Biomarkers in nutritional assessment.
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Biomarkers↗
Biomedical subjects
G van Poppel
Publications and source records attributed to G van Poppel.
Antioxidants and coronary heart disease.
This review briefly summarizes the scientific evidence for a possible role of antioxidants in the prevention of coronary heart disease (CHD). Antioxidants in our diet include vitamins E, C, and beta-carotene, whereas selenium is an integral part of the antioxidant enzyme glutathione peroxidase (GSHPx). Experimental evidence suggests that free-radical damage and antioxidant defence may play an important role in the development of coronary heart disease. Epidemiological studies have produced some intriguing results, but have not indicated unequivocally that a high intake of antioxidants leads to a decreased cardiovascular disease risk. We conclude that the antioxidant atherosclerosis hypothesis is promising, but that the results of long-term intervention studies are still to be awaited. Preventive action based on antioxidant supplementation is therefore not justifiable as yet. Nevertheless, the findings so far certainly do support the recommendations for a varied diet rich in vegetables and fruit.
Animals↗
[Nutrition and cancer: chemopreventive food ingredients].
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Calcium↗
Carotenoids and cancer: an update with emphasis on human intervention studies.
This article gives an overview of the current state of knowledge on the cancer preventive potential of carotenoids. Numerous retrospective and prospective epidemiological studies have shown that a high intake of carotenoid-rich fruits and vegetables is associated with a decreased risk of cancer at a number of common sites. For several other cancer sites, however, the epidemiological evidence is not very consistent. A number of mechanisms for the cancer preventive properties of carotenoids have been proposed. Conversion to retinol, possibly in posthepatic tissues, would allow an effect on cellular differentiation and proliferation, and on cell-to-cell communication. Antioxidant functions could prevent free radical-induced damage to cellular DNA and other macromolecules. Immunomodulatory effects could enhance immune surveillance in tumorigenesis. In addition, non-retinol-mediated effects of carotenoids on metabolism of carcinogens and cell-to-cell communication have been shown. Observational epidemiology cannot resolve whether associations are due to a specific carotenoid, or to an associated factor in fruits and vegetables, whereas interpretation of animal studies is hampered by uncertainties in extrapolation between species, more so because the metabolism of carotenoids in most animals differs notably from that in humans. Human intervention studies on biomarkers related to cancer risk and on cancer incidence are, therefore, necessary. Human intervention studies performed so far suggest that beta-carotene can affect carcinogenesis, though not at all stages and not at all cancer sites. Implications for future human intervention research are discussed.
Carotenoids↗
Effect of beta-carotene on immunological indexes in healthy male smokers.
To evaluate the immunomodulatory effects of beta-carotene we performed a randomized, double-blind trial in healthy male cigarette smokers. Lymphocyte subsets in peripheral blood were assessed by using double labeling with monoclonal antibodies before and after 14 wk beta-carotene (20 mg/d; n = 21) or placebo (n = 24) supplements. In addition we measured the ex vivo phytohemagglutinin and concanavalin A induced lymphocyte proliferation in a separate group (23 placebo, 24 beta-carotene). The beta-carotene and placebo groups were comparable on all initial characteristics. During the intervention plasma concentrations of beta-carotene increased 13-fold in the treatment group whereas retinol concentrations remained constant. Beta-carotene had no effect on lymphocyte subpopulations in peripheral blood. After treatment the beta-carotene group showed 12% higher PHA-induced lymphocyte proliferations than the placebo group (P = 0.02). For ConA induced proliferations no significant difference was observed. These results suggest that supplementary beta-carotene can moderately enhance certain aspects of immune response in healthy male cigarette smokers.
Adult↗
[Antioxidants and prevention of cardiovascular diseases].
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Antioxidants↗
Passive smoking and sister-chromatid exchanges in lymphocytes.
