question: How does hormonal imbalance cause weight gain?
comment: The most common hormone imbalance that most people think of in relation to weight is hypo/hyperthyroidism. Everybody has a basal metabolic rate, which is the amount of energy required by your body to carry out it's baseline daily functions. Your heart beating, food digesting, breathing, etc. Basically, the thyroid controls your metabolism. If you have an overactive thyroid gland (hyperthyroidism), your metabolism speeds up. This means your body requires more energy to function. Energy = Calories. People with hyperthyroidism may have trouble consuming enough calories to meet their BMR need, and therefore tend to see weight loss as the body breaks down fat for the energy it needs. On the flip side, low thyroid function (hypothyroidism) slows the metabolism down, so the body requires fewer calories to function. Eating more calories than your body needs results in weight gain.
passages: Section::::Causes.:Hormone and neurotransmitter imbalances.
  
  Weight gain is a common side-effect of certain psychiatric medications.
  
  Section::::Causes.:Pathologies.
  
  Pathological causes of weight gain include Cushing's syndrome, hypothyroidism, insulinoma, and craniopharyngioma. Genetic reasons can relate to Prader–Willi syndrome, Bardet–Biedl syndrome, Alström syndrome, Cohen syndrome, and Carpenter syndrome.
  
  Section::::Effects.
   FHA can affect women who are underweight, normal weight, or overweight. Risk factors for adolescents and young women generally include eating disorders, such as anorexia nervosa or bulimia nervosa. Even in normal-weight patients, it is important to watch for the presentation of symptoms of anorexia in both the physical and laboratory work-ups; this is especially true when recent encounters with emotional stress and conflicts are reported. Weight loss in the context of systemic illness may also cause FHA, especially in the presence of narcotics. These are known to inhibit GnRH pulsations and shut down the pituitary-ovarian axis, and therefore, the effects of narcotics on reproductive health should be considered for women of reproductive age. The risk of FHA due to weight-related factors increases across a series of four behaviors: 1) aesthetic dieting; 2) dieting due to obsessive ideals about diet and/or weight; 3) suppression of appetite, whether by drugs or self; 4) eating disorder, generally anorexia nervosa. Patients affected by eating disorders have overactive hypothalamic-pituitary systems, causing increased cortisol release and elevated β-endorphin concentrations. Hyperactivation of the hypothalamic-pituitary system appears to be manifested through increased secretion of CRH and beta-endorphin by the central nervous system, both of which can alter GnRH pulsatility. LH secretion may return to prepubertal levels, which is likely due to decreased GnRH secretion. While weight gain may restore patterns of LH and GnRH secretion, up to 50% may remain anovulatory; patients with anorexia nervosa additionally having a decrease in thyroid hormones. One reason for hypercortisolemia in these patients is due to an effort to maintain euglycemia in a low energy availability (EA) state, which works in conjunction with GH. Mobilization of lipid stores have been indicated by the inverse relationship between cortisol levels and fat free mass (FFM): AN patients with the lowest BMIs, FFM, and fasting glucose levels have been found to exhibit the highest levels of cortisol.
   In this case, since we are asking about the differential effects by gender, we see that gender might cause a certain amount of weight gain from the treatment, but that it also causes a larger initial weight for males which in turn might cause an increase in weight gain, meaning that it is mediated by initial weight. Then, the two statisticians are asking two different questions, with the first one asking about the total effect, and the second asking about the direct effect. The key here is that none of these variables are confounders, meaning variables that cause both the supposed cause and effect. Pearl is careful to note that confounders must always be controlled for, unlike mediating variables. Tu, Gunnell, and Gilthorpe use a similar causal framework, but counter that the conceptualization of direct and total effect is not the best framework in many cases because there are many different variables that could be controlled for, and without an experimental basis that these are separate causal paths, then separating out a total effect into direct effect and indirect effects has no real basis.
   In both September and June, the distribution of male weights is the same in September and June: the males' weights have the same mean and variance, and likewise for the distribution of female weights.
  
  Lord posits two statisticians who use different but respected statistical methods to reach opposite conclusions about the effects of the diet provided in the university dining halls on students' weights. 
   Energy imbalance and weight loss can disrupt menstrual cycles through several hormonal mechanisms. Weight loss can cause elevations in the hormone ghrelin which inhibits the hypothalamic-pituitary-ovarial axis. Elevated concentrations of ghrelin alter the amplitude of GnRH pulses, which causes diminished pituitary release of LH and follicle-stimulating hormone (FSH).
  
