Search results
Results From The WOW.Com Content Network
Developmental toxicity is any developmental malformation that is caused by the toxicity of a chemical or pathogen. It is the structural or functional alteration, reversible or irreversible, which interferes with homeostasis , normal growth , differentiation , development or behavior.
Poor diet in early childhood affects the number of neurons in parts of the brain. [1]Nutritional neuroscience is the scientific discipline that studies the effects various components of the diet such as minerals, vitamins, protein, carbohydrates, fats, dietary supplements, synthetic hormones, and food additives have on neurochemistry, neurobiology, behavior, and cognition.
It has been known that the liver organ is the main target of aflatoxins and chronic toxicity can result in immunosuppressive and carcinogenic effects. [25] However, there is currently conflicting evidence to pinpoint a connection between kwashiorkor and aflatoxins.
Myopathy: Exercise intolerance, symptoms tend to improve with rest. "Second wind" phenomenon in most. Some have hypertrophic calf muscles. [16] Rhabdomyolysis and myoglobinuria possible. Some have muscle weakness. Of those with muscle weakness, in two-thirds it worsens, however in some the muscle weakness is stable. Onset forms: infant, child ...
Symptoms of HFI include vomiting, convulsions, irritability, poor feeding as a baby, hypoglycemia, jaundice, hemorrhage, hepatomegaly, hyperuricemia and potentially kidney failure. [1] There are reported deaths in infants and children as a result of the metabolic consequences of HFI. Death in HFI is always associated with problems in diagnosis. [2]
Ketotic hypoglycemia classically presents in male young children, typically between the ages of 10 months and 6 years, in the morning after a prolonged overnight fast. Symptoms include those of neuroglycopenia, ketosis, or both. [6] [7] Neuroglycopenic symptoms usually include lethargy and malaise, but may include unresponsiveness or seizures.
Reported in 2001, a 13-year-old girl with short gut syndrome suddenly developed symptoms of intoxication after eating "excess carbohydrates and juices". She had no access to alcohol any time the symptoms were present. Her small intestine was colonized by two organisms: C. glabrata and S. cerevisiae. She was treated with fluconazole and her ...
These populations are at risk of developing ketoacidosis in the setting of metabolic stressors such as fasting, low-carbohydrate diets, or acute illness. [9] Children and infants have lower glycogen stores and may develop high levels of glucagon and counter-regulatory hormones during acute illness, especially gastrointestinal illness.