Iron and Heart Disease View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2005

AUTHORS

Christopher T. Sempos , Richard F. Gillum , Anne C. Looker

ABSTRACT

Key PointsIn 1981, Dr. Jerome Sullivan proposed the hypothesis that the risk of coronary heart disease (CHD) increases in a positive fashion as body iron stores increase. Nearly all of the research on this topic in humans has come through observational, epidemiological studies. Serum ferritin and other less precise measures of body iron stores have been used in those studies to test the hypothesis.Serum ferritin was not significantly related to risk of developing CHD in five of seven traditional cohort studies.Serum ferritin was not significantly related to having cardiovascular disease in 9 of 10 case-control and cross-sectional studies.Serum transferrin saturation was not significantly related to risk of developing CHD in six of seven cohort studies.In an experiment, 14 men who were heavy smokers donated 500 mL of blood three times over a 14-wk period and demonstrated reductions in serum ferritin and improvement in indices designed to measure low-density lipoprotein cholesterol oxidizability. The experiment has not been repeated.The presence of the Cys282Tyr mutation, which accounts for most of the cases of hemochromatosis, was found to be associated with CHD risk in three cohort studies but not in six case-control or cross-sectional studies—study designs that are considered to be scientifically weaker than the cohort study design.At present, the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD. In 1981, Dr. Jerome Sullivan proposed the hypothesis that the risk of coronary heart disease (CHD) increases in a positive fashion as body iron stores increase. Nearly all of the research on this topic in humans has come through observational, epidemiological studies. Serum ferritin and other less precise measures of body iron stores have been used in those studies to test the hypothesis. Serum ferritin was not significantly related to risk of developing CHD in five of seven traditional cohort studies. Serum ferritin was not significantly related to having cardiovascular disease in 9 of 10 case-control and cross-sectional studies. Serum transferrin saturation was not significantly related to risk of developing CHD in six of seven cohort studies. In an experiment, 14 men who were heavy smokers donated 500 mL of blood three times over a 14-wk period and demonstrated reductions in serum ferritin and improvement in indices designed to measure low-density lipoprotein cholesterol oxidizability. The experiment has not been repeated. The presence of the Cys282Tyr mutation, which accounts for most of the cases of hemochromatosis, was found to be associated with CHD risk in three cohort studies but not in six case-control or cross-sectional studies—study designs that are considered to be scientifically weaker than the cohort study design. At present, the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD. More... »

PAGES

173-190

References to SciGraph publications

Book

TITLE

Preventive Nutrition

ISBN

978-1-58829-445-6
978-1-59259-880-9

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-59259-880-9_7

DOI

http://dx.doi.org/10.1007/978-1-59259-880-9_7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1016833438


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110 schema:description Key PointsIn 1981, Dr. Jerome Sullivan proposed the hypothesis that the risk of coronary heart disease (CHD) increases in a positive fashion as body iron stores increase. Nearly all of the research on this topic in humans has come through observational, epidemiological studies. Serum ferritin and other less precise measures of body iron stores have been used in those studies to test the hypothesis.Serum ferritin was not significantly related to risk of developing CHD in five of seven traditional cohort studies.Serum ferritin was not significantly related to having cardiovascular disease in 9 of 10 case-control and cross-sectional studies.Serum transferrin saturation was not significantly related to risk of developing CHD in six of seven cohort studies.In an experiment, 14 men who were heavy smokers donated 500 mL of blood three times over a 14-wk period and demonstrated reductions in serum ferritin and improvement in indices designed to measure low-density lipoprotein cholesterol oxidizability. The experiment has not been repeated.The presence of the Cys282Tyr mutation, which accounts for most of the cases of hemochromatosis, was found to be associated with CHD risk in three cohort studies but not in six case-control or cross-sectional studies—study designs that are considered to be scientifically weaker than the cohort study design.At present, the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD. In 1981, Dr. Jerome Sullivan proposed the hypothesis that the risk of coronary heart disease (CHD) increases in a positive fashion as body iron stores increase. Nearly all of the research on this topic in humans has come through observational, epidemiological studies. Serum ferritin and other less precise measures of body iron stores have been used in those studies to test the hypothesis. Serum ferritin was not significantly related to risk of developing CHD in five of seven traditional cohort studies. Serum ferritin was not significantly related to having cardiovascular disease in 9 of 10 case-control and cross-sectional studies. Serum transferrin saturation was not significantly related to risk of developing CHD in six of seven cohort studies. In an experiment, 14 men who were heavy smokers donated 500 mL of blood three times over a 14-wk period and demonstrated reductions in serum ferritin and improvement in indices designed to measure low-density lipoprotein cholesterol oxidizability. The experiment has not been repeated. The presence of the Cys282Tyr mutation, which accounts for most of the cases of hemochromatosis, was found to be associated with CHD risk in three cohort studies but not in six case-control or cross-sectional studies—study designs that are considered to be scientifically weaker than the cohort study design. At present, the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD.
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