Health consequences of obesity

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Title of Part 1

Endocrine Changes in Obesity

Endocrine Changes

It is well documented that obesity is associated with changes in the normal endocrine profile. Many studies have focused particularly on the alterations in the sex steroid profile of obese individuals. This section of the article will briefly discuss the types of changes observed and their consequences on the health of the individual.

Oestrogens

Oestrogens are synthesized by aromatization of circulating testosterones. This conversion reaction is catalysed by the enzyme aromatase (Ali,) which is expressed at many sites throughout the body, including adipose tissue. Therefore, an increase in adipose tissue mass, results in a greater capacity for aromatization, and oestrogen levels rise.

The effects of obesity on oestrogen concentrations are augmented in postmenopausal women. In premenopausal, non-pregnant women, the principal site at which this takes place is the ovaries (Simpsom 2000) and so the contribution of adipose tissue to overall oestrogen synthesis is minor. However, after the menopause, adipose tissue becomes the main source of oestrogens (Simpson.)

Androgens

The increased capacity for aromatization results in hypoandrogenism in males, as a higher proportion of circulating testosterone is converted to oestrogen (Hammoud et al.) Other factors contributing to the decrease in circulating testoerone include insulin resistance and the suppression of the hypothalamic pituitary testicular axis (Hammoud.)

Most studies in premenopausal women have demonstrated that the concentration of free testosterone in the circulation increases with body weight. It has been proposed that the relationship between body weight and androgens is mediated by insulin and IGF-1, which are both increased in obese subjects.

Furthermore, as is the case for oestrogen, adipose tissue is an important site of peripheral testosterone production, due to local expression of 17 beta hydroxysteroid dehydroenase. Therefore there is a positive association between adipose tissue mass and androgen concentration.

SHBG

Sex steroids are highly lipophilic and are therefore carried in the circulation bound to proteins – sex hormone binding globulins (SHBG.) It is well documented that obesity results in a decreased concentration of SHBG. This is thought to be associated with the rise in insulin levels associated with obesity, as insulin inhibits hepatic synthesis of SHBG. The decreased concentration of binding protein results in an increase in the free fraction of sex steroids. (2)

Obesity and Cancer

It is estimated that 10% of all cancer deaths among non-smokers are related to obesity. Many hypotheses have been proposed to explain this, the most convincing of which is that alterations in endogenous hormone metabolism mediate the effects of obesity on cancer risk Kalle et al. This in part thought to be true due to the fact that sex steroids regulate the balance between cell proliferation, differentiation and apoptosis. 3

Many types of cancer are more prevalent in obese subjects, the most widely studied of which are breast and endometrial cancer. It has been observed that these types of cancer are associated with an increase in oestrogen concentration, decrease in plasma SHBG and an increase in androgen levels. (3, 2) These observations have led to the establishment of the unopposed oestrogen hypothesis. This hypothesis suggests that risk of cancer is due to increased exposure to oestrogen, which is unopposed by progestagens. This results in increased mitotic activity of cells. (Key et al) Increased mitosis, increases the risk of mutation accumulation, and thus the development of cancer.

Infertility

Obesity is thought to account for around 6% of primary infertiliy. (1)

Women

Many studies have observed increased number of atretic follicles in obese women. This reflects the increased risk of anovulatory infertility in obese women. * The anovulation is mainly due to hyperandrogenism. High androgen levels cause increased apoptosis of the granulosa cells, damage to the endometrium and developing oocytes. Excess oestrogen also contributes to infertility. This is partly due to increased negative feedback causing decreased gonadotrophin secretion (1,

PCOS

There is a well established link between PCOS and obesity. This syndrome is characterized by anovulatory infertility, obesity, hirsutism, multiple ovarian cysts and insulin resistance. ? It is unkown whether PCOS is a cause or effect of obesity (*.)

Men

Obese men generally express “hyperoestrogenic hypogonadotropic hypogonadism.” (hAMMOUD, one of other first ref) Essentially the high oestrogen levels, combined with low testosterone levels result in subfertility.

Many studies have reported a negative association between spermatogenesis and increasing BMI. The mechanism mediating this association is yet to be identified. However, it has been suggested that the gerneral hypoandrogenism observed in obese males, may reflect a reduced concentration of testosterone within the testes, which would cause a reduction in sperm count. Furthermore, the observed hyperoestrogenism causes inappropriate suppression of the hypothalamic-pituitary-gonadal axis, resulting in reduced spermatogenesis. The effects of obesity on spermatogenesis is thought to be qualitiative as well as quantitative. For example, .Ghanayem et al . . showed reduced sperm motlity and hyperactivated progression.

Obesity has also been associated with erectile dysfunction (hammoud, first). Feldman et al found that 79% of men suffering erectile dysunction were overweight or obese. Although erectile dysfunction is hought to be in part a result of hypoandrogenism, the main cause is thought to be related to endothelial dysfunction and disruption of the nitric oxide pathway.

In summary, alterations in sex steroid profiles as a result of obesity have many adverse effects on health. The most well documented health consequences are cancer and infertility.

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