Consumption of fish and coronary heart disease (CHD).

Background: Several randomized trials examined the association between fish oil consumption and CHD. Fewer randomized trials examined the relation with fish consumption. In two trials subjects were randomly allocated to a dietary advice to increase consumption of fatty fish to ≥ 2 portions/week. Both trials included men from the UK only (The DART study, and the DART II study).
The DART study included men with a history of MI. After 2 years of follow-up, fish advice significantly decreased risk of death from heart disease (Burr ML [9]), but no long-term benefit was found (Ness AR [9]). The DART II study included men with angina. Fish advice nonsignificantly increased risk of death from heart disease (Burr ML [25]).
In the past, several systematic reviews were published relating fish consumption to CHD. But lot's of cohorts were excluded from analysis, or not found by the authors, biasing associations towards a protective effect. Results from these systematic reviews are discussed briefly:

  • He K. 2004: Examined the relation with CHD death. 11 cohorts were included, and 7 studies (including data about 5 additional cohorts) were excluded. A total of 3,032 CHD deaths were included. 7 cohorts were not identified/discussed (Hirayama T [10], Dolecek TA [11], Knekt P [13], Gillum RF [17], Pietinen P [18], Whiteman D [21], Nagata C [23]). A strong protective effect was found: RR = 0.62 (0.45-0.82) for consumption ≥ 5 times/week vs < once/month.
  • Wang C. 2004: Examined the relation with CHD death. 15 cohorts were included. One cohort was excluded (Norell SE [5]), and 9 cohorts were not identified/discussed (Vollset SE [3], Hirayama T [10], Knekt P [13], Soinio M [16], Gillum RF [17], Yuan JM [19], Whiteman D [21], Nagata C [23], Erkkilä AT [28]).
    The authors of this review stated that among the large cohort studies, only the Physician's Health Study [15] failed to report a significant beneficial effect of fish consumption. But findings in their own tables contradict this statement. Tables 3.31 and 3.32 show results from prospective studies relating omega-3 fatty acids or fish to cardiac death (pages 65-66). Among the studies larger than the Physician's Health Study, no significant effects at any level of consumption were found in 3 cohorts (Fraser GE [8]; Pietinen P [18]; Egeland GM. 2001). Actually, a significant protective effect of high vs low consumption among the larger cohorts was found in only one cohort (Hu FB [14].
    Since a cod liver oil supplement was consumed in one of the cohorts (Egeland GM. 2001), this result was not included in my review examining dietary fish consumption.
  • König A. 2005: This review only included articles identified by Wang C. (2004) in the review mentioned above. And the authors wanted to describe the dose-response relationship for fish consumption and CHD death. Studies that limited attention to populations with particular risk/protective factors were excluded a priori, such as smokers and vegetarians. In addition, several other cohorts were excluded from the analysis, leaving only 6 out of 15 original cohorts (Kromhout D [1], Ascherio [14], Daviglus ML [2], Albert CM [15], Hu FB [14], Mozaffarian D [24]), and one subcohort (Oomen CM [2]), including a total of 1,927 cases.
    The authors of this review found that one servings of fish/week significantly decreased risk of CHD death (- 17%) relative to no consumption, and that each additional serving per week decreased risk incrementally by 3.9%.
  • Mozaffarian D. 2006: Examined the relation with CHD mortality. Both randomized trials and cohort studies were included. 14 cohorts examining fish intake were included And 14 cohorts were not identified/discussed (Vollset SE [3], Rodriguez BL [4], Norell SE [5], Hirayama T [10], Järvinen R [13], Salonen JT [16], Gillum RF [17], Pietinen P [18], Whiteman D [21], Nagata C [23], Erkkilä AT [28], Chang-Claude J [30], Ness AR [31], Nakamura Y [32]).
    The authors of this review found a significant protective effect from consumption of 1-2 servings fish/week (- 36%). Within the 14 cohorts included by the authors, a significant protective effect was found in 9 (sub)cohorts. But for "The Health Professionals Follow-up Study" [14] the authors chose to include a more recent publication in which a significant protective effect was found (Mozaffarian D. 2005; 218 cases), while an older publication about this cohort including more cases found absolutely no effect (Ascherio A. 1995; 264 cases). Also, for one of the randomized trials included [9], the authors chose to include data from an older publication in which a strong protective effect was found after 2 years of follow-up (Burr ML. 1989; 194 cases), while a more recent publication showed that no effect was found after > 10 years of follow-up (Ness AR. 2002; 738 cases).
    Noticeable is the fact that within the 14 cohorts excluded by the authors, significant protective effects were found in only 2 (sub)cohorts, and that significantly increased risks were found in 2 other cohorts.


