回顧發現:肥胖基因對減重無影響


  【24drs.com】根據線上發表於9月20日BMJ期刊的系統性回顧與統合分析,帶有脂肪量和肥胖相關基因(FTO)者,對於控制飲食、運動、藥物等減重治療的反應和其他人一樣好。
  
  澳洲維多利亞迪肯大學、英國泰恩河畔紐卡斯爾紐卡斯爾大學Katherine Livingstone博士等人寫道,我們發現,FTO基因型對於過重和肥胖成年人對介入方式之減重反應,並無可測得之影響。
  
  他們指出,重要的是,我們的研究結果顯示,肥胖的遺傳易感性和FTO次要等位基因有關,可以透過飲食、運動或以藥物為主的減重介入方式而達到至少有一部份的抵消,而帶有次要等位基因者對這些介入的反應一樣好。
  
  研究顯示,FTO基因和身體質量指數(BMI)之間有強烈關聯,該基因的主要作用被認為是降低對食慾之控制。作者們指出,相較於只有一組基因者,帶有這兩組基因者的體重重約3公斤,發生肥胖的機率增加1.7倍。
  
  不過,基因和環境對於減重的相對貢獻仍不清楚。全球約21億人口為過重或肥胖,所以,本研究的結果有重要的公衛影響。
  
  作者們強調,未來肥胖管理的公衛策略目標應是誘導生活型態行為的長期改善,主要是飲食模式與運動,因為這些將可有效達到持續減重,且與FTO基因組無關。   
  
  在系統回顧與統合分析中,Livingstone博士等人針對四個資料庫,搜尋從其成立開始到2015年11月為止、已發表的英文隨機控制試驗。
  
  他們確認了8篇在北美與南美以及歐洲進行的隨機控制試驗,共納入9,563名平均年齡51.6歲、平均BMI為32.2的研究對象,追蹤期範圍從8週到3年;只有1篇研究評估減重藥物。
  
  在開始時,相較於沒有前述基因者,帶有一組基因者有顯著增加的BMI (0.31, P < .001)、體重(0.89公斤, P < .001)與腰圍(0.63公分, P < .001)。
  
  不過,結果顯示,根據FTO基因狀態與介入類型,減重能力在整體上並無顯著差異。特別的是,相較於沒有FTO基因者,帶有FTO基因者參與飲食介入、運動、藥物等減重方式時,在BMI、體重、腰圍之變化上並無顯著差異。
  
  後續分析顯示,介入類型、研究期間長短、性別、種族或BMI都不會影響這些結果。
  
  作者們討論了幾項研究限制,雖然研究認為有幾個基因會影響肥胖與減重,這些研究並未評估其他肥胖相關基因對於減重的影響,而且,因為研究對象大多是白人,而未能評估FTO狀態與種族在減重上的差異。
  
  在相關的編輯評論中,英國倫敦英格蘭公共衛生署營養師主任 Alison Tedstone博士指出,這篇研究代表穩健地邁向揭開FTO如何影響減重。
  
  她觀察指出,肥胖的原因多元且複雜,但是Livingstone等人的研究增加證據認為,環境因素之影響可能大於常見的肥胖相關基因。
  
  瞭解飲食和生活型態如何與肥胖遺傳易感性相互影響,對於某些人將有幫助,特別是那些有罕見情況者。不過,對於大多數人而言,根據個人基因之減重介入方式並非解決方案。
  
  她強調,有鑑於肥胖和不良飲食習慣在英國是導致發病的原因,對整個系統方法之研究的再度平衡,包括環境驅動,對大眾可能有長期的更大效益;肥胖危機的解決方案必須是社會的,也要個人的。
  
  資料來源: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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