Higher levels of salivary alpha-amylase predict failure of cessation efforts in male smokers.

The ability to predict the success or failure of smoking cessation efforts will be useful for clinical practice. Stress response is regulated by two primary neuroendocrine systems. Salivary cortisol has been used as a marker for the hypothalamus-pituitary-adrenocortical axis and salivary alpha-amylase as a marker for the sympathetic adrenomedullary system. We studied 62 chronic smokers (34 women and 28 men with an average age of 45.2+/-12.9 years). The levels of salivary cortisol and salivary alpha-amylase were measured during the period of active smoking, and 6 weeks and 24 weeks after quitting. We analyzed the men separately from the women. The men who were unsuccessful in cessation showed significantly higher levels of salivary alpha-amylase over the entire course of the cessation attempt. Before stopping smoking, salivary cortisol levels were higher among the men who were unsuccessful in smoking cessation. After quitting, there were no differences between this group and the men who were successful in cessation. In women we found no differences between groups of successful and unsuccessful ex-smokers during cessation. In conclusions, increased levels of salivary alpha-amylase before and during smoking cessation may predict failure to quit in men. On the other hand, no advantage was found in predicting the failure to quit in women. The results of our study support previously described gender differences in smoking cessation.

The angiotensin converting enzyme I/D polymorphism in long distance runners.

AIM: There is an assumption that ACE I/D polymorphism represents one of the possible genetic factors that might be associated with sports excellence. Recent studies have identified an increased frequency of I allele in elite endurance athletes, long distance runners, rowers and mountaineers. The aim of this study was to test the hypothesis that the ACE I/D polymorphism is associated with enhanced endurance performance. METHODS: We examined this hypothesis by determining ACE I/D allele frequency in 215 marathon runners, 222 half-marathon runners and 18 inline skaters classified by performance (marathon competition results). ACE genotype and allele frequencies were compared with 252 healthy controls. RESULTS: ACE genotype frequency in the whole cohort did not differ from that in the sedentary controls (P < 0.56). However, there was an increase of the I/I genotype incidence amongst successful marathon runners scoring on places from 1st to 150th (P < 0.01). These findings were confirmed in the group of inline skaters, similarly demonstrating an increase of the I/I genotype (P < 0.01). There was no association found between half marathon runners and the ACE genotype (P < 0.59). CONCLUSIONS: An excess of the I allele in long distance runners confirms the association between the ACE I/D polymorphism and endurance sports performance.

The eNOS gene polymorphism does not have a major impact on lipid parameters and premature coronary artery disease in Slovene men (Caucasians).

eNOS affects the NO level in the blood vessel wall, and therefore eNOS might be considered as a candidate gene for CAD. In this cross-sectional case-control association study we tested the hypothesis whether the eNOS 4alb gene polymorphism is a genetic marker for premature CAD in Slovene men. The eNOS 4a/b gene polymorphism was tested in 403 Slovene men: 215 cases with premature CAD and 188 subjects with no history of CAD. The frequency of 4a/b genotypes did not differ between patients and controls: in CAD patients the frequencies of the 4aa, 4ab, or 4bb genotype were 5.0%, 27.9%, or 67.1%, respectively, and in controls the genotype frequencies were 5.3%, 30.9%, or 63.8%, respectively. In this study the aa genotype of the eNOS 4a/b polymorphism was not associated with premature CAD (OR = 1, 95% CI 0.4-2.3, P = 0.9). Moreover, there were no differences in lipid parameters (total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides) between the subjects with the aa genotype and the subjects with the ab or bb genotype. In conclusion, we failed to demonstrate that the eNOS 4a/b gene polymorphism was a genetic marker for premature CAD in Slovene men.

Haemochromatosis-causing mutations C282Y and H63D are not risk factors for coronary artery disease in Caucasians with type 2 diabetes.

Iron metabolism might be involved in the pathogenesis of CAD, and C282Y and H63D mutations in the HFE gene are associated with increased serum iron levels and net iron accumulation. The aim of this study was to look for a relationship between the C282Y and H63D gene mutations of the HFE gene and coronary artery disease (CAD) in a group of patients with type 2 diabetes lasting more than 10 years. The C282Y and H63D gene mutations were tested in 338 Caucasians with type 2 diabetes: 156 cases with CAD and 182 subjects with no history of CAD. The C282Y and the H63D HFE gene distributions in patients with CAD (C282Y: YY 0.6%, CY 9.0%, CC 90.4%; H63D: DD 3.8%, HD 21.8%, HH 74.4%) were not significantly different from those of diabetic subjects without CAD (C282Y: YY 0%, CY 8.2%, CC 91.8%; H63D: DD 2.2%, HD 20.3%, HH 77.5%). In conclusion, we failed to demonstrate that the C282Y and H63D HFE gene mutations were risk factors for CAD in Caucasians with type 2 diabetes lasting longer than 10 years.

The effects of smoking on steroid metabolism and fetal programming.