|Additional references:
Egeland GM. Cod liver oil consumption, smoking, and coronary heart disease mortality: three counties, Norway. Int J Circumpolar Health. 2001 Apr;60(2):143-9. Abstract
He K. Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies. Circulation. 2004 Jun 8;109(22):2705-11. Full text
König A. A quantitative analysis of fish consumption and coronary heart disease mortality. Am J Prev Med. 2005 Nov;29(4):335-46. Abstract
Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA. 2006 Oct 18;296(15):1885-99. Full text.
Wang C. Effects of omega-3 fatty acids on cardiovascular disease. Evid Rep Technol Assess (Summ). 2004 Mar;(94):1-8. Full text |



Coronary heart disease risk: Data about total fish consumption was provided by 37 cohorts, including 23,801 cases.
Significant protective effects were found in 4 cohorts (Daviglus ML [2], Dolecek TA [11], Kromhout D [12], Bernstein AM [14]), 3 of which were of (very) small size (2, 11, 12).
Significant protective effects were also found in 6 subcohorts: IHD among women only, and hypertensive heart disease among men only (Hirayama T [10]), women only (Järvinen R [13]), MI only (Yuan JM [19]), IHD death only (Mozaffarian D [24], de Goede J [34]), or "referents" only (Tomasallo C [45]). Four of these cohorts were of (very) small size also (13, 19, 24, 45). These analysis' included 6,393 cases (27% of all cases).
A significantly increased risk was found in one vegetarian cohort of very small size, including 60 cases (Chang-Claude J [30]).
The average RR could be calculated from 31 cohorts: RR = 0.88. Excluding the debatable results from Hirayama T [10], did not change the effect size.
Intermediate levels of consumption: Protective effects were stronger among higher levels of consumption (RR's are 0.95, 0.95, 0.89, and 0.90 for intakes < 1, 1, 2, and ≥ 3 servings/week, respectively). A more detailed analysis can be found here.
Effect modification: A detailed analysis can be found here. Briefly, stratified analysis showed the following effects:

  • Protective effects were somewhat stronger among women (RR = 0.84) than among men (RR = 0.90).
  • Protective effects were stronger among US (RR = 0.86) and Asian (RR = 0.85) cohorts, than among European (RR = 0.95) cohorts.
  • No (consistent) effect modification was found by other factors.

Coronary heart disease mortality: Data about total fish consumption was provided by 33 cohorts, including 15,347 cases.
Significant protective effects were found in 6 cohorts (Daviglus ML [2], Dolecek TA [11], Kromhout D [12], Hu FB [14], Mozaffarian D [24], de Goede J [34]), 4 of which were of (very) small size (2, 11, 12, 24).
Significant protective effects were also found in 4 subcohorts: IHD among women only, and hypertensive heart disease among men only (Hirayama T [10]), women only (Järvinen R [13]), MI only (Yuan JM [19]), or "referents" only (Tomasallo C [45]). Three of these cohorts were of (very) small size also (13, 19, 45). These analysis' included 3,715 cases (24% of all cases).
A significantly increased risk was found in one vegetarian cohort of very small size, including 60 cases (Chang-Claude J [30]).
Protective effects were stronger for higher levels of consumption (1.00, 0.93, 0.90, and 0.90 for < 1, 1, 2, and ≥ 3 servings/wk, respectively). The average RR could be calculated from 29 cohorts: RR = 0.88. Excluding the debatable results from Hirayama T [10], did not change the effect size.

