How to Stop Failing our Children
In the first survey of its kind, published on 14 February 2007, Unicef has accused the UK of failing its children. It comes at the bottom of a league table for child well-being across 21 industrialised countries. So what can we do?
According to Professor Nadir Farid, who runs The London Endocrine Centre and is an expert in women’s health, “We are fascinated with technology including assisted reproduction sustaining smaller and smaller might premature babies and stomach banding for grossly obese children. However, we, lose sight of important (seemingly mundane) home truths, that what happens to the foetus during gestation, shapes not only their adult health, but also that of generations descended from them.”
Sex is fun but reproduction is not an inconvenient downside of that most natural of activities. Reproduction is to be approached with caution, planning as well as joy. To paraphrase the Keanau Reeves character in the 1989 Ron Howard film Parenthood “You need a license to drive a motorbike but anyone can have kids”.
And it all starts from within. That what happens in utero determines future health has given rise to the concept of the foetal origins of adult disease. Because many of the shortcomings in health and fitness are not clearly determined by genes, and instead are shaped by the womb environment in which they are conceived - and into which they conceive their babies when they become mothers. This legacy is designated ”trans-generational transmission” as opposed to “genetic transmission”. It takes little imagination to surmise that the socially, economically and emotionally disadvantaged bear the brunt of the trans-generational predisposition to adult disease.
Foetal stress resulting from maternal psychological and /or physical stress ( as result of abuse or deprivation ) inappropriate nutrition, drug and alcohol and illegal drugs abuse as well as smoking can and does fashion organ development, function and the health of the conceptus. Apparently chemicals such as insecticides that we pick up from the environment, have with the ability to disrupt the endocrine system (endocrine disruptors) which can modify organ development and disease for up to 4 consecutive generations of experimental animals.
Eating high carbohydrate (high glycaemia index [GI]) foods, suboptimal calories for physiological requirement, stress, and physical inactivity leads, particularly in the genetically predisposed, to insulin resistance. Most obviously an “overdose” of maternal insulin crosses the placenta to influence foetal growth and the laying down of visceral fat, and more subtly, shaping the development and future responsiveness of the pancreas, hypothalamus and pituitary, to focus on two organs relevant to this piece.
Many insulin resistant pregnant women actually suffer from PCOS, and thus have high circulating testosterone augments the insulin-related deposition of visceral fat as well as modulate the responsiveness the pituitary, hypothalamus and likely other parts of the brain to sex steroids. This intra-uterine legacy ensures that the newborn are likely to be small for gestational age, and if over fed in infancy to catch up to their expected weight, by late childhood they are likely to be insulin resistant. Girls in particular, experience earlier sexual maturity and develop PCOS symptoms with the onset of the first periods or soon thereafter. Boys would present with obesity, unexplained fatigue, sugar-craving and so on. This trans-generational legacy is at the root of the epidemic of childhood obesity.
As adults they are more likely to be [centrally] obese, develop high blood pressure, abnormal blood fats predisposing to heart disease and, of course, to type 2 diabetes.
It has been argued that insulin resistance has had a survival advantage in the last snow age when the population had dwindled dramatically and access to carbohydrate was limited, accounting for the high prevalence of the genes associated with insulin resistance in the surviving population and their descendents. It has also been posited that women with high serum testosterone, as in PCOS, were more successful in fending for their newborn and thus assured their evolutionary success despite their reduced fertility.
It is likely that the foetal origin of adult disturbed metabolism and disease is due to the combination of genetic and non-genetic influence factors. Non-genetic factors prevailing in the womb modulate the development of organ, the level at which they respond to physiologic cues
As Professor Farid concludes “Our investment in the next generation needs to start at the time of conception, during pregnancy and in early infancy, not only to prevent many of the common diseases in the community, but also to ensure that the next generations will be the best they can be.”
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