Why do smokers need vitamin c




















The food-frequency-questionnaire data before and after the 3-mo supplementation period are shown. The data show that the subjects, as requested, were able to keep their dietary habits more or less unchanged during the study. Thus, no significant changes in total fruit and vegetable intake were observed. However, we did find significant increases in the dietary intake of vitamins C and E among supplemented nonsmokers and unsupplemented nonsmokers, respectively. Overall, a nonsignificant trend toward a better diet over the 3-mo supplementation period was observed for the cohort, as is frequently found in studies in which diet is not strictly controlled.

TAA increased markedly in the supplemented groups. However, because dietary vitamin C intakes increased during the study period in nonsmokers receiving the vitamin supplement, the effect of the supplementation itself cannot be properly evaluated in this group.

Among the smokers, no difference was observed in dietary vitamin C intakes increased whereas the plasma concentration showed a significant 3-fold increase after supplementation. Most likely, at least part of the better response among smokers could be attributed to their lower TAA concentration at baseline.

Thus, smokers in general seem to benefit more from vitamin C supplementation than do nonsmokers. Additionally, perhaps smokers have a higher homeostatic requirement, thereby contributing to a higher degree of supplement bioavailability in this group. No significant changes in dietary or plasma TAA were observed in the placebo groups over the course of the study. On the basis of the results of this study, we conclude that 1 of the major plasma antioxidants measured, ascorbic acid is the only plasma antioxidant depleted by smoking per se; 2 depleted plasma TAA concentrations can be normalized by moderate supplementation in smokers; and 3 smokers in particular seem to respond to this supplementation.

Of course, the conclusions can only legitimately be based on the original selection criteria of the study because the cohort differs from the average population. Extending this work to populations that have other dietary habits but differ only in smoking status is therefore desirable. Consequently, our study cohort may represent a large segment of the US population. We thank Gladys Block for her help in providing the customized prescreening fruit and vegetable intake questionnaire.

Free radicals in biology and medicine. Oxford, United Kingdom : Clarendon Press , Google Scholar. Google Preview. Mortality in relation to smoking: 40 years' observations on male British doctors. BMJ ; : — Gas phase oxidants of cigarette smoke induce lipid peroxidation and changes in lipoprotein properties in human blood plasma: protective effects of ascorbic acid.

Biochem J ; : — 8. Pryor WA , Stone K. Oxidants in cigarette smoke. Radicals, hydrogen peroxide, peroxynitrate, and peroxynitrite. Ann N Y Acad Sci ; : 12 — Leanderson P , Tagesson C. Cigarette smoke-induced DNA damage in cultured human lung cells: role of hydroxyl radicals and endonuclease activation. Chem Biol Interact ; 81 : — Cigarette smoking induces formation of 8-hydroxydeoxyguanosine, one of the oxidative DNA damages in human peripheral leukocytes. Free Radic Res Commun ; 11 : 23 — 7.

Smoking and low antioxidant levels increase oxidative damage to sperm DNA. Mutat Res ; : — Cigarette smoking as an inducer of oxidative stress. Exercise and oxygen toxicity. Amsterdam : Elsevier , : — Ascorbic acid and dehydroascorbic acid as biomarkers of oxidative stress caused by smoking. Am J Clin Nutr ; 65 : — National Research Council. Recommended dietary allowances. Ascorbic acid requirements for smokers: analysis of a population survey.

Am J Clin Nutr ; 53 : — Diet and health, implications for reducing chronic disease risk. US adults' fruit and vegetable intakes, to a revised baseline for the Healthy People objective. Am J Public Health ; 85 : — 9. Indicators of poor dietary habits in a high risk population. J Am Coll Nutr ; 14 : — Food intakes of US children and adolescents compared with recommendations.

Pediatrics ; : — 9. Diet and risk of renal cell cancer: a population-based case-control study. Cancer Epidemiol Biomarkers Prev ; 6 : — Case-control assessment of diet and lung cancer risk in African Americans and Mexican Americans. Nutr Cancer ; 29 : — La Vecchia C , Tavani A.

Fruit and vegetables, and human cancer. Eur J Cancer Prev ; 7 : 3 — 8. Effect of increased fruit and vegetable intake on the susceptibility of lipoprotein to oxidation in smokers. Eur J Clin Nutr ; 51 : — 6. The association between fruit and vegetable intake and chronic disease risk factors. Epidemiology ; 7 : — 5.

Morabia A , Wynder EL. Dietary habits of smokers, people who never smoked, and exsmokers. Am J Clin Nutr ; 52 : — 7. Science News. The research also suggests a possible mechanism by which smoking can cause cancer. ScienceDaily, 25 February Oregon State University. Retrieved November 9, from www. The anti-cancer effects of vitamin D are especially Healthy non-smokers who took vitamin B supplements nearly reversed any negative effects on their Print Email Share.

