Blaise C. Martin
University of Basel
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Arteriosclerosis, Thrombosis, and Vascular Biology | 1999
Eliseo Guallar; Antti Aro; F. Javier Jiménez; José M. Martín-Moreno; Irma Salminen; Pieter van’t Veer; A.F.M. Kardinaal; Jorge Gómez-Aracena; Blaise C. Martin; Lenore Kohlmeier; Jeremy D. Kark; Vladimir P. Mazaev; Jetmund Ringstad; José Guillén; Rudolph A. Riemersma; Jussi K. Huttunen; Michael Thamm; Frans J. Kok
Omega-3 fatty acids have potential antiatherogenic, antithrombotic, and antiarrhythmic properties, but their role in coronary heart disease remains controversial. To evaluate the association of omega-3 fatty acids in adipose tissue with the risk of myocardial infarction in men, a case-control study was conducted in eight European countries and Israel. Cases (n=639) included patients with a first myocardial infarction admitted to coronary care units within 24 hours from the onset of symptoms. Controls (n=700) were selected to represent the populations originating the cases. Adipose tissue levels of fatty acids were determined by capillary gas chromatography. The mean (+/-SD) proportion of alpha-linolenic acid was 0.77% (+/-0.19) of fatty acids in cases and 0.80% (+/-0.19) of fatty acids in controls (P=0.01). The relative risk for the highest quintile of alpha-linolenic acid compared with the lowest was 0.42 (95% confidence interval [CI] 0.22 to 0.81, P-trend=0.02). After adjusting for classical risk factors, the relative risk for the highest quintile was 0.68 (95% CI 0.31 to 1.49, P-trend=0.38). The mean proportion of docosahexaenoic acid was 0.24% (+/-0.13) of fatty acids in cases and 0.25% (+/-0.13) of fatty acids in controls (P=0. 14), with no evidence of association with risk of myocardial infarction. In this large case-control study we could not detect a protective effect of docosahexaenoic acid on the risk of myocardial infarction. The protective effect of alpha-linolenic acid was attenuated after adjusting for classical risk factors (mainly smoking), but it deserves further research.
BMJ | 1997
P. Van't Veer; I.E. Lobbezoo; Jose M. Martin-Moreno; Eliseo Guallar; Jorge Gómez-Aracena; A.F.M. Kardinaal; Lenore Kohlmeier; Blaise C. Martin; J.J. Strain; Michael Thamm; P. Van Zoonen; B. Baumann; Jussi K. Huttunen; F.J. Kok
Abstract Objective: To examine any possible links between exposure to DDE (1,1-dichloro-2,2-bis (p -chlorophenyl)ethylene), the persistent metabolite of the pesticide dicophane (DDT), and breast cancer. Design: Multicentre study of exposure to DDE by measurement of adipose tissue aspirated from the buttocks. Laboratory measurements were conducted in a single laboratory. Additional data on risk factors for breast cancer were obtained by standard questionnaires. Setting: Centres in Germany, the Netherlands, Northern Ireland, Switzerland, and Spain. Subjects: 265 postmenopausal women with breast cancer and 341 controls matched for age and centre. Main outcome measure: Adipose DDE concentrations. Results: Women with breast cancer had adipose DDE concentrations 9.2% lower than control women. No increased risk of breast cancer was found at higher concentrations. The odds ratio of breast cancer, adjusted for age and centre, for the highest versus the lowest fourth of DDE distribution was 0.73 (95% confidence interval 0.44 to 1.21) and decreased to 0.48 (0.25 to 0.95; P for trend=0.02) after adjustment for body mass index, age at first birth, and current alcohol drinking. Adjustment for other risk factors did not materially affect these estimates. Conclusions: The lower DDE concentrations observed among the women with breast cancer may be secondary to disease inception. This study does not support the hypothesis that DDE increases risk of breast cancer in postmenopausal women in Europe. Key messages Organochlorines such as polychlorinated biphenyls and DDT may increase the risk of breast cancer in women DDE concentrations among the women with cancer were lower than among the controls, and there was an inverse risk gradient with higher DDE concentrations which remained significant after adjustment for risk factors for breast cancer These results are clearly incompatible with an increased risk of breast cancer at increased concentrations of DDE, although associations with other organochlorines cannot be excluded
Arteriosclerosis, Thrombosis, and Vascular Biology | 1995
A.F.M. Kardinaal; Antti Aro; Jeremy D. Kark; Rudolph A. Riemersma; Pieter van’t Veer; Jorge Gómez-Aracena; Lenore Kohlmeier; Jetmund Ringstad; Blaise C. Martin; Vladimir P. Mazaev; Miguel Delgado-Rodriguez; Michael Thamm; Jussi K. Huttunen; Jose M. Martin-Moreno; Frans J. Kok
Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and alpha-tocopherol and beta-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For alpha-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) beta-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high beta-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that beta-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that alpha-tocopherol or selenium may protect against MI at any level of PUFA intake.Abstract Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and α-tocopherol and β-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For α-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) β-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high β-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that β-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that α-tocopherol or selenium may protect against MI at any level of PUFA intake.
