Gal Dubnov

Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study): a randomised single-blind trial.

BACKGROUND The rapid emergence of coronary artery disease (CAD) in south Asian people is not explained by conventional risk factors. In view of cardioprotective effects of a Mediterranean style diet rich in alpha-linolenic acid, we assessed the benefits of this diet for patients at high risk of CAD. METHODS We did a randomised, single-blind trial in 1000 patients with angina pectoris, myocardial infarction, or surrogate risk factors for CAD. 499 patients were allocated to a diet rich in whole grains, fruits, vegetables, walnuts, and almonds. 501 controls consumed a local diet similar to the step I National Cholesterol Education Program (NCEP) prudent diet. FINDINGS The intervention group consumed more fruits, vegetables, legumes, walnuts, and almonds than did controls (573 g [SD 127] vs 231 g [19] per day p<0.001). The intervention group had an increased intake of whole grains and mustard or soy bean oil. The mean intake of alpha-linolenic acid was two-fold greater in the intervention group (1.8 g [SD 0.4] vs 0.8 g [0.2] per day, p<0.001). Total cardiac end points were significantly fewer in the intervention group than the controls (39 vs 76 events, p<0.001). Sudden cardiac deaths were also reduced (6 vs 16, p=0.015), as were non-fatal myocardial infarctions (21 vs 43, p<0.001). We noted a significant reduction in serum cholesterol concentration and other risk factors in both groups, but especially in the intervention diet group. In the treatment group, patients with pre-existing CAD had significantly greater benefits compared with such patients in the control group. INTERPRETATION An Indo-Mediterranean diet that is rich in alpha-linolenic acid might be more effective in primary and secondary prevention of CAD than the conventional step I NCEP prudent diet.

Weight control and the management of obesity after menopause: the role of physical activity.

BACKGROUND Postmenopausal women have an increased tendency for gaining weight. The declines of endogenous estrogen, together with physical inactivity, are probably the major causes of this phenomenon. Postmenopausal overweight and obesity leads to increased rates of hypertension, diabetes mellitus, coronary artery disease, and all cause mortality. Additional consequences may include hormone-dependent cancer, gallstones, nephrolithiasis, and osteoarthritis. Weight loss can reverse many of these complications, reduce the number and dosages of medications used, and improve longevity. This difficult task requires lifestyle modification. OBJECTIVES To review the current information about the effects of physical activity on postmenopausal weight gain and its consequences and to provide basic strategies to treat obesity during the menopause transition. METHODS A Medline search together with a manual search of selected articles. CONCLUSION Several options for weight loss are available, yet lifestyle modification is essential in managing postmenopausal obesity and overweight. While this demands dietary and behavioral changes, a major element of this modification is regular physical activity, which reduces obesity-related morbidity and mortality. The amendment to a healthier lifestyle is achievable at the postmenopausal years. All medical personnel should advocate against overweight and obesity and provide tools for their management.

αMUPA mice: a transgenic model for longevity induced by caloric restriction

Caloric restriction (CR) is currently the only therapeutic intervention known to attenuate aging in mammals, but the underlying mechanisms of this phenomenon are still poorly understood. To get more insight into these mechanisms, we took advantage of the alphaMUPA transgenic mice that previously were reported to spontaneously eat less and live longer compared with their wild-type control mice. Currently, two transgenic lines that eat less are available, thus implicating the transgenic enzyme, i.e. the urokinase-type plasminogen activator (uPA), in causing the reduced appetite. This phenotypic change could have resulted from the ectopic transgenic expression that we detected in the adult alphaMUPA brain, or alternatively, from a transgenic interference in brain development. Here, we have summarized similarities and differences so far found between alphaMUPA and calorically restricted mice. Recently, we noted several changes in the alphaMUPA liver, at the mitochondrial and cellular level, which consistently pointed to an enhanced capacity to induce apoptosis. In addition, alphaMUPA mice showed a reduced level of serum IGF-1 and a reduced incidence of spontaneously occurring or carcinogen-induced tumors in several tissues. In contrast, alphaMUPA did not differ from wild type mice in the levels of low molecular weight antioxidants when compared in several tissues at a young or an old age. Overall, the alphaMUPA model suggests that fine-tuning of the threshold for apoptosis, possibly linked in part to modulation of serum IGF-1 and mitochondrial functions, could play a role in the attenuation of aging in calorically restricted mice.

High Prevalence of Iron Deficiency and Anemia in Female Military Recruits

Iron deficiency anemia has long been known to impair physical and mental performance. Iron deficiency itself, even without anemia, may also cause such an effect. Similar to female athletes, women in active military units may have increased risks for iron deficiency and its detrimental effects. Female recruits were screened for anemia and iron store status, and a questionnaire on lifestyle habits and menstruation was completed. Iron depletion (serum ferritin level of <20 microg/L) was found for 77% of study participants. Iron deficiency (ferritin level of <12 microg/L and transferrin saturation of <15%) was found for 15% of study participants. Anemia was found for 24% of subjects, and iron deficiency anemia was found for 10% of subjects. High prevalence of iron depletion, iron deficiency, anemia, and iron deficiency anemia was found among female recruits intended for active military duty. Therefore, a recommendation can be made to screen such female recruits for anemia and iron stores.

Polyunsaturated Fatty Acids, Insulin Resistance, and Atherosclerosis: Is Inflammation the Connecting Link?

We discuss the concept that the two essential (not produced by the body and obtained exclusively through the diet) polyunsaturated fatty acid families-n-6 and n-3-may play a role in the pathogenesis of insulin resistance through inflammatory pathways. Linoleic acid, the major n-6 fatty acid, is metabolized into pro-inflammatory arachidonic acid, which, in turn, gives rise to leukotrienes and protaglandins. N-3 fatty acids, found in plants and in fish, reduce the levels of arachidonic acid, thereby lowering inflammatory mediator concentrations and increasing insulin sensitization. We discuss these findings and their implications for insulin resistance and their possible effect on coronary heart disease.

Physical Activity and Mood

Various researchers have pointed out the affective changes brought about by physical activity (PA) (1–5). The mood changes documented are generally an increase in “positive” mood states, such as calmness and pleasantness, and a decrease in “negative” mood states, such as depression and anger. The improvement in overall mood scores is seen after most types of exercise, both aerobic and anaerobic, that last for a minimal period of time or intensity.

Stress in the Pathogenesis of Eating Disorders and Obesity

Eating disorders and obesity are multifactorial disease conditions with several accompanying comorbidities, including a shortened life span. Entangled among their risk factors and within their intricate pathogenesis is mental stress. This power of the mind has been repeatedly shown to affect somatic illnesses, most commonly coronary artery disease (Iso et al., 2002; Krantz, Shaps, Carrey, & Natelson, 2000; Sheps et al., 2002), so mental stress may convincingly result in physical harm. The center of appetite regulation is in close proximity to areas that control the stress response in the hypothalamus, hence the connection between feeding regulation and stress seems not to be by chance. It should be noted that the topic is broad, and the interrelationships within and between biological, psychological, and social factors are complex. This chapter will present several key issues regarding the role of stress in the pathogenesis and etiology of eating disorders, chiefly anorexia nervosa (AN), bulimia nervosa (BN), and obesity.