孕妇高脂肪饮食“危害”再次被证实:改变后代大脑发育,导致精神健康问题
2017/07/29
先前已有大量研究证明了孕妇高脂肪饮食对后代的危害,如增加患癌风险、引发代谢问题、自闭症等。近日,一项新发表的研究称,高脂肪饮食不仅会给孕妇带来健康问题,还会改变后代大脑和内分泌系统的发育,并对后代的行为具有长期的影响。
高脂肪饮食不仅会给孕妇带来健康问题,一项新的动物研究表明,它还会改变后代大脑和内分泌系统的发育,并对后代的行为具有长期的影响。这一新研究将怀孕期间不健康的饮食与后代的精神健康问题(如焦虑、抑郁等)联系了起来。相关成果于7月21日发表在Frontiers in Endocrinology杂志上。


图片来源:Frontiers in Endocrinology

该研究调查了孕妇高脂肪饮食对非人灵长类动物的影响。结果发现,后代行为的变化与大脑中中枢血清素系统(central serotonin system)发育受损有关。此外,研究还发现,在后代很小的时候就让他们采用健康饮食也未能逆转这种影响。

那么,研究究竟是如何进行的呢?

具体来说,研究人员将65只雌性日本猕猴分为两组:一组在孕期被给予高脂肪饮食;另一组被给予“对照饮食”(control diet)。随后,他们测量和比较了135个后代的焦虑样行为(anxiety-like behavior)。结果发现,与对照组相比,高脂肪饮食组的雌性和雄性后代都表现出更大的焦虑发生率。


Macronutrient composition of experimental diets.(图片来源:Frontiers in Endocrinology)

科学家们还检查了两组后代之间的生理学差异。结果发现,妊娠期和后代发育早期采用高脂肪饮食会损伤含有血清素(在发育大脑中一种重要的神经递质)的神经元的发育。

这项新研究首次证明,在发达国家中越来越普遍的高脂肪饮食会导致非人灵长类后代长期的精神健康影响。数据显示,在美国,64%的育龄女性是超重的,35%的育龄女性属于肥胖。作者们认为,鉴于发达国家的饮食脂肪摄入量和孕妇肥胖水平较高,这一发现对后代的精神健康具有重要意义。


图片来源:网络

多项研究证实孕妇高脂肪饮食危害大

事实上,关于孕妇高脂肪饮食的危害,探索君先前也有过不少报道。最近的一项发表在Breast Cancer Research杂志上研究(论文题目:Maternal intake of high n-6 polyunsaturated fatty acid diet during pregnancy causes transgenerational increase in mammary cancer risk in mice)证实,给怀孕小鼠喂食高脂肪饮食会增加其三代子孙患乳腺癌的概率。【详细

此外,去年6月16日,发表在Cell Reports杂志上题为“Maternal Metabolic Syndrome Programs Mitochondrial Dysfunction via Germline Changes across Three Generations”的研究表明,孕妇高脂肪和高糖饮食容易引发子孙后代的代谢问题,并且尽管后代健康饮食,这种影响也会存在。【详细

同日,发表在Cell杂志上题为“Microbial Reconstitution Reverses Maternal Diet-Induced Social and Synaptic Deficits in Offspring”的研究中,来自贝勒医学院的科学家们 揭示了孕妇高脂肪饮食导致孩子自闭的原理。【详细

参考资料:

High-fat diet in pregnancy can cause mental health problems in offspring

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  • Exposure to a High-Fat Diet during Early Development Programs Behavior and Impairs the Central Serotonergic System in Juvenile Non-Human Primates

    Perinatal exposure to maternal obesity and high-fat diet (HFD) consumption not only poses metabolic risks to offspring but also impacts brain development and mental health. Using a non-human primate model, we observed a persistent increase in anxiety in juvenile offspring exposed to a maternal HFD. Postweaning HFD consumption also increased anxiety and independently increased stereotypic behaviors. These behavioral changes were associated with modified cortisol stress response and impairments in the development of the central serotonin synthesis, with altered tryptophan hydroxylase-2 mRNA expression in the dorsal and median raphe. Postweaning HFD consumption decreased serotonergic immunoreactivity in area 10 of the prefrontal cortex. These results suggest that perinatal exposure to HFD consumption programs development of the brain and endocrine system, leading to behavioral impairments associated with mental health and neurodevelopmental disorders. Also, an early nutritional intervention (consumption of the control diet at weaning) was not sufficient to ameliorate many of the behavioral changes, such as increased anxiety, that were induced by maternal HFD consumption. Given the level of dietary fat consumption and maternal obesity in developed nations these findings have important implications for the mental health of future generations.

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