VITAMIN B1 (THIAMIN)



Table of Contents
image Incident pain caused by collapsed vertebrae in menopause. The logical background to a personal treatment protocol
image Vitamins and metals: Potential dangers for the human being
image Preventing Hypoglycemia
image [Criteria of supply of vitamins B1, B2, and B6 in children with insulin-dependent diabetes mellitus]
image [Vitamin metabolism in children with insulin-dependent diabetes mellitus. Effect of length of illness, severity, and degree of disruption of substance metabolism]
image [Metabolism of B group vitamins in patients with insulin-dependent and non-insulin dependent forms of diabetes mellitus]
image [Patients with type-II diabetes mellitus and neuropathy have nodeficiency of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folic acid]
image Relation between theophylline and circulating vitamin levels in children with asthma
image [The therapeutic approach in optic neuropathy due to methyl alcohol]
image Alcohol and brain damage.
image Acute ethanol poisoning and the ethanol withdrawal syndrome.
image Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.
image Thiamine status of institutionalised and non-institutionalised aged.
image [Vitamin B 1 deficiency in chronic alcoholics and its clinical correlation]
image Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation end-products: comparison with aminoguanidine.
image Vitamin status in patients with inflammatory bowel disease
image Chronic alcoholism in the absence of Wernicke-Korsakoff syndrome and cirrhosis does not result in the loss of serotonergic neurons from the median raphe nucleus
image Tissue concentrations of water-soluble vitamins in normal and diabetic rats.
image [Vitamin status in diabetic neuropathy (thiamine, riboflavin, pyridoxin, cobalamin and tocopherol)]
image Intakes of vitamins and minerals by pregnant women with selected clinical symptoms.
image Vitamins for seeing

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Incident pain caused by collapsed vertebrae in menopause. The logical background to a personal treatment protocol

ITALY MINERVA ANESTESIOL. (ITALY), 1984, 50/11 (573-576)

The physiopathological background to senile osteoporosis in women is reviewed with a reminder of possible complications like vertebral fractures and incident pain. The treatment protocols developed from these premises include the administration of oestroprogestins, vitamins D2, B1 and B6 and calcitonin. They also incorporate exposure to electromagnetic pulsation fields, ultraviolet and infrared rays as well as FANS and antidepressant treatment.



Vitamins and metals: Potential dangers for the human being

Schweizerische Medizinische Wochenschrift (Switzerland), 1996, 126/15 (607-611)

Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned.



Preventing Hypoglycemia

Anti-Aging News, January 1982 Vo.2, No. 1 pg 6-7

Cysteine is a strong reducing agent (it can prevent oxidation of some other substances). In fact, it has been found that too much cysteine in a cell culture medium can inactivate the hormone insulin contained in the medium. The insulin molecule contains three disulfide bonds, at least one of which can be reduced by cysteine. When this happens, the insulin molecule can no longer maintain the proper shape to function normally in stimulating the metabolism of sugar. In hypoglycemia attacks, there is too much insulin and too little sugar in the blood stream. Cysteine can inactivate insulin, thereby allowing the sugar level to begin to rise again. We and others have used the combination of vitamins B1, C, and cysteine to successfully abort severe attacks of hypoglycemia. A reasonable dose for a healthy adult is 5 grams of C, 1 gram of B1, and 1 gram cysteine. Although cysteine is a nutrient, it s use on a long-term basis should be considered experimental. Start with a low dose (250 milligrams per day) and work your way up. Always use at least three times as much vitamin C as cysteine. Be sure to consult with your physician and have regular clinical tests of basic body functions, especially liver and kidney. Diabetics should not use cysteine supplements due to its anti-insulin effects.



