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Anorexia nervosa is a primary psychiatric disease resulting in chronic starvation and serious medical complications, including severe bone loss in nearly 50% of affected adult women (1, 2). Testosterone administration did not improve BMD but increased lean body mass. If you or a loved one is struggling with an eating disorder and suspect low testosterone levels may be a contributing factor, it’s crucial to seek professional help. By increasing testosterone levels, TRT helps regulate appetite, enhance mood, and improve body composition.
In individuals with AN, leptin concentrations are lower because of reduced body weight and fat mass (71), and diurnal variation in leptin is decreased. However, vitamin D deficiency should be treated with oral supplementation to achieve serum 25-hydroxyvitamin D levels greater than 30 ng/mL to avoid further insult to bone metabolism. Generally, patients with AN have relatively low glucose and insulin levels and high glucagon levels during the active disease state with persistent abnormalities in glucose metabolism through recovery. Many patients with severe AN maintain normal albumin levels in contrast to patients with other marasmic conditions. Overall restoration and maintenance of a healthy weight have the greatest effect on bone density in patients with AN (41,42,58). Menatetrenone (vitamin K2) has shown some promise in patients with AN in terms of decreasing the loss of vertebral bone density, increasing markers of bone formation, and decreasing markers of bone resorption (55).
In a study by Stewart et al, 58% of women with either amenorrhea or oligomenorrhea had evidence of an eating disorder (15). Interestingly, this same degree of weight loss in postmenarchal women precedes amenorrhea in 20% of women with AN (3). Normal puberty and menarche are delayed with even a 10% to 15% loss of normal body weight. In females, androstenedione and testosterone are produced predominantly by the adrenal and ovary.38 Our analysis found that total testosterone levels are lower in AN compared with controls. DHEA supplementation has been studied in AN, and it may have some benefit in maintaining bone mineral density when administered with oestrogen replacement, although the overall benefits of treatment with DHEA in girls and women with AN have not been established.45,52,53 In addition, there are no studies measuring 11-oxoandrogen levels in this population.
The effect of hormone replacement therapy on eating disorder psychopathology with comorbid depression and anxiety is less clear. This finding suggests that normalization of reproductive function in addition to weight gain is necessary for maximal skeletal recovery. Despite a comparable amount of weight gained, those women who resumed menses had a mean annual increase in BMD of 3.1% at the spine, while those who did not recover menstrual function demonstrated a mean annual decline in BMD of –2.4% at the spine. In those who remained low weight and amenorrheic, the annual rate of decline was –2.4% at the hip and –2.6% at the spine in this study118. However, in a randomized controlled trial of bisphosphonate therapy in 32 adolescent girls with anorexia nervosa (mean age 16.9 ± 1.9 years), no increase in spine BMD was seen compared with placebo149. The relative contributions on these factors on impaired BMD and bone microarchitecture in anorexia nervosa is not well understood and is a focus of current research. Moreover, the effects of leptin on bone might not be uniform throughout the skeleton, as leptin-deficient ob/ob mice have decreased femoral BMD but increased spine BMD134.
We used the Q statistic and I2 to quantify the heterogeneity of effect size estimates across studies. We calculated the pooled MD by combining MDs of each study using the random-effects model. A subjective assessment of the methodological quality of observational studies was also performed using the Newcastle Ottawa Scale.7 The data are shown in Table S1.
No formal guidelines exist for BMD screening by DXA in patients with AN. A cross-sectional study in adolescent girls with active AN and an eight-year longitudinal study in adults with AN (regardless of current disease status) did not find an association between BMD by DXA and prevalent or incident fractures, respectively 101, 102. In later stages of chronic starvation, such as severe AN, where protein wasting can lead to death, bone marrow adipose tissue content is reduced as it is mobilized and metabolized as a final energy repository in a process called serous atrophy of bone marrow . Regardless, recombinant human leptin administration is not advised in women with AN. In addition to playing a role in functional hypogonadotropic hypogonadism in AN, deficits in the anorexigenic adipokine, leptin, have been hypothesized to promote starvation-induced hyperactivity in animals 84, 85, which is interesting to note as compulsive exercise is common in patients with AN. Adipokines and myokines are hormones produced by adipose tissue and muscle tissue, respectively.
To describe the hormonal adaptations and alterations in anorexia nervosa. Many of the studies were also conducted in Europe and the US, limiting generalizability regarding the results to other regions of the world. This heterogeneity likely reflects differences in study populations and differences in the use of laboratory assays. Several limitations need to be acknowledged such as the high between-study heterogeneity in several pooled analyses. The adrenal cortex is an important source of androgen production.38 The zona reticularis secretes DHEA, DHEA-S, androstenedione, testosterone, and other C19 steroids including androstenediol and the 11-oxoandrogens39 (Figure 11).