(Stroke. 1996;27:204-209.)
© 1996 American Heart Association, Inc.
Articles |
Fish Consumption and Stroke in Men
30-Year Findings of the Chicago Western Electric Study
From the Departments of Neurology (A.J.O.) and Preventive Medicine (A.J.O., M.L.D., A.R.D., J.S.), Northwestern University Medical School, Chicago, Ill, and the Department of Epidemiology, School of Public Health, University of Texas Health Science Center (Houston) (R.B.S.).
Correspondence to Anthony J. Orencia, MD, PhD, Indiana University, 541 Clinical Drive CL365, Indianapolis, IN 46202.
 |
Abstract |
|---|
 Top Abstract IntroductionSubjects and Methods Results Discussion References |
|---|
Background and Purpose Evidence of a relationship of fish intake to stroke incidence or mortality is weak. This report examines the association of fish consumption with stroke.
Methods A cohort of 2107 men aged 40 to 55 years from the
Chicago Western Electric Study who were free of coronary heart
disease and stroke through their first annual reexamination was
investigated in relation to baseline fish intake and 30-year risk of
fatal and nonfatal stroke. Data on baseline fish intake, categorized
into four levels (
35 g/d, 18 to 34 g/d, 1 to 17 g/d, and 0 g/d), were
available for 1847 men. Average values of macronutrients and
micronutrients from the first two examinations and major
coronary and stroke risk factors were assessed in relation to
fish consumption. Stroke mortality was ascertained from death
certificates and nonfatal stroke from records of the Health Care
Financing Administration.
Results During 46 426 person-years of follow-up,
76 stroke deaths occurred. Men consuming 35 g/d of fish (highest
level) had a higher age-adjusted death rate from stroke (23.5 per
10 000 person-years) than men in the three other categories of
fish consumption. Based on a Cox proportional hazards regression model
with adjustment for age, systolic blood pressure, cigarette
smoking, serum cholesterol level, diabetes,
electrocardiographic abnormalities, and table salt use, hazards ratios
(and 95% confidence intervals) for fish consumers compared with
nonconsumers were 1.34 (0.53 to 3.41) for 35 g/d, 0.96 (0.41 to 2.21)
for 18 to 34 g/d, and 1.00 (0.43 to 2.33) for 1 to 17 g/d.
Age-adjusted and multivariate analyses for
fatal and nonfatal strokes (n=222) yielded similar results.
Conclusions With stroke rates highest in the subgroup reporting highest fish intake, these data do not support the hypothesis of an inverse association of fish consumption with strokes.
Key Words: diet • epidemiology • risk factors
|
Introduction |
|---|
|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
Modifiable lifestyle risk factors1 2 3 4 such as dietary intake that are possibly related to risk factors for stroke and to stroke morbidity and mortality continue to come under investigation. Fish intake and its possible relations to chronic diseases have been of interest.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 However, data on fish consumption and stroke are sparse.3 4 Results do not clearly indicate whether fish consumption is associated with increased risk of hemorrhagic strokes or reduced risk of ischemic strokes or is not associated with stroke outcome.
Experimental studies in vitro and in humans16 17 18 19 20 indicate that fish abundant in eicosapentaenoic (20:5 n-3) and docosahexaenoic (22:6 n-3) acids may have an inhibitory effect on the n-6 polyunsaturated acid pathway synthesis of eicosanoids. n-3 polyunsaturated fatty acids reduce platelet aggregability and thrombosis via inhibition of cyclooxygenase, which leads to a diminution of thromboxane A2 content. n-3 polyunsaturated fatty acids possibly stabilize the phospholipid membrane through alteration of the cell membrane moiety and its enzymes and receptors16 and consequently protect the blood vessel wall from ischemic damage.