Subjects with prevalent diabetes: In one cohort, a significant protective effect was found among normoglycemic subjects (MR = 0.29), but not among glucose intolerant subjects (MR = 1.1; Feskens EJ [12]). In another cohort, risk tended to increase among men with diabetes (RR = 1.9), but not among men without diabetes (RR = 1.1; Morris MC [15]). In a third cohort, the protective effect was stronger among diabetic women (RR = 0.38), than among nondiabetic (RR = 0.78; Hu FB [14]).
But no significant effects were found among diabetic subjects in 2 cohorts (Ascherio A [14], Soinio M [16]. And no effect modification by prevalent diabetes was found in 2 other cohorts (Mozaffarian D [24], Folsom AR [29]).
Subjects with prevalent heart disease: One cohort included subjects with CAD only (Erkkilä AT [28]), and another cohort included subjects with suspected CAD only (Manger MS [46]). No associations were found with CHD risk or CHD mortality at any level of consumption.

Nonfatal MI: Data about total fish consumption was provided by 7 cohorts, including 2,787 cases.
Significant protective effects were found in 2 cohorts of moderate-large size (Hu FB [14], Iso H [33]), including 1,225 cases (44% of all cases). And a nonsignificant protective effect was found in a third cohort, which was of very small size (Mozaffarian D [24]). No (non)significantly increased risks were found. The average RR = 0.79.
Intermediate levels of consumption: Protective effects were stronger among higher levels of consumption (RR's are 0.88, 0.87, 0.80, and 0.78 for intakes < 1, 1, 2, and ≥ 3 servings/week). A more detailed analysis can be found here.
No (non)significantly increased risks were found at any level of consumption in any cohort. (non)significant protective effects were as follows:

  • 14) Ascherio A (1995). Nonsignificant at 1-3 servings/month, and significant at 2-3 servings/wk.
  • 14) Hu FB (2002). Nonsignificant at intake 1-3 times/month, and significant at intake 1-4 times/wk.
  • 24) Mozaffarian D (2003). The trend showed a nonsignificant protective effect, but no associations were found at any level of intake.
  • 33) Iso H (2006). Significant at 12 servings/wk.

Overlapping effects were found at intake 2-3 servings/wk in 2 cohorts of moderate-large size (Ascherio A [14], Hu FB [14]). These cohorts included 1,583 cases (57% of all cases).

Heart failure: Data about total fish consumption was provided by 6 cohorts, including 4,319 cases. A significant protective effect was found in one cohort of very small size, but with a very high prevalence of heart failure (> 20% of the population). No other significant associations were found, but all RR's were < 1. The average RR = 0.86.

Conclusion: High total fish consumption significantly decreased CHD risk in 10 out of 37 cohorts. But most cohorts were of small size, and protective effects were often restricted to subcohorts. Inconclusive evidence was found for an association between high vs low consumption of total fish and CHD risk, but the average effect size (- 12%) does not exclude the possibility of a small protective effect. Stratified analysis shows any small protective effect might be restricted to US and Asian populations.
High total fish consumption significantly decreased CHD mortality in 10 out of 33 cohorts. But most cohorts were of small size, and protective effects were sometimes restricted to subcohorts. Inconclusive evidence was found for an association between high vs low consumption of total fish and CHD mortality, but the average effect size (- 12%) does not exclude the possibility of a small protective effect. For both CHD risk and CHD mortality, effect sizes were stronger for higher levels of consumption, but similar for intakes of 2 and ≥ 3 servings/week.
High total fish consumption significantly decreased risk of nonfatal MI in 2 cohorts of moderate-large size, but these cohorts included only a minority of all cases. Suggestive evidence was found that high vs low consumption of total fish is protective against nonfatal MI (- 21%). Analysis of intermediate levels of consumption showed significant protective effects against nonfatal MI were found in 2 cohorts of moderate-large size at intake 2-3 servings/wk. These cohorts included the majority of all cases. Consumption of 2-3 servings fish/wk possibly protects against nonfatal MI (- 20 to 22%).
High total fish consumption significantly decreased risk of heart failure in 1 out of 6 cohorts. Inconclusive evidence was found for an association between high vs low consumption of total fish and risk of heart failure, but the average effect size (- 14%) does not exclude the possibility of a small protective effect.



