食慾(和遺傳)會造成早期體重增加


  【24drs.com】根據線上發表於2月17日JAMA小兒科期刊的兩篇研究結果,基因會影響幼童的食慾和飲食行為,導致加速體重增加,最後造成肥胖。
  
  用來評估多基因遺傳性狀(家庭、領養和雙胞胎研究)的傳統工具認為,體重超過50%是得自遺傳;英國倫敦大學院和倫敦國王學院的兩組研究者,進行了釐清早期體重增加之可能遺傳機轉的研究。
  
  自2008年來,有許多研究認為食慾高張和身體質量指數較高有關;具體而言,有風險者的食物反應(FR)高於平均值,而飽足感反應(SR)低於平均值。
  
  FR是食物(嗅覺或外觀)促成進食行為和反映出腦部神經回饋路徑的程度;SR是進食後的飽足感與滿意感,反映出與腦部受體產生作用之荷爾蒙飽足因子有關的神經內分泌回饋環;飽足感上的差異,被視為個人如何盡快停止進食之遺傳差異的原因。
  
  第一篇研究中,倫敦國王學院研究員Cornelia H. M. van Jaarsveld博士等人檢視了15個月大、同性、異卵雙胞胎的食慾和體重增加情況,研究設計排除了家庭飲食行為差異的影響。
  
  研究者在2007年3月1日至2007年12月15日間,對800對雙胞胎使用「嬰兒飲食行為問卷」評估了FR和SR,前15個月內的評估權重是平均11.5倍,偏差定義為至少1個標準差的配對差異內。
  
  這800對雙胞胎中,172對的SR達到偏差定義,121對的FR達到偏差定義;不過,這些達到偏差的雙胞胎在出生時體重並無差異,FR值較高和SR值較低者生長得比另一個手足快。
  
  6個月大時,FR值較高者平均重了654 g (95%信心區間[CI],395 - 913 g),15個月時,平均重了991 g (95% CI,484 - 1498 g);至於SR達到偏差的雙胞胎,在6個月時體重差異平均637 g (95% CI,438 - 836 g),15個月時平均差異918 g (95% CI,569 - 1267 g)。
  
  15個月時的平均體重為10.3公斤,各對雙胞胎的體重差異將近1公斤視為顯著;研究者結論指出,這篇研究證實了嬰兒時期食慾旺盛是體重快速增加的危險因素。
  
  研究限制包括,體重和身長之些微差異的影響,以及資料來源得自家長。
  
  第二篇研究中,倫敦國王學院助理研究員Clare H. Llewellyn博士等人,聚焦在有遺傳肥胖風險因素孩童的低飽足反應,他們使用橫斷面觀察型設計,對1994至1996年間出生的雙胞胎,每對挑1名、共選定2,258名孩童,這些研究對象曾經參與蒐集食慾、體重和基因型資料的兩篇研究。
  
  研究者根據基因組關聯研究結果統合分析獲得的28個肥胖相關基因單核苷酸多態性,區分多基因風險分數(PRS);這篇研究探討單核苷酸多態性類型之間的關聯;家長使用評量表評估飽足反應;以及身體測量(身體質量指數和腰圍)。
  
  這些結果認為,進食後無法快速感到飽足是受基因影響的,基因差異性和飽足反應呈現負相關(β係數,-0.060;95% CI,-0.019 至-0.101),和肥胖呈正相關(β係數,0.177 [95% CI,0.136 - 0.218]之於身體質量指數標準差;β係數,0.167 [95% CI,0.126 - 0.208]之於腰圍標準差)。處於PRS前四分之一的孩童,比最後四分之一者更多屬於過重(18.5% vs 7.2%;勝算比,2.90 [95% CI,1.98 - 4.25])。
  
  研究限制包括,無法確認因果關係,雙胞胎之間的體重差異可能無法代表一般人,還有一個限制是依賴家長進行測量。研究者結論指出,他們的結果支持「食慾調節系統是基因差異影響肥胖的一種方式」這項假設。
  
  杜克大學醫學中心老化與人類發展研究中心Daniel W. Belsky博士在編輯評論中表示,許多小孩面對的是普遍持續存在的「致胖環境」,他認為,因為食物獲得方式是穩定的,遺傳因素或許正可以解釋體重增加模式的差異。
  
  編輯結論指出,食慾和肥胖多基因風險的關聯認為,用這種方法確認哪些小孩可以對預防性介入方式有反應而促進健康生活型態;觀察型研究表示肥胖多基因風險會因為不良飲食而擴大,而可以透過積極的生活方式來緩解。
  
  資料來源:http://www.24drs.com/professional/list/content.asp?x_idno=7055&x_classno=0&x_chkdelpoint=Y
  

Appetite (and Genes) May Drive Early Weight Gain

By Ricki Lewis, PhD
Medscape Medical News

Genetics may influence appetite and eating behavior in young children in ways that lead to accelerated weight gain that can, in turn, lead to obesity, according to results from 2 studies published online February 17 in JAMA Pediatrics.