This study is a prospective population-based investigation of the association of fish intake with stroke. Its a priori hypothesis is that fish consumption is inversely related to stroke risk.
|
Subjects and Methods |
|---|
|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
The Western Electric Study is a long-term prospective population study principally of coronary heart disease.21 22 In 1957, 3102 men were randomly selected from the population of 5397 men aged 40 to 55 years and employed for at least 2 years at the Hawthorne Works of the Western Electric Co in Chicago, Ill; 2080 (67.1%) agreed to participate. Another 27 men served as a pilot group, bringing the total number initially examined from October 1957 through December 1958 to 2107. Approximately 65% were first- or second-generation Americans, predominantly of German, Polish, or Bohemian ancestry. Most of the other men were descendants of earlier emigrants from Great Britain and Ireland. The men worked at various occupations associated with manufacture of telephones and related products. Selection, examination, and follow-up procedures have been described.21 22
Dietary data were obtained at the initial examination and at the second examination 1 year later by two nutritionists who used standardized interviews and questionnaires based on Burke's diet history method.23 The interview, which lasted about 1 hour, asked about the usual eating pattern (what, when, and where) on a typical workday and on a typical weekend, special diets followed now and previously, and changes in eating habits during the preceding 20 years. This was followed by a detailed cross-check of 195 specific food items to determine the number of times in the previous 28 days each food item had been eaten and the quantity per serving. As an aid in determining portion sizes, wax models of commonly used foods and dishes of varying sizes were used for reference. This was further assisted by information obtained from the dietary department of the Western Electric Co regarding standard portions and types of foods served in the cafeteria. Supplementary information regarding food preparation was obtained from a questionnaire mailed to wives and returned by participants at the time of interview. Information on food preparation was also obtained from neighborhood restaurants and bakeries. The list of 195 specific foods was compiled so that it would be adequate for most participants, but when a man reported habitual consumption of a dish not on that list, the recipe was obtained and analyzed into its component parts so that the contribution of that dish to his nutrient intake would be represented.
Dietary information was coded by the nutritionists to indicate kinds and quantities of foods and beverages (alcoholic and nonalcoholic) consumed by each participant during the past 28 days. These data were analyzed based on a food table derived from several sources24 25 26 27 to obtain each man's usual daily caloric intake and consumption of animal and vegetable protein, animal and vegetable fat, total carbohydrate, total saturated fatty acids, total unsaturated fatty acids, linoleic acid, linolenic acid, arachidonic acid, cholesterol, calcium, phosphorus, iron, vitamins (A, C, and D), thiamine, riboflavin, and niacin. Quantities of linoleic, linolenic, and arachidonic acid were added to estimate total polyunsaturated fatty acids.
The dietary histories are no longer available, but food profile scores
were used at the second examination to indicate consumption of 26
separate foods or food groups: soft drinks; whole milk; skim milk;
cream; cheese; eggs; ice cream; puddings and custards; soups; fish;
beef, veal, and lamb; pork, ham, and bacon; liver; poultry; mixed
dishes; vegetables; breads and cereals; potatoes; fruits; pastries;
sweets and sugars; butter; margarine; and fried foods. Each was coded
on a 4-point scale on which 0 indicated none, and codes 1 through 3
indicated increasing levels of consumption. For instance, consumption
of fish in 120-g units per 28 days was coded as 0 (none), 1 (<4), 2 (4
to 8), and 3 (>8). Averaged over a 28-day period, these categories
corresponded to average daily intakes of none, 1 to 17 g/d, 18 to 34
g/d, and 35 g/d. Since each participant was classified only by this
score, no actual mean grams per day of fish was recorded. During
that survey year (calendar year 1959), per capita consumption of fish
(expressed in edible weight) in the United States was 13.3
g/d28 ; this national data estimate deals with fish sales
rather than intake.
Men continuing to participate in the study were reexamined annually until 1966. Afterward, vital status was determined periodically by mailed questionnaire and telephone interview through the 25th anniversary of the initial examination, when vital status was known for all 2107 men. Subsequently, vital status at the 30th anniversary of the participant's initial examination was ascertained through the National Death Index. Death certificates of all decedents were obtained and coded for multiple causes.
Ascertainment of cause of death from death certificates was made without knowledge of other information on the participant. Transient ischemic attack was considered a nondefinitive end point for purposes of this study, particularly since ascertainment of transient ischemic attack through medical records (including death certificates) is not comprehensive.29 After exclusion of one case of transient ischemic attack, all death certificates with cerebrovascular disease codes (ICD codes [adapted for use in the United States, 8th Revision] 430 through 434 and 436 through 438)30 were reviewed. Only causes of death in Part I of the death certificate were considered definitive end points. Stroke mentioned as immediate or underlying cause of death was excluded as a definitive end point for any of the following reasons: cerebrovascular insufficiency or ischemia without further qualification (n=1), strokes due to secondary coagulopathies such as myeloblastic leukemia or lymphoma (n=2), progressive cerebral degeneration (without any mention of stroke) (n=1), subdural hematoma (n=1), cerebral arteriosclerosis (n=4), and intracerebral hemorrhage due to brain tumor or trauma (n=2). After review of death certificates, 76 stroke end points were identified for inclusion in the analyses.
