Humanity is being subjected to a toxic soup of contaminants that cause disease. Dangerous contaminants in cosmetics that are added to others with endocrine health risks, allergies, etc., and carcinogens, to which we must add environmental damage. In addition, these contaminants act as enhancers in the multiplication of the Spike protein.
Phthalates, like other endocrine-disrupting chemicals, can alter the homeostasis and action of hormones and signaling molecules, causing adverse health outcomes. This is especially true for babies, who are more exposed and sensitive to its effects. Phthalates are particularly harmful when exposure occurs during certain critical developmental time windows, such as the prenatal and early postnatal phases. Phthalates may also interfere with neuroendocrine systems (e.g., thyroid hormone signaling or metabolism), causing disruption of neuronal differentiation and maturation, increasing the risk of behavioral and cognitive disorders (ADHD and autistic behaviors, reduced mental, psychomotor and IQ development, and emotional problems) and the reproductive system. Di(2-ethylhexyl) phthalate (DEHP), an environmental endocrine disruptor, has hormone-like activity and endocrine-disrupting effects. Overall, in men, DEHP was positively correlated with sex hormone binding globulin (SHBG) and negatively correlated with total testosterone (TT), free androgen index (FAI), and follicle-stimulating hormone (FSH). Among women, it revealed that postmenopausal women were more vulnerable to DEHP, which was associated with lower total testosterone and estradiol.
There is a relationship between exposure to phthalates and fatty liver disease, coronary heart disease, associated metabolic dysfunction, and mitochondrial dysfunction.
Phthalate exposure was associated with accelerated biological aging promoted by inflammation. Tuberculosis is linearly linked to exposure to individual or combined phthalates.
Significant biological aging-related interactions were found between specific phthalate metabolites and dietary nutrient intake (carotenoids, vitamins A, B 1, B 2, B 6, B 12, niacin, and selenium) that mitigated this effect.
These reviews analyze the occurrence and main metabolic pathways of six typical phthalates (PAEs) (DMP, DEP, DBP, BBP, DEHP and DOP) in water, soil and atmosphere, degradation and metabolic pathways under environmental conditions. aerobic and anaerobic in immunotoxicity. PAEs affect immune system function through regulation of the expression of immune genes and enzymes, increased ROS, immune signaling pathways, specific and nonspecific immunosuppression, and interference with the complement system. Phthalates that accumulate in the intestine can influence the gut microbiome by altering its composition, resulting in intestinal dysbiosis, immune system imbalance, and altered glucose metabolism. Exposure during pregnancy can promote obesity phenotypes. Phthalates can also cause autoimmune diseases,
Humanity is being subjected to a toxic soup of contaminants that cause disease. Dangerous contaminants in cosmetics that are added to others with endocrine health risks, allergies, etc., and carcinogens, to which we must add environmental damage. In addition, these contaminants act as enhancers in the multiplication of the Spike protein.
Phthalates, like other endocrine-disrupting chemicals, can alter the homeostasis and action of hormones and signaling molecules, causing adverse health outcomes. This is especially true for babies, who are more exposed and sensitive to its effects. Phthalates are particularly harmful when exposure occurs during certain critical developmental time windows, such as the prenatal and early postnatal phases. Phthalates may also interfere with neuroendocrine systems (e.g., thyroid hormone signaling or metabolism), causing disruption of neuronal differentiation and maturation, increasing the risk of behavioral and cognitive disorders (ADHD and autistic behaviors, reduced mental, psychomotor and IQ development, and emotional problems) and the reproductive system. Di(2-ethylhexyl) phthalate (DEHP), an environmental endocrine disruptor, has hormone-like activity and endocrine-disrupting effects. Overall, in men, DEHP was positively correlated with sex hormone binding globulin (SHBG) and negatively correlated with total testosterone (TT), free androgen index (FAI), and follicle-stimulating hormone (FSH). Among women, it revealed that postmenopausal women were more vulnerable to DEHP, which was associated with lower total testosterone and estradiol.
There is a relationship between exposure to phthalates and fatty liver disease, coronary heart disease, associated metabolic dysfunction, and mitochondrial dysfunction.
Phthalate exposure was associated with accelerated biological aging promoted by inflammation. Tuberculosis is linearly linked to exposure to individual or combined phthalates.
Significant biological aging-related interactions were found between specific phthalate metabolites and dietary nutrient intake (carotenoids, vitamins A, B 1, B 2, B 6, B 12, niacin, and selenium) that mitigated this effect.
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These reviews analyze the occurrence and main metabolic pathways of six typical phthalates (PAEs) (DMP, DEP, DBP, BBP, DEHP and DOP) in water, soil and atmosphere, degradation and metabolic pathways under environmental conditions. aerobic and anaerobic in immunotoxicity. PAEs affect immune system function through regulation of the expression of immune genes and enzymes, increased ROS, immune signaling pathways, specific and nonspecific immunosuppression, and interference with the complement system. Phthalates that accumulate in the intestine can influence the gut microbiome by altering its composition, resulting in intestinal dysbiosis, immune system imbalance, and altered glucose metabolism. Exposure during pregnancy can promote obesity phenotypes. Phthalates can also cause autoimmune diseases,
https://www.sciencedirect.com/science/article/abs/pii/S0269749122013872 (2022)
https://www.mdpi.com/1422-0067/25/1/675 (2024).--
https://www.besjournal.com/fileSWYXYHJKX/journal/article/swyxyhjkx/2024/5/PDF/23381.pdf (2024).-