Just a Game? Living Well. Demographic characteristics and BMI of children exposed or not exposed to environmental tobacco smoke 1. Chi-square test of homogeneity of proportions between exposed and unexposed groups. Note that the midpoint value for BMI in our study population was 22 Table 1.

Our midpoint for BMI is not necessarily the same as that of other pediatric or adult populations because age, sex, ethnicity, and maturation stage can all independently contribute to the percentage body fat Ratio of cotinine to creatinine in urine of children exposed or not exposed to environmental tobacco smoke 1. In the multifactorial ANOVA, the ratio of cotinine to creatinine differed significantly between the exposed and unexposed groups, but the interaction between exposure and each of the other variables age, sex, and BMI was not significant.

Amounts of exposure to ETS were quantified by using the biomarker cotinine; these results are shown in Table 2. For all age groups and BMI groups and for both sexes, children exposed to ETS had significantly higher concentrations of the biomarker in their urine than did the unexposed children. The mean values of 4. There were no significant differences between the different age or BMI groups or the sexes.

Comparisons for dietary vitamin C are adjusted for the other covariates age, sex, and BMI. None of the two-factor or three-factor interaction terms were statistically significant. Comparisons for plasma vitamin C are adjusted for dietary vitamin C and the other covariates. Separate analyses for male and female children yielded P values of 0. As previously reported elsewhere, there is an inverse relation between age and cotinine excretion in children residing in households where someone smokes The mean values of The low values of the biomarker that we found in Puerto Rican children are most likely a result of our open tropical environment, which allows maximum ventilation and dilution of cigarette smoke.

However, there were highly significant differences between the different age groups, with the median for the youngest age group being more than twice that of the other 2 age groups. Before we conducted separate analyses for different age, sex, and exposure groups, a multifactor analysis of variance was performed to examine the role of interaction effects.

The results of the analysis of covariance for variables associated with plasma and dietary vitamin C are shown in Table 3. For the overall population, vitamin C intakes did not differ significantly between the ETS-exposed and unexposed groups, but plasma vitamin C concentrations were lower by 3.

The mean plasma concentration for the entire combined sample was There were no significant effects of age or BMI on dietary intake of vitamin C. In addition, plasma values were not related to ETS exposure in boys but were In the multiple regression analysis, exposure to ETS was the most important predictor of plasma vitamin C in girls, explaining more of the total variation than was explained by either BMI or age.

Regression lines plotting plasma vitamin C against vitamin C intake in children either exposed or not exposed to ETS are shown in Figure 1. Curves relating vitamin C intake and blood vitamin C were published for adults 12 , Information gained from this research was used to estimate the additional recommended dietary allowance for vitamin C in smokers Although the subjects' values for vitamin C intake were within the normal ranges reported by other investigators 37 , it should be recognized that the h recall method most often underestimates intakes and it may not be representative of a typical day.

However, the purpose of this study was to compare group means in a large population, and therefore the h recall method was appropriate because it can provide adequate estimates of intakes of individual nutrients in this type of study Exposure of children to ETS is a major concern because of its long-term consequences in terms of increased disease risk and morbidity This situation is even more distressing when exposure occurs in very young children who have little mobility and thus are unable to avoid the exposure; young children are also unaware of the health risks.

The current investigation addressed the question of whether vitamin C status is compromised in smoke-exposed children. It is well known that smokers typically consume a less healthy diet than do nonsmokers 11 , 13 , so one might suspect that the same foods consumed by smokers would be offered to children in their households. However, children are not entirely dependent on home-prepared meals and have the freedom to choose foods high in vitamin C. This study showed that blood ascorbate concentrations of ETS-exposed children were below those of children not exposed to ETS.

Although the magnitude of this difference was small 3. When we analyzed the data separately for boys and girls, there was no significant difference in plasma vitamin C concentrations between exposed and unexposed boys, but girls with ETS exposure had significantly lower ascorbate concentrations than unexposed girls.

This discrepancy between the sexes is difficult to explain. One might expect that girls spend more time at home and close to their parents, which could lead to more ETS exposure if parents smoke. However, the values of the biomarker urinary cotinine did not differ significantly between the sexes, and so this issue remains unresolved.

Our results also merit comparison with 5 studies on ETS exposure in nonsmoking adults. The effects of chronic exposure were described by Tribble et al 17 , who found that plasma ascorbate concentrations in nonsmokers exposed to ETS were intermediate between those of active smokers and those of nonsmokers not exposed to ETS, even when dietary intakes were similar.

These findings were confirmed in a recent study by Farchi et al 20 , who reported an inverse dose-response relation between plasma ascorbate in nonsmoking Italian women and the intensity of exposure to their husbands' cigarette smoke, after controlling for dietary vitamin C intake. Further evidence of impaired ascorbate status was presented by Ayaori et al 18 , who found that nonsmoking soldiers exposed to ETS had higher ratios of oxidized ascorbate to total ascorbate in the plasma than did nonsmoking, unexposed soldiers; no group differences in vitamin C intake were found.

