All original studies centered on food habits, nutritional status, and eating disorders among the transgender population, from inception until May 2024, were included in this systematic review. A systematic review by Gomes et al. reported body image and weight control, food and nutrition security, nutritional status, nutritional health assistance, and the perception of healthy eating . Animal and human data also point to notable sex differences in neural responsivity to highly palatable food cues that may contribute to sex-differentiated risk for eating pathology. In females, the lack of early testosterone exposure in combination with lower estradiol during gonadarche and in young adulthood, increases genetic and phenotypic risk for eating pathology. Lower risk for eating pathology among males appears to arise from an initial bout of testosterone exposure during prenatal/perinatal development and subsequent exposure to moderate-to-high levels of circulating testosterone after pubertal onset and in young adulthood. Intact female rats show higher binge-like eating when estradiol levels low (i.e., diestrous) and lower binge-like eating when estradiol levels are high (i.e., estrous).72 Similarly, women show higher binge eating and emotional eating in post-ovulatory phases (midluteal and premenstrual) when estradiol action is low1 and lower binge/emotional eating in pre-ovulatory phases (follicular/ovulatory) when estradiol action is high, independent of BMI or negative affect.73–77 Furthermore, data indicate that ovarian hormones exert direct effects on dysregulated eating symptoms (e.g., emotional eating, binge eating)73–76, whereas cycle/hormone influences on body-related concerns (e.g, body dissatisfaction, weight preoccupation) have been less robust78–82 and occur indirectly, e.g., secondary to emotional/binge eating or mediated by other cycle-based changes (e.g., water retention; overestimation of body size).79,80,82Together, these data highlight ovarian hormones as sex-specific biological factors that can enhance eating pathology, particularly emotional/binge eating, in women. In contrast to the prenatal/perinatal organization (e.g., masculinizing and defeminizing effects) from testosterone, ovarian hormones are not elevated in prenatal/perinatal development and do not play a major role at this stage of life.54 Thus, our review of ovarian hormones focuses on their organizational and activational actions on eating pathology during puberty, young adulthood, and midlife (perimenopause/menopause), and we only cover within-sex effects in females given a general absence of male data. The natural testosterone exposure during prenatal/perinatal development in males appears to impact sex differences in eating pathology by reducing risk in males relative to females; however, between-person variation in levels of circulating sex steroids, during and after puberty, could exert sex-specific effects that impact individual variation in risk among males and females and further contribute to sex-based differentiation in risk. Indeed, sex steroids facilitate organizational (i.e., long-lasting, permanent changes) and activational (i.e., transient alterations) effects on the central nervous system (CNS) that are known to drive between-sex differences and within-sex variation in the development of several sex-differentiated phenotypes (e.g., aggression, food intake, body weight).16,33,37 Hormone-dependent organization begins during prenatal/perinatal development, ends with the refinement of the CNS during puberty, and alters CNS responsiveness to the activational effects of circulating hormones on behavioral outcomes during adolescence/adulthood.33,38,39 Notably, because steroid hormones exert some of their action via intracellular genomic signaling (e.g., activation/inhibition of target genes)33,37,39, they are one set of biological factors that could uniquely contribute to the observed developmental and qualitative sex-based differences in genetic effects on eating pathology described above. A high BMI was also reported to be a risk factor influencing the choice and dosage of HT in Hojbjerg et al.’s questionnaire survey and gender confirmation surgery in Martison et al.’s cross-sectional study. Referencing Vilas et al.’s cohort study, 12% of the trans women sample and 15.1% of trans men were overweight . Around 4.3% of the trans women and 6.0% of the trans men samples were underweight in the Vilas et al. prospective cohort study . In Maheshwari et al.’s case study, the BMI was only assessed in case 1, revealing that the patient was underweight (17.2 kg/m2) . Body mass index (BMI) was the most referenced nutritional status indicator reported in twenty-five of the twenty-seven articles screened 28,30,31,32,33,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53. Twenty-seven studies were selected for this review with a combined number of 8827 participants, with 3557 confirmed to be under the trans umbrella 27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53. 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. Effects in males are less described but likely have a similar mechanism leading to hypogonadotropic hypogonadism of hypothalamic origin. Throughout history, luteal deficiency and infertility have been observed in times of food rationing during wars and reduced seasonal availability in nomadic populations (18). Infertility and impaired sexual function appear to be a protective adaptation to prevent pregnancy in a setting of impaired nutrition. The amenorrhea seen in AN is due to hypothalamic dysfunction with low levels of FSH, LH, and estradiol. Sexual orientation was not fully assessed in our patients, although the majority had reported being in heterosexual relationships. The evidence indicates that the severe multiple endocrinopathies in these patients were due to failure to seek treatment and a lack of early diagnosis, as all 4 men initially denied the severity of their weight loss. In our group, half of the patients became malnourished with the goal of losing weight or fear of weight gain.
