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According to most prospective studies, being underweight (BMI<18·5 kg/m2) is associated with significantly higher mortality than being of normal weight, especially among smokers. We aimed to explore in a generally lean population whether being underweight is significantly associated with increased all-cause mortality.
Prospective cohort study.
Korea Medical Insurance Corporation study with 14 years of follow-up.
After excluding deaths within the first 5 years of follow-up (1993–1997) to minimize reverse causation and excluding participants without information about smoking and health status, 94 133 men and 48 496 women aged 35–59 years in 1990 were included.
We documented 5411 (5·7 %) deaths in men and 762 (1·6 %) in women. Among never smokers, hazard ratios (HR) for underweight individuals were not significantly higher than those for normal-weight individuals (BMI=18·5–22·9 kg/m2): HR=0·87 (95 % CI 0·41, 1·84, P=0·72) for underweight men and HR=1·12 (95 % CI 0·76, 1·65, P=0·58) for underweight women. Among ex-smokers, HR=0·86 (95 % CI 0·38, 1·93, P=0·72) for underweight men and HR=3·77 (95 % CI 0·42, 32·29, P=0·24) for underweight women. Among current smokers, HR=1·60 (95 % CI 1·28, 2·01, P<0·001) for underweight men and HR=2·07 (95 % CI 0·43, 9·94, P=0·36) for underweight women.
The present study does not support that being underweight per se is associated with increased all-cause mortality in Korean men and women.
Epidemiological studies have reported that higher education (HE) is associated with a reduced risk of incident Alzheimer's disease (AD). However, after the clinical onset of AD, patients with HE levels show more rapid cognitive decline than patients with lower education (LE) levels. Although education level and cognition have been linked, there have been few longitudinal studies investigating the relationship between education level and cortical decline in patients with AD. The aim of this study was to compare the topography of cortical atrophy longitudinally between AD patients with HE (HE-AD) and AD patients with LE (LE-AD).
We prospectively recruited 36 patients with early-stage AD and 14 normal controls. The patients were classified into two groups according to educational level, 23 HE-AD (>9 years) and 13 LE-AD (≤9 years).
As AD progressed over the 5-year longitudinal follow-ups, the HE-AD showed a significant group-by-time interaction in the right dorsolateral frontal and precuneus, and the left parahippocampal regions compared to the LE-AD.
Our study reveals that the preliminary longitudinal effect of HE accelerates cortical atrophy in AD patients over time, which underlines the importance of education level for predicting prognosis.
The present study was designed to define how dietary fat type regulates body adiposity in dietary obesity-susceptible (DOS) Sprague–Dawley (SD) rats. Eighty-three SD rats received a purified diet containing 50 g maize oil (MO)/kg for 3 weeks and then thirty-nine of the rats, designated as the DOS rats, were allotted to diets containing 160 g MO (DOS-MO), beef tallow (DOS-BT) or fish oil (DOS-FO)/kg for 9 weeks. As a result of the experiment, the DOS-FO rats had significantly (P<0·05) reduced weight gain and abdominal and epididymal fat-pad mass than the DOS-MO and DOS-BT rats. Serum leptin level was also significantly (P<0·05) lower in the DOS-FO rats; however, hypothalamic leptin receptor (a and b) mRNA and neuropeptide Y expressions were not altered by dietary fat sources. A lower acetyl-CoA carboxylase mRNA expression in the liver was observed in the DOS-FO group, whereas hepatic peroxisome proliferator-activated receptor-γ mRNA and protein expressions were markedly elevated in the DOS-FO group compared with those in the other groups. We did not observe differences in acetyl-CoA carboxylase and peroxisome proliferator-activated receptor-γ expressions in epididymal fat of the DOS rats consuming MO, BT or FO. It is concluded from our present observations that dietary fat type, especially that rich in FO, plays a potential role in down-regulation of adiposity by altering hepatic lipogenic genes, rather than feeding behaviour, in the DOS-SD rats.
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