The effects of acute exposure to ETS on blood ascorbate concentrations are even more dramatic. Valkonen and Kuusi 19 reported on the effects of passive smoking in 10 healthy adults who spent 30 min in a room where 16 cigarettes were smoked by active smokers. Passive smoking caused an acute decrease in blood ascorbate 1.

In a subsequent study by Valkonen and Kuusi 42 , a similar group of nonsmokers was supplemented with 3 g vitamin C, and this prevented the drop in plasma ascorbate that had occurred after ETS exposure in the previous study.

The magnitude of the adverse effect of ETS exposure on vitamin C status is largely dependent on the amount of smoke exposure, according to the studies of adults and our work in children.

Obviously, the greater the concentration of ambient smoke, the greater its effect will be on vitamin C status.

In the current study, very low levels of the biomarker appeared in the urine of our exposed children. Only 2 of the 5 previously cited studies in adults provided biomarker measurements.

Ayaori et al 18 reported that blood thiocyanate concentrations are greater in smoke-exposed nonsmokers than in nonsmokers without smoke exposure. Tribble et al 17 mentioned that the plasma cotinine concentrations in nonsmokers exposed to ETS were below detectable quantities when analyzed with an HPLC method.

Valkonen and Kuusi 19 , 42 did not report any biomarker information. Consequently, the current study is the first to show a reduction in plasma vitamin C in children with minimal exposure to ETS, as confirmed by urinary cotinine values. Data from our study also support the theory that persons exposed to ETS require more dietary vitamin C than do persons with no ETS exposure.

In the current study, the children exposed to ETS had lower plasma ascorbate concentrations at a given intake of vitamin C than did the children not exposed to ETS.

Although these data are not sufficient to allow estimation of a specific vitamin C requirement for children regularly exposed to ETS, these children should be urged to eat more vitamin C—rich foods or they should take supplemental vitamin C.

Among all the predictors in our model, with the exception of dietary vitamin C intake, smoke exposure had the greatest effect on plasma ascorbate concentrations. This finding raises the question of whether a small, but statistically significant, decrease in plasma ascorbate resulting from exposure to ETS has clinical importance.

The present study cannot provide a definitive answer to this question because long-term health effects were not measured.

Yet it is reasonable to assume that reduced antioxidant concentrations could be meaningful in vulnerable populations. It is unlikely that smoke-exposed children ingesting high amounts of vitamin C would experience significant reductions in plasma concentrations. It is known that active smokers taking supplemental vitamin C maintain blood ascorbate concentrations similar to or above those of nonsupplemented nonsmokers In summary, we have confirmed and extended previous studies of vitamin C status in ETS-exposed populations.

Smoking depletes these shields, making it easier for free radicals to damage the body. Put together, the combination of increased free radicals caused by smoking and a reduced supply of vitamins also due to smoking packs a double wallop against us.

Free radicals are atoms or molecules that have an odd number of electrons. These unhappy free radicals, therefore, travel around the body looking for an electron to grab from other molecules so that they can stabilize their energy. Depending on where they find the electron they need, they can wreak havoc on healthy tissue. When they interfere with collagen, they cause the notorious "smoker's wrinkles. And when the source becomes DNA in the cells of our bodies, damage gene mutations may occur.

It is this accumulation of gene mutations that is responsible for the formation of a cancer cell. The body's defense system uses antioxidants to combat the damage caused by free radicals.

In this way, they are able to slow the destructive impact that free radicals have on the body. Science has identified upwards of 4, antioxidants, some of which are produced in the human body naturally.

Two important antioxidant champions are vitamin C and vitamin E. They help fight off inflammation and toxins in the body and are critical for a healthy immune system. When there are too many free radicals and not enough antioxidants in the body, a condition known as oxidative stress occurs.

Vitamin C is a water-soluble vitamin. Unlike fat-soluble vitamins, the body is unable to store water-soluble vitamins and must get them daily from the foods we eat. Vitamin C is needed to make collagen, a protein responsible for growing and repairing cells in our bodies that produce everything from skin to muscle, and from ligaments to blood vessels.

It also has the unique quality of being able to help with the regeneration of other antioxidants such as vitamin E.

Studies have found that people who smoke, and those who are exposed to secondhand smoke, have reduced amounts of vitamin C in their bodies. It's thought that smokers require 35 mg more vitamin C daily than non-smokers. Unfortunately, simply taking a supplement isn't the answer at least with regard to heart disease. People who took a vitamin C supplement still suffered the damage to blood vessels that occurs with low vitamin C levels.

There have been arguments that supplements of vitamin C do not reduce cancer risk and this can be confusing. Overloading the body taking much more than you need is not likely to be helpful. But even a small deficiency in vitamin C may put you at greater risk. And since vitamin C levels are lower in people who smoke, this appears to be the case.



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