High long-term cortisol levels, measured in scalp hair, are associated with a history of cardiovascular disease.

"Abstract

BACKGROUND:

Stress is associated with an increased incidence of cardiovascular disease. The impact of chronic stress on cardiovascular risk has been studied by measuring cortisol in serum and saliva, which are measurements of only 1 time point. These studies yielded inconclusive results. The measurement of cortisol in scalp hair is a novel method that provides the opportunity to measure long-term cortisol exposure. Our aim was to study whether long-term cortisol levels, measured in scalp hair, are associated with cardiovascular diseases.

METHODS:

A group of 283 community-dwelling elderly participants were randomly selected from a large population-based cohort study (median age, 75 y; range, 65-85 y). Cortisol was measured in 3-cm hair segments, corresponding roughly with a period of 3 months. Self-reported data concerning coronary heart disease, stroke, peripheral arterial disease, diabetes mellitus, and other chronic noncardiovascular diseases were collected.

RESULTS:

Hair cortisol levels were significantly lower in women than in men (21.0 vs 26.3 pg/mg hair; P < .001). High hair cortisol levels were associated with an increased cardiovascular risk (odds ratio, 2.7; P = .01) and an increased risk of type 2 diabetes mellitus (odds ratio, 3.2; P = .04). There were no associations between hair cortisol levels and noncardiovascular diseases.

CONCLUSIONS:

Elevated long-term cortisol levels are associated with a history of cardiovascular disease. The increased cardiovascular risk we found is equivalent to the effect of traditional cardiovascular risk factors, suggesting that long-term elevated cortisol may be an important cardiovascular risk factor."

http://www.ncbi.nlm.nih.gov/pubmed/23596141

Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.

Abstract

"The negative impact of consuming sugar-sweetened beverages on weight and other health outcomes has been increasingly recognized; therefore, many people have turned to high-intensity sweeteners like aspartame, sucralose, and saccharin as a way to reduce the risk of these consequences. However, accumulating evidence suggests that frequent consumers of these sugar substitutes may also be at increased risk of excessive weight gain, metabolic syndrome, type 2 diabetes, and cardiovascular disease. This paper discusses these findings and considers the hypothesis that consuming sweet-tasting but noncaloric or reduced-calorie food and beverages interferes with learned responses that normally contribute to glucose and energy homeostasis. Because of this interference, frequent consumption of high-intensity sweeteners may have the counterintuitive effect of inducing metabolic derangements."

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Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic

Abstract

"Xenobiotic and dietary compounds with hormone-like activity can disrupt endocrine signaling pathways that play important roles during perinatal differentiation and result in alterations that are not apparent until later in life. Evidence implicates developmental exposure to environmental hormone-mimics with a growing list of health problems. Obesity is currently receiving needed attention since it has potential to overwhelm health systems worldwide with associated illnesses such as diabetes and cardiovascular disease. Here, we review the literature that proposes an association of exposure to environmental endocrine disrupting chemicals with the development of obesity. We describe an animal model of developmental exposure to diethylstilbestrol (DES), a potent perinatal endocrine disruptor with estrogenic activity, to study mechanisms involved in programming an organism for obesity. This experimental animal model provides an example of the growing scientific field termed “the developmental origins of adult disease” and suggests new targets of abnormal programming by endocrine disrupting chemicals."

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The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.

Abstract

"A fat diet, rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA), is said to be an important cause of atherosclerosis andcardiovascular diseases (CVD). The evidence for this hypothesis was sought by reviewing studies of the direct link between dietary fats and atherosclerotic vascular disease in human beings. The review included ecological, dynamic population, cross-sectional, cohort, and case-controlstudies, as well as controlled, randomized trials of the effect of fat reduction alone. The positive ecological correlations between national intakes of total fat (TF) and SFA and cardiovascular mortality found in earlier studies were absent or negative in the larger, more recent studies. Secular trends of national fat consumption and mortality from coronary heart disease (CHD) in 18-35 countries (four studies) during different time periods diverged from each other as often as they coincided. In cross-sectional studies of CHD and atherosclerosis, one group of studies (Bantu people vs. Caucasians) were supportive; six groups of studies (West Indians vs. Americans, Japanese, and Japanese migrants vs. Americans, Yemenite Jews vs. Yemenite migrants; Seminole and Pima Indians vs. Americans, Seven Countries) gave partly supportive, partly contradictive results; in seven groups of studies (Navajo Indians vs. Americans; pure vegetarians vs. lacto-ovo-vegetarians and non-vegetarians, Masai people vs. Americans, Asiatic Indians vs. non-Indians, north vs. south Indians, Indian migrants vs. British residents, Geographic Study of Atherosclerosis) the findings were contradictory. Among 21 cohort studies of CHD including 28 cohorts, CHD patients had eaten significantly more SFA in three cohorts and significantly less in one cohort than had CHD-free individuals; in 22 cohorts no significant difference was noted. In three cohorts, CHD patients had eaten significantly more PUFA, in 24 cohorts no significant difference was noted. In three of four cohort studies of atherosclerosis, the vascular changes were unassociated with SFA or PUFA; in one study they were inversely related to TF. No significant differences in fat intake were noted in six case-control studies of CVD patients and CVD-free controls; and neither total or CHD mortality were lowered in a meta-analysis of nine controlled, randomized dietary trials with substantial reductions of dietary fats, in six trials combined with addition of PUFA. The harmful effect of dietary SFA and the protective effect of dietary PUFA on atherosclerosis and CVD are questioned."

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