HCFA tapes (Part A, inpatient, and Part B, outpatient) were obtained for study participants for the period 1984 through 1989. These tapes contain a record of each Medicare-reimbursed healthcare encounter. Because all surviving study participants were Medicare eligible (age 65 years or older) by 1983, costs for essentially all major events were eligible for Medicare reimbursement by the HCFA. The data available for each encounter included date of service and up to five ICD (9th revision; ICD-9) diagnostic codes. Stroke was defined as any mention of cerebrovascular disease (ICD-9 codes 430 through 438), with the exception of transient cerebral ischemia (ICD-9 435), in either HCFA Part A or Part B encounter records (n=147). With events on the death certificate combined with nonoverlapping events from the HCFA, there were 222 men with nonfatal or fatal strokes.
Exclusions from the original 2107 participants were made for one or more of the following reasons: coronary heart disease or stroke at initial examination (n=44) and/or missing data for dietary nutrients (n=187), serum cholesterol (n=6), or body mass index (n=9) at initial examination and/or reexamination. At baseline, five participants included in the analysis had atrial fibrillation, a well-established risk factor for stroke and stroke mortality.31 32 None of these men had a stroke (nonfatal or fatal) during the 30-year follow-up. Analyses were based on fish consumption data available for 1847 men. Rates of stroke incidence and mortality per 10 000 person-years of follow-up were computed for each category of fish consumption. Fish consumers were compared with nonfish consumers in regard to average baseline dietary intake and stroke risk factor profile from the 1958 and 1959 examinations. Multivariate proportional hazards regression models were used to adjust for potential confounding variables, including age, systolic blood pressure, cigarette smoking, serum cholesterol, diabetes (yes or no), ECG abnormalities (present or absent), table salt use (salt before and after food tasting versus no salt use at table), and macronutrients and micronutrients.
|
Results |
|---|
|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
Table 1
presents baseline characteristics by
category of fish intake and for the whole cohort. The Western Electric
men on average had elevated body mass index and higher than desirable
serum cholesterol level, blood pressure, and intake of
total fat, saturated fatty acids, and cholesterol. A
clinical diagnosis of diabetes or codable ECG abnormality (Minnesota
code) was present in 1.5% and 18.4% of participants,
respectively. Prevalence of cigarette smoking was high (57.9%).
Alcohol intake was reported by 85.2% of participants. Significant
differences among the four groups according to fish consumption were
found for the following dietary variables: total energy; percent
kilocalories from polyunsaturated fatty acids, linoleic acid,
arachidonic acid, total protein, animal protein,
and carbohydrate; amounts per day of iron, thiamine, riboflavin,
niacin, vitamin C, beta-carotene, and retinol; and alcohol intake
(milliliters per day) (P<.01). Established or
putative stroke risk factors measured at baseline, such as body
mass index, systolic and diastolic blood pressure,
cigarette smoking, heart rate, education, and ECG abnormalities, did
not differ significantly across the four groups.
|
During the 30-year follow-up, 76 stroke deaths meeting inclusion
criteria occurred among the 1847 men. The large proportion of
participants without information about stroke types (namely,
ischemic stroke and intracerebral
hemorrhage) and the sparse number of
intracerebral hemorrhagic stroke deaths precluded
stratified analyses according to stroke type. The cohort
experience represented a total of 46 426 person-years
of follow-up. Table 2 presents mortality rates
of stroke per 10 000 person-years of observation by categories of
fish consumption. Persons consuming at least 35 g/d of fish had a
higher age-adjusted rate of stroke death (23.5 per 10 000
person-years) than persons consuming 1 to 17 g/d of fish or 18 to
34 g/d of fish and than nonconsumers. Mortality rates among men
consuming 1 to 17 g/d of fish or 18 to 34 g/d (15.5 and 15.3 per
10 000 person-years, respectively) were similar to those of
nonconsumers (15.6 per 10 000 person-years).