Traditional tools to assess polygenic traits (family, adoption, and twin studies) identify heritability greater than 50% for body weight. Two overlapping groups of researchers from University College London and King's College London, United Kingdom, have conducted studies that tease out possible genetic mechanisms behind early weight gain.

Since 2008, several studies have associated hearty appetite with higher body mass index. Specifically, those at risk have higher than average food responsiveness (FR) coupled with lower than average satiety responsiveness (SR).

FR is the degree to which food cues (smell or appearance) compel eating behavior and reflects neural reward pathways in the brain. SR is the feeling of fullness and satisfaction after eating and reflects neuroendocrine feedback loops involving hormonal satiety factors that interact with receptors in the brain. Differences in satiety are thought to underlie some of the inherited differences seen in how soon individuals stop eating.

In the first study, Cornelia H. M. van Jaarsveld, PhD, a research fellow at King's College London, and colleagues, examined appetite and weight gain in same-sex, nonidentical twin pairs during the first 15 months of life. The design removed the confounding effects of differences in eating behavior among families.

The researchers assessed FR and SR using the Baby Eating Behavior Questionnaire among 800 twin pairs born between March 1, 2007, and December 15, 2007, assessing weight an average of 11.5 times for the first 15 months. Discordance was defined as a within-pair difference of at least 1 standard deviation unit.

Of the 800 twin pairs, 172 pairs were discordant for SR and 121 pairs for FR. Although there was no difference in weight at birth among discordant pairs, the infants with higher FR and lower SR grew faster than their siblings.

At 6 months of age, babies with higher FR were an average of 654 g (95% confidence interval [CI], 395 - 913 g) heavier, and at 15 months, they were an average of 991 g (95% CI, 484 - 1498 g) heavier, than their siblings. For twins discordant for SR, weights differed by a mean of 637 g (95% CI, 438 - 836 g) at 6 months and a mean of 918 g (95% CI, 569 - 1267 g) at 15 months.

Considering that mean weight at 15 months is 10.3 kg, the finding that the twins at opposite extremes differed by nearly a kilogram is significant. The investigators conclude that the study "corroborates the hypothesis that a hearty appetite in infancy is a risk factor for faster weight gain."

Limitations of the study include the effects of small differences in birth weight and body length and the parental source of the data.

Low Satiety a Risk

In the second study, Clare H. Llewellyn, PhD, a research associate at King's College London, and coworkers focused on low satiety responsiveness as a genetic risk factor for obesity in children. They used a cross-sectional observational design on twins born between 1994 and 1996, selecting 2258 unrelated children, 1 from each pair. The participants had previously participated in 2 studies that gathered data on appetite and weight, and on genotype.

The researchers derived a polygenic risk score (PRS) based on single nucleotide polymorphisms in 28 obesity-related genes from a meta-analysis of genome-wide association study findings. The study looked for associations among single nucleotide polymorphisms patterns; satiety responsiveness that parents assessed, using a rating scale; and anthropometric measures (body mass index and waist circumference).

These results suggest that inability to feel full soon after eating is genetically influenced. The gene variants were associated negatively with satiety responsiveness (β coefficient, ?0.060; 95% CI, ?0.019 to ?0.101) and positively with adiposity (β coefficient, 0.177 [95% CI, 0.136 - 0.218] for body mass index standard deviation; β coefficient, 0.167 [95% CI, 0.126 - 0.208] for waist standard deviation scores). More children in the top quartile of the PRS were overweight than in the lowest quartile (18.5% vs 7.2%; odds ratio, 2.90 [95% CI, 1.98 - 4.25]).

Limitations of the study include an inability to determine causality, the fact that weight among twins may not represent the general population, and the fact that parents obtained the measurements. The researchers conclude that their results support the hypothesis that the appetite regulatory system is one way that gene variants influence adiposity.

Lifestyle Factors Contribute

In an accompanying editorial, Daniel W. Belsky, PhD, from the Center for the Study of Aging and Human Development at the Duke University Medical Center, Durham, North Carolina, discusses the pervasive and persistent "obesogenic environment" that many children face. Because the availability of food is constant, he argues, genetic factors may explain differences in weight gain patterns.

"The link between appetite and polygenic risk for obesity suggests that children identified in this way may be responsive to preventive interventions that promote healthy lifestyle practices; observational studies indicate that polygenic risk for obesity is amplified by poor diet and can be mitigated by active lifestyle," the editorial concludes.

The investigators and commentator have disclosed no relevant financial relationships.

JAMA Pediatr. Published online February 17, 2014.

    
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