Prospective studies of total fish and coronary heart disease risk:
AuthorCohort nameCasesEnd pointRelative Risk (RR)
46) Manger MS (2010)The WENBIT Study210RiskHR = 0.93 (0.63-1.40; P = 0.72)
45) Tomasallo C (2010)No cohort name defined34 captains, and

26 referents
MortalityCaptains: HR = 1.81 (0.53-6.16).

Referents: HR = 0.31 (0.10-0.96; P = < 0.05).
44) Holmberg S (2009)No cohort name defined138RiskOR = 1.00 (0.49-2.06)
38) Kaushik S (2008)The Blue Mountains Eye Study184MortalityHR = 0.91 (0.64-1.28)
36) Yamagishi K (2008)The JACC Study419 IHD,

107 cardiac arrest, and

307 heart failure
MortalityIHD: HR = 0.86 (0.62-1.19; P = 0.41).

Cardiac arrest: HR = 0.73 (0.36-1.46; P = 0.16).

Heart failure: HR = 0.76 (0.53-1.07; P = 0.10).
34) de Goede J (2010)The Dutch part of the EPIC Study82 CHD mortality, and

252 nonfatal MI
RiskCHD mortality: HR = 0.52 (0.28-0.95; P = 0.02).

Nonfatal MI: HR = 1.01 (0.71-1.45; P = 0.14).
34) Bjerregaard LJ (2010)The Danish part of the EPIC Study854 men, and

268 women
RiskMen: HR = 0.87 (0.69-1.10).

Women: HR = 0.85 (0.55-1.32).
34) Buckland G (2009)The Spanish part of the EPIC Study606RiskHR = 0.83 (0.68-1.02; P = 0.82)
33) Iso H (2006)The JPHC Study258RiskHR = 0.63 (0.38-1.04; P = 0.25)
32) Nakamura Y (2005)The NIPPON DATA80124MortalityRR = 0.86 (0.33-2.23; P = 0.51) for the highest vs second quintile of consumption (RR reference group = 1.45).
31) Ness AR (2005)The Boyd Orr Cohort298MortalityRR = 1.18 (0.80-1.76; P = 0.6)
30) Chang-Claude J (2005)The German Vegetarian Study60MortalityRR = 2.11 (1.13-3.96; P = 0.03)
29) Folsom AR (2004)The Iowa Women's Health Study922MortalityRR = 1.04 (0.80-1.34; P = 0.31)
28) Erkkilä AT (2003)The EUROASPIRE Study34RiskRR = 0.49 (0.17-1.41; P = 0.21)
26) Osler M (2003)No cohort name defined491RiskHR = 0.93 (0.68-1.27; P = 0.55) for the highest vs third quartile of consumption
(RR reference group = 1.02)
24) Mozaffarian D (2003)The Cardiovascular Health Study247 IHD death, and

363 nonfatal MI
RiskIHD death: HR = 0.47 (0.27-0.82; P = 0.002).

Nonfatal MI: HR = 0.67 (0.42-1.07; P = 0.10).
23) Nagata C (2002)The Takayama Study63 men, and

52 women
MortalityMen: HR = 1.05 (0.56-1.97; P = 0.91).

Women: HR = 0.73 (0.37-145; P = 0.37).
22) Wennberg M (2011)The NSHDS263RiskOR = 1.21 (0.43-3.33; P = 0.52)
21) Whiteman D (1999)The OXCHECK Study93MortalityRR = 1.36 (0.57-3.25)
20) Mann JI (1997)The Oxford Vegetarian Study64MortalityDRR = 123 (70-217; P = NS)
19) Yuan JM (2001)The Shanghai Cohort Study113 MI, and

74 other IHD
MortalityMI: RR = 0.35 (0.17-0.72; P = 0.02).

