance were seen in subjects in the high category of cotinine exposure (>0.215 ng/mL). The increased levels of fibrinogen and homocysteine seen in relation to secondhand smoke exposure were equivalent to ~ 30% to 45% of those seen for active smoking.

Conclusions--Passive smokers appear to have disproportionately increased levels of 2 biomarkers of cardiovascular disease risk, fibrinogen and homocysteine. This finding provides further evidence to suggest that low-level exposure to secondhand smoke has a clinically important effect on susceptibility to cardiovascular disease.

Smoking has 'heroin effect' on brain

SMOKING causes long-lasting changes in the brain similar to changes seen in animals when they are given cocaine, heroin and other addictive drugs. A US study of the brain tissue of smokers and nonsmokers who had died showed that smokers had the changes, even if they had quit years before, the team at the National Institute on Drug Abuse said. "The data show that there are long-lasting chemical changes in the brains of humans," Michael Kuhar of Emory University in Atlanta, who was not involved in the study, said. "The chemical changes alone suggest a physiological basis for nicotine addiction."

A team led by Bruce Hope of NIDA, one of the National Institutes of Health, analysed levels of two enzymes found inside brain cells known as neurons. These enzymes help the neurons use chemical signals such as those made by the message-carrying compound dopamine. Smokers and former smokers had high levels of these enzymes. Hope said other studies had seen the same thing in animals given cocaine and heroin - and it was clear that the drugs were causing the effects. "This strongly suggests that the similar changes observed in smokers and former smokers contributed to their addiction," he said.

Experts on smoking have long said that nicotine is at least as addictive as heroin. The US Centers for Disease Control and Prevention estimate that 20.9 per cent of all adults smoke in the US, which adds up to 45 million people. More than 20 per cent of high school students smoke.



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.