[Criteria of supply of vitamins B1, B2, and B6 in children with insulin-dependent diabetes mellitus]

Vopr Med Khim (RUSSIA) Nov-Dec 1995, 41 (6) p58-62

By mathematically analysing the curves of urinary excretion of vitamins, their plasma and erythrocytic concentrations or of TDP-effect, by constructing and mathematically interpreting the variation curves of distribution of a given plasma concentration of riboflavin and pyridoxal phosphate for 10-14-old-year children suffering from insulin-dependent diabetes mellitus after supplementation of vitamin, as a criterion of normal requirement for vitamin B2, the authors are prone to recommend the concentration of riboflavin over 10 micrograms/ml in plasma and over 96 micrograms/ml in erythrocytes, the hourly excretion of more than 27 micrograms. It has been ascertained that the criteria for the optimal body's requirements for vitamins in diabetes mellitus children do not differ from those in healthy age-matched children. Thus, the value of TDP-effect is less than 1.25, the concentration of pyridoxal phosphate is over 8.4 micrograms/ml plasma, the excretion values of thiamine and 4-pyridoxic acid are 13.5 and 64.0 micrograms/h, respectively.



[Vitamin metabolism in children with insulin-dependent diabetes mellitus. Effect of length of illness, severity, and degree of disruption of substance metabolism]

Vopr Med Khim (RUSSIA) Jul-Aug 1994, 40 (4) p33-8

Correlation between the state of vitamin metabolism and the impairments in carbohydrate, lipid and protein metabolism was studied in 35 children of 9-13 years of age with diabetes mellitus of various severity standing for up to 7 years. Deterioration of riboflavin metabolism in insulin-dependent diabetes mellitus, expressed as an increase of the vitamin excretion with urine, was augmented with prolongation of the disease duration; the deterioration was sometimes related to the value of glycemia and glucosuria, being the indicative symptom of the disease. In spite of some limitations in validity of experiments related to insufficient number of children in some groups, a decrease in excretion of 1-methyl nicotinamide with urine was detected in all the children with the comatose state, in acidoketosis and glucosuria (above 20 g/day), whereas normal content of nicotinamide coenzymes was found in erythrocytes. Deficiency in vitamins B1, B6 and C was observed more often (5-100%) in children with elevated content of cholesterol as compared with 7-67% of children exhibiting normal level of cholesterol. Optimization of vitamins B and C consumption in children as well as use of any means for correction of these vitamins deficiency are discussed.



[Metabolism of B group vitamins in patients with insulin-dependent and non-insulin dependent forms of diabetes mellitus]

Vopr Med Khim (RUSSIA) Sep-Oct 1993, 39 (5) p26-9

Metabolism of vitamins B, involving evaluation of these vitamins content in blood and excretion of their metabolites with urine, was studied in adult healthy persons as well as in patients with insulin-dependent and -independent forms of diabetes mellitus. Distinct alterations in metabolism of vitamin B2 were detected in the insulin-dependent diabetes: its content in erythrocytes and the rate of excretion with urine were increased. This phenomenon made some problems in evaluation of riboflavin consumption in patients with diabetes mellitus of the I type, while parameters of vitamin consumption in insulin-independent diabetes were similar to those of healthy persons. Parameters of metabolism of vitamins B1, B6 and PP were not different in patients with insulin-dependent and -independent forms of diabetes mellitus. Rates of excretion of 4-pyridoxic acid, 1-methyl nicotinamide, thiamine with urine as well as concentration of the corresponding vitamins in blood were similar to those parameters of healthy persons.



[Patients with type-II diabetes mellitus and neuropathy have nodeficiency of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folic acid]

