Reports used to determine a healthy intake of a-linolenic acid:

1. Adult intakes of ALA of Australians of 1.17 g/day, median intake 0.95 g/day from Meyer et al (2003), national food intake survey of 10,851 adults, used fatty acid data base developed in Australia (no health statistics collected).  Where data was available, the ALA intakes as % energy was 0.46 to 0.50.
2. Adult intakes France. Astorg et al (2004) have reported the ALA intake in 2099 men and 2785 women collected from ten 24-hr diet records over a 30-month period in the years from 1994 to 1998.  The ALA intakes as a % energy were 0.36 (0.2-1.11) for men [mean (minimum-maximum)] and 0.38 (0.18-1.04) for women.
3. Adult intakes in Japan, referred to by Dolecek (see below): 1946 intake 0.67 g/day up to 2.08 g/day in 1985 (source Dr H Okuyama, probably based on National disappearance data).
4. Prospective Cohort studies examined the effect of the intake of dietary fat and w3 PUFA from plants on coronary heart disease in humans.  In the first study, 43 757 healthy male professionals aged 40 to 75 years free of diagnosed cardiovascular disease or diabetes were followed-up for six years from 1986 (Ascherio et al 1996). Each subject completed a food frequency questionnaire at the beginning of the study. The subjects returned food frequency questionnaires in each two-year follow-up cycle. During the follow-up 505 non-fatal myocardial infarctions and 229 deaths were documented. After adjustment for non-dietary risk factors and total fat intake, intake of ALA was significantly negatively correlated with risk of myocardial infarction (relative risk 0.41 for a 1% increase in energy from ALA, P < 0.01). The median ALA intake range (quintiles) was from 0.8 to 1.5 g/day (no total caloric intake).
5. In the second study, the dietary intake of ALA was calculated from a food frequency questionnaire completed in 1984 by 76,283 nurses aged 38-63 years, free from previously diagnosed cardiovascular disease and cancer. There were 597 cases of nonfatal myocardial infarction and 232 cases of fatal ischemic heart disease documented during 10 years of follow-up. After the adjustment of confounding factors, such as age, standard coronary risk factors, dietary intake of LA and other nutrients, the results showed that women who had a higher intake of ALA (≥ 5-6 times per week) were significantly associated with reduced risk of fatal ischemic heart disease compared with women who consumed ALA less than once per month in this study population (P < 0.001) (Hu et al 1999).  The major foods contributing to ALA in this study were mayonnaise or other creamy salad dressings and oil and vinegar salad dressings. The mean ALA intake range (quintiles) was from 0.71 to 1.36 g/day (0.32-0.61% en, based on 2000kcal diet).
6. In the third study, 667 men aged 64-84 yr from the Zutphen Elderly Study who were free of CAD at baseline were followed up for 10 years.  After adjustment for age, standard CHD risk factors, the intake of trans fatty acids and other nutrients, it was found that dietary ALA as assessed by cross-check diet history was not significantly associated  with CAD risk (Oomen et al 2001). The tertiles of ALA intake ranged from <0.45% en to >0.58% en. The authors noted that this study was complicated by the positive association between dietary ALA and trans fatty acids.
7. The final study, The Multiple Risk Factor Intervention Trial (MRFIT), was a study of 12,866 men who were randomly assigned to either usual care or special intervention group who received advice and programs regarding reduction in smoking, blood pressure and blood cholesterol.  Multivariate regression analysis was used to determine the effect of dietary PUFA intakes on 10-year mortality rates in 6250 usual care men (Dolecek 1992). Dietary PUFA intake was calculated from 4 dietary 24-hr recall interviews at baseline and at 1-, 2-, and 3-year follow-up. Dietary intake of the ALA was significantly negatively associated with CHD mortality rates (P<0.04), total CVD (P<0.03) and all-cause mortality (P<0.02). The mean ALA intakes (quintiles) were from 0.873 to 2.802 g/day (0.424 to 0.980% energy)
8. Cross sectional studies; The Family Heart Study, a cross-sectional study from USA National Heart, Lung, and Blood Institute, found that higher intakes of either ALA or LA were inversely related to the prevalence of coronary artery disease (CAD) (Djousse et al 2001). Dietary intakes of 4584 volunteers were assessed with a semi-quantitative food-frequency questionnaire. After adjustment for confounding factors such as age, LA, and anthropometric, lifestyle and metabolic factors, the prevalence odds ratios of CAD from the lowest to the highest quintile of ALA intake were 1.0, 0.77, 0.61, 0.58, and 0.60 for the men (P = 0.012) and 1.0, 0.57, 0.52, 0.30, and 0.42 for the women (P = 0.014). LA was also inversely related to the prevalence odds ratios of CAD in the multivariate model (0.60 and 0.61 in the second and third quintiles, respectively) after adjustment for ALA.  It was noted that the combined effects of LA and ALA were stronger than either of the fatty acids individually.  The mean ALA intakes (quintiles) were from 0.53 to 1.14 g/day for males and 0.46 to 0.96 g/day for females (0.2 – 0.5%en, based on 2000kcal diet).
9.  A second cross sectional study was the MARGARIN prevention project of CHD. Baseline data from this project was investigated for the association between dietary intake of ALA and LA, assessed by food frequency questionnaire and plasma cholesterol ester (CE), with CHD risk factors. The study involved 266 subjects with hypercholesterolemia (6.0-8.0 mmol/L) and at least two other CHD risk factors (Bemelmans et al 2000). In multivariate analysis, CE ALA was inversely associated with diastolic blood pressure (r = -0.13; P<0.05) and positively with serum TAG levels (P<0.01), while the CE LA was inversely associated with serum TAG (P<0.01). In the lowest quintile of CE ALA, mean dietary intake was 0.4% energy of ALA (1.2 g/day), 8.4% energy of LA and an LA/ALA ratio of 21, and in the highest quintile 0.6% energy of ALA (1.7 g/day), 6.8% energy of LA and an LA/ALA ratio of 12.  In the highest quintile of CE ALA, the diastolic BP was 4 mm Hg lower and the serum TAG 0.3 mmol/L higher compared with the top quintile, suggesting that replacing LA with ALA might decrease diastolic blood pressure. Note that this study did not have CHD as an outcome.  
