Karolin Virgo
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簡介
The effects of HT related to the nutritional status of transgender individuals taking HT have been researched 11,12,13,14. The effects of HT include weight gain, eating disorders, altered lipid profiles, and cardiovascular risk 1,2,3. High food insecurity frequency, restricted eating behaviors, high fat intake, and low levels of vegetable, grain, and fruit consumption were also observed.
These changes disrupt signals of fullness to the brain which can be a contributing factor in the development of an eating disorder. If the body is not producing ghrelin in appropriate quantities and at the right times, a person may have trouble distinguishing feelings of fullness and satiety. There are a variety of hormones that control feelings of hunger and satiety, metabolism, and digestive processes.
Existing literature on male anorexia is sparse, and a review of the endocrine effects of AN in males has not previously been published. Conversely, in preovulatory phases of the cycle, estradiol levels increase while progesterone remains low – a hormonal milieu that would permit estradiol’s protective effects on binge/emotional eating to be expressed. While no studies have explored if/how development (e.g., puberty) may impact these neural processes, emerging data in females indicates that brain activity is modulated, in part, via estradiol. Studies have also not yet explored whether natural reductions in androgens during mid-to-late life influence differential risk for eating pathology among men. Interestingly, the detected sex-differentiated effects may be driven, in part, by estradiol modulation of neural responsivity to food cues. Moreover, while the propensity for binge eating appears to be organized during gonadarche (see above), OVX in adult female rats and mice leads to immediate increases in PF consumption whereas estradiol treatment reverses the effect.69–72 Pathological eating also varies with natural fluctuations in ovarian hormones across the estrous (in rats) and menstrual (in women) cycle. In regards to activational effects of ovarian hormones, early work was critical in demonstrating that estradiol exerts direct and anorexic effects on general eating behavior, whereas progesterone’s stimulatory effects largely occur indirectly via its antagonism of estradiol.16 More recent research has demonstrated that ovarian hormones also influence pathological eating symptoms.
When these hormones fluctuate during menstrual cycles, due to contraception, or for other reasons, the body’s signals can become dysregulated, potentially lending to the development of eating disorders. Lastly, testosterone, a hormone that regulates sex drive and tissue development, has been found to stimulate hunger and food intake. This chemical can have significant effects on food intake when in the presence of estradiol in the body. Those who experience eating disorders often experience altered eating habits, obsessions and negative associations with food and eating, and an intense fixation on weight, size, or musculature. An eating disorder is a serious mental health condition characterized by intense, persistent changes in one’s relationship with food, eating, and/or body image.
In other cases, lower to medium BMI values were also reported, partly related to restrictive eating behaviors. Nutritional status is perceived as a relevant factor when administering HT and seems to be influenced by this therapy. Transgender health is a new area in the field of nutrition, given the unique gender experience of this population, which may not follow the standard dietary and nutritional recommendations, as well as the specific nutritional concerns related to HT.
Most research on ovarian hormones and eating pathology has focused on the pubertal or young adulthood periods of development. These experimental animal studies test whether female rodents perinatally exposed to testosterone show more male-typical eating behavior. The strongest evidence of perinatal testosterone’s organizational effects on eating behavior come from non-human animal data, where exposure to exogenous testosterone can be experimentally manipulated and behavioral outcomes can be monitored across development. Indeed, sex-specific considerations in genetic variants/expression and the role of genes/proteins in CNS activity may be necessary for fully elucidating the biological basis of eating pathology. We refer to distinct diagnoses or symptoms if/when findings have been unique to certain outcomes (e.g., binge eating vs. weight/shape concerns). Eating disorders are broadly characterized by disturbances in eating and weight focused cognitions (e.g., undue influence of weight/shape on one’s self-evaluation) and behaviors (e.g., over-control or under-control of eating).