Chronic stress could induce adrenaline to activate lactate dehydrogenase A (LDHA) to produce lactic acid. Systemic lactic acidosis is associated with an extremely poor prognosis for survival in cancer. Chronic stress and stress hormones can upregulate the expression of stress-related proinflammatory genes in circulating white blood cells, which increases the release of proinflammatory cells and the production of proinflammatory cytokines, and may activate aging. inflammatory response without the trigger of exogenous inflammation, leading to the promotion of tumorigenesis and metastasis. Stress hormones promote the onset and development of cancers through several mechanisms, such as inducing DNA damage, increasing p53 degradation, and regulating the tumor microenvironment.
Chronic stress can also activate the inflammatory response and the interaction between inflammatory cells and cancer cells to form the tumor microenvironment, thereby promoting all stages of tumorigenesis. Animal and human studies have reported that systemic cortisol levels are increased by acid-base disruption through transiently induced metabolic acidosis. Acidosis mediates cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis.
Many studies suggest that acidosis induced by the Western diet may play a role in modulating systemic cortisol levels, and that neutralizing the acid load through alkalinization may reduce cortisol levels. Excessive or chronic cortisol production acquired from a “Western” dietary lifestyle could play a role in upregulating the tryptophan metabolism pathway and driving downstream molecular events that promote carcinogenesis. Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance.
Chronic hyperglucocorticoidism increases visceral obesity while reducing insulin sensitivity primarily in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher levels of glucocorticoid receptor expression. Visceral adipocytes also show increased activity that converts cortisone to bioactive cortisol. Glucocorticoids stimulate visceral adipocytes to increase lipoprotein lipase activity, while suppressing insulin-mediated glucose uptake. Acute induction of systemic acidosis appears to reduce serum IGF-1 levels.
Chronic stress could induce adrenaline to activate lactate dehydrogenase A (LDHA) to produce lactic acid. Systemic lactic acidosis is associated with an extremely poor prognosis for survival in cancer. Chronic stress and stress hormones can upregulate the expression of stress-related proinflammatory genes in circulating white blood cells, which increases the release of proinflammatory cells and the production of proinflammatory cytokines, and may activate aging. inflammatory response without the trigger of exogenous inflammation, leading to the promotion of tumorigenesis and metastasis. Stress hormones promote the onset and development of cancers through several mechanisms, such as inducing DNA damage, increasing p53 degradation, and regulating the tumor microenvironment.
Chronic stress can also activate the inflammatory response and the interaction between inflammatory cells and cancer cells to form the tumor microenvironment, thereby promoting all stages of tumorigenesis. Animal and human studies have reported that systemic cortisol levels are increased by acid-base disruption through transiently induced metabolic acidosis. Acidosis mediates cortisol activity through the pituitary-adrenal cortex-renal glutaminase axis.
Many studies suggest that acidosis induced by the Western diet may play a role in modulating systemic cortisol levels, and that neutralizing the acid load through alkalinization may reduce cortisol levels. Excessive or chronic cortisol production acquired from a “Western” dietary lifestyle could play a role in upregulating the tryptophan metabolism pathway and driving downstream molecular events that promote carcinogenesis. Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance.
Chronic hyperglucocorticoidism increases visceral obesity while reducing insulin sensitivity primarily in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher levels of glucocorticoid receptor expression. Visceral adipocytes also show increased activity that converts cortisone to bioactive cortisol. Glucocorticoids stimulate visceral adipocytes to increase lipoprotein lipase activity, while suppressing insulin-mediated glucose uptake. Acute induction of systemic acidosis appears to reduce serum IGF-1 levels.
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