回顾发现:肥胖基因对减重无影响


  【24drs.com】根据在线发表于9月20日BMJ期刊的系统性回顾与统合分析,带有脂肪量和肥胖相关基因(FTO)者,对于控制饮食、运动、药物等减重治疗的反应和其它人一样好。
  
  澳洲维多利亚迪肯大学、英国泰恩河畔纽卡斯尔纽卡斯尔大学Katherine Livingstone博士等人写道,我们发现,FTO基因型对于过重和肥胖成年人对介入方式之减重反应,并无可测得之影响。
  
  他们指出,重要的是,我们的研究结果显示,肥胖的遗传易感性和FTO次要等位基因有关,可以透过饮食、运动或以药物为主的减重介入方式而达到至少有一部份的抵消,而带有次要等位基因者对这些介入的反应一样好。
  
  研究显示,FTO基因和身体质量指数(BMI)之间有强烈关联,该基因的主要作用被认为是降低对食慾之控制。作者们指出,相较于只有一组基因者,带有这两组基因者的体重重约3公斤,发生肥胖的机率增加1.7倍。
  
  不过,基因和环境对于减重的相对贡献仍不清楚。全球约21亿人口为过重或肥胖,所以,本研究的结果有重要的公卫影响。
  
  作者们强调,未来肥胖管理的公卫策略目标应是诱导生活型态行为的长期改善,主要是饮食模式与运动,因为这些将可有效达到持续减重,且与FTO基因组无关。   
  
  在系统回顾与统合分析中,Livingstone博士等人针对四个资料库,查找从其成立开始到2015年11月为止、已发表的英文随机控制试验。
  
  他们确认了8篇在北美与南美以及欧洲进行的随机控制试验,共纳入9,563名平均年龄51.6岁、平均BMI为32.2的研究对象,追踪期范围从8周到3年;只有1篇研究评估减重药物。
  
  在开始时,相较于没有前述基因者,带有一组基因者有显著增加的BMI (0.31, P < .001)、体重(0.89公斤, P < .001)与腰围(0.63公分, P < .001)。
  
  不过,结果显示,根据FTO基因状态与介入类型,减重能力在整体上并无显著差异。特别的是,相较于没有FTO基因者,带有FTO基因者参与饮食介入、运动、药物等减重方式时,在BMI、体重、腰围之变化上并无显著差异。
  
  后续分析显示,介入类型、研究期间长短、性别、种族或BMI都不会影响这些结果。
  
  作者们讨论了几项研究限制,虽然研究认为有几个基因会影响肥胖与减重,这些研究并未评估其它肥胖相关基因对于减重的影响,而且,因为研究对象大多是白人,而未能评估FTO状态与种族在减重上的差异。
  
  在相关的编辑评论中,英国伦敦英格兰公共卫生署营养师主任 Alison Tedstone博士指出,这篇研究代表稳健地迈向揭开FTO如何影响减重。
  
  她观察指出,肥胖的原因多元且复杂,但是Livingstone等人的研究增加证据认为,环境因素之影响可能大于常见的肥胖相关基因。
  
  了解饮食和生活型态如何与肥胖遗传易感性相互影响,对于某些人将有帮助,特别是那些有罕见情况者。不过,对于大多数人而言,根据个人基因之减重介入方式并非解决方案。
  
  她强调,有监于肥胖和不良饮食习惯在英国是导致发病的原因,对整个系统方法之研究的再度平衡,包括环境驱动,对大众可能有长期的更大效益;肥胖危机的解决方案必须是社会的,也要个人的。
  
  资料来源:http://www.24drs.com/
  
  Native link:Obesity Gene Shows No Effect on Weight Loss, Review Suggests

Obesity Gene Shows No Effect on Weight Loss, Review Suggests

By Veronica Hackethal, MD
Medscape Medical News

People who carry the fat mass and obesity associated (FTO) gene respond as well as the rest of the population to weight-loss treatments that use diet, physical activity, or medication, according to a systematic review and meta-analysis published online on September 20 in the BMJ.

"We found that the FTO genotype had no detectable effect on weight loss in overweight and obese adults in response to intervention," write Katherine Livingstone, PhD, of Newcastle University, Newcastle upon Tyne, United Kingdom, and Deakin University, Victoria, Australia, and colleagues.

"Importantly, our findings show that the genetic predisposition to obesity associated with the FTO minor allele can be at least partly counteracted through dietary, exercise, or drug-based weight-loss interventions and that those carrying the minor allele respond equally well to such interventions," they add.

Research has shown strong associations between the FTO gene and body mass index (BMI), with the gene's main effect thought to be on decreasing appetite control. People who carry two copies of the gene weigh about 3 kg more and have 1.7 times increased odds of being obese, compared with those who have one copy of the gene, the authors note.

However, the relative contribution of genes and environment to weight loss remains unclear. Over 2.1 billion people worldwide are overweight or obese, so the findings from this study may have important public-health implications.

"Future public-health strategies for the management of obesity should aim to induce long-term improvements in lifestyle behaviors, principally eating patterns and physical activity, since these will be effective in achieving sustained weight loss irrespective of FTO genotype," the authors emphasize.

In the systematic review and meta-analysis, Dr Livingstone and colleagues searched four databases from inception until November 2015 for randomized controlled trials published in English only.

They identified eight randomized controlled trials conducted in North and South America and Europe, which included 9563 participants with a mean age of 51.6 years and a mean BMI of 32.2. Follow-up ranged from 8 weeks to 3 years; only one study evaluated weight-loss medications.

At baseline, individuals who carried one copy of the gene had significantly increased BMI (0.31, P < .001), weight (0.89 kg, P < .001), and waistline circumference (0.63 cm, P < .001), compared with those without it.

However, results showed no overall significant differences in the ability to lose weight based on FTO gene status and type of intervention. Specifically, changes in BMI, body weight, and waist circumference were not significantly different in carriers of the FTO gene who had participated in weight-loss interventions using diet, exercise, or medication, compared with those without the gene.

Further analyses showed that these results were not affected by intervention type, study length, sex, race/ethnicity, or BMI.

The authors discussed several limitations of the study. While research suggests that multiple genes may play a role in obesity and weight loss, the study could not evaluate the effect of other obesity-related genes on weight loss. Also, because studies included mostly white participants, the study could not evaluate differences in weight loss based on FTO carrier status and ethnicity.

In a linked editorial, Alison Tedstone, PhD, chief nutritionist at Public Health England, London, United Kingdom, notes that this study represents a "substantial step toward" unraveling how FTO may influence weight loss.

"The causes of obesity are multiple and complex, but the study by Livingstone et al adds to the evidence suggesting that environmental factors might dominate over at least common obesity-linked genes," she observed.

Understanding how diet and lifestyle interact with genetic predisposition for obesity may help some people, especially those with a rare condition. However, weight-loss interventions based on an individual's genes may not be the answer for the larger population, she explained.

"Given that obesity and poor diet are leading causes of morbidity in Britain, a rebalancing of research toward whole systems approaches, including environmental drivers, may be of greater benefit to the population in the long term," she emphasized. "The solutions to the obesity crisis must be societal, as well as individual."

The authors report no relevant financial relationships. Dr Tedstone reports meeting regularly with charities, academics, food companies, and other commercial interests as part of her work with Public Health England, although she receives no remuneration from these meetings.

For more diabetes and endocrinology news, follow us on Twitter and on Facebook.

BMJ. Published online September 20, 2106.

    
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