  Secondary amenorrhea is caused by low levels of the hormone leptin in females with low body weight. Like ghrelin, leptin signals energy balance and fat stores to the reproductive axis. Decreased levels of leptin are closely related to low levels of body fat, and correlate with a slowing of GnRH pulsing.
   Weight gain is the primary effect of diet-induced obesity, but there are a variety of additional physiological side effects. One such side effect is that the body gains more fat cells. The increased number of fat cells persists even after the diet becomes lower in fat. Weight put on during the high-fat diet also tends to persist. Changes in the composition of the body are accompanied by hormonal changes. High levels of leptin and insulin are produced; at the same time, the body becomes resistant to both. Insulin resistance in particular is fed by the addition of more fat cells.
   Section::::Causes.
  
  Section::::Causes.:Hormonal imbalance.
   Section::::Key components of weight management.:Thermogenic Effect of Food.
  
  The thermogenic effect of food is another component of a person's daily energy expenditure and refers to the amount of energy it takes the body to digest, absorb, and metabolize nutrients in the diet. The amount of energy expended while processing food differs by individual but on average it amounts to about 10% the number of calories consumed during a given time period. Processing proteins and carbohydrates has more of a thermogenic effect than does processing fats.
  
  Section::::Key components of weight management.:Genetics.
   Decrease in overall thyroid function is correlated with fetal hypoxemia. Serum glucagon, adrenaline, noradrenaline levels increase, eventually causing peripheral glycogenolysis and mobilization of fetal hepatic glycogen stores.
  
  Section::::Pathophysiology.:Fetal effects.:Fetal hematologic changes.
   One statistician does not adjust for initial weight; using analysis of variance (ANOVA), and treating gain scores (June - September) as the outcome, s/he finds no significant difference between dining halls. "[A]s far as these data are concerned, there is no evidence of any interesting effect of diet (or of anything else) on student weights. In particular, there is no evidence of any differential effect on the two sexes, since neither group shows any systematic change." (Lord 1967, p. 305) 
   Both significant weight loss and weight gain can cause FHA through insulin. Significant weight loss, as in eating disorders and chronic malnutrition, is characterized by low insulin levels. Significant weight gain can lead to obesity and insulin resistance, which mimics low insulin levels via functional hypoinsulinaemia. As insulin assists in regulating the HPO axis, these low, or functionally low, levels of insulin can cause FHA, as mice models suggest that low insulin levels decrease levels of circulating LH.
   Section::::Function.:Control of food intake.
  
  The extreme lateral part of the ventromedial nucleus of the hypothalamus is responsible for the control of food intake. Stimulation of this area causes increased food intake. Bilateral lesion of this area causes complete cessation of food intake. Medial parts of the nucleus have a controlling effect on the lateral part. Bilateral lesion of the medial part of the ventromedial nucleus causes hyperphagia and obesity of the animal. Further lesion of the lateral part of the ventromedial nucleus in the same animal produces complete cessation of food intake.
  
  There are different hypotheses related to this regulation:
   The process of regaining weight and especially body fat is further promoted by the high metabolic plasticity of skeletal muscle. The "Summermatter Cycle" explains how skeletal muscle persistently reduces energy expenditure during dieting. In addition, food restriction increases physical activity which further supports body weight loss initially. Such weight regain in the form of preferential catch-up-fat is well documented after weight loss due to malnutrition, cancer, septic shock or AIDS and thus constitutes a general phenomenon related to weight loss.
  
  Section::::Effects on health.
   Section::::Deficiencies.
   Growing cells require synthesis of new nucleotides, membranes and protein components. These materials can be obtained from carbon metabolism (e.g. glucose metabolism) or from peripheral metabolism. The enhanced flux observed in abnormally growing cells is brought about by high glucose uptake.
  
  Section::::Roles of metabolic flux in cells.:Regulation of mammalian cell growth.:Cancer.
   Endocrinopathy is usually the result of improper insulin regulation, and is most commonly seen with pituitary pars intermedia dysfunction (also called equine Cushing's syndrome) and equine metabolic syndrome (EMS), as well as obesity and glucocorticoid administration. In cases of EMS, most episodes occur in the spring when the grass is lush.
  