Med Klin (GERMANY) Aug 15 1993, 88 (8) p453-7

The present study was aimed to determine the vitamin status of vitamins A, E, beta-carotene, B1, B2, B6, B12 and folate in plasma using HPLC and vitamins B1, B2 and B6 in erythrocytes using the apoenzyme stimulation test with the Cobas-Bio analyzer in 29 elderly type II diabetic women with (G1: n = 17, age: 68.6 +/- 3.2 years) and without (G2: n = 12, age: 71.8 +/- 2.7 years) diabetic polyneuropathy. The basic parameters as age, hemoglobin A1c, fructosamine and duration of the disease did not differ in both groups. Furthermore, retinopathy was assessed with fundoscopy and nephropathy with creatinine clearance. The creatinine clearance (G1: 50.6 +/- 3.4 vs. G2: 63.6 +/- 3.7 ml/min, 2p < 0.025) and the percentage of retinopathy (G1: 76.5% vs. G2: 16.7%, 2p = 0.002) were different indicating that G1 had significantly more severe late complications than G2. Current plasma levels of all measured vitamins (A, E, beta-carotene, B1, B2, B6, B12 and folate) and the status of B1, B2 and B6 in erythrocytes did not vary between the two groups (2p > 0.1). In summary, we found a lack of association between the actual vitamin condition in plasma and erythrocytes and diabetic neuropathy.



Relation between theophylline and circulating vitamin levels in children with asthma

Pharmacology (Switzerland), 1996, 53/6 (384-389)

We investigated the effect of theophylline administration on circulating vitamin levels in children with asthma. Twenty-three asthmatic children, ranging in age from 7 to 15 with a mean of 10.8 years and including 16 patients who were treated with slow-release theophylline and 7 patients not receiving any type of theophylline preparation, were enrolled in this study. They all were inpatients who had been hospitalized for the control of asthma. Steady-state serum theophylline and vitamin A, B1, B2, B6, B12 and C levels were evaluated in these patients. Circulating vitamin B1 and B6 levels were depressed in asthmatic children treated with theophylline compared to those not receiving the agent (38.4 plus or minus 1.6 (mean plus or minus SEM) vs. 46.4 plus or minus 3.5 ng/ml and 7.1 plus or minus 0.5 vs. 11.8 plus or minus 2.1 ng/ml, respectively, p < 0.05). A significant negative correlation between theophylline and circulating levels of vitamin B6 was demonstrated in the subjects of this study (r(s) = -0.657, p < 0.001). In contrast, no relationship was noted between theophylline and circulating vitamin B1 levels. Theophylline did not affect circulating vitamin A, B1, B12 or C levels. We conclude that theophylline induces depression of circulating vitamin B1 and B6 levels in asthmatic children, although a dose-dependent interaction between theophylline and vitamin B1 would be unlikely.



[The therapeutic approach in optic neuropathy due to methyl alcohol]

Oftalmologia (ROMANIA) Jan-Mar 1991, 35 (1) p39-42

The paper reports on the case of a 44-year-old patient suffering from toxic optic neuropathy produced by ingestion of a drink brought at second hand. The eye examination revealed the installment of bilateral blindness without the perception of light and with alteration of the general state. After the treatment with 3 perfusions/day with 22 ml ethylic alcohol, 90 degrees, in 250 ml glucosed serum 10%, 200 mg vitamin B1, 500 mg vitamin B6, nicotined xanthnol, vials II for six days, the evolution was good: VOD = 2/3 n.c.; VOS = 1/8 n.c.



Alcohol and brain damage.

Hum Toxicol (ENGLAND) Sep 1988, 7 (5) p455-63

1. The safe limits of alcohol intake are difficult to define because of individual variations in susceptibility to damage. The present recommendations are based largely on epidemiological studies of liver damage. 2. Recent investigations indicate that alcoholic brain damage is much more common than previously suspected. More information is required about its natural history and the characteristics of individuals most likely to suffer damage. 3. Thiamin (vitamin B1) deficiency has long been associated with brain damage and may result from a number of additive causes in the alcoholic patient. New information indicating damage to the protein moeity of some of the thiamin-using enzymes has been reviewed, as have possible mechanisms of brain cell necrosis.



Acute ethanol poisoning and the ethanol withdrawal syndrome.

Med Toxicol Adverse Drug Exp (NEW ZEALAND) May-Jun 1988, 3 (3) p172-96

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol- ependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.



Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.

