'Failure to thrive' is an outdated medical diagnosis masking the failure on doctors' role in addressing the underlying conditions contributing to poor health.
Excellent report that provides us with an overview of cellular damage from food and environmental toxins. A diet that avoids the promotion of endotoxins related to metabolic diseases, including cardiovascular, neurodegenerative diseases and cancer. Excessive intake of fructose and linoleic acid in the usual human diet is related to a global increase in metabolic disorders. Chronic endotoxemia commonly occurs in obesity and is an important factor inducing systemic inflammation leading to metabolic syndrome. Healthy dietary choices, such as consumption of fish, fresh vegetables, and fruits and berries, may be associated with positive health outcomes. by reducing systemic endotoxemia. Vitamin D restriction and/or a high-fat diet increases the risk of metabolic endotoxemia. Phytochemicals reduce endotoxins.
Specific components of the Western diet, such as PUFAS, monosaccharides, processed fats, gluten, alcohol and additives, can affect the tight junctions between enterocytes, leading to increased permeability and the movement of endotoxins into the bloodstream. blood. These endotoxins include lipopolysaccharides derived from gram-negative bacteria.
In particular, a high-fructose diet can increase intestinal permeability and circulatory endotoxins by changing intestinal barrier function and microbial composition. Excess fructose causes inflammation and de novo lipogenesis. Lipogenesis leads to hepatic steatosis, thus causing abdominal adiposity and insulin resistance.
Serum endotoxin levels are elevated in patients with liver cirrhosis, diabetes, cardiovascular diseases, chronic infections and aging, amyotrophic lateral sclerosis, and Alzheimer's disease. The highest levels of plasma endotoxin are found in patients with sepsis, around 500 pg/ml.
Endotoxin levels in blood plasma are normally low, but rise during infections, intestinal inflammation, gum disease, and neurodegenerative diseases.
Leaky gut causes the release of bacterial metabolites and endotoxins, such as lipopolysaccharide, into the circulation, causing bacterial infections, oxidative stress. Diet rich in polyunsaturated fats, exposure to alcohol or chronic allergens, and dysbiosis are highly related to development and/or progression. of several systemic metabolic and autoimmune diseases, neurodegenerative disease, cardiovascular disease, inflammatory bowel disease, cancer and the development of metastases.
Increases in blood endotoxin levels were associated with increases in C-reactive protein concentrations and increases in intestinal permeability markers such as zonulite.
Probiotics help modify the intestinal microbiota, promote the growth of beneficial bacteria and are an alternative source of SCFAs and reduce LPS expression, intestinal inflammation and tumor size in CRC. Among them, Akkermansia muciniphila has the ability to reduce the expression of LPS, improving metabolic endotoxemia.
Excellent report that provides us with an overview of cellular damage from food and environmental toxins. A diet that avoids the promotion of endotoxins related to metabolic diseases, including cardiovascular, neurodegenerative diseases and cancer. Excessive intake of fructose and linoleic acid in the usual human diet is related to a global increase in metabolic disorders. Chronic endotoxemia commonly occurs in obesity and is an important factor inducing systemic inflammation leading to metabolic syndrome. Healthy dietary choices, such as consumption of fish, fresh vegetables, and fruits and berries, may be associated with positive health outcomes. by reducing systemic endotoxemia. Vitamin D restriction and/or a high-fat diet increases the risk of metabolic endotoxemia. Phytochemicals reduce endotoxins.
Specific components of the Western diet, such as PUFAS, monosaccharides, processed fats, gluten, alcohol and additives, can affect the tight junctions between enterocytes, leading to increased permeability and the movement of endotoxins into the bloodstream. blood. These endotoxins include lipopolysaccharides derived from gram-negative bacteria.
In particular, a high-fructose diet can increase intestinal permeability and circulatory endotoxins by changing intestinal barrier function and microbial composition. Excess fructose causes inflammation and de novo lipogenesis. Lipogenesis leads to hepatic steatosis, thus causing abdominal adiposity and insulin resistance.
Serum endotoxin levels are elevated in patients with liver cirrhosis, diabetes, cardiovascular diseases, chronic infections and aging, amyotrophic lateral sclerosis, and Alzheimer's disease. The highest levels of plasma endotoxin are found in patients with sepsis, around 500 pg/ml.
Endotoxin levels in blood plasma are normally low, but rise during infections, intestinal inflammation, gum disease, and neurodegenerative diseases.
Leaky gut causes the release of bacterial metabolites and endotoxins, such as lipopolysaccharide, into the circulation, causing bacterial infections, oxidative stress. Diet rich in polyunsaturated fats, exposure to alcohol or chronic allergens, and dysbiosis are highly related to development and/or progression. of several systemic metabolic and autoimmune diseases, neurodegenerative disease, cardiovascular disease, inflammatory bowel disease, cancer and the development of metastases.
Increases in blood endotoxin levels were associated with increases in C-reactive protein concentrations and increases in intestinal permeability markers such as zonulite.
Probiotics help modify the intestinal microbiota, promote the growth of beneficial bacteria and are an alternative source of SCFAs and reduce LPS expression, intestinal inflammation and tumor size in CRC. Among them, Akkermansia muciniphila has the ability to reduce the expression of LPS, improving metabolic endotoxemia.
https://www.mdpi.com/2076-2607/11/2/267 (2023).--
https://www.sciencedirect.com/science/article/pii/S002231662304525X (2023).-
https://www.mdpi.com/2304-8158/12/19/3706 (2023).-
https://www.cghjournal.org/article/S1542-3565(22)01110-7/fulltext (2023).-
https://www.mdpi.com/2076-2607/11/2/267 (2023).-
https://www.sciencedirect.com/science/article/pii/S002231662304525X (2023)
https://www.mdpi.com/2304-8158/12/19/3706 (2023).-
https://www.sciencedirect.com/science/article/pii/S2405844023061042 (2023).-
https://link.springer.com/article/10.1007/s11739-023-03374-w (2024).--
https://onlinelibrary.wiley.com/doi/full/10.1111/eci.14224 (2024).---
https://www.cell.com/trends/endocrinology-metabolism/abstract/S1043-2760(24)00087-0 (2024).—
https://ejhm.journals.ekb.eg/article_349082.html (2024).--
The future looks grim...... groups.google.com/g/zcsd3/c/qA1O9ECDVds?=87hg4