  BULLET::::- Trauma
   Section::::Medications.:Concerns regarding stimulants.:Side effects.
  
  Section::::Medications.:Concerns regarding stimulants.:Side effects.:Growth delay and weight loss.
  
  There is some evidence of mild reductions in growth rate with prolonged stimulant treatment in children, but no causal relationship has been established and reductions do not appear to persist long-term. Weight loss almost always corresponds with loss of appetite, which may result from the medication. Severe weight loss is very uncommon though. Loss of appetite is very temporary and typically comes back as daily effects of stimulates wear off. Nausea, dizziness, and headaches, other side effect, can also indirectly affect appetite and result in weight loss.
   Certain medications can cause either weight loss or weight gain. These side effects are often listed for each medication and should be considered when attempting to manage a person's weight.
  
  Section::::Key components of weight management.:Diseases.
  
  As previously stated, acute illnesses can effect weight management by increasing a person's BMR. There are also several other medical conditions that are associated with either weight loss or weight gain. Examples of conditions that are associated with weight gain include hypothyroidism and Cushing's Syndrome. Examples of conditions that are associated with weight loss include hyperthyroidism and many cancers.
  
  Section::::Body Mass Index (BMI).
   "Zugunruhe" has been artificially induced in experiments by simulating long days. Some studies on White-crowned Sparrows have suggested that prolactin is involved in the pre-migratory hyperphagia (feeding), fattening and "Zugunruhe". However, others have found that prolactin may merely be associated with lipogenesis (fat accumulation).
  
  Researchers have been able to study the endocrine controls and navigational mechanisms associated with migration by studying "Zugunruhe".
   Exercise is increased in non-laminitic horses. Animals resistant to weight loss, despite diet and exercise changes, can be placed on levothyroxine to increase metabolism. Metformin can also be used to reduce glucose absorption through the intestinal tract.
  
  Section::::Treatment.
   It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNF-α and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-α has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNF-α receptor that may lead to insulin resistance. An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.
   According to this new theory, homeostatic imbalance includes the 'Circle of Discontent', a system of feedback loops linking weight gain, body dissatisfaction, negative affect and over-consumption. The theory is consistent with an extensive evidence-base of cross-sectional and prospective studies. A four-armed strategy to halt the obesity epidemic consists of: (1) Putting a stop to victim-blaming, stigma and discrimination; (2) Devalorizing the thin-ideal; (3) Reducing consumption of energy-dense, low nutrient foods and drinks; (4) Improving access to plant-based diets. If fully implemented, interventions designed to restore homeostasis would halt the obesity epidemic.
  
  Section::::Consciousness research.
   Environment can have large impact on the HPG axis. One example is women with eating disorders suffer from oligomenorrhea and secondary amenorrhea. Starvation from anorexia nervosa or bulimia causes the HPG axis to deactivate causing women's ovarian and uterine cycles to stop. Stress, physical exercise, and weight loss have been correlated with oligomenorrhea and secondary amenorrhea. Similarly environmental factors can also affect men such as stress causing impotence. Prenatal exposure to alcohol can affect the hormones regulating fetal development resulting in foetal alcohol spectrum disorder.
  
  Section::::Comparative anatomy.
   Section::::Simulations.:Gene/reaction deletion and perturbation studies.:Growth media optimization.
   Conversely, leptin is reduced in patients with FHA and this may suppress GnRH through a kisspeptin-mediated pathway. Leptin and adiponectin are secreted by adipocytes and are directly related to FFM, with the former being directly related and the latter being inversely related. Leptin coordinates metabolic and hormonal signals with reproductive function, and decreased levels of leptin have been shown to decrease LH pulsatile frequency. As leptin is mainly decreases feeding behavior, negative energy states have been linked to decreased leptin levels when fat mass is at critically low levels. Thus, hypoleptinemia is often representative of the chronic negative energy balance associated with FHA, and this trend holds true when compared to age-, weight-, and body fat-matched eumenorrheic controls Further, the arcuate nucleus of the hypothalamus, which is known for its regulation of food intake, is considered to be the most concentrated source of both leptin and GnRH receptors in the brain. While GnRH receptors in the hypothalamus do not contain receptors for leptin, a positive correlation has been shown to exist between leptin receptor mRNA and the kisspeptin-expressing cells which are known to stimulate GnRH release. 
  