Arteriosclerosis, Thrombosis, and Vascular Biology | 1995
A.F.M. Kardinaal; Antti Aro; Jeremy D. Kark; R.A. Riemersma; P. van 't Veer; Jorge Gómez-Aracena; Lenore Kohlmeier; Jetmund Ringstad; Blaise C. Martin; Vladimir P. Mazaev; Miguel Delgado-Rodriguez; Michael Thamm; Jussi K. Huttunen; Jose M. Martin-Moreno; F.J. Kok
Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and alpha-tocopherol and beta-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For alpha-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) beta-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high beta-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that beta-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that alpha-tocopherol or selenium may protect against MI at any level of PUFA intake.Abstract Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and α-tocopherol and β-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For α-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) β-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high β-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that β-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that α-tocopherol or selenium may protect against MI at any level of PUFA intake.
Arteriosclerosis, Thrombosis, and Vascular Biology | 1995
A.F.M. Kardinaal; Antti Aro; Jeremy D. Kark; Rudolph A. Riemersma; Pieter van’t Veer; Jorge Gómez-Aracena; Lenore Kohlmeier; Jetmund Ringstad; Blaise C. Martin; Vladimir P. Mazaev; Miguel Delgado-Rodriguez; Michael Thamm; Jussi K. Huttunen; Jose M. Martin-Moreno; Frans J. Kok
Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and alpha-tocopherol and beta-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For alpha-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) beta-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high beta-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that beta-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that alpha-tocopherol or selenium may protect against MI at any level of PUFA intake.Abstract Because antioxidants may play a role in the prevention of coronary heart disease by inhibiting the peroxidation of polyunsaturated fatty acids (PUFAs), the combined association of diet-derived antioxidants and PUFAs with acute myocardial infarction (MI) was investigated. This multicenter case-control study included 674 patients and 725 control subjects in eight European countries and Israel. Fatty acid composition and α-tocopherol and β-carotene levels were determined in adipose tissue; selenium level was determined in toenails. For α-tocopherol no association with MI was observed at any PUFA level. The overall multivariate odds ratio (OR) for low (10th percentile) versus high (90th percentile) β-carotene was 1.98 (95% confidence interval [CI], 1.39 to 2.82). The strength of this inverse association with MI was dependent on PUFA levels (in tertiles): for low PUFA, the OR for low versus high β-carotene was 1.79 (95% CI, 0.98 to 3.25), for medium PUFA the OR was 1.76 (95% CI, 1.00 to 3.11), and for high PUFA 3.47 (95% CI, 1.93 to 6.24). For selenium increased risk was observed only at the lowest PUFA tertile (OR, 2.49; 95% CI, 1.22 to 5.09). This interaction between selenium and PUFAs was not significant and may at least partly be explained by a higher proportion of smokers at the low PUFA level. These findings support the hypothesis that β-carotene plays a role in the protection of PUFAs against oxidation and subsequently in the protection against MI. No evidence was found that α-tocopherol or selenium may protect against MI at any level of PUFA intake.
American Journal of Epidemiology | 1997
Lenore Kohlmeier; Jeremy D. Kark; Enrique Gomez-Gracia; Blaise C. Martin; Susan E. Steck; A.F.M. Kardinaal; Jetmund Ringstad; Michael Thamm; Victor Masaev; Rudolf Riemersma; Jose M. Martin-Moreno; Jussi K. Huttunen; Frans J. Kok
American Journal of Epidemiology | 1998
Neal Simonsen; Pieter van’t Veer; J.J. Strain; Jose M. Martin-Moreno; Jussi K. Huttunen; Joaquin Femández-Crehuet Navajas; Blaise C. Martin; Michael Thamm; A.F.M. Kardinaal; Frans J. Kok; Lenore Kohlmeier
Cancer Epidemiology, Biomarkers & Prevention | 1997
Lenore Kohlmeier; N.R. Simonson; P. van 't Veer; J.J. Strain; Jose M. Martin-Moreno; B. Margolin; Jussi K. Huttunen; J. Fernandez-Crehuet Navajas; Blaise C. Martin
American Journal of Epidemiology | 1997
A.F.M. Kardinaal; Frans J. Kok; Lenore Kohlmeier; Jose M. Martin-Moreno; Jetmund Ringstad; Jorge Gómez-Aracena; Vladimir P. Mazaev; Michael Thamm; Blaise C. Martin; Antti Aro; Jeremy D. Kark; Miguel Delgado-Rodriguez; Rudolph A. Riemersma; Pieter 't van Veer; Jussi K. Huttunen
Cancer Epidemiology, Biomarkers & Prevention | 1998
L.-C. J. Su; Mai Bui; A.F.M. Kardinaal; Jorge Gómez-Aracena; Jose M. Martin-Moreno; Blaise C. Martin; Michael Thamm; Neal Simonsen; P. van 't Veer; F.J. Kok; S. Strain; Lenore Kohlmeier