|
Results on fish intake and stroke mortality were adjusted for age and
then for age, systolic blood pressure, cigarette smoking, serum
cholesterol, diabetes, ECG abnormalities, table salt use,
macronutrients, and micronutrients (Table 2
). Study
participants who
never consumed fish served as the comparison group. Age-adjusted
risk of stroke death among men who consumed 35 g/d of fish was 47%
greater than that of those who never ate fish (95% CI for hazards
ratio, 0.60 to 3.61). In the risk factor–adjusted model, risk for
stroke death among consumers of 35 g/d was 34% higher compared with
participants who never ate fish (95% CI for hazards ratio, 0.53 to
3.41) (Table 2). Neither the age-adjusted analyses nor the
multivariate risk factor–adjusted analyses
showed a significant increase or decrease in risk of stroke death with
higher levels of fish consumption.
Analyses were repeated for nonfatal plus fatal strokes derived
from both HCFA data and death certificates (Table 2). The risk
factor–adjusted model for fatal and nonfatal strokes showed a
relative risk of 1.26 for fish consumers in the 35-g/d category
compared with participants who never ate fish (95% CI, 0.74 to 2.16).
Fish intake was not significantly related to nonfatal and fatal
strokes.
As expected, baseline age, blood pressure, and cigarette smoking were significantly related to stroke. Multivariate proportional hazards coefficients (rounded to three decimal places) for stroke mortality were 0.129±0.029 for age, 0.028±0.006 for systolic pressure, and 0.020±0.010 for cigarette smoking. Hazards ratio estimates and 95% CIs were as follows: age (per 5 years older) adjusted for systolic blood pressure and cigarette use, 1.91 (95% CI, 1.43 to 2.53); systolic blood pressure (per 20 mm Hg higher) adjusted for age and cigarette use, 1.75 (1.38 to 2.22); and cigarette smoking (per 20 cigarettes higher) adjusted for age and systolic pressure, 1.49 (1.01 to 2.21).
|
Discussion |
|---|
|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
Our main finding is that differences in fish consumption from none to
35 g/d, as noted by a dietary intake evaluation at the beginning
of the study in 1957, were not significantly associated with increased
or decreased risk of stroke in the Western Electric sample of 1847
middle-aged men followed up for 30 years. There was no significant
relationship between fish consumption and stroke; however, the lower
limits of the CIs (0.53 and 0.74, Table 2) show that a modest
protective effect could have been present. On the other hand, the
upper limits of the CIs (3.41 and 2.16, Table 2) show that an
adverse
effect could have been present. These findings have to be interpreted with respect to the potential limitations in the study. Although trained interviewers who were nutritionists collected dietary data 2 years in a row with standardized interviews and questionnaires based on Burke's in-depth diet history, measurement of fish intake was available from one examination only. These estimates of fish consumption by the individual men would have been more stable if two or more measurements were available. Fish consumption may also have increased or decreased over the course of follow-up. Trends toward a more healthy lifestyle that include exercise, a modified fat diet, reduced salt intake, and avoidance of cigarette smoking and excessive alcohol intake did not begin until the 1970s and beyond in the United States. Long-term data on such possible trends are not available for this cohort. However, the available data did show a significant inverse association between baseline fish intake and 19-year coronary heart disease mortality (probability value for trend, P=.008),6 a finding that persisted with 30-year follow-up.
As to potential limitations in stroke ascertainment, death certificates are a main source for stroke deaths in epidemiological investigations.33 34 35 36 The follow-up methods used in the Western Electric cohort were comprehensive (eg, annual examinations of the participants during the early years of the study, letters and questionnaires, and death-certificate requests through the National Death Index). The finding that the established major risk factors for stroke (age, blood pressure, and cigarette use) were significantly related to long-term risk of stroke death in this cohort lends credence to the judgment that ascertainment of stroke as a cause of death was of high validity.
Annual examinations for the Western Electric men were conducted through 1966; between 1966 and 1983, no follow-up on stroke incidence was done. In 1984, HCFA data became available for research purposes. Although the HCFA method of outcome ascertainment has limitations because it is difficult to verify incident stroke cases, analyses for fatal and nonfatal strokes (n=222) yielded hazards ratios similar to those for fatal stroke (n=76).
The results on fish intake and stroke risk prevailed with adjustment for multiple possible confounders and were not accounted for by significant differences across the groups in several dietary variables. The nonsignificantly higher stroke rates for the group with highest fish intake may thus be a chance finding. In any case, these data lend no support to the hypothesis that fish intake is associated with lower stroke risk.