The object of this study was to determine whether exposure to environmental tobacco smoke is associated with DNA damage reflected by the frequency of sister-chromatid exchange (SCE) in lymphocytes. Within a cross-sectional design, 106 male non-smoking adults, employees of two administrative companies, were divided on the basis of self-reported exposure into high and low passive smoking groups. The high exposed subjects (passive smokers, n = 50) lived with smokers, worked with smokers and were exposed to tobacco smoke for an average of 70 h/week. The low exposed non-smokers (n = 56) were exposed for an average of 5 h/week. Plasma cotinine levels for the passive smokers ranged between 0.4 and 9.0 ng/ml (median 1.4 ng/ml), and for the low exposed group between 0.0 and 1.9 ng/ml (median 0.4 ng/ml) (p less than 0.0001; Mann-Whitney test). No difference was observed between the two groups in the frequency of SCEs in lymphocytes: 4.66 +/- 0.05 for passive smokers and 4.68 +/- 0.04 for low exposed non-smokers (mean +/- SEM) (p = 0.80; t-test). Reclassification of subjects on the basis of plasma cotinine levels did not change the results substantially. These results are in accordance with observations that the increase in cancer risk due to passive smoking is small in comparison with the increase due to active smoking. The SCE test may be too insensitive to be useful for the evaluation of possible cytogenetic effects related to passive smoking.
Adult↗
Decreased excretion of thioethers in urine of smokers after the use of beta-carotene.
Epidemiologic studies have demonstrated an inverse relation between vitamin A intake and lung cancer rate. There is strong evidence that the provitamin A, beta-carotene, plays a more important role in the protective effect than vitamin A itself. The anticarcinogenic properties of beta-carotene have so far been attributed to its scavenger properties in deactivating or trapping reactive chemical species such as singlet oxygen and certain organic free radicals. Smoking results in increased excretion of detoxification products of electrophilic agents (mercapturic acids) in urine. Since reactive electrophilic intermediates are involved in carcinogenesis, we performed a double-blind, placebo-controlled intervention trial to investigate whether the intake of beta-carotene by smokers would affect urinary thioether excretion. Before the intervention the beta-carotene group (n = 62) and the placebo group (n = 61) had similar thioether excretion levels in urine (4.2 vs 4.3 mmolSH/mol creatinine). During the intervention (20 mg beta-carotene daily for 14 weeks) the placebo group showed a 12% increase, whereas the beta-carotene group showed a 5% decrease (P = 0.004). After the intervention the beta-carotene group had a 15% lower thioether excretion level than the placebo group (4.1 vs 4.7 mmolSH/mol creatinine; P = 0.0017). Our study shows that urinary thioether excretion varies considerably over time, and that smokers have a decreased excretion of thioethers in urine after the use of beta-carotene.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Beta-carotene supplementation in smokers reduces the frequency of micronuclei in sputum.
beta-carotene has been hypothesised to reduce lung cancer risk. We studied the effect of 14 weeks of beta-carotene supplementation (20 mg d-1) on the frequency of micronuclei in sputum in 114 heavy smokers in a double-blind trial. Micronuclei reflect DNA damage in exfoliated cells and may thus provide a marker of early-stage carcinogenesis. Pre-treatment blood levels of cotinine, beta-carotene, retinol and vitamins C and E were similar in the placebo group (n = 61) and the treatment group (n = 53). Plasma beta-carotene levels increased 13-fold in the treatment group during intervention. Initial micronuclei counts (per 3,000 cells) were higher in the treatment group than in the placebo group (5.0 vs 4.0, P < 0.05). During intervention, the treatment group showed a 47% decrease, whereas the placebo group showed a non-significant decrease (16%). After adjustment for the initial levels, the treatment group had 27% lower micronuclei counts than the placebo group at the end of the trial (95% CI: 9-41%). These results indicate that beta-carotene may reduce lung cancer risk in man by preventing DNA damage in early-stage carcinogenesis.
Adult↗
Increased cytogenetic damage in smokers deficient in glutathione S-transferase isozyme mu.
Reduced expression of the mu-isozyme of glutathione S-transferase (GST; EC 2.5.1.18) has been associated with increased lung cancer risk. We studied the association between GST-mu expression and DNA damage as measured by sister chromatid exchanges (SCE) in healthy male smokers. SCE levels were higher in the 71 GST-mu-deficient smokers compared to the 83 non-deficient smokers (5.24 versus 4.97 SCE/lymphocyte; P = 0.09). In smokers having high plasma cotinine levels (greater than median of 315 ng/ml), this mu-related difference was more pronounced (5.50 versus 4.97; P = 0.01), whereas it was absent in smokers having low cotinine levels (4.95 versus 4.97; P = 0.92). Increased cytogenetic damage in GST-mu-deficient heavy smokers may thus explain the association between GST-mu expression and lung cancer.
