Secondhand Smoke Raises Heart Disease Risk
|LE Magazine July 2004|
|Secondhand Smoke Raises Heart Disease Risk|
Although cigarette smoking remains the leading cause of preventable deaths in the US, claiming some 440,000 Americans each year, approximately 25% of adult men and 20% of adult women in the US continue to smoke.
While cigarette smoking is known to increase the risk of a heart attack, secondhand smoke (or environmental tobacco smoke) also increases the risk of a heart attack by about 30%.1 For those continually exposed to environmental tobacco smoke in the home or workplace, the risk of heart attack doubles. In fact, of the 40,000 annual deaths attributable to environmental tobacco smoke, 35,000 result from heart disease. The American Heart Association estimates that some 90% of nonsmokers are routinely exposed to environmental tobacco smoke.
Within minutes of exposure to cigarette smoke, the capacity of the blood vessels that nourish the heart is impaired, the aorta stiffens, normal heart rate variability is reduced, and antioxidant efficacy is decreased. Within 30 minutes of exposure, secondhand smoke causes an increase in platelet clumping and damages the lining of blood vessels, increasing the risk of heart attack and stroke.2
In June 2002, the city of Helena, MT, enacted a public smoking ban based on an analysis of hospital admissions data for a six-month period during which a public smoking ban was enforced.3 In a sample comprising smokers, nonsmokers, and former smokers in roughly equal percentages, hospital admissions due to myocardial infarction declined 40% during the six-month period.
This landmark study demonstrated for the first time the immediate benefits of protection from environmental tobacco smoke and may provide the impetus for universal smoke-free environments in public areas.
—Dean S. Cunningham, MD, PhD
1. He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passive smoking and the risk of coronary heart disease—a meta-analysis of epidemiologic studies. N Engl J Med. 1999 Mar 25;340(12):920-6.
2. Glantz SA, Parmley WW. Passive smoking and heart disease. Mechanisms and risk. JAMA. 1995 Apr 5;273(13):1047-53.
3. Sargent RP, Shepard RM, Glantz SA. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: before and after study. BMJ. 2004 Apr 5. [Epub ahead of print.]
|DHEA Shown to Boost Brain Cell Growth|
Dehydroepiandrosterone (DHEA) is one of the most active and plentiful circulating hormones in both men and women. DHEA levels peak, however, around the age of 30, then decline by as much as 80% by the age of 80. As a result, many anti-aging researchers recommend supplemental DHEA as a way to forestall many of the deleterious effects of aging, such as decreased libido, muscle mass, and brain function.
esearchers at the University of Wisconsin found that DHEA boosts brain cell growth.* When DHEA was added to human neural stem cells, these embryonic brain cells showed a remarkable increase in their growth rate. These findings, published in the Proceed-ings of the National Academy of Sciences USA, offer the first direct proof of DHEA’s beneficial effect on human brain cells.
Study director Dr. Clive Svendsen and his colleagues grew human neural stem cells in culture and then exposed the cells to either a mixture of DHEA, growth factors, and inhibitory factors or a mixture of the growth and inhibitory factors minus DHEA. The cells exposed to the mixture containing DHEA demonstrated a 29% increase in new brain cells compared to the mixture without DHEA.
The researchers noted that DHEA was the only hormone tested that had such a direct effect on neural stem cell growth and new neuron formation. Since adult human brains have neural stem cells that continue to make new neurons in some parts of the brain, this study may point to one way in which DHEA works as anti-aging supplement.
—Edward R. Rosick, DO, MPH, MS
* Suzuki M, Wright LS, Marwah P, Lardy HA, Svendsen CN. Mitotic and neurogenic effects of dehydroepiandrosterone (DHEA) on human neural stem cell cultures derived from the fetal cortex. Proc Natl Acad Sci USA. 2004 Mar 2;101(9):3202-7. Epub 2004 Feb 18.
|Fruits and Vegetables Cut Non-Hodgkin’s Lymphoma Risk|
Diets that are high in fibrous fruits and vegetables such as tomatoes, broccoli, and cauliflower reduce the risk of developing non-Hodgkin’s lymphoma, according to Yale University researchers. Conversely, consuming foods that are high in animal protein, saturated fat, eggs, and dairy products leads to an increased risk of developing the disease. Non-Hodgkin’s lymphoma is a cancer that attacks the lymphatic system, part of the body’s immune system.
“An association between dietary intake and [non-Hodgkin’s lymphoma] is biologically plausible because diets high in protein and fat may lead to altered immunity, resulting in increased risk of [non-Hodgkin’s lymphoma],” said principal investigator Tongzhang Zheng, MD. “The antioxidants found in vegetables and fruits may result in reduced risk of about 40%.”
The study was conducted between 1995 and 2001 on 601 Connecticut women aged 21 to 84 who were diagnosed with varying subtypes of non-Hodgkin’s lymphoma. Each participant was asked to complete a questionnaire characterizing her usual diet in the year prior to being interviewed. After completion, the questionnaires were analyzed to calculate average daily nutrient intakes. Results were compared to a control group of 717 women.
“So far, risk of [non-Hodgkin’s lymphoma] associated with animal protein and fat intakes has only been investigated in American women, in three studies,” said Zheng. “If the association could also be demonstrated in American men, it would provide important information towards understanding the cause of [non-Hodgkin’s lymphoma].”
* Zheng T, Holford TR, Leaderer B, et al. Diet and nutrient intakes and risk of non-Hodgkin’s lym- phoma in Connecticut women. Am J Epidemiol. 2004 Mar 1;159(5):454-66.
|Vitamin D Deficiency More Common than Thought|
Aside from sources such as cod liver oil and oily fish such as salmon, vitamin D is hard to come by in the diet. This is partly why milk, orange juice, and some cereals are fortified with vitamin D.
While many people are able to satisfy their vitamin D requirements through dietary intake and intermittent exposure to sunlight, a vitamin D deficiency during growth and development causes rickets. A similar deficiency during adulthood may lead to secondary hyperparathyroidism, which in turn gives rise to osteoporosis. Vitamin D deficiency also is associated with an increased risk of prostate, colon, breast, and other cancers, as well as multiple sclerosis and high blood pressure.
Once considered rare, vitamin D deficiency is in fact quite common. Breastfed infants, the elderly, the obese, and even otherwise healthy young adults are known to be at risk. Indeed, in one Boston-based study, up to 84% of the elderly subjects were vitamin D deficient.1 In another Boston-based study, 32% of healthy adults under the age of 30 were shown to be vitamin D deficient.2
Vitamin D deficiency is properly assessed by serum 25(OH)D levels and should be measured annually. To optimize health and reduce the risk of these common diseases, the ideal value for 25(OH)D is 30-40 ng/ml.3 For those with adequate exposure to the sun, a vitamin D-containing multivitamin and a vitamin D supplement (containing either 400 or 1000 IU) are recommended. Those without adequate exposure to sunlight should take 1000 IU of vitamin D daily.
—Dean S. Cunningham, MD, PhD
1. Holick MF. Vitamin D: the underappreciated D- lightful hormone that is important for skeletal and cellular health. Curr Opin Endocrinol Diabetes. 2002;9:87-98.
2. Tangpricha V, Pearce EN, Chen TC, Holick MF. Vitamin D insufficiency among free-living healthy young adults. Am J Med. 2002 Jun 1;112(8):659-62.
3. Holick MF. Vitamin D: importance in the preven- tion of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004 Mar;79(3):362-71.