Life Extension Magazine®
Caloric Restriction Reduces Atherosclerosis Risk | |
Caloric restriction in humans is associated with a reduced risk for atherosclerosis, according to a study recently published in the Proceedings of the National Academy of Sciences USA.* Caloric restriction has been shown to prolong life and reduce the incidence of certain diseases in animals, though little is known about its long-term effects on cardiovascular risk factors in humans. Investigators from the Washington University School of Medicine in St. Louis, MO, examined 18 adults (average age of 50) who had practiced caloric restriction for an average of six years, along with 18 age-matched healthy adults following a typical American diet. The caloric restriction group consumed a balance of foods designed to exceed the recommended daily intake of all essential nutrients while minimizing energy intake. They consumed 1,100-2,000 calories per day, with approximately 26% of calories derived from protein, 28% from fat, and 46% from complex carbohydrates. The caloric restriction group avoided eating processed foods and trans fats. By contrast, the control group consumed nearly twice as many calories (2,000-3,500 calories a day), with approximately 18% of calories derived from protein, 32% from fat, and 50% from carbohydrates. Compared to the control group, the caloric restriction group had a lower average body mass index (19.6 vs. 25.9), lower percentage of body fat (8.7% vs. 24%), higher levels of beneficial high-density lipoprotein (HDL), and lower levels of total cholesterol, low-density lipoprotein (LDL), triglycerides, fasting glucose, fasting insulin, C-reactive protein, and systolic and diastolic blood pressure. Furthermore, carotid artery intima-media thickness was 40% less in the caloric restriction group than in the control group. Based on a range of risk factors and measurement of carotid artery intima-media thickness, the practice of caloric restriction in adults appears to offer powerful protection against atherosclerosis, the major cause of death in Americans. —Elizabeth Wagner, ND | |
Reference | |
* Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci USA. 2004 Apr 27;101(17):6659-63. | |
Calcium, Vitamin D May Lower Risk of PMS | |
Consuming calcium and vitamin D may reduce a woman’s risk of developing premenstrual syndrome, according to a recent study published in the Archives of Internal Medicine.* Up to 90% of women experience PMS at some point during their childbearing years. PMS is marked by physical and psychological symptoms such as headache, edema, anxiety, depression, and irritability during the 7-10 days before onset of menstruation. These symptoms can range from mild to debilitating, and usually disappear soon after menses begins. Researchers examined calcium and vitamin D intake among more than 3,000 women aged 27-44 years, using a food-frequency questionnaire that was administered three times over an eight-year period. Comparing dietary intake data with participants’ incidence of PMS, they found that women with the highest intake of calcium and vitamin D had a 30-40% lower risk of developing clinical PMS than women with the lowest intake of calcium and vitamin D. While this study examined only calcium and vitamin D intake from dietary sources, the researchers hope to investigate the effects of calcium and vitamin D supplements in relation to PMS incidence. “At this point, I hesitate to say that there really is a difference between these two sources,” lead researcher Dr. Elizabeth Bertone-Johnson of Brigham and Women’s Hospital and Harvard Medical School told Life Extension. “Our findings, together with those from several small randomized trials that found calcium supplements to be effective in treating PMS, suggest that a high intake of calcium and vitamin D may reduce the risk of PMS,” the researchers concluded. “Clinical trials of this issue are warranted. In the interim, given that calcium and vitamin D may also reduce the risk of osteoporosis and some cancers, clinicians may consider recommending these nutrients even for younger women.” —Marc Ellman, MD | |
Reference | |
* Bertone-Johnson ER, Hankinson SE, Bendich A, Johnson SR, Willett WC, Manson JE. Calcium and vitamin D intake and risk of incident premenstrual syndrome. Arch Intern Med. 2005 Jun 13;165(11):1246-52. | |
Broccoli Protects Against Bladder Cancer | |
Compounds in broccoli may help prevent or slow the progression of bladder cancer, according to Ohio State University researchers.1,2 Previous research has shown that men who eat two or more servings of broccoli per week are less likely to develop bladder cancer, which kills more than 13,000 Americans each year. The researchers isolated compounds called glucosinolates from broccoli sprouts. The process of chopping, chewing, and digestion transforms these compounds into biochemicals called isothiocyanates. The Ohio State team used an enzyme process to convert the broccoli glucosinolates into isothiocyanates. In the laboratory, the scientists treated two lines of human bladder cancer cells and one mouse cell line with varying amounts of glucosinolates and isothiocyanates. They found that the isothiocyanates decreased proliferation of all three cancer cell lines. In fact, the isothiocyanates exerted the strongest effect on the most aggressive cell line examined, human invasive transitional cell carcinoma. Surprisingly, the glucosinolates did not demonstrate an effect against the bladder cancer cells.1,2 The researchers are not sure how biochemicals in broccoli prevent cancer cells from proliferating, noting that at least a dozen compounds in broccoli could have anti-cancer effects. Other cruciferous vegetables—including cabbage, cauliflower, kale, and Brussels sprouts—may also contain similar disease-fighting phytochemicals. “Eat a variety of vegetables in your diet,” study author Dr. Steven Schwartz advised. “Because there’s all sorts of compounds we’re finding can be healthy and disease preventive.”2 —Elizabeth Wagner, ND | |
References | |
1. Available at: http://researchnews.osu.edu/archive/goodbroc.htm. Accessed August 18, 2005. | |
DHEA Helps Resolve Cervical Dysplasia | |
Intravaginal use of dehydroepiandrosterone (DHEA) promotes regression of low-grade cervical dysplasia, according to women’s cancer specialists at Boston’s Massachusetts General Hospital.* Defined as abnormal cells on the surface of the female cervix, cervical dysplasia is considered a pre-cancerous condition that, if left untreated, may progress to cervical cancer. Most pre-malignant and malignant lesions of the cervix result from infection with the human papilloma virus (HPV), which is spread through sexual contact. Treatment options for cervical dysplasia include cryotherapy, laser treatment, loop excision, and cone biopsy. Supporting the body’s immune response to the HPV virus may be an effective therapeutic tool in managing cervical dysplasia. Scientists theorized that because DHEA is known to help modulate immune activity in laboratory animals, topical DHEA might help women combat an early infection with HPV. The MGH pilot study enrolled 12 women with low-grade cervical dysplasia, who were instructed to insert one vaginal tablet containing 150 mg of DHEA next to the cervix each day at bedtime for six months. Between three and six months later, cervical dysplasia completely regressed in 10 of the 12 patients, and incompletely regressed to a non-normal, non-dysplatic lesion in the remaining two patients. DHEA was well tolerated and did not result in significant elevation of testosterone levels. This study suggests that intravaginal DHEA is a safe, well-tolerated therapeutic tool that may help promote the regression of low-grade cervical dysplasia by supporting the local immune response to the HPV virus. —Linda M. Smith, RN | |
Reference | |
* Suh-Burgmann E, Sivret J, Duska LR, Del Carmen M, Seiden MV. Long-term administration of intravaginal dehydroepiandrosterone on regression of low-grade cervical dysplasia—a pilot study. Gynecol Obstet Invest. 2003;55(1):25-31. | |