This study is one of the few population-based investigations of
fish consumption and stroke. Two other studies—one in Zutphen, The
Netherlands, and one in Perth, Australia—have reported findings
seemingly different from the Western Electric cohort
results.3 4 The prospective Zutphen Study, of 552 men
experiencing 42 strokes during 15-year follow-up, presented
data indicating a nonsignificant inverse relationship between fish
intake (20 versus <20 g/d, or "always" versus
"never"
ate fish) and stroke incidence. Compared with men in the Zutphen Study,
the Western Electric men were younger at initial examination. The
method used in the two studies to assess diet was essentially the same,
with relatively minor modifications for local
use.3 5 21 22 37
With respect to baseline dietary profiles
for fish consumers and nonconsumers, total energy, total fat, saturated
fatty acids, monounsaturated fatty acids, and
carbohydrate intake did not differ in the Zutphen and Western Electric
cohorts. Intake of polyunsaturated fatty acids was lower in the Western
Electric than the Zutphen men. These minor differences do not seem
capable of explaining the possibly diverse findings of the two studies
on fish and stroke. Given that results in each of the two studies were
not statistically significant, the seemingly disparate trends may be
due to chance.
The case-control study of lifestyle risk factors for stroke in the Perth, Western Australia, region reported an inverse relation of fish consumption (more than twice per month compared with less than this amount) to first strokes (odds ratio, 0.60; 95% CI, 0.36 to 0.99).4 In identical multivariate risk-factor models for ischemic stroke and for intracerebral hemorrhage, a significant inverse relation with fish consumption was found for intracerebral hemorrhage but not for ischemic stroke. Possible reasons are not apparent for the difference in the findings of the Chicago and Perth studies.
The Physicians' Health Study38 reported that men who had five or more servings of fish per week had a nonsignificantly lower risk of fatal and nonfatal stroke compared with men consuming less than one serving per week (relative risk, 0.6; 95% CI, 0.3 to 1.6). Because this study is a clinical trial related to myocardial infarction and cancer outcomes, findings may not be generalizable to the natural history of stroke. In addition, the study population for this clinical trial is more restrictive and homogeneous (eg, persons with liver or renal disease, peptic ulcer, and gout or who were currently using aspirin, other platelet-active drugs, or nonsteroidal anti-inflammatory agents were excluded at baseline screening). Therefore, results from the Physicians' Health Study are not directly comparable with the Zutphen, Chicago, and Perth studies.
In summary, the Chicago Western Electric Study data show no significant relationship between fish intake and stroke mortality. With stroke rates highest in the subgroup reporting highest fish intake, these data do not support the hypothesis of an inverse relationship between fish consumption and risk of stroke.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This research was supported by the American Heart Association and its Chicago and Illinois affiliates; the National Heart, Lung, and Blood Institute (HL-15174 and HL-21010); the Chicago Health Research Foundation; the Otho S. Sprague Foundation; the Research and Education Committee of the Presbyterian-St Luke's Hospital; and the Illini Foundation. We are pleased to express appreciation to the officers, executive leadership, and labor force of the Western Electric Co, Chicago, Ill; their cooperation made this study possible. We are also gratified to acknowledge the role of Oglesby Paul, MD, and Mark Lepper, MD, in the initiation of the Western Electric Study and in its leadership for many years, of Anne MacMillan Shryock, BS, in the collection of the nutrition data for the Western Electric men, and of the many physicians who participated in the annual examinations of the cohort (Maurice Albala, Harry Bliss, Herschel Browns, Marvin Colbert, Henry De Young, Peter Economou, Sanford Franzblau, Robert Felix, John Graettinger, Buford Hall, Wallace Kirkland, Joseph Muenster, Hyman Mackler, Adrian Ostfield, Robert Parsons, Charles Perlia, William Phelan, Norman Roberg, Marvin Rosenberg, George Saxton, Armin Schick, John Sharp, Jay Silverman, Donald Tarun, and Walter Wood). We are also pleased to thank Daniel Garside and Douglas K. Morris for assistance with WE data files and analyses and Carol Maliza for supervising the 20- and 25-year follow-up surveys. Acknowledgment is also gratefully extended to Ronald Prineas, MD, PhD, and members of the ECG Coding Laboratory, Division of Epidemiology, School of Public Health, University of Minnesota (Minneapolis) for the ECG coding and quality control. It is also a pleasure to acknowledge the years-long contributions to the study of colleagues in the Department of Preventive Medicine, Northwestern University Medical School, particularly David M. Berkson, MD, Patricia Collette, MA, Dan Garside, MA, Kiang Liu, PhD, Mary Newman, Rose Stamler, MA, and Linda Van Horn, PhD.