J Neurol Neurosurg Psychiatry (ENGLAND) Apr 1986, 49 (4) p341-5

A recent necropsy study has shown that 80% of patients with the Wernicke-Korsakoff syndrome were not diagnosed as such during life. Review of the clinical signs of these cases revealed that only 16% had the classical clinical triad and 19% had no documented clinical signs. The incidence of clinical signs in this and other retrospective pathological studies is very different from that of prospective clinical studies. This discrepancy may relate to "missed" clinical signs but the magnitude of the difference suggests that at least some cases of the Wernicke-Korsakoff syndrome may be the end result of repeated subclinical episodes of vitamin B1 deficiency. In order to make the diagnosis, clinicians must maintain a high index of suspicion in the "at risk" group of patients, particularly alcoholics. Investigations of thiamine status may be helpful and if the diagnosis is suspected, parenteral thiamine should be given.



Thiamine status of institutionalised and non-institutionalised aged.

Int J Vitam Nutr Res (SWITZERLAND) 1977, 47 (4) p325-35

Thiamine status of 196 institutionalised (in hospital, residential accommodation and sheltered dwelling) and non-institutionalised Caucasian aged subjects was assessed by combined dietary, biochemical and clinical studies. Fourteen subjects (7.1 per cent) consumed less than two-thirds of recommended vitamin B1/DAY. Erythrocyte transketolas activity coefficient (a) test indicated biochemical deficiency of thiamine in 17.6 per cent males and 12.5 per cent females. The incidence of deficiency was highest in subjects of sheltered dwelling. Multivitamin supplementation failed to raise the biochemical thiamine status to normal in 2.9 per cent subjects. No characteristic clinical features of thiamine deficiency were noted, though extreme loss of appetite was reported by 3 subject with activity coefficient greater than 1.30. Dietary intake was not always associated with deficient biochemical indices. The possible factors such as alcohol intake and low folate status affecting the biochemical status of thiamine are discussed.



[Vitamin B 1 deficiency in chronic alcoholics and its clinical correlation]

Schweiz Med Wochenschr (SWITZERLAND) Oct 23 1976, 106 (43) p1466-70

50 chronic alcoholics reporting to the medical emergency ward of Basle University Hospital with alcohol-related illness were examined with respect to thiamine nutritional status by means of the transketolase activation test of erythrocytes (ETK). 46% of the chronic alcoholics, compared to only 2% of the control population (1152 healthy adults), had transketolase activation quotients indicating a strong probability of thiamine deficiency (alphaETK greater than 1.25). The most important symptoms associated with the biochemical parameters of thiamine deficiency were: anemia, pathologic liver functions (bilirubin, gamma-globulins), low diastolic blood pressure and Wernicke's encephalopathy. There was a statistically significant correlation (p less than 0.05) between these symptoms and the biochemical parameters for thiamine deficiency. Therefore, when treating chronic alcoholics, these symptoms should direct attention to a possible vitamin B1 deficiency. Since the enzymatic vitamin B1 parameters correlate with the patients' hemoglobin, our results would be consistent with anemia influenced by provision of thiamine.



Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation end-products: comparison with aminoguanidine.

Biochem Biophys Res Commun (UNITED STATES) Mar 7 1996, 220 (1) p113-9

Nonenzymatic glycation of proteins by glucose leading to the formation of toxic and immunogenic advanced glycation end products (AGEs) may be a major contributor to the pathological manifestations of diabetes mellitus, aging, and, possibly, neurodegenerative diseases such as Alzheimer's. We tested the in vitro inhibition of antigenic AGE formation on bovine serum albumin, ribonuclease A, and human hemoglobin by various vitamin B1 and B6 derivatives. Among the inhibitors, pyridoxamine and thiamine pyrophosphate potently inhibited AGE formation and were more effective than aminoguanidine, suggesting that these two compounds may have novel therapeutic potential in preventing vascular complications of diabetes. An unexpected finding was that aminoguanidine inhibited the late kinetic stages of glycation much more weakly than the early phase.



