来源:Hellokid在线英语丨2017-08-01 09:41:10


    High-Risk Scenario 1: When Early Life Undernutrition is Followed by Adult Weight Gain


        The above text discussed the hypothesis that the fetus has a capacity to "anchor" its nutritional expectations to a gestational signal (e.g. hormones, nutrients) of average recent nutrition as experienced by the mother. This might allow the developing organism to modify its own nutritional expenditure, as reflected in its growth rate, body size and other traits, as locally experienced nutritional conditions change. It is easy to see how metabolic changes that could be favorable to a nutritionally stressed fetus or infant—such as sparing glucose or depositing more fat in the abdomen – might also plant the seeds for heightened risk of developing metabolic diseases if that individual ends up gaining weight during childhood or as an adult. Thus, any context in which individuals routinely face nutritional stress before birth or during infancy but then gain excess weight during later childhood or as an adult should be associated with a high susceptibility of developing metabolic disease.  The now common finding that CVD risk is highest among individuals who were born small but later put on weight is consistent with this idea. Under what societal conditions might this pattern of early dearth followed by later excess be especially prominent or influential within a population? One way is as a result of rapid cultural, political or economic transition. In many societies, industrialization of farming is increasing affordability of cheap calories, while populations are also increasingly relying upon automobiles and other forms of transportation to move from place to place. As individuals take in more calories while expending fewer during the day, weight gain is inevitable. When the transition to relative caloric excess takes place within a single generation individuals raised under austere nutritional conditions during early life may go on to gain excess weight as older children or adults and have heightened CVD risk as a result. Consistent with this model, stunting – a measure of early life undernutrition—has been shown to be a risk factor for metabolic syndrome and obesity in populations experiencing rapid nutritional transition.   Poor early life nutrition may also coexist with adult overnutrition simply because nutritional stressors are often concentrated during periods of heightened nutritional vulnerability early in the life cycle. In contrast to trends towards positive adult energy balance and weight gain in many global populations, the nutritional experiences of infants and young children are often more strongly influenced by common communicable diseases and their underlying social determinants, such as sanitation, crowding and the availability of clean water. That nutritional stress around the age of weaning is often severe is revealed by the mammalian strategy of depositing extra body fat after birth in preparation for weaning. Among mammals, humans give birth to the fattest babies on record, which may help us to prepare for this weaning stress, which is accentuated in our species owing to the need to provide a constant supply of energy for our unusually large and energetically fragile brains.





    It is an unfortunate fact that in many developing economies today, nutritionalstressors at this early age tend to be common—tracing to factors such as diarrhea and respiratory tract infections—despite the fact that those same individuals may later experience excess weight gain as adults. Because infancy nutrition remains tightly linked to social conditions related to poverty while the availability of cheap calories is increasingly common and driving adult weight gain, many individuals may how experience early life nutrition stress followed by adult caloric excess even in the absence of rapid societal transition. This is reflected, for instance, in the common co-occurrence of obese and malnourished individuals in the same household within some low-income populations. The body’s developmental response to early nutritional stressors can help to explain why these populations often have high rates of cardiovascular and other metabolic diseases.









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