Smoking linked to earlier menopause
New York, NY, United States (AHN) – And yet another reason for women not to light up.
Researchers say that women who smoke may hit menopause about a year earlier than non-smokers.
The study, published in the journal Menopause, reviewed data from several pervious studies that included roughly 6,000 women from the United States, Poland and Turkey and Iran.
On average, non-smokers hit menopause between the ages of 46-51. Smokers however, reached menoucpase overall at around 43-50.
Both early and late menopause have been linked with health problems. Women who hit menopause later in life are believed to be at a greater risk for breast cancer because one risk for the disease is exposure to estrogen.
Earlier menopause is linked to a host of medical conditions including osteoporosis, cardiovascular disease, diabetes mellitus, obesity, Alzheimer’s disease and others. Also, smoking may, overall, slightly increase of woman’s risk of death in years to follow.
In addition to smoking. alcohol use, weight gain or loss, and whether a woman has ever given birth may also effect a woman’s timing of menopause. The evidence for all the risk factors, except smoking, have been mixed.
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Some cases of Alzheimer’s may be transmitted
Houston, TX, United States (AHN) – Some cases of Alzheimer’s disease may be transmitted similar to other infectious illnesses, according to a new study.
Researchers with the University of Texas Health Science Center at Houston said that the brain damage associated with Alzheimer’s may originate in a way similar to that of what are known as infectious prion diseases such as mad cow disease, or bovine spongiform.
“Our findings open the possibility that some of the sporadic Alzheimer’s cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease,” researcher Claudio Soto said in a statement.
Soto said the underlying mechanism of Alzheimer’s disease is “very similar” to the prion diseases.
“It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones. The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer’s,” Soto said.
Soto and his colleagues injected the brain tissue of a confirmed Alzheimer’s patient into mice and compared the results with a group of mice injected with the tissue of someone without the disease. None of the mice injected with the control showed signs of Alzheimer’s, but all of the rodents injected with Alzheimer’s brain extracts developed plaques and other alterations associated with the disease.
“The mouse developed Alzheimer’s over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure,” Soto said in a statement.
A full report on the study appears in the Oct. 4 online issue of the journal Molecular Psychiatry.
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