haimarcotte350/hai2006
1
0
Code Issues Actions Packages Projects Wiki

Add Current Health News & Updates For the Mind & Body

Hai Marcotte 2026-04-02 21:22:09 +08:00
commit b8790960e8
1 changed files with 7 additions and 0 deletions
Show Stats Download Patch File Download Diff File Expand all files Collapse all files

7
Current-Health-News-%26-Updates-For-the-Mind-%26-Body.md Normal file

@ -0,0 +1,7 @@
<br>
<br>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.
Those who experience eating disorders have an increased risk of thyroid problems and reduced fat stores, which has numerous impacts on the hormones that regulate reproduction, hunger and satiety, [music.crone.es](https://music.crone.es/@gennieventura6?page=about) sleep cycles, and more. When a person is restricting their food intake, like in the case of eating disorders, the body is left with lower fat stores, reduced protein stores, and decreased availability of essential nutrients and vitamins. Someone with fluctuating weight or extreme changes in body fat may experience drastic changes in leptin levels. Patients at highest risk for refeeding syndrome are those with minimal or no nutritional intake for more than 3 days, more than 15% weight loss over the past 3 months, low weight for height, and abnormal electrolytes prior to refeeding (2). Body fat percentage may be predictive of menstrual restoration, as women with a higher percentage of body fat maintained menses despite low body weight (21). The other 2 patients’ weight loss and starvation states were unintentional effects of underlying depression and psychosis, with less concern about their body image.
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 [buy testosterone without prescription](http://207.180.227.11:3001/madelinemountg) 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 [buy testosterone cream online](http://106.55.0.66:31807/luisbruner8523) 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).
Ewan et al.’s case report had a patient showing a decrease from 26.8 kg/m2 to 13.8 kg/m2, indicating an undernutrition status . Regarding the case studies, only one, performed by Linsenmeyer et al. , had an extensive description of the statistical methods used in the analysis and the results obtained. Some studies had a small community sample, such as the Kirby and Linde cross-sectional survey with 26 college students or the Sánchez Amador et al. comparative survey with 37 TW in 105 participants . Regarding the geographical area, fifteen studies were from Europe, eleven were from America, and one was from Asia. The studies screened included sixteen cohort studies 28,29,30,31,32,33,36,37,43,44,45,48,49,50,51,52, seven cross-sectional studies 27,34,38,39,42,47,53, and four case studies 35,40,41,46. The remaining participants’ gender identities were either not specified or were grouped into a broad term, such as "transgender individuals" or "written-in different identity" .
Non-human animal data indicate that female rodents have a greater propensity to overconsume PF, independent of their physiological state (hunger vs. satiated)102,103, and may experience PF as inherently more rewarding than males.103,104 For example, female rats worked harder to obtain PF than males and were also more sensitive to the stimulatory/palatability effects of an opioid agonist (morphine).103 Compared to males, female rats have also been found to show stronger motivation for PF, and show greater neural activation of mesocoticolimibic reward circuit regions (e.g., nucleus accumbens, medial prefrontal cortex) following PF consumption.104 Although some sex similarities in neural activation in response to PF do occur (e.g., increased activation in hypothalamic and amygdala regions; orexin/hypocretin neurons in hypothalamus)102,104, sex-differentiated action in key neural substrates (e.g., reward regions) likely underlie sex differences in hedonic and motivational responses to PF. Both estradiol and progesterone play a role in late adolescence and adulthood, and their activational and interactive effects (especially hormonal milieus that result in low estradiol action) further facilitate risk for eating pathology in women. Second, pre-pubertal OVX in female rats increases the proportion of binge eating prone phenotypes during adolescence and adulthood68, whereas adult OVX increases PF consumption in all female rats but the relative proportion classified as binge eating prone versus binge eating resistant is not changed.69 This maintenance of classification status (binge eating prone vs binge eating resistant) even after adult OVX suggests that individual differences in binge-proneness might be permanently organized earlier in development.68,69 Given that genetic contributions to eating pathology in girls emerge during gonadarche (independent of BMI)18,26–30 and the fact that steroid hormones can regulate gene transcription, recent research has explored whether pubertal ovarian hormones moderate genetic effects on eating pathology. Following administration of an antiandrogenic oral contraceptive, women with BN showed significant reductions in circulating testosterone levels, and this hormonal change was related to decreases in appetite (e.g., hunger) and binge-purge symptoms, particularly in women who had hyperandrogenic levels and greater severity of bulimic symptoms at baseline.60 Similarly, reduction in binge-purge symptoms have also been found in patients with BN following treatment with a [buy testosterone propionate](https://opensourcebridge.science/wiki/User:Gabriele44P) blocker (i.e., the androgen receptor antagonist, flutamide)61,62, whereas relapse of symptoms occurred when the drug was withdrawn.61 Together, findings suggest that high [buy testosterone propionate](https://koseongnam.com/francescocazar) may enhance risk for pathological eating in adult women, and systematic reductions in [order testosterone online](http://shinhwaspodium.com/bbs/board.php?bo_table=free&wr_id=4831597) may be effective at reducing vulnerability to binge-purge behavior in some women with BN.
<br>