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Vitamin smoking

Uses. Inactive dried yeasts are used as iagredients ia many formulated foods baby foods, soups, gravies, and meat extenders as carriers of spice and smoke flavors and ia baked goods. Yeasts used ia the health food iadustry are geaeraHy fortified with minerals and contain higher concentrations of the B vitamins, especially thiamin, riboflavin, and niacia (see Vitamins). [Pg.394]

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). [Pg.33]

Some osteoporosis risk factors (see Table 53-1) are non-modifiable, including family history, age, ethnicity, sex, and concomitant disease states. However, certain risk factors for bone loss may be minimized or prevented by early intervention, including smoking, low calcium intake, poor nutrition, inactivity, heavy alcohol use, and vitamin D deficiency. [Pg.857]

A somewhat related situation can be used to explain the well-publicized lung-cancer inducing effects of P-carotene in heavy smokers. This subpopulation will have low vitamin C levels and hence damage due to smoke components, such as N02 can produce P-CAR which will reach the lung and initiate damage. In nonsmokers, the vitamin C (or other water-soluble antioxidant) is likely to be present in sufficient concentration to preclude this damaging process. Indeed, this speculation has been promoted by the American Chemical Society as the subject of a press release in 1997 (Bohm et al. 1997). [Pg.304]

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). [Pg.104]

Persons with a metabolic disturbance in the conversion of cyanide to thiocyanate may be at greater risk. A defect in the rhodanese system and vitamin B12 deficiency have been associated with tobacco amblyopia and Leber s hereditary optic atrophy in persons exposed to cyanide in tobacco smoke (Wilson 1983). [Pg.116]

Some drugs, including oral contraceptives, and smoking tobacco, increase the body s demand for vitamins B, C and E. [Pg.334]

Several lifestyle factors predispose to cancer development, including smoking tobacco and exposure to sunlight (especially for children and the fair-skinned). It should be noted that low levels of continuous sun exposure may protect against breast and colon cancer, perhaps as a result of raising vitamin D levels which has already been discussed described. [Pg.504]

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. 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.
On the basis of a few reports, it is assumed that a "local vitamin A deficiency exists in meta- and dysplastic areas. Measurements of vitamin A concentrations in metaplastic areas of the respiratory epithelium and the cervix epithelium actually proved that vitamin A in comparison to the surrounding tissues was not found (Biesalski, 1996). Clearly one cannot say what is cause and effect. Studies carried out by Edes et al. (1991) confirm an induction of a vitamin A deficit. These studies showed that a depletion of vitamin A ester stores is caused by toxins, present in cigarette smoke (predominantly polyhalogenated compounds), in different tissues. [Pg.183]

Forty healthy participants, 25 female and 15 males, aged 19-33 years with a body mass index between 18 and 24 kg/m took part in the study. Excluding criteria were smoking, current dental surgery, illness of the pharynx or the cavity of the mouth, malabsorption, long-time medication, use of a toothpaste with vitamin A during the last 2 months prior to the study, pregnancy, and metabolic diseases. [Pg.195]

Bacterial colonization of lower respiratory tract. Cigarette smoke, administered for 3 days before and after intratracheal instillation of bacterial suspension containing six bacterial species (Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumonia, Proteus mirabilis, Haemophilus influenza, Peptostreptococcus spp.) to male Wistar albino rats with or without vitamin E supplements (100 mg/kg/day), signifi-... [Pg.290]

Cytochrome C oxidase inhibition. Smoke extract, in the mouse brain mitochondria culture in the presence or absence of vitamin C for 60 minutes, inhibited mitochon-... [Pg.301]

GST activity. Cigarette smoke, administered intranasally to young male C57BL mice fed 0, 5, and 100 ppm of vitamin E, 20 minutes/day for 8 weeks, produced no effect... [Pg.312]


See other pages where Vitamin smoking is mentioned: [Pg.3887]    [Pg.166]    [Pg.3887]    [Pg.166]    [Pg.22]    [Pg.285]    [Pg.1295]    [Pg.29]    [Pg.288]    [Pg.307]    [Pg.304]    [Pg.1326]    [Pg.470]    [Pg.199]    [Pg.30]    [Pg.18]    [Pg.914]    [Pg.91]    [Pg.300]    [Pg.342]    [Pg.181]    [Pg.186]    [Pg.187]    [Pg.188]    [Pg.214]    [Pg.269]    [Pg.173]    [Pg.290]    [Pg.291]    [Pg.292]    [Pg.297]    [Pg.301]    [Pg.307]    [Pg.311]    [Pg.312]   
See also in sourсe #XX -- [ Pg.380 ]

See also in sourсe #XX -- [ Pg.380 ]

See also in sourсe #XX -- [ Pg.380 ]




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