食慾(和遗传)会造成早期体重增加


  【24drs.com】根据在线发表于2月17日JAMA小儿科期刊的两篇研究结果,基因会影响幼童的食慾和饮食行为,导致加速体重增加,最后造成肥胖。
  
  用来评估多基因遗传性状(家庭、领养和双胞胎研究)的传统工具认为,体重超过50%是得自遗传;英国伦敦大学院和伦敦国王学院的两组研究者,进行了厘清早期体重增加之可能遗传机转的研究。
  
  自2008年来,有许多研究认为食慾高张和身体质量指数较高有关;具体而言,有风险者的食物反应(FR)高于平均值,而饱足感反应(SR)低于平均值。
  
  FR是食物(嗅觉或外观)促成进食行为和反映出脑部神经回馈路径的程度;SR是进食后的饱足感与满意感,反映出与脑部受体产生作用之荷尔蒙饱足因子有关的神经内分泌回馈环;饱足感上的差异,被视为个人如何尽快停止进食之遗传差异的原因。
  
  第一篇研究中,伦敦国王学院研究员Cornelia H. M. van Jaarsveld博士等人检视了15个月大、同性、异卵双胞胎的食慾和体重增加情况,研究设计排除了家庭饮食行为差异的影响。
  
  研究者在2007年3月1日至2007年12月15日间,对800对双胞胎使用「婴儿饮食行为问卷」评估了FR和SR,前15个月内的评估权重是平均11.5倍,偏差定义为至少1个标准差的配对差异内。
  
  这800对双胞胎中,172对的SR达到偏差定义,121对的FR达到偏差定义;不过,这些达到偏差的双胞胎在出生时体重并无差异,FR值较高和SR值较低者生长得比另一个手足快。
  
  6个月大时,FR值较高者平均重了654 g (95%信心区间[CI],395 - 913 g),15个月时,平均重了991 g (95% CI,484 - 1498 g);至于SR达到偏差的双胞胎,在6个月时体重差异平均637 g (95% CI,438 - 836 g),15个月时平均差异918 g (95% CI,569 - 1267 g)。
  
  15个月时的平均体重为10.3公斤,各对双胞胎的体重差异将近1公斤视为显著;研究者结论指出,这篇研究证实了婴儿时期食慾旺盛是体重快速增加的危险因素。
  
  研究限制包括,体重和身长之些微差异的影响,以及资料来源得自家长。
  
  第二篇研究中,伦敦国王学院助理研究员Clare H. Llewellyn博士等人,聚焦在有遗传肥胖风险因素孩童的低饱足反应,他们使用横断面观察型设计,对1994至1996年间出生的双胞胎,每对挑1名、共选定2,258名孩童,这些研究对象曾经参与搜集食慾、体重和基因型资料的两篇研究。
  
  研究者根据基因组关联研究结果统合分析获得的28个肥胖相关基因单核苷酸多态性,区分多基因风险分数(PRS);这篇研究探讨单核苷酸多态性类型之间的关联;家长使用评量表评估饱足反应;以及身体测量(身体质量指数和腰围)。
  
  这些结果认为,进食后无法快速感到饱足是受基因影响的,基因差异性和饱足反应呈现负相关(β系数,-0.060;95% CI,-0.019 至-0.101),和肥胖呈正相关(β系数,0.177 [95% CI,0.136 - 0.218]之于身体质量指数标准差;β系数,0.167 [95% CI,0.126 - 0.208]之于腰围标准差)。处于PRS前四分之一的孩童,比最后四分之一者更多属于过重(18.5% vs 7.2%;胜算比,2.90 [95% CI,1.98 - 4.25])。
  
  研究限制包括,无法确认因果关系,双胞胎之间的体重差异可能无法代表一般人,还有一个限制是依赖家长进行测量。研究者结论指出,他们的结果支持「食慾调节系统是基因差异影响肥胖的一种方式」这项假设。
  
  杜克大学医学中心老化与人类发展研究中心Daniel W. Belsky博士在编辑评论中表示,许多小孩面对的是普遍持续存在的「致胖环境」,他认为,因为食物获得方式是稳定的,遗传因素或许正可以解释体重增加模式的差异。
  
  编辑结论指出,食慾和肥胖多基因风险的关联认为,用这种方法确认哪里些小孩可以对预防性介入方式有反应而促进健康生活型态;观察型研究表示肥胖多基因风险会因为不良饮食而扩大,而可以透过积极的生活方式来缓解。
  
  资料来源: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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