Other IHD: RR = 0.92 (0.41-2.06; P = 0.34).
18) Pietinen P (1997)The ATBC Study635MortalityRR = 1.12 (0.87-1.45; P = 0.09)
17) Gillum RF (2000)The NHANES I StudyNot defined
(2,007 total)
RiskWhite men: RR = 0.86 (0.65-1.13).

Black men: RR = 1.05 (0.50-2.19).

White women: RR = 0.97 (0.74-1.28).

Black women: RR = 0.90 (0.51-1.60).
16) Soinio M (2003)No cohort name defined117RiskNo significant association
15) Albert CM (1998)The Physician's Health Study737RiskRR = 1.00 (0.62-1.60; P = 0.67)
14) Bernstein AM (2010)The Nurses' Health Study3,162RiskRR = 0.81 (0.72-0.90; P = < 0.001)
14) Ascherio A (1995)The Health Professionals Follow-up Study811RiskRR = 0.90 (0.63-1.28; P = 0.70)
13) Järvinen R (2006)The Finnish Mobile Clinic Health Survey335 men, and

163 women
MortalityMen: RR = 1.00 (0.70-1.43; P = 0.83).

Women: RR = 0.59 (0.36-0.99; P = 0.02).
12) Kromhout D (1995)No cohort name defined58MortalityRR = 0.51 (0.29-0.89)
11) Dolecek TA (1992)The Multiple Risk Factor Intervention Trial175MortalityRR = 0.61 (P = < 0.05)
10) Hirayama T (1990)No cohort name definedIHD: 2,170 men, and 1,378 women.

Hypertensive heart disease: 559 men, and 613 women.

Rheumatic heart disease: 364.

Other heart disease: not defined
MortalityIHD: RR's for low vs high consumption are 1.20 (0.76-1.90) for men, and 1.49 (1.02-2.19) for women.

Hypertensive heart disease: RR's for low vs high consumption are 2.14 (1.07-4.27) for men, and 0.52 (0.20-1.31) for women.

Rheumatic heart disease: RR = 0.95 (0.79-1.14).

Other heart disease: RR's for low vs high consumption are 1.02 (0.60-1.75) for men, and 1.36 (0.97-1.92) for women.
8) Fraser GE (1992)The Adventist Health Study134 nonfatal MI, and

463 CHD death
RiskNonfatal MI: RR = 1.04 (0.55-1.96).

CHD death: RR = 1.09 (0.73-1.61).
7) Tanaka H (1987)The Shibata Studynot definedRiskRR = 1.23
6) Lapidus L (1986)No cohort name defined23RiskNo significant association
5) Norell SE (1986)The Cohort of Swedish Twins800MortalityRR = 0.85 (0.69-1.06)
4) Rodriguez BL (1996)The Honolulu Heart Programnot definedRiskNo significant association
3) Vollset SE (1985)No cohort name defined967MortalityNo significant association (P = 0.93)
2) Daviglus ML (1997)The Western Electric Study430MortalityRR = 0.62 (0.40-0.94; P = 0.04)
1) Streppel MT (2008)The Dutch part of the Seven Countries Study336MortalityHR = 0.73 (0.47-1.13; P = 0.16)
1) Oomen CM (2000)The Finnish & Italian part of the Seven Countries Study242 Finland, and

116 Italy
MortalityFinland: RR = 1.25 (0.89-1.76; P = 0.20).

Italy: RR = 0.67 (0.33-1.39; P = 0.33).
Total number of cases: 23,801Average RR = 0.88
Excluding data from Hirayama T [10].Total number of cases: 18,717Average RR = 0.88


Prospective studies of total fish and coronary heart disease mortality:
AuthorCohort nameCasesEnd pointRelative Risk (RR)
46) Manger MS (2010)The WENBIT Study76CHDHR = 1.03 (0.54-1.94; P = 0.94)
45) Tomasallo C (2010)No cohort name defined34 captains, and

26 referents
CHDCaptains: HR = 1.81 (0.53-6.16).