Received July 20, 1995; revision received September 26, 1995; accepted October 9, 1995.
|
References |
|---|
|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
- Davis PH, Dambrosia JM, Schoenberg BS, Schoenberg DG, Pritchard DA, Lilienfeld AM, Whisnant JP. Risk factors for ischemic stroke: a prospective study in Rochester, Minnesota. Ann Neurol. 1987;22:319-327. [Medline] [Order article via Infotrieve]
-
Ellekjaer EF, Wyller TB, Sverre JM, Holmen J.
Lifestyle factors and risk of cerebral infarction.
Stroke. 1992;23:829-834.
[Abstract/Free Full Text] - Keli SO, Feskens EJM, Kromhout D. Fish consumption and risk of stroke: the Zutphen Study. Stroke. 1994;25:328-332. [Abstract]
- Jamrozik K, Broadhurst RJ, Anderson CS, Stewart-Wynne EG. The role of lifestyle factors in the etiology of stroke: a population-based case-control study in Perth, Western Australia. Stroke. 1994;25:51-59. [Abstract]
- Kromhout D, Bosschieter EB, de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med. 1985;312:1205-1209. [Abstract]
- Shekelle RB, Missell LV, Paul O, Shryock AM, Stamler J. Fish consumption and mortality from coronary heart disease. N Engl J Med. 1985;313:820. Letter. [Medline] [Order article via Infotrieve]
- Vollset SE, Heuch I, Bjelke E. Fish consumption and mortality from coronary heart disease. N Engl J Med. 1985;313:820-821. Letter.
- Curb JD, Reed D. Fish consumption and mortality from coronary heart disease. N Engl J Med. 1985;313:821-822. Letter.
- Norell SE, Ahlbom A, Feytching M, Pedersen NL. Fish consumption and mortality from coronary heart disease. Br Med J. 1986;293:426. Abstract.
-
Ascherio A, Rimm EB, Stampfer MJ, Giovannucci EL,
Willet WC. Dietary intake of marine n-3 fatty acids, fish
intake, and the risk of coronary disease among men.
N Engl J Med. 1995;332:977-982.
[Abstract/Free Full Text] - Feskens EJM, Bowles CH, Kromhout D. Inverse association between fish intake and risk of glucose intolerance in normoglycemic elderly men and women. Diabetes Care. 1991;14:935-941. [Abstract]
-
Shahar E, Folsom AR, Melnick SL, Tockman MS, Comstock
GW, Gennaro V, Higgins MW, Sorlie PD, Ko WJ, Szklo M, for the
Atherosclerosis Risk in Communities Study
Investigators. Dietary n-3 polyunsaturated fatty acids and
smoking-related chronic obstructive pulmonary disease.
N Engl J Med. 1994;331:228-233.
[Abstract/Free Full Text] - Kromann N, Green A. Epidemiological studies in the Upernavik District, Greenland. Acta Med Scand. 1980;208:401-406. [Medline] [Order article via Infotrieve]
- Feskens EJM, Kromhout D. Epidemiologic studies on Eskimos and fish intake. Ann N Y Acad Sci. 1993;683:9-15. [Abstract]
- Shekelle RB, Stamler J. Fish and coronary heart disease: the epidemiological evidence. Nutr Metab Cardiovasc Dis. 1993;3:46-51.
-
Kinsella JE, Lokesh B, Stone RA. Dietary N-3
polyunsaturated acids and amelioration of
cardiovascular disease: possible mechanisms.
Am J Clin Nutr. 1990;52:1-28.
[Abstract/Free Full Text] - van Houwelingen AC, Hornstra G, Kromhout D, de Lezenne-Coulander C. Habitual fish consumption, fatty acids of serum phospholipids and platelet function. Atherosclerosis. 1989;75:157-165. [Medline] [Order article via Infotrieve]
-
Bonaa KH, Bjerve KS, Nordoy A. Habitual fish
consumption, plasma phospholipid fatty acids, and serum lipids: the
Tromso Study. Am J Clin Nutr. 1992;55:1126-1134.
