Can persistent organic pollutants explain the association between serum γ-glutamyltransferase and type 2 diabetes?

The results of several epidemiological studies of serum γ-glutamyltransferase (GGT) led us to hypothesise that associations of GGT within its normal range with type 2 diabetes may reflect detrimental effects of xenobiotics found in the environment, such as persistent organic pollutants (POPs). Epidemiological observations showed that serum GGT activity within its normal range strongly predicted future type 2 diabetes; the predictability of diabetes from obesity was low with GGT at the low end of the normal range; and GGT showed a positive association with known markers of oxidative stress or inflammation. Experimental findings on cellular GGT suggest that serum GGT levels within the normal range may reflect oxidative stress related to the re-synthesis of intracellular glutathione; however, this interpretation is not completely satisfying because, in its role of regenerating intracellular glutathione, GGT activity should be antioxidative. Alternatively, serum GGT activity may reflect amounts of glutathione conjugates formed during the metabolism of xenobiotics. Accordingly, we postulate a two-part hypothesis: that the association of serum GGT with type 2 diabetes reflects exposure to POPs, as these substances, which have a very long half-life, may influence diabetes risk by residing in adipose tissue as endocrine disruptors; and that POPs or similar substances may interact with obesity to cause type 2 diabetes. Supporting this hypothesis, cross-sectional investigation of background exposure to POPs in the National Health and Nutrition Examination Survey showed relationships similar to those observed for GGT, including a powerful association with prevalent diabetes and no association between obesity and diabetes for very low POP concentrations. Our hypothesis can be tested in both prospective studies and toxicological studies.     

Can persistent organic pollutants distinguish between two opposite metabolic phenotypes in lean Koreans?

Aims

This study investigated the association of persistent organic pollutants (POPs), an emerging new risk factor for type 2 diabetes and the metabolic syndrome, with the presence of opposite phenotypes of glucose and lipid metabolism among normal-weight Koreans of similar body composition.

Can vitamin D deficiency cause diabetes and cardiovascular diseases? Present evidence and future perspectives

Several studies have shown that vitamin D may play a role in many biochemical mechanisms in addition to bone and calcium metabolism. Recently, vitamin D has sparked widespread interest because of its involvement in the homeostasis of the cardiovascular system. Hypovitaminosis D has been associated with obesity, related to trapping in adipose tissue due to its lipophilic structure. In addition, vitamin D deficiency is associated with increased risk of cardiovascular disease (CVD) and this may be due to the relationship between low vitamin D levels and obesity, diabetes mellitus, dyslipidaemia, endothelial dysfunction and hypertension. However, although vitamin D has been identified as a potentially important marker of CVD, the mechanisms through which it might modulate cardiovascular risk are not fully understood. Given this background, in this work we summarise clinical retrospective and prospective observational studies linking vitamin D levels with cardio-metabolic risk factors and vascular outcome. Moreover, we review various randomised controlled trials (RCTs) investigating the effects of vitamin D supplementation on surrogate markers of cardiovascular risk. Considering the high prevalence of hypovitaminosis D among patients with high cardiovascular risk, vitamin D replacement therapy in this population may be warranted; however, further RCTs are urgently needed to establish when to begin vitamin D therapy, as well as to determine the dose and route and duration of administration.     

Primary and secondary prevention in cardiovascular disease: an old‐fashioned concept?

Abstract. van Venrooij FV, Stolk RP, Banga JD, Erkelens DW, Grobbee DE (Julius Centre for General Practice and Patient Oriented Research, University Medical Center, Utrecht, The Netherlands). Primary and secondary prevention in cardiovascular disease: an old‐fashioned concept? (Review). J. Intern Med 2002; 251: 301–306. Objective. Is the concept of primary and secondary cardiovascular prevention an old‐fashioned concept that needs to be re‐defined? Design. Discussion paper. Results. Cardiovascular prevention means reduction of absolute risk for cardiovascular disease (CVD), irrespective of clinical stage. Conclusion. For the calculation of an individual probability to develop CVD all factors that contribute to the risk must be taken into account, including previous CVD events.     

Does hypoglycemia cause cardiovascular events?

Hypoglycemia is a very common side effect of insulin therapy and, to a lesser extent, of treatment with oral hypoglycemic agents. Severe hypoglycemia can precipitate adverse cardiovascular outcomes such as myocardial ischemia and cardiac arrhythmia. These are mainly secondary to autonomic activation which results in hemodynamic changes, vasoconstriction and rise in intravascular coagulability and viscosity.     

Coeliac disease: the cause of the various associated disorders?

The advent of the endomysial antibody test has allowed the true association between coeliac disease and at least 12 other disorders to be established. There is evidence suggesting that coeliac disease is a cause of these disorders; a mechanism for this is proposed.     

Is self‐rated health associated with ideal cardiovascular health? The Multi‐Ethnic Study of Atherosclerosis

Background

Self‐rated health (SRH) is an indicator of health status—a determinant of health‐promoting behaviors and a predictor of morbidity/mortality. Little is known about the association between SRH and ideal cardiovascular health (CVH), as measured by the AHA Life's Simple 7 (LS7) metrics, or whether the relationship between SRH and CVH differs by race/ethnicity.

Hypothesis

Favorable SRH is associated with better CVH.

Methods

We conducted a cross‐sectional analysis of 6457 men and women (4 race/ethnicities) who participated in the Multi‐Ethnic Study of Atherosclerosis. SRH was measured on a 5‐point Likert scale (excellent, very good, good, fair, and poor). CVH was assessed using the LS7 metrics, each scored from 0 to 2, with a total score of 0 to 14. Scores of 0 to 8 indicate inadequate, 9 to 10, average, and 11 to 14, optimal CVH. ORs and 95% CIs were calculated for associations between SRH and CVH scores using multinomial logistic regression, adjusted for age, sex, race/ethnicity, education, income, marital status, health insurance, and chronic diseases.

Results

Mean age of participants was 62 ± 10 years; 53% were female. Odds of ideal CVH increased as SRH improved. Compared with poor–fair SRH, adjusted ORs and 95% CIs for optimal CVH by SRH status were excellent, 4.9 (3.4–7.0); very good, 2.2 (1.6–3.1); and good, 1.5 (1.1–2.1). Results were similar by race/ethnicity, sex, and age groups.

Conclusions

More favorable SRH was associated with better CVH, irrespective of sex, race/ethnicity, or age. Further research could explore whether optimization of SRH predicts CVH.