Adult↗
Supplementation with vitamin E but not beta-carotene in vivo protects low density lipoprotein from lipid peroxidation in vitro. Effect of cigarette smoking.
Several lines of evidence suggest that oxidatively modified low density lipoprotein (LDL) is atherogenic and that antioxidants may protect LDL against oxidation. In addition, cigarette smoking is known to induce oxidant stress. We have examined the effect of ingestion of the antioxidants D,L-alpha-tocopherol (vitamin E) and beta-carotene and of smoking on the resistance of LDL against copper-mediated oxidation. Six healthy nonsmoking volunteers ingested 1,000 IU/day D,L-alpha-tocopherol acetate for 7 days. After vitamin E ingestion concentrations of alpha-tocopherol in plasma and LDL increased 3.0- and 2.4-fold, respectively. Simultaneously, the oxidation resistance of LDL was elevated significantly (+41%), and the rate of oxidation was decreased significantly (-19%). The increase in alpha-tocopherol content of LDL and the increase in resistance time were highly correlated (rs = 0.89, p = 0.014). Eight weeks after termination of the vitamin E intake, alpha-tocopherol concentrations in plasma and LDL and oxidation resistance of LDL had returned to baseline values. In smokers (n = 46), plasma levels of vitamin C (-26%) and concentrations of beta-carotene (-44%, -43%) and total carotenoids (-23%, -29%) in plasma and LDL, respectively, were significantly lower compared with nonsmokers (n = 23). No differences were found in alpha-tocopherol content of LDL and the susceptibility of LDL to lipid peroxidation in both groups. Supplementation of a group of smokers in a 14-week randomized, double-blind, placebo-controlled intervention trial with beta-carotene resulted in a 16.6- and 5.0-fold increase of LDL beta-carotene and total carotenoid content, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Do antioxidants and polyunsaturated fatty acids have a combined association with coronary atherosclerosis?
To evaluate the antioxidant hypothesis with regard to atherosclerosis, we compared plasma selenium, serum alpha-tocopherol, serum polyunsaturated fatty acids (PUFA), and the ratios of selenium and alpha-tocopherol to PUFAs in subjects with varying degrees of coronary atherosclerosis. Cases had more than 85% stenosis in at least one coronary vessel and controls had less than 50% stenosis in all three vessels. Plasma selenium was significantly lower in cases than controls (95.1 +/- 21.0 micrograms/l and 108.8 +/- 29.3 micrograms/l, respectively). Though alpha-tocopherol and PUFA levels were similar in both groups, the ratios Se/linoleic acid, Se/total PUFA and Se/total n-6 acids were significantly lower in cases. In particular, these differences were observed in subjects with low serum alpha-tocopherol level (below the median; 1452 micrograms/dl). Moreover, in this subgroup the ratio Se/PUFA was significantly lower in cases than in controls for all PUFAs except eicosapentaenoic and docosahexaenoic acid. Though definitive conclusions cannot be drawn from our data, it is hypothesized that high PUFA levels, when insufficiently protected by antioxidants against peroxidation, may indicate a higher risk of atherosclerosis.
Coronary Artery Disease↗
[Socioeconomic differences in nutrition and nutritional status in 10-11-year-old boys].
The relation between socio-economic status and food consumption and nutritional status was investigated in boys aged 10-11 yr (n = 125) who participated in a survey in 1987. Based on the parents' education and profession, boys were categorized in three levels of socio-economic status. In the lower socio-economic category (n = 59) body mass index and skinfold thickness are higher (p less than 0.05) than in the highest category (n = 41) and caries is more prevalent (83% vs 51%). In comparison with both higher groups, dairy products, vegetables and fruit are less frequently used in the lower category, and consumption of protein, calcium and riboflavin is lower (p less than 0.05). These results indicate an increased risk of caries and obesity in the lower socio-economic group. The other differences clearly have an unfavourable tendency, but do not indicate directly increased risk of nutritional deficiencies or nutrition-related diseases in the lower socio-economic group.
