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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 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 ...
Vitamin B 6 Excess, Hypervitaminosis B 6, Vitamin B 6 Toxicity [1] [2] Specialty: Neurology, toxicology: Symptoms: Peripheral sensory neuropathy: Usual onset: Gradual onset with slow progression, in the usual case of chronic vitamin B 6 supplementation. [3] Duration: Usually, but not always, resolves within six months from the cessation of ...
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]
That makes sense, since, according to the Cleveland Clinic, some of the top symptoms of vitamin D deficiency in adults are fatigue, muscle weakness, and low mood, which can lead to feeling down ...
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.
Hypervalinemia has an autosomal recessive pattern of inheritance.. Hypervalinemia is inherited in an autosomal recessive manner. [1] This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder.
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