Thursday, September 06, 2007



DOES THE PILL STOP MS?

Popular summary followed by journal abstract below:

ESTROGEN may be the next treatment for multiple sclerosis (MS), with research published online in the Proceedings of the National Academy of Sciences this week showing that the hormone can protect the brain from degeneration without increasing the risk of breast and endometrial cancers. Previous studies have shown that the symptoms of MS greatly improve in women during pregnancy, when estrogen levels are high. In the current study, scientists studied young adult female mice aged five to six weeks old with a condition similar to human MS called encephalomyelitis. Some mice were given a specific form of estrogen, while a control group received an inactive placebo. Those receiving estrogen did not develop any of the disease symptoms seen in the control group, including slower movement, difficulty maintaining balance and nerve damage.

Source

Differential neuroprotective and anti-inflammatory effects of estrogen receptor (ER)beta ligand treatment

By Seema Tiwari-Woodruff et al.

Abstract

Treatment with either estradiol or an estrogen receptor (ER)alpha vs. an ERbeta ligand treatment abrogated disease at the onset and throughout the disease course. In contrast, ERalpha ligand treatment was antiinflammatory in the systemic immune system, whereas ERalpha ligand treatment reduced CNS inflammation, whereas ERalpha or the ERbeta selective ligand, we have dissociated the antiinflammatory effect from the neuroprotective effect of estrogen treatment and have shown that neuroprotective effects of estrogen treatment do not necessarily depend on antiinflammatory properties. Together, these findings suggest that ERbeta ligand treatment should be explored as a potential neuroprotective strategy in multiple sclerosis and other neurodegenerative diseases, particularly because estrogen-related toxicities such as breast and uterine cancer are mediated through ERalpha

Proc. Natl. Acad. Sci. USA, Sept, 2007




Some gene damage from smoking is permanent: study

The sample is derisory but there is probably something in it nonetheless

A new study may help explain why former smokers are still more prone to lung cancer than those who have never smoked. It found that smoking causes some permanent genetic damage. Quitting still offers huge health benefits, researchers stressed, as the risk to former smokers is much lower than for current smokers.

A team led by Wan Lam and Stephen Lam from the BC Cancer Agency in Vancouver, Canada, took samples from the lungs of 24 current and former smokers, as well as from people who have never smoked.

They used the samples to create libraries using a technique called serial analysis of gene expression, which helps to identify patterns of gene activity. Only about a fifth of the genes in a cell are switched on at any given time, but smoking leads to changes in gene activity. The researchers found that some of these changes, though not all, persisted even years after quitting smoking.

The reversible genes were particularly involved in "xenobiotic" functions -- managing chemicals not produced in the body and metabolism of genetic material and mucus secretion, scientists found. The irreversible damage was to some DNA repair genes, and to the activity of genes that help fight lung cancer development.

"Those genes and functions which do not revert to normal levels upon smoking cessation may provide insight into why former smokers still maintain a risk of developing lung cancer," said Raj Chari, first author of the study. Tobacco smoking accounts for 85 percent of lung cancers, and former smokers account for half of those newly diagnosed with the disease.

The gene findings are published in the Aug. 29 issue of the online research journal BMC Genomics.

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].

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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