Vitamin status in patients with inflammatory bowel disease

Fernandez-Banares F.; Abad-Lacruz A.; Xiol X.; Gine J.J.; Dolz C.; Cabre E.; Esteve M.; Gonzalez-Huix F.; Gassull M.A.

Department of Gastroenterology, Hospital de Bellvitge 'Princeps d'Espanya', Barcelona Spain

AM. J. GASTROENTEROL. (USA), 1989, 84/7 (744-748)

The status of water- and fat-soluble vitamins was prospectively evaluated in 23 patients (13 men, 10 women, mean age 33 plus or minus 3 yr) admitted to the hospital with acute or subacute attacks of inflammatory bowel disease. Protein-energy status was also assessed by means of simultaneous measurement of triceps skin-fold thickness, mid-arm muscle circumference, and serum albumin. Fifteen patients (group A) had extensive acute colitis (ulcerative or Crohn's colitis), and eight cases (group B) had small bowel or ileocecal Crohn's disease. Eighty-nine healthy subjects (36 men, 53 women, mean age 34 plus or minus 2 yr) acted as controls. In both groups of patients, the levels of biotin, folate, beta-carotene, and vitamins A, C, and B1 were significantly lower than in controls (p < 0.05). Plasma levels of vitamin B12 were decreased only in group B (p < 0.01), whereas riboflavin was lower in group A (p < 0.01). The percentage of patients at risk of developing hypovitaminosis was 40% or higher for vitamin A, beta-carotene, folate, biotin, vitamin C, and thiamin in both groups of patients. Although some subjects had extremely low vitamin values, in no case were clinical symptoms of vitamin deficiency observed. Only a weak correlation was found between protein-energy nutritional parameters and vitamin values, probably due to the small size of the sample studied. The pathophysiological and clinical implications of the suboptimal vitamin status observed in acute inflammatory bowel disease are unknown. Further studies on long-term vitamin status and clinical outcome in these patients are necessary.



Chronic alcoholism in the absence of Wernicke-Korsakoff syndrome and cirrhosis does not result in the loss of serotonergic neurons from the median raphe nucleus

Metabolic Brain Disease (USA), 1996, 11/3 (217-228)

Previous studies have identified alcohol, thiamine deficiency and liver disease as contributing to the neuropathology of alcohol-related brain damage. In order to examine the effects of alcohol toxicity and thiamine deficiency on serotonergic neurons in the median raphe nucleus (MnR), alcoholic and previously published Wernicke-Korsakoff syndrome (WKS) cases without liver disease, were compared with age-matched non-alcoholic controls. While there was no difference between the estimated number of serotonergic neurons in either controls or alcoholics without WKS (means of 63,010plus or minus8,900 and 59,560plus or minus8,010 respectively), a substantial loss of serotonergic neurons was previously found in WKS cases (mean of 19,050plus or minus13,140). Further analysis revealed a significant difference in the maximum daily alcohol consumption between these groups. However, analysis of covariance showed that the number or serotonergic neurons in the MnR did not correlate with the amount of alcohol consumed. Therefore, our results suggest that cell loss in the MnR can be attributed to thiamine deficiency rather than alcohol per se.



Tissue concentrations of water-soluble vitamins in normal and diabetic rats.

Int J Vitam Nutr Res (SWITZERLAND) 1993, 63 (2) p140-4

Changes in circulating and tissue concentrations of several vitamins have been reported in diabetic animals and human subjects. In this study, the effect of short-term (2 weeks) streptozotocin diabetes on folate, B6, B12, thiamin, nicotinate, pantothenate, riboflavin and biotin in liver, kidney, pancreas, heart, brain and skeletal muscle of rats was investigated. The tissue distribution of vitamins varied widely in normal rats. Diabetes significantly lowered folate in kidney, heart, brain, and muscle; B6 in brain; B12 in heart; thiamin in liver and heart; nicotinate in liver, kidney, heart and brain; pantothenate in all tissues; riboflavin in liver, kidney, heart, and muscle. These results indicate that experimental diabetes causes a depression of several water-soluble vitamins in various tissues of rats.



