Vitamin insufficient supply

Recently we published data that even in countries with excellent food sources and availability, insufficient vitamin A supply will occur (Schulz et ah, 2007). The aim of this trial was to analyze vitamin A and p-carotene status and investigate the contribution of nutrition to vitamin A and p-carotene supply in mother-infant pairs of multiparous births or births within short birth rates. Twenty-nine volimteers aged between 21 and 36 years were evaluated for 48 hours after delivery. In order to establish overall supply, retinol and p-carotene were determined in maternal plasma, cord blood, and colostrum via HPLC analysis. A food frequency protocol was obtained from all participants. Regardless of the high-to-moderate socioeconomic background, 27.6% of participants showed plasma retinol levels below 1.4 pmol/liter, which can be taken as borderline deficiency. In addition, 46.4% showed retinol intake <66% of RDA and 50.0% did not consume liver at all, although liver contributes as a main source for preformed retinol. Despite a high total carotenoid intake of 6.9 3.9mg/day, 20.7% of mothers showed plasma levels <0.5 pmol/liter p-carotene. 

What is more frequent than vitamin E deficiency is vitamin E insufficiency, with suboptimal vitamin E supply in the diet or inefficient uptake and distribution of vitamin E. The normal average plasma concentration of vitamin E is 23.2 pM a plasma level below 11.6 pM is regarded as deficient. Certain diseases, like abe-talipojjroteinemia, chronic cholestatic liver disease, cystic fibrosis, chronic pancre-... 

A disease resulting from a deficiency of one or more vitamins is hypovitaminosis (if vitamin is supplied in insufficient quantity) or avitaminosis (complete lack of vitamin manifested by some biochemical processes disorder). Deficiency of vitamins was formerly one of the main causes of many diseases and deaths. Pellagra (deficiency of some B-complex vitamins), scurvy (vitamin C), beriberi (thiamine), rickets (vitamin D), pernicious anaemia associated with reduced ability to absorb vitamin Bj2 (corrinoids) and xerophthalmia (vitamin A) are now well-known diseases caused by vitamin deficiency. Excessive intake of one or more vitamins (especially of lipophilic vitamins A and D) also causes an abnormal state resulting from disturbances of biochemical processes and can lead to severe diseases known as hypervitaminosis. 

Vitamins become a pharmacological concern when there is an imbalance in the body s vitamin supply. Dehciency diseases can result from insufficient vitamin ingestion, irregular absorption, or impaired metabolic use of these nutrients. The ingestion or administration of excessive quantities of vitamins, also known as hy-pervitaminosis, may result in toxicity. 

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. 

A vitamin deficiency occurs when there is an insufficient quantity of vitamins for metabolism, such as when the patient s intake of vitamins is less than that required for his or her metabolism. Patients such as alcoholics and elderly people may not have a well-balanced diet or have difficulty absorbing food. Patients who have conditions that increase metabolism may use up their vitamin supply quicker than they can absorb food. 

The body s storehouse of calcium is bone tissue. When the supply of calcium from external sources, the diet, is insufficient, the body uses a mechanism to compensate for this shortage. With vitamin D in a critical role, this mechanism removes calcium from bone to enable other functions to continue to take place. It is evident then that prolonged dietary calcium deficiency can weaken the bone structure. Unfortunately, current studies show that as many as 75% of the American population may not be consuming sufficient amounts of calcium. Develop-... 

Lewis etal, 1981), and that remaining in the critically depleted pool is released at a reduced rate. The consequence is a relative accumulation of hepatic apo-RBP owing to the limited availability of retinol from internal and external supplies. At an intermediate level of hepatic vitamin A nutriture (Fig. 3B), a portion of newly absorbed retinol is mobilized, presumably to satisfy any peripheral tissue insufficiency that may be transiently created by fasting the remainder, however, enters the hepatic pools for short- or long-term storage (Sewell et al., 1967 Varma and Beaton, 1972 Lewis et al., 1981). It is generally believed that the hepatic pools serve to buffer dietary fluctuations in supply and to match circulating levels of RBP-retinol with rates of tissue utilization (Underwood et al., 1979). 

The daily requirement is shown in Table 6.3. An indicator of insufficient vitamin supply in the diet is a low level in blood plasma (0.65 mg/100 ml). Vitamin C is present in all animal and plant cells, mostly in free form, and it is probably bound to protein as well. Vitamin C is particularly abundant in rose hips, black and red currants, strawberries, parsley, oranges, lemons (in peels more than in pulp), grapefruit, a variety of cabbages and potatoes. Vitamin C loss during storage of... 

In treating persons with protein deficiency, the supply of some vitamins and minerals appears to be more critical than that of others. In particular enough niacin, potassium, and phosphorus should be given to ensure that they are not limiting factors in protein replenishment. Thus, in a niacin deficiency, not only is tryptophan converted to niacin when present in excess but there is evidence that some conversion may occur even when there is insufficient tryptophan for protein synthesis. 

A 4 oz (114 g) serving of pumpkin pie plus an 8 oz (244 g) glass of milk constitute a nutritious meal for a growing child, except that insufficient iron is provided unless dark molasses is used as the sweetener in the pie. The pie supplies ample calories and vitamin A, a moderate amount of protein, and fair amounts of calcium and phosphorus whereeis the milk is rich in protein, calcium, phosphorus, and the vitamin B complex. 

Vitamin K intake in average U.S. diet— The average mixed diet in the United States supplies 300 to 500 meg of vitamin K per day hence, there is little danger of insufficiency under normal conditions. 

The symptoms of vitamin K deficiency are a tendency to bleed and disturbances in blood clotting. Of the many clotting factors (end of Chapt. IV-9), prothrombin is affected primarily it is produced in insufficient amounts in vitamin K deficiency. In man the deficiency symptoms are rather rare, because the intestinal flora produces enough of the vitamin to contribute materially in the supply. 

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