Child↗
Biochemical and anthropometric evaluation of the nutritional status of 35-year-old Dutch men with reference to smoking and drinking habits.
In 1986, sixty 35-year-old Dutch men (response 87%) provided information on medications, alcohol consumption and smoking habits. Length, body weight and blood pressure were determined. A blood sample was taken to determine serum cholesterol, HDL cholesterol and biochemical parameters of the vitamin, iron and trace element status (hematology, ferritin, vitamins A, B6, B12, folate, Zn, Se). Prevalence of overweight (body mass index greater than 27 kg/m2) was 15%, whereas 12% had high-risk cholesterol levels (greater than 6.4 mmol/l). Except for possibly selenium, no marginal values for the vitamin, iron and trace element status were found. Smokers had a higher hematocrit reading and mean corpuscular volume and lower mean corpuscular hemoglobin concentration (p less than 0.05). The nutritional status was not negatively influenced by (predominantly moderate) alcohol consumption (mean = 21 g/day). Positive associations with alcohol consumption were found for plasma folic acid (p less than 0.01) and plasma pyridoxal-5'-phosphate (p less than 0.001). This study shows that the most important nutritional risks in 35-year-old Dutch men are related to cardiovascular disease.
Adult↗
Multiple overnight urine collections may be used for estimating the excretion of electrolytes and creatinine.
We studied the excretion of sodium, potassium, calcium, magnesium, and creatinine in overnight and 24-h urines collected over a period of seven consecutive days from 28 Dutch boys, ages eight and nine years. The correlation coefficients for the relation between true mean overnight and true mean 24-h excretion ranged between 0.94 and 1.00 for sodium, calcium, magnesium, and creatinine and was equal to 0.61 for potassium. Generally the within-person coefficients of variation for overnight excretions (range, 33-52%) were greater than for 24-h excretions (range 16-35%). We conclude that overnight collections may replace 24-h collections in the case of young boys, but that generally more overnight than 24-h urine specimens are required to achieve a similar degree of precision. The exact number of urine specimens required varies with the aims of the study.
Calcium↗
[Morbidity and subjective wellbeing in young adults with obesity].
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Adult↗
Markers for cytogenetic damage in smokers: associations with plasma antioxidants and glutathione S-transferase mu.
Biomarkers for increased cytogenetic damage in smokers include sister chromatid exchanges (SCE) in peripheral lymphocytes and micronuclei in sputum cells. These markers may reflect increased cancer risk. Increased cancer risk has also been associated with lower blood levels of the antioxidants beta-carotene and vitamin C and with genetic deficiency of the detoxification enzyme glutathione S-transferase mu (GST-mu). We therefore evaluated the associations of plasma antioxidants, GST-mu phenotype, and indices for tobacco exposure with SCEs and micronuclei in a group of 156 male cigarette smokers and 38 nonsmokers. As expected, smokers as compared with nonsmokers had higher SCE levels (5.08 versus 4.71 SCE/lymphocyte) and lower levels of plasma beta-carotene (0.31 versus 0.48 mumol/liter) and blood vitamin C (36.6 versus 33.8 mumol/liter). In smokers, SCEs were weakly correlated with plasma cotinine (r = 0.186) but not with plasma antioxidants (all r < 0.04). Micronuclei in smokers were not correlated with either cotinine or antioxidants (all r < 0.14). As reported previously, SCEs were higher (5.24 versus 4.97 SCE/lymphocyte) in GST-mu-deficient smokers than in nondeficient smokers. Micronuclei, however, were similar in both GST-mu phenotypes (4.3 versus 4.9 micronuclei/3000 cells). No correlation was observed between micronuclei and SCEs (r = -0.025). Large random variations in both SCEs and micronuclei make it difficult to interpret the absence of relations unambiguously. The results indicate that SCEs and micronuclei have only limited sensitivity to variations in cigarette smoke exposure. The association between GST-mu and cancer risk may be mediated through increases in certain forms of smoking-induced DNA damage in GST-mu deficiency.
Adult↗