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DHEA and Cortisol

DHEA and Cortisol

 DHEA (dehydroepiandrosterone) is a precursor to male and female sex steroids. Treating women with DHEA will help increase their serum testosterone to a youthful range and can make testosterone replacement unnecessary. DHEA can boost mood, cognitive function. Boost immune function, boost bone density, increase strength and enhance well-being. Many adverse clinical outcomes are associated with low levels of DHEA, such as cognitive and immune dysfunction, some cancers, inflammatory diseases, type II diabetes and cardiovascular disorders. Many people over 40 have DHEAS levels lower than youthful levels. Serum laboratory testing is required to order DHEA sulfate levels, the level that gives us an accurate DHEA assessment. Unsulfated DHEA levels differ greatly during the day, and serum levels are useless (A4M, 2013-2018, p. 346). Optimal levels of DHEA can improve sex, increase muscle mass, decrease body fat, enhance memory, improve cognition, decrease depression and boost the immune system's response by regulating cortisol and adrenaline levels ((2012), 2013-2018, p. 347). The metastatic cycle in breast tumor cell lines is inhibited with dehydroepiandrosterone. Dehydroepiandrosterone (DHEA), an adrenal hormone, plays a protective role against cancer. DHEA blocked transwells migration (an assay commonly used test or study the migratory response of endothelial cells to certain angiogenic inducers or inhibitors) and Matrigel invasion of the cells MCF-7 and MDA-MB-231. In addition, DHEA inhibited the anchorage-independent growth of agar and decreased the size of spheroids, and also decreased the secretion of IL-1α,IL-6,IL-8 and TNF-α in all cell lines (Lopez-Marure et al., 2016). Dehydroepiandrosterone defends human keratinocytes by binding membrane sites against apoptosis. DHEA, utilizing non-immortalized human HaCaT cells, has a defensive function against apoptosis in keratinocytes. DHEA transmits its signal via different protein-coupled, membrane-binding sites and prevents apoptosis by preventing mitochondrial disruption and altering the Bcl-2 protein balance (Alexaki et al., 2009). When our heart rate and blood pressure rise quickly and we feel a trembling sensation, it is the response of our body to stressful situations. Cortisone is responsible for such scenarios. Cortisol is produced and release by the adrenal glands. It is a glucocorticoid hormone whose release is tightly controlled by the hypothalamus-pituitary-adrenal axis. It induces either a cortisol syndrome and Addison’s disease respectively under conditions of overproduction and underproduction. Cortisol is the only human hormone that increases with age. Like DHEA, cortisol is produced by your adrenal glands which make all our sex hormones after menopause. Cortisol is generally called the "stress hormone," due to its role in your reaction to stress (Thau & Sharma, 2020). Cortisol Influences bone turnover plays a vital role in the immune system response, Influences pituitary / thyroid / adrenal system and stress reaction. Cortisol helps balance blood sugar levels and controls body weight, protein synthesis, sleep, improvement in mood, influences DHEA to insulin ratio, influences estrogen to testosterone ratio, has anti-inflammatory actions (D. Y. Lee, Kim, & Choi, 2015).

 There is a strong interrelation between hypothalamic-pituitary-adrenal axis activation and energy homeostasis. Cortisol levels are high in patients with abdominal obesity. Stress and glucocorticoids also regulate the consumption of food as well as energy. The consumption of foods enriched with fat and sugar is well known to increase glucocorticoids. Cortisol responses to stress or adrenocorticotropin are widely considered to be extremely variable in all animals (Hewagalamulage, Lee, Clarke, & Henry, 2016). A rise in serum cortisol / DHEA-S ratio demonstrated higher cortisol values and lower DHEA-S values in sarcopenia patients relative to nonsarcopenic patients leading the study authors to conclude that a relative increase in cortisol may indicate stress and promote muscle catabolism, while a relative decrease in DHEA-S may cause a decrease in DHEA's anabolic action on muscle; combining these factors can contribute to scoping (Yanagita et al., 2019). Evidence suggests that glucocorticoids and catecholamines inhibit the development of proinflammatory cytokines such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, while stimulating the development of anti-inflammatory cytokines such asIL-10, IL-4andgrowth factor (TGF)-beta (Elenkov & Chrousos, 2002). Hence, when we encounter an excessive immune response through the activation of the stress system, an essential negative feedback mechanism is activated that protects the organism the tissue-damaging proinflammatory cytokines and other activated macrophages (Elenkov & Chrousos, 2002).