Vitamin excessive intake

There is only a limited capacity to metabolize vitamin A, and excessive intakes lead to accumulation beyond the capacity of binding proteins, so that unbound vitamin A causes tissue damage. Symptoms of toxicity affect the central nervous system (headache, nausea. 

In the Artie Eskimos depended historically on fish for their supply of vitamin D, whereas in the tropics a supply is unnecessary. Excessive intakes of vitamins A and D can be lethal. The liver is the storage organ for fat-soluble vitamins Eskimos avoided hypervitaminoses by discarding livers of polar bears which get a surfeit of vitamins A and D from their diet of seals and fish. 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

No adverse effects have been associated with excess vitamin B12 intake from food or supplements in healthy individuals [417]. 

Historically choline, inositol and carnitine have been considered to be part of the vitamin B complex. However, for the general population there has been no demonstration of a dietary need for these agents and also for none of them has there been a therapeutic role established. Vitamins of the B family are found in many food ingredients like in yeast, in meat, in dairy products and also in eggs and grain cereals and separate vitamin B deficiencies are unlikely to occur. Excessive intake of these vitamins is eliminated in the urine because of the fact that they are water-soluble. 

Avitaminosis A results in the loss of night vision nyctalopia). Furthermore, the removal of vitamin A from the diet causes the cornea of the eye to dry out xerophthalmia). However, excessive intake of vitamin A can result in severe and even fatal toxicity. 

The physiological role of vitamin K is in blood clotting and is essential for the synthesis of at least four of the proteins (including prothrombin) involved in this process. Vitamin K also plays a role in the synthesis of a protein (osteocalcin) in bone. Vitamin K deficiency is rare but can result from impaired absorption of fat. Vitamin K levels in the body are also reduced if the intestinal flora is killed (e.g. by antibiotics). Vitamin K toxicity is rare but can be caused by excessive intake of vitamin K supplements. Symptoms include erythrocyte haemolysis, jaundice, brain damage and reduced effectiveness of anticoagulants. 

Phytic acid, although restricted to a more narrow range of food products, mainly grains, complexes a broader spectrum of minerals than does oxalic acid. Decreased availability of P is probably the most widely recognized result of excessive intakes of phytic acid, yet Ca. Cu, Zn, Fe. and Mn are also complexed and rendered unavailable hy this compound. High intakes of both calcium and vitamin D help to offset ihe deleterious effects of oxalates. 

Excessive intake of vitamin D Toxic effect of vitamin D, as opposed to vitamin D3... 

Excessive intake of vitamin A (hyper-vitaminosis A), like too little intake, can result in adverse health consequences. Approximately 60%-80% of vitamin A is stored in the liver in hepatic stellate cells (also called Ito cells and fat-storing cells). Retinyl esters are the main storage form of vitamin A in the liver and are found in lipid droplets present in the hepatic... 

Mrs TY should try to maintain a healthy balanced diet with adequate calcium and vitamin D intake, avoid excessive alcohol, reduce her caffeine intake, increase her vegetable consumption and try to take up some weight-bearing exercise. She should also take steps to avoid trips or falls, such as having her eyesight tested regularly and assessing her home environment for risks. 

Vitamin C occurs in all fruit, citrus, green vegetables, tomatoes, peppers, sprouts, broccoli, etc. This water-soluble vitamin is easily lost from the body and so needs constant replacement by eating fresh vegetables and fruit. On the other hand, excessive intake of it can adversely affect the working of vitamin B12 and also cause a loss of calcium from the bones. Excessive vitamin supplements are not usually required if a balanced diet is eaten. 

Hypercalcemia persists for many months after the cessation of excessive intakes of vitamin D, because of the accumulation of the vitamin in adipose tissue and its slow release into the circulation. The introduction of calcitriol and 1 a -hydroxycalcidiol for the treatment of such conditions as hypoparathyroidism, renal osteodystrophy, hypophosphatemic osteomalacia, and vitamin D-dependent rickets has meant that hypercalcemia is less of a problem than when high doses of vitamin D were used in the treatment of these conditions. Because calcitriol has a short half-life in the circulation, the resultant hypercalcemia is of shorter duration than after cholecalciferol, and adjustment of the dose is easier. 

Hypercalcemia can result from an excessive intake of vitamin D. Prolonged immobilization can also result in hypercalcemia, as bone resorption increases with this immobilization, especially where there is concurrent renal failure (where the kidneys cannot excrete the excess calcium). Sudden, severe hypercalcemia results in vomiting, coma, and possibly death. Prolonged hypercalcemia can result in the formation of kidney stones and in the calcification of soft tissues, such as the eye. Stone formation and caiciheahon are more likely to occur with concurrent hyperphosphatemia. 

Calcium is normally considered to be safe in parenteral nutrition, and relatively high quantities are often included in neonatal and pediatric formulations. However, there is a risk of hjrpercalciuria. The pathogenesis of hjrpercal-ciuria is not readily explicable on the basis of endocrine or metabolic effects, but it has been postulated to be due to excessive calcium or vitamin D intake or aluminium overload. 

Hypervitaminosis A and D have also been associated with bone abnormalities. Vitamin D can cause resorption of calcium from bone. Chronic vitamin D intoxication may result in increased mineralization on bone and metastatic calcifications including joints, periarticular, and the kidney. Excessive vitamin D intake can cause demineralization of bone resulting in multiple fractures from very slight trauma. 

The findings of these and other studies have led the Food and Nutrition Board of the U.S. Institute of Medicine to recommend a tolerable upper intake level of3000 tg/day of preformed vitamin A for men of 19 years and older, with lower levels for women of child-bearing age, infants, children, and adolescents. Carotenemia results from a chronic excessive intake of carotene-rich foods, principally carrots. This condition, in which yellowing of skin is observed, is benign, because the excess carotene is deposited rather than converted to vitamin A. 

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