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harlanmcgrew0

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This figure synthesizes key findings from animal and human research exploring sex steroid and genetic effects on eating pathology in males (displayed at top) and females (displayed at bottom) across the lifespan. Nonetheless, these data likely have relevance to sex-differentiated risk for eating pathology since core symptoms (e.g., binge eating) occur on a dimensional spectrum12 and neural disruptions in food-cue and appetite-related processes have been found in eating disorder samples.100,101 Data suggest that estradiol may exert organizational effects on binge eating during gonadarche; lower levels enhance genetic influences and may lead to increased risk for eating pathology after puberty. Lower testosterone is predictive of more eating pathology in males, whereas in adult females, higher testosterone might be related to increased eating pathology risk. Medical conditions that involve elevated prenatal/perinatal androgen exposure (e.g., congenital adrenal hyperplasia) are rare and have been linked to a number of other outcomes (e.g., overweight/obesity, HPA-axis dysregulation, body/appearance-based concerns) that might affect eating disorder risk beyond the effects of early testosterone.10 Given these methodological challenges, researchers have primarily relied on two biomarkers that capture between-person variability in prenatal testosterone exposure and can be assessed in the general population. The natural exposure to testosterone during prenatal/perinatal in males results in organizational effects on the body and CNS that drive the development of several male-typical physical, physiological, and behavioral phenotypes, including eating behavior.16,33,37 Conversely, the relative absence of prenatal/perinatal testosterone exposure in normal-developing females prevents their CNS from becoming masculinized and allows for more female-typical physical, physiological, and behavioral phenotypes to develop. In the following sections, we review evidence of organizational and activational influences of sex steroid hormones on variability in risk for eating pathology across different life stages.
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.
For TM, there was an adverse effect of HT on the lipid profile, although the risk of cardiovascular disease was not above the general non-transgender male population . In masculinizing transitions, an increase in lean body mass and a decrease in fat mass was observed . However, no guidelines regarding nutritional care in the transgender population exist, and the conditions that influence the nutrients and energy needs of this target population have yet to be determined 5,6,7,8. To achieve the goal of adjusting their physical body to their gender identity, transgender individuals may resort to the use of hormone replacement therapy (HT) to alter physical attributes depending on the gender identity in question. Understanding the basics of how your body works and what your body needs to function is important, especially if you or a loved one is experiencing an eating disorder. When an eating disorder disrupts hormonal levels, there can be a variety of health impacts. If someone is experiencing an eating disorder, there can be significant impacts to hormone production and regulation, and therefore the bodily processes that those hormones control.
In the Giltay et al. study, body fat decreased by 24% in the TM sample and increased by 38% in the TW sample . Eight studies screened fat mass to determine changes in body composition after HT administration 28,36,43,44,45,50,51,52. High body fat values were obtained by bioelectrical bioimpedance in the Sánchez Amador et al. cross-sectional study . Furthermore, after one year of administration, body weight increased, partly due to an increase in lean body mass, most frequently observed in the TM sample of Van Caenegem et al.’s prospective controlled study . In four studies, higher values of BMI, indicating overweight and obesity status, were also found 27,40,42,51. In three studies, similarly to the gender identity, broader terms were used, such as "hormone replacement therapy" , "sex-steroid hormones" , or "gonadotropin-releasing hormone agonist therapy" .
In fact, a female bias is evidenced by previous diagnostic criteria, which include amenorrhea but not low testosterone or decreased libido. Increased awareness of AN in males is vital, as its prevalence is likely underestimated and appropriate diagnosis and treatment can ameliorate the metabolic dysfunction in a majority of cases. This small case series highlights the importance of AN as a potential cause of multiple endocrinopathies in males. Most of the clinical effects from these endocrinopathies resolved with improved caloric intake and nutrition, although symptoms of hypogonadism persisted.
Often, these changes in hormones and ensuing eating disorders can produce a feedback loop of increased changes in hormones due to the eating disorder behaviors. As previously explored, there is a variety of hormones that can play a role in the development of an eating disorder. An eating disorder can develop for a variety of reasons, and hormones may have a key role. It is clear that hormones are critical to the various bodily systems involved in eating disorders.
The same endocrinopathies seen in females with AN can also occur in males. In summary, AN is not only a disease in females but should also be suspected in males with multiple endocrine dysfunction. Biochemical parameters such as bone turnover markers, total and free testosterone, prolactin, LH, FSH, ACTH, IGF-1, GH, and total and free T3 levels were not universally assessed in all 4 patients during their admission and would have possibly provided an opportunity for further analysis and conclusions. Low levels of testosterone and dehydroepiandrosterone may contribute to low bone mass during puberty. Additionally, the loss of body fat leads to decreased aromatization of androgens to estrogens. A decrease in normal body weight by 10 to 15% can cause amenorrhea (17). The hypothalamic-pituitary-gonadal axis has welldescribed alterations in females with AN, which is similar to males with AN, as in our cohort.
Some of the articles screened for this review were case reports and studies with a smaller sample size. Consequently, it does not allow for an accurate extrapolation of the general transgender population regarding food habits. In addition, few studies have used a standardized protocol to analyze diet or food habits. They also illustrate the need for more research to be conducted on food habits and eating intakes in the trans adult population, outside of compensatory behaviors related to EDs. The focus on food habits/intake and the potential relation with HT is a major difference between the present review and those referenced. Body weight values were compared between the TW and TM groups before and after starting HT, and no significant differences were found . Cost, access, and food preparation were seen as barriers to including healthy foods in the diet, which is in line with previous reviews.
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