Referents: HR = 0.31 (0.10-0.96; P = < 0.05)
38) Kaushik S (2008)The Blue Mountains Eye Study184CHDHR = 0.91 (0.64-1.28)
36) Yamagishi K (2008)The JACC Study419 IHD,

107 cardiac arrest, and

307 heart failure
IHD,

cardiac arrest, and

heart failure
IHD: HR = 0.86 (0.62-1.19; P = 0.41).

Cardiac arrest: HR = 0.73 (0.36-1.46; P = 0.16).

Heart failure: HR = 0.76 (0.53-1.07; P = 0.10).
34) de Goede J (2010)The Dutch part of the EPIC Study82CHDHR = 0.52 (0.28-0.95; P = 0.02)
33) Iso H (2006)The JPHC Study62CHDHR = 1.08 (0.42-2.76; P = 0.31)
32) Nakamura Y (2005)The NIPPON DATA80124CHDRR = 0.86 (0.33-2.23; P = 0.51) for the highest vs second quintile of consumption (RR reference group = 1.45)
31) Ness AR (2005)The Boyd Orr Cohort298CHDRR = 1.18 (0.80-1.76; P = 0.6)
30) Chang-Claude J (2005)The German Vegetarian Study60IHDRR = 2.11 (1.13-3.96; P = 0.03)
29) Folsom AR (2004)The Iowa Women's Health Study922CHDRR = 1.04 (0.80-1.34; P = 0.31)
28) Erkkilä AT (2003)The EUROASPIRE Study16CADRR = 1.04 (0.25-4.31; P = 0.73)
26) Osler M (2003)No cohort name defined247CHDHR = 0.98 (0.62-1.52; P = 0.74) for the highest vs third quartile of consumption
(RR reference group = 1.09).
24) Mozaffarian D (2003)The Cardiovascular Health Study247IHDHR = 0.47 (0.27-0.82; P = 0.002)
23) Nagata C (2002)The Takayama Study63 men, and

52 women
IHDMen: HR = 1.05 (0.56-1.97; P = 0.91).

Women: HR = 0.73 (0.37-145; P = 0.37).
21) Whiteman D (1999)The OXCHECK Study93IHDRR = 1.36 (0.57-3.25)
20) Mann JI (1997)The Oxford Vegetarian Study64IHDDRR = 123 (70-217; P = NS)
19) Yuan JM (2001)The Shanghai Cohort Study113 MI, and

74 other IHD
MI, and

other IHD
MI: RR = 0.35 (0.17-0.72; P = 0.02).

Other IHD: RR = 0.92 (0.41-2.06; P = 0.34).
18) Pietinen P (1997)The ATBC Study635CHDRR = 1.12 (0.87-1.45; P = 0.09)
17) Gillum RF (2000)The NHANES I Study752CHDNo significant association
16) Soinio M (2003)No cohort name defined65CHDNo significant association
15) Albert CM (1998)The Physician's Health Study308CHDRR = 0.81 (0.41-1.61; P = 0.49)
14) Hu FB (2002)The Nurses' Health Study484CHDRR = 0.55 (0.33-0.90; P = 0.01)
14) Ascherio A (1995)The Health Professionals Follow-up Study264CHDRR = 0.77 (0.41-1.44; P = 0.14)
13) Järvinen R (2006)The Finnish Mobile Clinic Health Survey335 men, and

163 women
CHDMen: RR = 1.00 (0.70-1.43; P = 0.83).

Women: RR = 0.59 (0.36-0.99; P = 0.02).
12) Kromhout D (1995)No cohort name defined58CHDRR = 0.51 (0.29-0.89)
11) Dolecek TA (1992)The Multiple Risk Factor Intervention Trial175CHDRR = 0.61 (P = < 0.05)
10) Hirayama T (1990)No cohort name definedIHD: 2,170 men, and 1,378 women.

