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Low and high birth weight have been associated with increased risk of type 2 diabetes and CVD. Diet could partly mediate this association, e.g. by intra-uterine programming of unhealthy food preferences. We examined the association of birth weight with diet in Finnish children.
Birth weight standard deviation score (SDS) was calculated using national birth register data and Finnish references. Dietary factors were assessed using 4 d food records. Diet quality was defined by the Finnish Children Healthy Eating Index (FCHEI).
The Physical Activity and Nutrition in Children (PANIC) study.
Singleton, full-term children (179 girls, 188 boys) aged 6–8 years.
Birth weight was inversely associated (standardized regression coefficient β; 95 % CI) with FCHEI (−0·15; −0·28, −0·03) in all children and in boys (−0·27; −0·45, −0·09) but not in girls (−0·01; −0·21, 0·18) after adjusting for potential confounders (P=0·044 for interaction). Moreover, higher birth weight was associated with lower fruit and berries consumption (−0·13; −0·25, 0·00), higher energy intake (0·17; 0·05, 0·29), higher sucrose intake (0·19; 0·06, 0·32) and lower fibre intake (−0·14; −0·26, −0·01). These associations were statistically non-significant after correction for multiple testing. Children with birth weight >1 SDS had higher sucrose intake (mean; 95 % CI) as a percentage of energy intake (14·3 E%; 12·6, 16·0 E%) than children with birth weight of −1 to 1 SDS (12·8 E%; 11·6, 14·0 E%) or <−1 SDS (12·4 E%; 10·8, 13·9 E%; P=0·036).
Higher birth weight may be associated with unhealthy diet in childhood.
Androgen insensitivity syndromes (AIS) arise from target tissue resistance to androgen action. The clinical manifestations of androgen resistance vary from external genitalia that are completely female to degrees of partial masculinization. These syndromes are the most common identifiable cause of male undermasculinization.
Role of androgens in sex determination
After development of the testis (sex determination), which is not androgen dependent, the events of male sex differentiation involve two pathways, one inhibitory and one stimulatory. The principal function of the inhibitory pathway is to cause regression of the Müllerian ducts and thus to repress the development of female internal genitalia (Fallopian tubes, uterus, and upper third of the vagina). This process occurs between six and eight weeks' gestation, mediated by anti-Müllerian hormone (Josso and Clemente, 2003). The stimulatory events of male sex differentiation require high levels of androgens and a functional androgen receptor (AR). Testosterone is thought to be critical in stabilizing the Wolffian duct system to prevent its involution and to induce differentiation into the epididymides, vasa deferentia and seminal vesicles. Stabilization of the Wolffian ducts occurs between 9 and 13 weeks' gestation, when testosterone is secreted from the testes, mostly under the control of placental chorionic gonadotrophin. Dihydrotestosterone (DHT) cannot be involved in this process, as the 5α-reductase enzyme that converts testosterone into DHT is not yet expressed in these tissues (Wilson et al., 1993).
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