Weight loss from lifestyle interventions and severity of sleep apnoea: a systematic review and meta-analysis

Background

Excess body weight is a risk factor for obstructive sleep apnoea (OSA). The aim of the systematic review was to establish whether weight loss via lifestyle interventions such as diet and exercise are useful in the treatment of OSA.

Methods

A literature search was conducted between 1980 and February 2012. Systematic reviews and randomised controlled trials (RCTs) with participants who had OSA, were overweight or obese, and who had undergone lifestyle interventions with the aim of improving sleep apnoea were included. Meta analyses were conducted for a subset of RCTs with appropriate data.

Results

Two systematic reviews and eight RCTs were included. Meta-analyses were conducted for four RCTs comparing intensive lifestyle interventions to a control. The overall weighted mean differences for weight change, change in apnoea -hypopnoea index (AHI) and change in oxygen desaturation index of ≥4% were as follows: −13.76 kg (95% confidence interval (CI) −19.21, −-8.32), −16.09 (95% CI −25.64, −6.54) and −14.18 (95% CI −24.23, −4.13), respectively. Although high heterogeneity within the meta analyses, all studies favoured the interventions. Long-term follow-up data from three RCTs suggest that improvements in weight and AHI are maintained for up to 60 months.

Conclusions

Intensive lifestyle interventions are effective in the treatment of OSA, resulting in significant weight loss and a reduction in sleep apnoea severity. Weight loss via intensive lifestyle interventions could be encouraged as a treatment for mild to moderate OSA.     

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The Role of Cognitive Function in Postoperative Weight Loss Outcomes: 36-Month Follow-Up

Background

Cognitive dysfunction is associated with reduced postoperative weight loss up to 2 years following surgery, though the role of cognition at more extended follow-up is not yet understood. Thirty-six months following bariatric surgery, we retrospectively compared obese and non-obese patients on 12-week postoperative cognitive performance. We hypothesized that early postoperative cognitive dysfunction would predict higher body mass index (BMI) and lower percent weight loss (%WL) in the total sample at 36 month follow-up.

Materials and Methods

Fifty-five individuals undergoing bariatric surgery completed cognitive testing at preoperative baseline and serial postoperative timepoints, including 12 weeks and 36 months. Cognitive test scores were normed for demographic variables. Percent weight loss (%WL) and body mass index (BMI) were calculated at 36-month follow-up.

Results

Adjusting for gender, baseline cognitive function, and 12-week %WL, 12-week global cognitive test performance predicted 36 month postoperative %WL and BMI. Partial correlations revealed recognition memory, working memory, and generativity were most strongly related to weight loss.

Conclusion

Cognitive function shortly after bariatric surgery is closely linked to extended postoperative weight loss at 36 months. Further work is necessary to clarify mechanisms underlying the relationship between weight loss, durability, and cognitive function, including contribution of adherence, as this may ultimately help identify individuals in need of tailored interventions to optimize postoperative weight loss.     

Middle-aged women's awareness of cholesterol as a risk factor: Results from a national survey of Korean Middle-aged Women's Health Awareness (KomWHA) study

Background

Dyslipidemia, a risk factor for cardiovascular disease (CVD), is more prevalent in middle-aged women than in men of the same age in Korea. This study, the first national survey that focused on cholesterol in Korean women, aimed to: (1) assess their awareness and knowledge of cholesterol, (2) evaluate their risk reduction behavior, and (3) examine differences in these variables among geographical regions in Korea.

Methods

A questionnaire survey study was conducted in a randomly selected national sample of 1304 Korean women, aged 40-64 years in 3 geographic regions.

Results

High cholesterol was identified as a cause of CVD by 54.4% of respondents, however, 95.4% did not know their own values. Only 4.1% of respondents were aware of desirable level of total cholesterol. Eight percent of respondents perceived correctly the meaning of high-density lipoprotein cholesterol (HDL-C) as good cholesterol. And 32.9% had cholesterol check at least once a year. No significant regional differences were found in women's awareness and knowledge on cholesterol. No smoking (93.6%), low salt diet (52.5%) and weight management (50.6%) were the most prevalent risk reduction behaviors. Women in the rural area performed less risk reduction behaviors than those in urban area.

Conclusions

Given the low level of awareness and knowledge about cholesterol in these women, nurses need to increase their education about cholesterol and risk reduction behaviors of CVD for middle-aged Korean women, particularly those in rural area. To resolve identified disparities in women's risk reduction behaviors between the rural and urban area, a national-level health policy can result in a successful effort to promote women's awareness of cholesterol and risk reduction behaviors for the cardiovascular health of the public.     

