Dataset Information

The effect of smoking and sex on the association between long-term alcohol consumption and metabolic syndrome in middle-aged and older population.

ABSTRACT:

Background

The effect of smoking and sex on the relationship between alcohol consumption and risk of developing metabolic syndrome (MetS) and its components has not been investigated.

Methods

A total of 5,629 Korean adults aged 40-69 years without MetS were recruited at baseline. Alcohol consumption was assessed biennially and classified as light, moderate or heavy drinker. Smoking status was examined at baseline and categorized into non-smokers and current smokers. Risk of incident MetS and its components according to alcohol consumption was examined by smoking status and sex using a multivariate Cox proportional hazards model.

Results

During a follow-up of 12 years, 2,336 participants (41.5%) developed MetS. In non-smokers, light or moderate alcohol drinkers had a lower risk of developing MetS, abdominal obesity, hyperglycemia, hypertriglyceridemia, and low HDL-C compared with never drinkers. Heavy alcohol consumption was associated with a higher risk of incident elevated blood pressure (hazard ratio [HR] = 1.48; 95% confidence interval [CI], 1.07-2.06; P = 0.020) in men and abdominal obesity (HR = 1.86; 95% CI, 1.06-3.27; P = 0.030) in women. However, in smokers, the inverse association of light or moderate alcohol consumption with hypertriglyceridemia and abdominal obesity was not present, whereas a positive association between heavy alcohol consumption and hyperglycemia (HR = 1.39; 95% CI, 1.07-1.80; P = 0.014) was observed.

Conclusions

Smoking status and sex strongly affects the association between long-term alcohol consumption and MetS and its components by the amount of alcohol consumed.

SUBMITTER: Lee K

PROVIDER: S-EPMC7940979 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Although clinical data support an association between paternal alcohol use and deficits in child neurocognitive development, the relationship between paternal drinking and alcohol-induced growth phenotypes remains challenging to define. Using an established mouse model of chronic exposure, previous work by our group has linked preconception paternal alcohol use to sex-specific patterns of fetal growth restriction and placental dysfunction. The aim of the present study was to investigate the long-term impact of chronic preconception paternal alcohol use on offspring growth and metabolic programming. RESULTS:Preconception paternal alcohol exposure induced a prolonged period of fetal gestation and an increased incidence of intrauterine growth restriction, which affected the male offspring to a greater extent than the females. While the female offspring of ethanol-exposed males were able to match the body weights of the controls within the first 2 weeks of postnatal life, male offspring continued to display an 11% reduction in weight at 5 weeks of age and a 6% reduction at 8 weeks of age. The observed growth deficits associated with insulin hypersensitivity in the male offspring, while in contrast, females displayed a modest lag in their glucose tolerance test. These metabolic defects were associated with an up-regulation of genes within the pro-fibrotic TGF-? signaling pathway and increased levels of cellular hydroxyproline within the livers of the male offspring. We observed suppressed cytokine profiles within the liver and pancreas of both the male and female offspring, which correlated with the up-regulation of genes in the LiverX/RetinoidX/FarnesoidX receptor pathways. However, patterns of gene expression were highly variable between the offspring of alcohol-exposed sires. In the adult offspring of alcohol-exposed males, we did not observe any differences in the allelic expression of Igf2 or any other imprinted genes. CONCLUSIONS:The impact of paternal alcohol use on child development is poorly explored and represents a significant gap in our understanding of the teratogenic effects of ethanol. Our studies implicate paternal exposure history as an additional and important modifier of alcohol-induced growth phenotypes and challenge the current maternal-centric exposure paradigm.