Alpha-Linolenic acid versus sudden cardiac death

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Hi All,

Take your flaxseed or flaxseed oil. " [alpha]-Linolenic acid (ALA) is an

intermediate-chain n-3 fatty acid found in high concentrations in flaxseed,

soybean,

and canola oils and other foods of plant origin. After ingestion, ALA is partly

converted (~4% to 8%) into the long-chain n-3 fatty acids found in fish. "

See the pdf-available not in Medline yet paper excerpts and title, for a paper

describing how much taking ALA may protect us from sudden cardiac death (SCD).

For me, the most interesting results were the not numbered figure data on the

SCD

for the correlations between quintiles of ALA for high versus low long-chain n-3

fatty acid intake. " Compared with those with the lowest intakes, the relative

hazard for SCD was 0.41 (95% CI, 0.21 to 0.79, P=0.008) among those in the

highest

quintile of ALA intake who were also above the median for EPA+DHA intake. We

found

no evidence for an interaction between ALA intake and aspirin use, n-6 fatty

acid

intake, or age (<60 versus 60+ years). " Relative to the risk of those with the

lowest intake of ALA and long-chain n-3 fatty acids, the risks were 0.75 for

those

subjects with the lowest intakes of ALA and the highest intake of long-chain

fatty

acids. Relative to the risk of those with the lowest intake of ALA and

long-chain

n-3 fatty acids, the risks were 0.54 for those subjects with the highest intakes

of

ALA and the lowest intake of long-chain fatty acids.

Dietary {alpha}-Linolenic Acid Intake and Risk of Sudden Cardiac Death and

Coronary

Heart Disease

M. Albert, Kyungwon Oh, Whang, JoAnn E. Manson, U.

Chae,

Meir J. Stampfer, Walter C. Willett, and B. Hu

Circulation 2005;112 3232-3238

Abstract

Background—: [alpha]-Linolenic acid, an intermediate-chain n-3 fatty acid found

primarily in plants, may decrease the risk of fatal coronary heart disease (CHD)

through a reduction in fatal ventricular arrhythmias and sudden cardiac death

(SCD).

Methods and Results—: We prospectively examined the association between dietary

intake of [alpha]-linolenic acid assessed via updated food-frequency

questionnaires

and the risk of SCD, other fatal CHD, and nonfatal myocardial infarction (MI)

among

76 763 women participating in the Nurses’ Health Study who were free from cancer

and

completed a dietary questionnaire at baseline in 1984. During 18 years of

follow-up,

we identified 206 SCDs, 641 other CHD deaths, and 1604 nonfatal MIs. After

controlling for coronary risk factors and other fatty acids, including

long-chain

n-3 fatty acids, the intake of [alpha]-linolenic acid was inversely associated

with

the risk of SCD (P for trend, 0.02) but not with the risk of other fatal CHD or

nonfatal MI. Compared with women in the lowest quintile of [alpha]-linolenic

acid

intake, those in the highest 2 quintiles had a 38% to 40% lower SCD risk. This

inverse relation with SCD risk was linear and remained significant even among

women

with high intakes of long-chain n-3 fatty acids.

Conclusions—: These prospective data suggest that increasing dietary intake of

[alpha]-linolenic acid may reduce the risk of SCD but not other types of fatal

CHD

or nonfatal MI in women. The specificity of the association between

[alpha]-linolenic acid and SCD supports the hypothesis that these n-3 fatty

acids

may have antiarrhythmic properties.

.... cardiac deaths were considered sudden if the death or cardiac arrest that

precipitated death occurred within 1 hour of symptom onset. To increase our

specificity for “arrhythmic death,” we excluded women with evidence of

circulatory

collapse (hypotension, exacerbation of congestive heart failure, or altered

mental

status) before the disappearance of the pulse.21 Unwitnessed deaths that could

have

occurred within 1 hour of symptom onset and with autopsy findings consistent

with

SCD were considered probable SCDs (10%) and were included in the analysis.

Analyses

excluding these events revealed similar results.

Fatal CHD was defined as ICD-9 codes 410 to 412 if confirmed by hospital records

or

autopsy or if CHD was the most probable cause and was listed as the cause of

death

on the death certificate, along with evidence of prior CHD. We designated as

presumed CHD (24% of fatal cases) those cases in which CHD was the underlying

cause

on the death certificate but for which no medical records concerning the death

were

available. CHD deaths that did not also fulfill the criteria for SCD described

earlier were designated “other CHD deaths” for these analyses.

.... Table 2 and 3

===============================

Quintiles of Linolenic Fatty Acids

Median (% Energy) 1 (0.37) 2 (0.45) 3 (0.52) 4 (0.60) 5 (0.74) P for Trend

===============================

SCD

No. of cases 54 44 40 32 36

Multivariate II‡ 1.0 0.86 (0.57–1.29) 0.76 (0.50–1.16) 0.62 (0.39–0.98) 0.60

(0.37–0.96) 0.02

Other fatal CHD

No. of cases 146 144 116 112 123

Multivariate II‡ 1.0 1.13 (0.89–1.43) 0.92 (0.71–1.18) 0.96 (0.74–1.25) 1.01

(0.77–1.33) 0.74

===============================

‡Adjusted for age and for calories (continuous), smoking status (never, past,

current 1–14 cigarettes/d, 15–24 cigarettes/d, =/>25 cigarettes/d), body mass

index

(<22, 22–22.9, 23–24.9, 25–28.9, =/>29 kg/m 2 ), alcohol intake (0, <5, 5–14,

=/>15

g/d), menopausal status and postmenopausal hormone use, vigorous to moderate

activity (<2, 2–3.9, =/>4 h/wk), usual aspirin use (<1/wk, 1–6/wk, and =/>7/wk),

multivitamin use (yes vs no), vitamin E supplement use (yes vs no), history of

hypertension (yes vs no), hypercholesterolemia (yes vs no), diabetes (yes vs

no),

family history of MI (no, before age 60 y, after age 60 y), and history of prior

CVD

(yes vs no). Adjusted for factors cited above and for intakes of

trans-unsaturated

fat, ratio of polyunsaturated fat to saturated fat, and omega-3 fatty acids (all

in

quintiles).

===============================

SCD, no prior history of CVD

No. of cases 40 34 34 24 27

Multivariate† 1.0 0.89 (0.56–1.41) 0.86 (0.54–1.39) 0.60 (0.35– SCD

SCD, prior history of CVD

No. of cases 1.03) 0.59 (0.34–1.02) 0.03

Multivariate† 1.0 0.68 (0.28–1.64) 0.38 (0.14–1.06) 0.76 (0.30–1.88) 0.53

(0.19–1.45) 0.33

===============================

†Adjusted for age, calories (continuous), smoking status (never, past, current

1–14

cigarettes/d, 15–24 cigarettes/d, =/>25 cigarettes/d), body mass index (<22,

22–22.9, 23–24.9, 25–28.9, =/>29 kg/m 2 ), alcohol intake (0, <5, 5–14, =/>15

g/d),

menopausal status and postmenopausal hormone use, vigorous to moderate activity

(<2,

2–3.9, =/>4 h/wk), usual aspirin use (<1/wk, 1–6/wk, and =/>7/wk), multivitamin

use

(yes vs no), vitamin supplement use (yes vs no), history of hypertension (yes vs

no), hypercholesterolemia (yes vs no), diabetes (yes vs no) family history of MI

(no, before age 60 y, after age 60 y), intakes of trans-unsaturated fat, ratio

of

polyunsaturated fat to saturated fat, and omega-3 fatty acids (all in

quintiles).

===============================

Al Pater, PhD; email: old542000@...

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