[Vitamin status in diabetic neuropathy (thiamine, riboflavin, pyridoxin, cobalamin and tocopherol)]

Z Ernahrungswiss (GERMANY, WEST) Mar 1980, 19 (1) p1-13

Investigations on the vitamin pattern of diabetic neuropathy: thiamine, riboflavin, pyridoxine, cobalamin and tocopherol. The contents of the vitamins mentioned above have been measured in the blood of 119 patients (53 diabetic neuropathies, 66 diabetics without neuropathy). The incidence of neuropathy shows a strong correlation with the duration of the diabetic state, but not with sex, nor with concomitant diseases such as adipositas, hypertension, heart and circulatory diseases, except retinopathia diabetica. Most of the diabetics in our study are well supplied with vitamins B1, B2, and E; B6 and B12 are occasionally low, but there is no statistically relevant difference between diabetic controls and neuropathies. Adipose patients have neither a markedly different vitamin content nor a different calory uptake from non-adipose patients. A general trend towards reduced total calory uptake is seen in old age, men (lower protein intake) and women (lower carbohydrate intake) obviously differing somewhat in their habits. The influence of therapy on the vitamin pattern is not clear cut, except for patients under diet and biguanide-therapy showing a higher proportion of low or subnormal B12 values. The increased frequency of neuropathies in patients treated with sulfonyl-urea approaches only the limits of significance and needs further investigations.



Intakes of vitamins and minerals by pregnant women with selected clinical symptoms.

J Am Diet Assoc (UNITED STATES) May 1981, 78 (5) p477-82

Toxemia in pregnancy is characterized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In this study the dietary intakes of young pregnant women attending a Maternal and Infant Care Program at Tuskegee Institute were evaluated for selected vitamins and minerals. Women with toxemia were identified, and women without toxemia served as controls. The toxemia group generally consumed lesser amounts of vitamins and minerals than the controls. However, both groups were deficient (less than two-thirds RDA) in calcium, magnesium, vitamin B6, vitamin B12, and thiamin. Milk, meat, and grains supplied an appreciable proportion of each vitamin except vitamin A, which was found primarily in the two vegetable groups. Meat and grains contained the greatest quantities of minerals, but milk provided a relatively good proportion of potassium, calcium, magnesium, and phosphorus. Anemia was not related to the incidence of toxemia. Women exhibiting anemia consumed smaller amounts of vitamins studied than did women without anemia.



Vitamins for seeing

COMPR. THER. (USA), 1990, 16/4 (62)

It has long been known that an inadequate diet lacking in certain essential vitamins can cause ocular disorders. On an Egyptian papyrus dated about 1500 BC, it is recorded that liver was used as a food to cure night blindness. Healthy eyes depend on a well-balanced diet. Vitamin A maintains the normal function of the epithelial cells of the eye and is essential for the synthesis of visual photosensitive pigments. Deficiencies of vitamin A lead to clinical manifestations including night blindness, conjunctival pigmentation, and dry eyes. The B vitamins are important for maintaining good vision. Vitamin B1 (thiamine) deficiency produces optic nerve dysfunction. Vitamin B12 deficiency can produce vascular changes in the retina. Deficiency of riboflavin (part of the B complex) has been implicated in the formation of cataracts and may also be a factor in producting xerophthalmia (dry eyes). Vitamin C is necessary to prevent scurvy. The scorbutic manifestations in the eyes are bleeding from the lids, conjunctiva, anterior chamber, and retina. Vitamin C deficiency may also be a factor in cataract formation. Finally, vitamin K deficiency causes retinal hemorrhages in neonates. Deficiencies of vitamin D and E have not been shown to have a negative effect on the visual process, but vitamin E therapy improves retrolental fibroplasia (retinopathy of prematurity).

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