10. A case-control study in Costa Rica examined the association between adipose tissue ALA levels and non-fatal acute myocardial infarction (Baylin et al 2003). The study matched 482 case patients (first non-fatal acute myocardial infarction) with 482 control subjects. It was found that subjects in the top quintiles of adipose tissue ALA had significantly lower risk of MI than those in the lowest quintile (P<0.001). The association was strengthened after adjustment for established MI risk factors and for other dietary variables.
11. A primary prevention study conducted in Norway (Natvig et al 1968), where men were randomised to receive either 10 mL of sunflower oil (n=6690) or 10 mL linseed oil (n=6716) for a year. In effect, this meant that the ALA intake from the two treatments were 0.14 g/day and 5.5 g/day over-and-above the ALA of the background diet. Deaths from all causes were fewer than expected in both groups, based on a comparison with population mortality data. Deaths from CHD were intermediate between expected numbers compared with mortality in Oslo and in Norway. There was no difference between the two diet groups in terms of all causes and CHD mortality.  This data do not support a benefit for increased ALA intake of approx. 5.5 g/day over that provided by the linoleic acid in the sunflower oil (6.3 g/day).  The combined PUFA levels in the two treatments were 7.6 g/day and 7.0 g/day, respectively, for the sunflower and linseed oil groups.
12. Secondary Prevention studies: The Lyon diet-heart study concluded that ALA prevented secondary CHD ( de Logeril et al 1994). In this study the diet chosen was associated with a low mortality rate from CHD and all causes in the Seven-Countries Study (Keys 1980). The Cretan diet had a high intake of ALA and was rich in anti-oxidants since it was rich in fruits and vegetables. Crete had a lower mortality rate from CHD compared with similar cohorts in other countries. Cretan participants had 3-fold higher serum concentrations of ALA compared with a similar cohort from the Netherlands (Sandker et al 1993). In the Lyon study, 605 patients who had suffered a first myocardial infarction were randomly divided into two groups, the experimental (n=302) and control (n=303). Patients in experimental group received a Mediterranean style diet (rapeseed oil and rapeseed oil based margarine) which was rich in ALA (ALA: LA ratio of 1: 4), total fat provided 30.5% of energy with S: M: P ratio of 0.9: 1.4: 1. The control group consumed a habitual diet which was poor in ALA (ALA: LA was 1: 20) and total fat contributed 32.7% of energy with S: M: P ratio of 1.2: 1: 1. After 27 months of follow up, there were 16 cardiac deaths in the control and 3 in the experimental groups, 17 non-fatal myocardial infarction in control and 5 in the experimental groups and the relative risk ratio for cardiac deaths and non-fatal myocardial infarction in ALA rich group was 0.27 (P=0.001). This study was continued after the original conclusion because there was a high adherence of the experimental group to the program over the total 46 months of mean follow-up for each patient (de Lorgeril et al 1999). It was found that three composite outcomes (cardiac death and non-fatal myocardial infarction; the preceding plus major secondary endpoints including unstable angina, stroke, heart failure, pulmonary or peripheral embolism; or the preceding plus minor events requiring hospital admission) were significantly reduced in the Mediterranean diet group compared with the Western diet group. The traditional risk factors such as high blood cholesterol and raised blood pressure were significantly and independently associated with recurrence of events. Plasma ALA, measured at 2 months after randomization, was the only fatty acid which was significantly negatively associated with myocardial infarction plus cardiac death after adjustment for age sex, smoking, total cholesterol, blood pressure, leukocyte count and aspirin use. The control diet had an ALA intake of 0.64 g/day (0.27% en) and the experimental diet had an ALA intake of 1.74 g/day (0.81% en). A cautionary note on this study is that the dietary change did not involve just changing the ALA intake, therefore the data need to interpreted carefully in terms of the relevance to determining ALA requirements.
13. Another secondary prevention study of CHD which involved dietary interventions was that by Singh et al (1997). In this study, 360 patients less than 1 day after acute myocardial infarction (AMI) were randomized to 1 of 3 dietary groups: fish oil capsules (EPA, 1.08 g/d, and DHA, 0.72 g/d), mustard seed oil, 20 g/d (ALA, 2.9 g/d), and a control group (aluminum hydroxide, 100 mg/d). After 1 year, this study showed that there was a significant reduction in cardiac events in the fish oil and mustard oil groups compared with the control group (24.5% and 28.2%, respectively, vs. 34.7%; P<0.01). Non-fatal infarctions were also significantly lower in the fish oil and mustard oil groups compared with placebo (13.0% and 15.0% vs. 25.4%, P<0.05). Total cardiac deaths were significantly reduced in the fish oil group but not in the mustard oil group compared with placebo. The fish oil and mustard oil groups also showed significant reductions in total cardiac arrhythmias, left ventricular enlargement and angina pectoris compared with the placebo group. The ALA intake of the placebo group was not reported. The data need to be interpreted cautiously since the background diet was non-western.
14. Intakes in infants from Mitoulas et al (2003), who monitored daily breast milk FA content over 12 months (LA 2.38 and ALA 0.194 g/day).