Alcohol's effects on female puberty: the role of insulin-like growth factor 1

Abstract

Research suggests that alcohol consumption during early adolescence may delay the onset of female puberty. Alcohol's effect on sexual development is associated with altered function of insulin-like growth factor 1 (IGF-1). This hormone, which is produced in the liver, travels through the bloodstream to the brain, where it helps coordinate overall physical growth with the maturation of the reproductive system. Long-term alcohol consumption inhibits the production of IGF-1 in the liver. Short-term alcohol administration alters IGF-1 function within the brain, ultimately suppressing the release of specific reproductive hormones that initiate puberty. Large proportions of young girls develop drinking habits that place them at risk for alcohol-related endocrine disorders at a crucial time in female pubertal development.

Figure 1

Proposed action of IGF-1 in females as puberty approaches. (A) As puberty approaches, growth hormone stimulates the synthesis of IGF-1 by the liver. The liver releases IGF-1 into the bloodstream. (B) IGF-1 induces the release of LHRH from the median eminence of the hypothalamus. (C) LHRH induces the pituitary gland to secrete FSH and LH into the bloodstream. (D) On reaching the ovaries, FSH and LH help regulate the synthesis of steroid reproductive hormones. (E) In addition to its direct effects on the reproductive cycle, the ovarian steroid hormone estradiol contributes to the regulation of LHRH and LH levels. NOTE: ⊕ = stimulates; ⊖ = inhibits; FSH = follicle-stimulating hormone; IGF-1 = insulin-like growth factor 1; LH = luteinizing hormone; LHRH = luteinizing hormone-releasing hormone.

Figure 2

Alcohol blocks the ability of IGF-1 to induce the release of LH in prepubertal female rats. Rats were administered either a single dose of alcohol or a corresponding amount of alcohol-free salt solution (i.e., saline) immediately following determination of their baseline LH levels. Blood was sampled again after 90 minutes, before IGF-1 was injected directly into the brain in the region of the hypothalamus of each rat. Levels of LH decreased in the alcohol-fed rats and failed to increase in response to IGF-1 injection, potentially suppressing LH-induced ovulation. NOTE: ETOH = alcohol; IGF-1 = insulin-like growth factor 1; LH = luteinizing hormone; ng/mL = nanograms per milliliter.