[Abstract/Free Full Text] - Fischer S, Weber PC. Thromboxane A3(Txa3) is formed in human platelets after dietary eicosapentaenoic acid (C20:5w3). Biochem Biophys Res Commun. 1983;116:1091-1099. [Medline] [Order article via Infotrieve]
- Dyerberg J, Bang HO, Stofferson E, Moncada S, Vane JR. Eicosapentaenoic acid and prevention of thrombosis and atherosclerosis? Lancet. 1978;2:117-119. [Medline] [Order article via Infotrieve]
- Paul O, Lepper MH, Phelan WH, Dupertuis GW, MacMillan A, McKean H, Park H. A longitudinal study of coronary heart disease. Circulation. 1963:28:20-31.
- Stamler J, Dyer AR, Shekelle RB, Neaton J, Stamler R. Relationship of baseline major risk factors to coronary and all-cause mortality, and to longevity: findings from long-term follow-up of Chicago cohorts. Cardiology. 1993;82:191-222. [Medline] [Order article via Infotrieve]
- Burke BS. The dietary history as a tool in research. J Am Diet Assoc. 1947;23:1041-1046.
- Hayes OB, Rose G. Supplementary food composition table. J Am Diet Assoc. 1957;33:26-29. [Medline] [Order article via Infotrieve]
- Hardinge MG, Crooks H. Fatty acid composition of food fats. J Am Diet Assoc. 1958;34:1065-1071. [Medline] [Order article via Infotrieve]
-
Department of Nutrition. Food Composition
Table
No. 3. Boston, Mass: Harvard School of Public Health; 1957.
- Bowes A De P, Church CF. Food Values of Portions Commonly Used. Philadelphia, Pa: JB Lippincott Co; 1956.
- US Department of Commerce. Statistical Abstract of the United States (82nd edition). Washington, DC: Economics and Statistics Administration, Bureau of the Census; 1961.
- Whisnant JP, Melton LJ, Davis PH, O'Fallon WM, Nishimaru K, Schoenberg BS. Comparison of case ascertainment by medical record linkage and cohort follow-up to determine incidence rates for transient ischemic attacks and stroke. J Clin Epidemiol. 1990;43:791-797. [Medline] [Order article via Infotrieve]
- ICDA: Eighth Revision, International Classification of Diseases, Adapted for Use in the United States. Washington, DC: US Government Printing Office; 1968. US Public Health Service publication 1693.
-
Stroke Prevention in Atrial Fibrillation Investigators.
Stroke Prevention in Atrial Fibrillation Study: final results.
Circulation. 1991;84:527-539.
[Abstract/Free Full Text] -
Broderick JP, Phillips SJ, O'Fallon M, Frye RL,
Whisnant JP. Relationship of cardiac disease to stroke
occurrence, recurrence, and mortality.
Stroke. 1992;23:1250-1256.
[Abstract/Free Full Text] - Howard G, Anderson R, Sorlie P, Andrews V, Backlund E, Burke GL. Ethnic differences in stroke mortality between non-Hispanic whites, Hispanic whites, and blacks: the National Longitudinal Mortality Study. Stroke. 1994;25:2120-2125. [Abstract]
- McGovern PG, Burke GL, Sprafka M, Xue S, Folsom A, Blackburn H. Trends in mortality, morbidity and risk factor levels for stroke from 1960 through 1990: the Minnesota Heart Survey. J Am Med Assoc. 1992;268:753-759. [Abstract]
- Neaton JD, Wentworth DN, Cutler J, Stamler J, Kuller L, for the Multiple Risk Factor Intervention Trial Research Group. Risk factors for death from different types of stroke. Ann Epidemiol. 1993;3:493-499. [Medline] [Order article via Infotrieve]
- Neaton JD, Kuller L, Stamler J, Wentworth DN. Impact of systolic and diastolic blood pressure on cardiovascular mortality. In: Laragh JH, Brenner BM, eds. Hypertension: Physiology, Diagnosis, and Management. 2nd ed. New York, NY: Raven Press Publishers; 1995;chap 9:127-144.