Immunodetection of Tau microtubule-associated protein in human sperm and testis

Dear Editor,
The cytosolic protein Tau is naturally present in human neurons, where it has a pivotal role in controlling microtubule stability. Hyperphosphorylation of Tau （observed during neurodegenerative diseases, such as Alzheimer＇s disease） impairs the protein＇s ability to bind microtubules. This results in microtubule disassembly and the formation of Tau aggregates, Tau protein is also widely expressed in peripheral tissues. In the male reproductive system, screening for Tau has focused solely on the rodent and bovine testis. In the present study, we used immunofluorescence and immunoenzymatic techniques （with a Tau-specific antibody） to investigate the presence of Tau protein in human ejaculated sperm and testicular tissue.     

Glucuronidation of monohydroxylated warfarin metabolites by human liver microsomes and human recombinant UDP-glucuronosyltransferases

Our understanding of human phase II metabolic pathways which facilitate detoxification and excretion of warfarin (Coumadin) is limited. The goal of this study was to test the hypothesis that there are specific human hepatic and extrahepatic UDP-glucuronosyltransferase (UGT) isozymes, which are responsible for conjugating warfarin and hydroxylated metabolites of warfarin. Glucuronidation activity of human liver microsomes (HLMs) and eight human recombinant UGTs toward (R)- and (S)-warfarin, racemic warfarin, and major cytochrome P450 metabolites of warfarin (4'-, 6-, 7-, 8-, and 10-hydroxywarfarin) has been assessed. HLMs, UGT1A1, 1A8, 1A9, and 1A10 showed glucuronidation activity toward 4'-, 6-, 7-, and/or 8-hydroxywarfarin with K(m) values ranging from 59 to 480 microM and V(max) values ranging from 0.03 to 0.78 microM/min/mg protein. Tandem mass spectrometry studies and structure comparisons suggested glucuronidation was occurring at the C4'-, C6-, C7-, and C8-positions. Of the hepatic UGT isozymes tested, UGT1A9 exclusively metabolized 8-hydroxywarfarin, whereas UGT1A1 metabolized 6-, 7-, and 8-hydroxywarfarin. Studies with extrahepatic UGT isoforms showed that UGT1A8 metabolized 7- and 8-hydroxywarfarin and that UGT1A10 glucuronidated 4'-, 6-, 7-, and 8-hydroxywarfarin. UGT1A4, 1A6, 1A7, and 2B7 did not have activity with any substrate, and none of the UGT isozymes evaluated catalyzed reactions with (R)- and (S)-warfarin, racemic warfarin, or 10-hydroxywarfarin. This is the first study identifying and characterizing specific human UGT isozymes, which glucuronidate major cytochrome P450 metabolites of warfarin with similar metabolic rates known to be associated with warfarin metabolism. Continued characterization of these pathways may enhance our ability to reduce life-threatening and costly complications associated with warfarin therapy.     

Evidence that the LRRK2 ROC domain Parkinson's disease‐associated mutants A1442P and R1441C exhibit increased intracellular degradation

Mutations in the leucine‐rich repeat kinase 2 (lrrk2) gene are the leading genetic cause of Parkinson's disease (PD). In characterizing the novel ROC domain mutant A1442P, we compared its steady‐state protein levels, propensity to aggregate, and toxicity with the pathogenic R1441C mutant and wild‐type (WT) LRRK2. Mutant (R1441C and A1442P) and WT LRRK2 fused to green fluorescent protein (GFP) and FLAG were transiently expressed in HEK293 cells using plasmid constructs. Western analysis and fluorescence microscopy consistently demonstrated lower mutant LRRK2 protein levels compared with WT. A time‐course expression study using flow cytometry showed that WT LRRK2 expression increased initially but then plateaued by 72 hr. Conversely, R1441C and A1442P mutant expression attained 85% and 74% of WT levels at 24 hr but fell to 68% and 55% of WT levels by 72 hr, respectively. We found that proteasome inhibition markedly increased mutant LRRK2 to levels approaching those of WT. Taken together, our findings reveal increased intracellular degradation for both mutants. Furthermore, the impact of mutant and WT LRRK2 expression on HEK293 cell viability was assessed under normative and oxidative (hydrogen peroxide) conditions and found not to differ. Expression of WT and mutant LRRK2 protein gave rise to intracellular aggregates of similar appearance and cellular localization. In summary, we provide evidence that the novel A1442P mutant and the previously investigated R1441C pathogenic mutant exhibit increased intracellular degradation, a property reportedly demonstrated for the pathogenic LRRK2 kinase domain mutant I2020T. © 2013 Wiley Periodicals, Inc.