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Hypervitaminosis A refers to the toxic effects of ingesting too much preformed vitamin A (retinyl esters, retinol, and retinal). Symptoms arise as a result of altered bone metabolism and altered metabolism of other fat-soluble vitamins. Hypervitaminosis A is believed to have occurred in early humans, and the problem has persisted throughout ...
Urolithin A is not known to be found in any food but rather forms as the result of transformation of ellagic acids and ellagitannins by the gut microflora in humans. [ citation needed ] Sources of ellagitannins are: pomegranates, nuts, some berries (raspberries, strawberries, blackberries, cloudberries), tea, muscadine grapes, many tropical ...
Hypervitaminosis is a condition of abnormally high storage levels of vitamins, which can lead to various symptoms as over excitement, irritability, or even toxicity. Specific medical names of the different conditions are derived from the given vitamin involved: an excess of vitamin A, for example, is called hypervitaminosis A.
Chemical structure of urolithin A.. Urolithins are microflora metabolites of dietary ellagic acid derivatives, such as ellagitannins. [1] They are produced in the gut, and found in the urine in the form of urolithin B glucuronide after absorption of ellagitannins-containing foods, such as pomegranate. [2]
Symptom severity appears to be dose-dependent (higher doses cause more severe symptoms) [24] and the duration of supplementation with vitamin B 6 before the onset of systems appears to be inversely proportional to the amount taken daily (the smaller the daily dosage, the longer it will take for symptoms to develop).
Local and systemic symptoms can appear immediately or several hours after consuming a meal prepared with the toxic wintered grain. Local symptoms include a bitter taste in the mouth, which leads to a complete loss of taste, tongue numbness or swelling, a burning sensation in the mouth, and pain when swallowing. If no more hazardous grain was ...
Symptoms appear several months after excessive doses of vitamin D are administered. A mutation of the CYP24A1 gene can lead to a reduction in the degradation of vitamin D and thus to vitamin toxicity without high oral intake (see Vitamin D: Excess). Symptoms of vitamin D toxicity may include the following: [2] Dehydration; Vomiting; Diarrhea
Treatment options for protein toxicity can include renal replacement therapies like hemodialysis and hemofiltration. [25] Lifestyle modifications like a diet low in protein, decreased sodium intake, and exercise can also be in incorporated as part of a treatment plan. Medications may also be prescribed depending on symptoms.