Tuesday, December 16, 2008

Here we go again: Breast cancer from HRT claim

If it all depends on how you analyse the same data -- which it does -- the effect is not one to be relied upon. If you look at any body of data long enough, you can generally find something -- but that does not mean that the observation is generalizable.

Hormone replacement therapy could double your risk of breast cancer, scientists say - just months after researchers gave the drugs the all-clear. The new warning follows a study in 2002 that led to a million women coming off HRT when it reported that those taking a particular type had a [minimally] higher risk of breast cancer, heart disease and stroke. Then last year, re-analysis of the data found the risks only applied to those in their sixties and seventies, older than most Britons taking the therapy. And this year, experts said HRT was safe for women in their fifties too. But the latest study, by U.S. scientists, shows the breast cancer threat may be higher than previously thought.

Women who took HRT for as little as two years were at an increased danger, they found. When the patients stopped the therapy, however, their odds quickly improved, returning to a normal risk level two years later. For their research, the team looked again at the 2002 findings of the Women's Health Initiative study and followed women who took part, to find out what happened after they stopped taking 'combined' HRT pills, which contain oestrogen and progestogen. The original study had looked at the risk of breast cancer over five years.

But the most recent research calculated the risk at points before, during and for three years after, the women were taking HRT pills. It rose with the start of use, and peaked when the women had been on HRT for five years. At that stage, the risk for women who had been on HRT for five years, was twice that of those not on the pills. The risk fell again after most stopped taking it.

Researchers said the results were 'worrisome', but Dr Claudine Isaacs, of Georgetown University, in Washington DC, who led the study, said some of the findings were positive. 'You can still diminish the risk by quitting, even if you've been on hormones for a long time. It's not like smoking where you have to wait ten or 15 years for the risk to come down.' However, the average age of the women in the study was 63, much older than the majority taking HRT. So the findings may only apply to older women.

Drug company Wyeth, which manufactures the combined drug, said: 'Hormone therapy remains a good healthcare choice to relieve moderate to severe menopausal symptoms.' British women reach the menopause at 52 on average. HRT is normally prescribed to combat symptoms such as hot flushes and mood changes.

A treatment for women with breast cancer can reduce the chance of the disease spreading to other parts of the body by a fifth, scientists said last night. Women given the hormone exemestane after surgery were 19 per cent less likely to see their cancer spread than those receiving standard chemotherapy with the drug tamoxifen, the San Antonio Breast Cancer Symposium, in Texas, found. It is not licensed for use on breast cancer in the UK.


Compulsion to overeat is mainly in the genes, study shows

The genetic roots of obesity lie mainly in the brain, according to research that implicates inherited eating tendencies as one of the strongest influences over waistlines. The discovery of seven genetic variants linked to obesity has suggested that DNA affects body shape mainly by changing eating behaviour, rather than by regulating fat storage. Of the seven, five seem to be active in the brain, making it likely that work by fine-tuning appetite, the sense of fullness after eating, or even preferences for some foods over others.

The findings indicate that although genetic differences can help to explain why some people are overweight while others are slim, obesity cannot generally be blamed on genes that slow metabolism and allow fat to be laid down more easily. Most of the genetic factors linked to obesity, which were found by two independent research teams, seem rather to work by altering the amount people eat. Some DNA profiles may simply make it easier or harder to control food consumption.

This insight demonstrates how nature and nurture are intertwined in the origins of common biological effects such as obesity. It is also encouraging for therapy, as it means that something people can control - their food intake - is ultimately responsible for weight gain even when genetic predisposition is also involved. "In cases like this, the line between nature and nurture begins to blur," said Kari Stefansson, of deCODE Genetics, an Icelandic company that conducted one of the studies. "Genetic factors seem to be influencing environmental risk factors."

Joel Hirschhorn, of the Children's Hospital, Boston, who led the other study, by the international Genetic Investigation of Anthropometric Traits (Giant) consortium, said:"The genes near these variants are all active in the central nervous system, suggesting that inherited variation in appetite regulation may have something to do with predisposition to obesity."

Genetic factors are known to influence obesity risk, as twin studies have shown that 40 to 70 per cent of the variation in body mass index is inherited. But it was only 18 months ago that scientists identified a first genetic variant involved, in a gene called FTO. The discoveries, published in Nature Genetics, bring the total number of variants firmly linked to obesity to nine.

All seven variants were detected by the deCODE study and six were also identified by the Giant consortium. Each of the variants has a modest effect on obesity risk. The 1 per cent of people who have the riskier version of all of them would typically be 2kg (4lb) heavier than an average person, and 4.5kg (10lb) heavier than a person with the least risky genetic profile.


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