Hypertensive heart disease: 559 men, and 613 women.

Rheumatic heart disease: 364.

Other heart disease: not defined
IHD,

hypertensive heart disease,

rheumatic heart disease, and

other heart disease
IHD: RR's for low vs high consumption are 1.20 (0.76-1.90) for men, and 1.49 (1.02-2.19) for women.

Hypertensive heart disease: RR's for low vs high consumption are 2.14 (1.07-4.27) for men, and 0.52 (0.20-1.31) for women.

Rheumatic heart disease: RR = 0.95 (0.79-1.14).

Other heart disease: RR's for low vs high consumption are 1.02 (0.60-1.75) for men, and 1.36 (0.97-1.92) for women.
8) Fraser GE (1992)The Adventist Health Study463CHDRR = 1.09 (0.73-1.61)
5) Norell SE (1986)The Cohort of Swedish Twins800CHDRR = 0.85 (0.69-1.06)
4) Rodriguez BL (1996)The Honolulu Heart Programnot definedCHDlowest 2 tertiles of smoking: no significant association.

highest tertile of smoking: RR = 0.50 (0.28-0.91).
3) Vollset SE (1985)No cohort name defined967CHDNo significant association (P = 0.93)
2) Daviglus ML (1997)The Western Electric Study430CHDRR = 0.62 (0.40-0.94; P = 0.04)
1) Streppel MT (2008)The Dutch part of the Seven Countries Study336CHDHR = 0.73 (0.47-1.13; P = 0.16)
1) Oomen CM (2000)The Finnish & Italian part of the Seven Countries Study242 Finland, and

116 Italy
CHDFinland: RR = 1.25 (0.89-1.76; P = 0.20).

Italy: RR = 0.67 (0.33-1.39; P = 0.33).
Total number of cases: 15,347Average RR = 0.88
Excluding data from Hirayama T [10].Total number of cases: 10,263Average RR = 0.88


Prospective studies of total fish and nonfatal coronary heart disease:
AuthorCohort nameCasesEnd pointRelative Risk (RR)
34) de Goede J (2010)The Dutch part of the EPIC Study252Nonfatal MIHR = 1.01 (0.71-145; P= 0.14)
33) Iso H (2006)The JPHC Study196Nonfatal CHDHR = 0.43 (0.23-0.81; P = 0.02)
24) Mozaffarian D (2003)The Cardiovascular Health Study363Nonfatal MIHR = 0.67 (0.42-1.07; P = 0.10)
15) Morris MC (1995)The Physician's Health Study259Nonfatal MIRR = 0.8 (0.4-1.7; P = 0.79)
14) Hu FB (2002)The Nurses' Health Study1,029Nonfatal MIRR = 0.73 (0.51-1.04; P = 0.03)
14) Ascherio A (1995)The Health Professionals Follow-up Study554Nonfatal MIRR = 0.96 (0.63-1.47; P = 0.62)
8) Fraser GE (1992)The Adventist Health Study134Nonfatal MIRR = 1.04 (0.55-1.96)
Total number of cases: 2,787Average RR = 0.79


Prospective studies of total fish and heart failure:
AuthorCohort nameCasesEnd pointRelative Risk (RR)
43) Dijkstra CS (2009)The Rotterdam Study669RiskRR = 0.96 (0.78-1.18; P = 0.39)
42) Levitan EB (2010)The Swedish Mammography Cohort651RiskRR = 0.81 (0.63-1.05)
42) Levitan EB (2009)The Cohort of Swedish Men597RiskHR = 0.89 (0.60-1.33)
39) Nettleton JA (2008)The ARIC Study1,140RiskRR = 0.99 (0.81-1.22)
36) Yamagishi K (2008)The JACC Study307MortalityHR = 0.76 (0.53-1.07; P = 0.10).
24) Mozaffarian D (2005)The Cardiovascular Health Study955RiskHR = 0.68 (0.45-1.03; P = 0.009)
Total number of cases: 4,319Average RR = 0.86