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glutamates and glucose? what could go wrong?
Quote from
Joe2 on November 25, 2025, 8:30 pm
https://x.com/tnseyfried/status/1993370662635782407
Thomas N. Seyfried on X: "Acute myeloid leukemia (AML) is dependent on the sugar glucose and the amino acid glutamine for growth and cannot replace these metabolic fuels with fatty acids or ketone bodies. The greater the malignancy, the greater the dependency on glucose and glutamine. Consequently, the" / X
Thomas N. Seyfried
@tnseyfried
Acute myeloid leukemia (AML) is dependent on the sugar glucose and the amino acid glutamine for growth and cannot replace these metabolic fuels with fatty acids or ketone bodies. The greater the malignancy, the greater the dependency on glucose and glutamine. Consequently, the simultaneous targeting of glycolysis and glutaminolysis while the body is under nutritional ketosis becomes a logical adjuvant therapeutic strategy for managing AML. Unfortunately, the current standard of care fails to consider metabolism as a target. Chronic insufficiency of oxidative phosphorylation coupled to a compensatory increase in substrate level phosphorylation is the origin of most malignant cancers, including AML. The scientific evidence supporting these statements is presented in these papers (PMID: 28250801), (https://doi.org/10.1007/s10863-025-10059-w).
https://x.com/tnseyfried/status/1993370662635782407
Thomas N. Seyfried on X: "Acute myeloid leukemia (AML) is dependent on the sugar glucose and the amino acid glutamine for growth and cannot replace these metabolic fuels with fatty acids or ketone bodies. The greater the malignancy, the greater the dependency on glucose and glutamine. Consequently, the" / X
Thomas N. Seyfried
@tnseyfried
Acute myeloid leukemia (AML) is dependent on the sugar glucose and the amino acid glutamine for growth and cannot replace these metabolic fuels with fatty acids or ketone bodies. The greater the malignancy, the greater the dependency on glucose and glutamine. Consequently, the simultaneous targeting of glycolysis and glutaminolysis while the body is under nutritional ketosis becomes a logical adjuvant therapeutic strategy for managing AML. Unfortunately, the current standard of care fails to consider metabolism as a target. Chronic insufficiency of oxidative phosphorylation coupled to a compensatory increase in substrate level phosphorylation is the origin of most malignant cancers, including AML. The scientific evidence supporting these statements is presented in these papers (PMID: 28250801), (https://doi.org/10.1007/s10863-025-10059-w).
Quote from
Joe2 on November 25, 2025, 8:31 pm
What would happen to someone eating a high fiber low fat low calcium diet for years if they added in high doses of niacin, monosodium glutamate and aluminum silicate?
What would happen to someone eating a high fiber low fat low calcium diet for years if they added in high doses of niacin, monosodium glutamate and aluminum silicate?
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