Foetal programming Sample Clauses

Foetal programming. The foetal origins of adult disease (FOAD) hypothesis is the notion that exposure to intrauterine insults during gestation affects foetal brain development, leading to vulnerabilities for a variety of neuropsychiatric and chronic physical health diseases in adult life. This concept was initially termed the “Xxxxxx Hypothesis”, in acknowledgement of the late Xxxxx Xxxxxx, who, in his seminal 1995 paper presented the argument for an association between poor foetal growth and elevated cardiovascular disease (CVD) in adulthood. Xxxxxx and colleagues’ research was predominantly drawn from a series of studies on a British cohort of men and women that demonstrated an inverse relationship between low birth weight and death from CVD, and elevated markers of the metabolic syndrome (X Xxxxxx, Xxxxxxxx, et al., 1993; X Xxxxxx, Xxxxx, et al., 1993). Xxxxxx’x original hypothesis (X Xxxxxx & Xxxxx, 1997; X Xxxxxx, 1995) postulates that offspring exposure to adverse conditions during gestation, especially malnutrition, ultimately leads to “programming” of insulin resistance and glucose intolerance. This phenomenon resonates with an evolutionary adaptation, functioning to enhance the foetus’ ability to retain as much nutritional energy as possible, resulting in the development of the “thrifty phenotype”. It is argued that this physiological reprogramming translates into a risk for metabolic diseases in later life in scenarios where high-energy food becomes readily available. This concept of “mismatch” between the foetal environment and post birth environment in predicting pathological conditions has been replicated in animal studies. It is worth noting that “mismatch” is argued to be a U-shaped phenomenon in which both overabundance and scarcity in gestational environmental conditions can result in the foetus making short-term adaptations that are non- beneficiary in the long run. For example, studies in rodents have shown that maternal high fat diet during pregnancy leads to the greatest obesity in pups fed a normal diet after birth, whilst a maternal low calorie diet leads to obesity in offspring that go on to be fed a high fat diet postnatally (Xxxxx, Xxxxxxx, Xxxxx, & Xxxxxxx, 2009; Xxxxxxxx et al., 2007). Since its inception into the wider research field, the Xxxxxx Hypothesis has been applied to a variety of offspring in utero risk exposures, as well as to a variety of later neuropsychiatric conditions, including emotional and behavioural psychopathology. Specificall...