- den Hartog C, van Schaik TH, Dalderup LM, Drion EF, Mulder T. The diet of volunteers participating in a long term epidemiological field survey on coronary heart disease in Zutphen, The Netherlands. Voeding. 1965;26:184-208. [Medline] [Order article via Infotrieve]
-
Morris M, Manson J, Rosner B, Buring J, Willett W,
Hennekens C. Fish consumption and cardiovascular
disease in the Physicians' Health Study: a prospective study.
Am J Epidemiol. 1995;142:166-175.
[Abstract/Free Full Text]
This article has been cited by other articles:
 |
|
 |
|
  C. Wang, W. S Harris, M. Chung, A. H Lichtenstein, E. M Balk, B. Kupelnick, H. S Jordan, and J. Lau n-3 Fatty acids from fish or fish-oil supplements, but not {alpha}-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review Am. J. Clinical Nutrition, July 1, 2006; 84(1): 5 - 17. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. K Gebauer, T. L Psota, W. S Harris, and P. M Kris-Etherton n-3 Fatty acid dietary recommendations and food sources to achieve essentiality and cardiovascular benefits Am. J. Clinical Nutrition, June 1, 2006; 83(6): S1526 - 1535S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. C. Morris, D. A. Evans, C. C. Tangney, J. L. Bienias, and R. S. Wilson Fish Consumption and Cognitive Decline With Age in a Large Community Study Arch Neurol, December 1, 2005; 62(12): 1849 - 1853. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Mozaffarian, W. T. Longstreth Jr, R. N. Lemaitre, T. A. Manolio, L. H. Kuller, G. L. Burke, and D. S. Siscovick Fish Consumption and Stroke Risk in Elderly Individuals: The Cardiovascular Health Study Arch Intern Med, January 24, 2005; 165(2): 200 - 206. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. He, Y. Song, M. L. Daviglus, K. Liu, L. Van Horn, A. R. Dyer, U. Goldbourt, and P. Greenland Fish Consumption and Incidence of Stroke: A Meta-Analysis of Cohort Studies Stroke, July 1, 2004; 35(7): 1538 - 1542. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Fraser Commentary: Protection from stroke by eating animal foods? Surely not! Int. J. Epidemiol., August 1, 2003; 32(4): 543 - 545. [Full Text] [PDF]
|
|
|
|
 |
|
 P. M. Kris-Etherton, W. S. Harris, L. J. Appel, and for the Nutrition Committee Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease Arterioscler. Thromb. Vasc. Biol., February 1, 2003; 23(2): e20 - 30. [Full Text] [PDF]
|
|
|
|
 |
|
 K. He, E. B. Rimm, A. Merchant, B. A. Rosner, M. J. Stampfer, W. C. Willett, and A. Ascherio Fish Consumption and Risk of Stroke in Men JAMA, December 25, 2002; 288(24): 3130 - 3136. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. M. Kris-Etherton, W. S. Harris, L. J. Appel, and for the Nutrition Committee Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease Circulation, November 19, 2002; 106(21): 2747 - 2757. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Angerer, W. Kothny, S. Stork, and C. von Schacky Effect of dietary supplementation with {omega}-3 fatty acids on progression of atherosclerosis in carotid arteries Cardiovasc Res, April 1, 2002; 54(1): 183 - 190. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Iso, K. M. Rexrode, M. J. Stampfer, J. E. Manson, G. A. Colditz, F. E. Speizer, C. H. Hennekens, and W. C. Willett Intake of Fish and Omega-3 Fatty Acids and Risk of Stroke in Women JAMA, January 17, 2001; 285(3): 304 - 312. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Jamrozik, R. J. Broadhurst, S. Forbes, G. J. Hankey, and C. S. Anderson Predictors of Death and Vascular Events in the Elderly : The Perth Community Stroke Study Stroke, April 1, 2000; 31(4): 863 - 868. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Smith, P. Mitchell, and S. R. Leeder Dietary Fat and Fish Intake and Age-Related Maculopathy Arch Ophthalmol, March 1, 2000; 118(3): 401 - 404. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. R. Artalejo, P. Guallar-Castillon, J. R. B. Banegas, B. d. A. Manzano, and J. d. R. Calero Consumption of Fruit and Wine and the Decline in Cerebrovascular Disease Mortality in Spain (1975–1993) Stroke, August 1, 1998; 29(8): 1556 - 1561. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||