Hormone intake

Excess thyroid hormone intake (thyrotoxicosis factitia)... 

Careful anamnesis (with meticulous precision and detailed detective work) allows important information to be gathered for the distinction between intrahepatic and extrahepatic cholestasis. Questions about medication and hormone intake, chemicals (occupation, hobbies, house and garden), alcohol, teas (containing alkaloids), cosmetics, etc. as well as about fever, arthralgia, pruritus and discolouration of the stools or urine are mandatory in this context, (s. tab. 12.5) (s. p. 76)... 

Postmenopausal hormone Exogenous hormone intake decreases... 

In a 1996 review, the Committee of Toxicity of Chemicals in Food, Consumer Products and the Environment (COT) estimated the intake of isoflavones from soya-milk to be approximately 4 mg/kg/day over the first 4 months of life. This is greater than that associated with hormonal effects in premenopausal women, but the COT nonetheless supported the existing Department of Health s advice that... 

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Hormones, peptides and neurotransmitters Effect of ICV injection on food intake Effect of gene deletion on food intake Response to adiposity signals Receptor Effect of receptor defect on food intake... 

CART (cocaine- and amphetamine-regulated transcript) is a hypothalamic peptide that inhibits both normal and starvation-induced feeding when injected into cerebral ventricles of rats. CART is co-localized with the anorexigenic peptide a-melanocyte-stimulating hormone in neurons of the arcuate nucleus. Secretion of CART is stimulated by leptin and CART may be an endogenous inhibitor of food intake. 

Vasopressin (Rtressin Synthetic) and its derivatives, namely lypressin (Diapid) and desmopressin (DDAVP), regulate the reabsorption of water by the kidneys. Vasopressin is secreted by the pituitary when body fluids must be conserved. An example of this mechanism may be seen when an individual has severe vomiting and diarrhea with little or no fluid intake. When this and similar conditions are present, die posterior pituitary releases the hormone vasopressin, water in die kidneys is reabsorbed into die blood (ie, conserved), and die urine becomes concentrated. Vasopressin exhibits its greatest activity on die renal tubular epithelium, where it promotes water resoqition and smooth muscle contraction throughout die vascular bed. Vasopressin has some vasopressor activity. 

MANAGING SODIUM AND WATER RETENTION. Sodium and water retention may occur during female hormone therapy, hi addition to reporting any swelling of die hands, ankles, or feet to the primary health care provider, die nurse weighs the hospitalized patient daily, keeps an accurate record of die intake and output, encourages ambulation (if not on bed rest), and helps the patient to eat a diet low in sodium (if prescribed by the primary health care provider). 

Metallothioneins are a group of small proteins (about 6.5 kDa), found in the cytosol of cells, particularly of liver, kidney, and intestine. They have a high content of cysteine and can bind copper, zinc, cadmium, and mercury. The SH groups of cysteine are involved in binding the metals. Acute intake (eg, by injection) of copper and of certain other metals increases the amount (induction) of these proteins in tissues, as does administration of certain hormones or cytokines. These proteins may function to store the above metals in a nontoxic form and are involved in their overall metaboHsm in the body. Sequestration of copper also diminishes the amount of this metal available to generate free radicals. 

Obviously, regulation of food intake depends on many neurotransmitters and hormones but this final section will outline the role played by central 5-HT transmission in this process. It had been the belief for some time that increased 5-HT transmission in the brain reduces food intake (Blundell 1977) and this certainly explains the satiety in rats that follows infusion of 5-HT into the paraventricular nucleus (PVN) of the hypothalamus. However, recent studies using microdialysis have found that 5-HT efflux in the lateral hypothalamus is itself increased by food intake, suggesting the existence of a feedback control system. In fact, because the increase in 5-HT efflux is greater in genetically obese rats than in their lean counterparts, it has been proposed that there is a deficiency in the 5-HT inhibition of food intake in obesity. 

KEY T J A, THOROGOOD M, KEENAN J, LONG A (1992) Raised thyroid stimulating hormone associated with kelp intake in British vegan men. J Hum Nutr Diet. 5 323-6. 

In addition to fiber and carbohydrate content, protein intake from legumes may have weight-loss benefits for obese individuals just because proteins enhance post-meal satiety (Rolls, 1995). However, a possible specific role for phytoestrogens in obesity has been postulated through the modulation of the satiety response, a neuroendocrine mechanism controlled by leptin (a hormone secreted by adipose tissue and already known to be regulated by... 

The determination of an acceptable dose for humans involves the application of uncertainty factors to reflect the fact that, unlike the experimental animal, there is wide variability and susceptibility of response in the genetically diverse human population. Variations in gender, age, hormonal and disease status can affect the response to a chemical. In order to minimise any potential risks, uncertainty factors are applied to the NOAEL to arrive at a reduced exposure that is considered tolerable - namely the acceptable daily intake or ADI. These are usually tenfold for variations in susceptibility amongst the human population (the intra-species factor) and tenfold for the potential... 

The common causes of thyrotoxicosis are shown in Table 41-6.29,30 Thyrotoxicosis can be related to the presence or absence of excess hormone production (hyperthyroidism). Graves disease is the most common cause of hyperthyroidism. Thyrotoxicosis in the elderly is more likely due to toxic thyroid nodules or multinodular goiter than to Graves disease. Excessive intake of thyroid hormone may be due to overtreatment with prescribed therapy. Surreptitious use of thyroid hormones also may occur, especially in health professionals or as a self-remedy for obesity. Thyroid hormones can be obtained easily without a prescription from health food stores or Internet sources. 

Osteoporosis Oral calcium supplementation (1000-5000 mg/day) Oral vitamin D Calcifediol (1000 lU/day) Calcitriol (0.5 mcg/day) Hormone-replacement therapy Calcitonin or oral bisphosphonates If daily intake less than 1000 mg elemental calcium Documented deficiency If kidney functioning If kidney not functioning Post-menopausal women without contraindications Documented loss in bone mineral density greater than 3% Data lacking for bisphosphonates in patients with Rl... 

Electrolytes are involved in many metabolic and homeostatic functions, including enzymatic and biochemical reactions, maintenance of cell membrane structure and function, neurotransmission, hormone function, muscle contraction, cardiovascular function, bone composition, and fluid homeostasis. The causes of electrolyte abnormalities in patients receiving PN may be multifactorial, including altered absorption and distribution excessive or inadequate intake altered hormonal, neurologic, and homeostatic mechanisms altered excretion via gastrointestinal and renal losses changes in fluid status and fluid shifts and medications. 

Cholelithiasis can develop as a result of decreased gallbladder contractility, especially in the absence of enteral or oral intake. Lack of intestinal stimulation reduces secretion of cholecys-tokinin, a peptide hormone secreted in the duodenum that induces gallbladder contractility. The best prevention of cholelithiasis is early initiation of enteral or oral feeding, as stated earlier (to stimulate secretion of cholecystokinin, gallbladder contraction and emptying, and intestinal motility). 

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