Tobacco addiction is a serious psychosocial and health problem. A pregnant woman who smokes not only influences the maternal organism, but also passes health risks on to the unborn child. A fetus exposed to maternal smoking is not only directly influenced, but is also endangered by a wide range of diseases up to his or her adult years. The components of tobacco smoke play a significant role in the development of a number of diseases for a large proportion of the smoking population, as well as among those pregnant. This article summarizes findings regarding the impacts on the production of steroid hormones - first describing the smoking-related changes in steroidogenesis in women, and then focusing on the influence of maternal smoking on the fetus's developing steroidogenesis. We assume that if during prenatal development the fetus has already been exposed to the effect of endocrine disruptors at the time fetal steroidogenesis begins fetal programming, this exposure can have serious pathophysiological effects both in the pregnancy as well as later in life. An example of such effects might be a delay in the creation of kidney adrenal androgens, which could also be evident on the level of steroid neuroactive metabolites that may influence the individual's psychological state and lead to later addictions.

Effects of smoking cessation on hormonal levels in men.

Chronic smoking can cause imbalance in endocrine homeostasis and impairment of fertility in both sexes. The male reproductive system is more resilient, still the literature provides conflicting results about the influence of smoking on the steroid hormone levels. The data about smoking cessation are limited; there has not yet been a study primarily focused on changes in steroids levels. In our study, we analyzed levels of testosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), cortisol and sex hormone-binding globulin (SHBG) in male smokers and during smoking cessation. Monitored analytes were determined by RIA. The free testosterone index was calculated. Basal samples of men successful and unsuccessful in smoking cessation did not differ and monitored hormones could hardly predict success of smoking cessation. After one year without smoking, a significant BMI increase and SHBG decrease in former smokers was observed. The decrease in total testosterone was non-significant. Changes in SHBG and testosterone did not correlate with BMI, presumably due to the direct effect of smoking cessation.

Dehydroepiandrosterone in the type 1 diabetes mellitus.

OBJECTIVE: Dehydroepiandrosterone (DHEA) is believed to exert, besides others, positive effects on the insulin resistance or its secretion and glucose metabolism. There are several reports dealing with the DHEA levels and its effects in the type 2 diabetes mellitus, but less information is available on the type 1 diabetic subjects. Recently, a report dealing with the lack of the age-dependent decline of the DHEA levels in the type 2 diabetic subjects was published. The aim of the present study was to answer the question whether a comparable change in the aging pattern of the DHEA and its sulphate could be detected in the type 1 diabetes mellitus. METHODS: The data regarding the DHEA and dehydroepiandrosterone sulphate (DHEA-S) concentrations in the serum obtained from 116 patients with the type 1 diabetes mellitus and 259 controls were gathered from the database of the Institute of Endocrinology (Prague, Czech Republic). RESULTS: No significant differences in the level of the DHEA-S were found between the type 1 diabetics and controls either in men or women. However, lower DHEA levels were found in the type 1 diabetic women, but not in men. The age-dependent declines of both the DHEA and DHEA-S were similar to those in controls. CONCLUSION: In contrast to the type 2 diabetes, the levels of DHEA-S in the type 1 diabetic patients were practically identical with those in controls. In contrast to men, in women, the DHEA basal levels were lower than those seen in controls. The age dependence of both hormones followed the pattern of the decline in controls.

Chronic cigarette smoking alters circulating sex hormones and neuroactive steroids in premenopausal women.

Chronic smoking alters the circulating levels of sex hormones and possibly also the neuroactive steroids. However, the data available is limited. Therefore, a broad spectrum of free and conjugated steroids and related substances was quantified by GC-MS and RIA in premenopausal smokers and in age-matched (38.9+/-7.3 years of age) non-smokers in the follicular (FP) and luteal phases (LP) of menstrual cycle (10 non-smokers and 10 smokers, in the FP, and 10 non-smokers and 8 smokers in the LP). Smokers in both phases of the menstrual cycle showed higher levels of conjugated 17-hydroxypregnenolone, 5alpha-dihydroprogesterone, conjugated isopregnanolone, conjugated 5alpha-pregnane-3beta,20alpha-diol, conjugated androstenediol, androstenedione, testosterone, free testosterone, conjugated 5alpha-androstane-3alpha/beta,17beta-diols, and higher free testosterone index. In the FP, the smokers exhibited higher levels of conjugated pregnenolone, progesterone, conjugated pregnanolone, lutropin, and a higher lutropin/follitropin ratio, but lower levels of cortisol, allopregnanolone, and pregnanolone. In the LP, the smokers exhibited higher levels of free and conjugated 20alpha-dihydropregnenolone, free and conjugated dehydroepiandrosterone, free androstenediol, 5alpha-dihydrotestosterone, free and conjugated androsterone, free and conjugated epiandrosterone, free and conjugated etiocholanolone, 7alpha/beta-hydroxy-dehydroepiandrosterone isomers, and follitropin but lower levels of estradiol and sex hormone binding globulin (SHBG) and lower values of the lutropin/follitropin ratio. In conclusion, chronic cigarette smoking augments serum androgens and their 5alpha/beta-reduced metabolites (including GABAergic substances) but suppresses the levels of estradiol in the LP and SHBG and may induce hyperandrogenism in female smokers. The female smokers had pronouncedly increased serum progestogens but paradoxically suppressed levels of their GABA-ergic metabolites. Further investigation is needed concerning these effects.