Achieving Optimal Essential Fatty Acid Status in Vegetarians
4th International Congress of Vegetarian Nutrition
Achieving Optimal Essential Fatty Acid Status in Vegetarians:
Current Knowledge and Practical Implications
Brenda Davis, RD1 and Penny Kris-Etherton, PhD, RD2
1Private Practice Nutrition Consultant, Kelowna BC, Canada
2Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802
Abstract
While vegetarian diets are generally lower in total fat, saturated fat and cholesterol than are nonvegetarian diets, they provide comparable levels of essential fatty acids. Vegetarian, especially vegan diets, are relatively low in ALA compared with LA, and provide little, if any, EPA and DHA. Clinical studies suggest that tissue levels of long-chain omega-3 fatty acids are depressed in vegetarians, and particularly in vegans. Omega-3 fatty acids have numerous physiological benefits, including potent cardioprotective effects. These effects have been demonstrated for ALA as well as EPA and DHA, although the response is generally less for ALA than for EPA and DHA. Conversion of ALA by the body to the more active longer-chain metabolites is inefficient - approximately 5-10% for EPA and 2-5% for DHA. Thus, total omega-3 requirements may be higher for vegetarians than for nonvegetarians, as vegetarians must rely on conversion of ALA to EPA and DHA. Because of the beneficial effects of omega-3 fatty acids, it is recommended that vegetarians make dietary changes to optimize omega-3 fatty acid status.
It is widely recognized that overall morbidity and mortality are lower in vegetarians compared to omnivores.1 The dietary patterns of vegetarians as well as their healthful lifestyle practices, at least in part are thought to explain these differences. One notable difference relates to the type and amount of fat in the diet. Vegetarian diets are slightly lower in total fat than omnivorous diets (30-34% for lacto-ovo vegetarians; 28-32% for vegans, and 34-36% for omnivores).2 However, vegetarians eat about one-third less saturated fat (vegans about one half), and about one half as much cholesterol (vegans consume none) as omnivores.3-5 Intake of trans fatty acids is highly dependent on the amount of processed foods in the diet. Limited research comparing trans fatty acid intake of omnivores and vegetarians suggests that vegetarians consume slightly smaller amounts, with more pronounced differences for vegans eating whole foods diets.3 One study found that vegetarians had one third less trans fatty acids in subcutaneous adipose tissue than non-vegetarians and that vegans (eating no refined foods) had no detectable levels.6
With respect to essential fatty acid (EFA) intake and balance, vegetarian diets appear to offer no advantages over omnivorous dietary patterns. Some have suggested that vegetarians could be at a significant disadvantage, as consumption of alpha-linolenic acid (ALA – an omega-3 fatty acid) is low relative to linoleic acid (LA – an omega-6 fatty acid) - resulting in limited conversion of ALA to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In addition, vegetarians consume very little EPA and DHA.7
The purpose of this paper is to review the EFA intake and status of vegetarians, compare the biological effects of ALA and its long-chain metabolites, EPA and DHA, and explore the practical implications of this knowledge as it relates to optimal EFA status in this population. In addition, the scientific justification for assuring an adequate EFA status with respect to cardiovascular disease will be reviewed.
Essential Fatty Acid Conversion
There are two essential fatty acids, both polyunsaturated fats – linoleic acid (the parent omega-6 fatty acid) and alpha-linolenic acid (the parent omega-3 fatty acid). Humans have the ability to convert LA and ALA to more physiologically active fatty acids through a series of elongation and desaturation reactions (LA to arachidonic acid (AA) and alpha-linolenic acid to EPA and DHA). The resulting highly unsaturated fatty acids (HUFAs) are necessary for cell membrane function, the proper development and functioning of the brain and nervous system, and for the production of eicosanoids (thromboxanes, leucotrienes, prostaglandins and prostacyclins). While conversion of LA to AA is typically very efficient, conversion of ALA to EPA and DHA is much less. In healthy individuals, about 5-10% of alpha-linolenic acid is converted to EPA, but only about 2-5% to DHA.8, 9, 10 The long chain members of the omega-6 and omega-3 families generally are not considered essential because we have the capacity to make them from “parent” fatty acids. Omega-6 and omega-3 fatty acids compete for enzymes responsible for their conversion; since they are not interchangeable we must consume both. This takes on special importance in people with diabetes or other metabolic disorders where conversion enzymes may be compromised as well as in those who have inherited a limited ability to produce these enzymes.11
Recommended EFA Intakes
While the US has not yet established Dietary Reference Intakes (DRIs) for essential fatty acids, the National Research Council recommends that 7% of total energy come from polyunsaturated fats.12 In 1999, NIH (National Institutes of Health) sponsored an international workshop on the essentiality and recommended dietary intakes of omega-6 and omega-3 fatty acids. The NIH Working Group proposed Adequate Intakes (AI) of 2-3% of total calories for linoleic acid, 1% of total calories for alpha-linolenic acid and 0.3% of total calories for EPA and DHA. The Working Group further recommended intakes of EPA and DHA of at least 650 mg/day and a minimum of 300 mg of DHA/day during pregnancy and lactation.13 Health Canada suggests a minimum of 3% of energy from omega-6 fatty acids and 0.5% from omega-3 fatty acids or 1% for infants who do not receive a preformed source of EPA and DHA. 14 The United Kingdomrecommends that1% of energy be from ALA and 0.5% from EPA and DHA combined15. While there are no official recommendations for vegetarians and vegans, it is not possible for this population to achieve the NIH Working Group’s proposed AI’s for EPA and DHA. Even with the use of DHA-enriched eggs, some seaweed and/or DHA supplements, the best vegetarians could do is to meet the recommended intakes for DHA. Some experts suggest that vegetarians (and others receiving no direct sources of EPA and DHA) at least double the recommended intakes for ALA16. This would suggest an intake of ALA in the range of 1-2%.
The ratio of omega-6 to omega-3 fatty acids is often used to assess the balance between EFA in the diet, although there is some controversy as to its practical significance. For vegetarians, and others who consume little, if any, EPA and DHA, the n-6:n-3 ratio is of greater relevance than for individuals who consume significant daily sources of EPA and DHA. A number of recommendations have been made on the basisof the ratio of n-6 to n-3 fatty acids. The WHO/FAO suggests a ratio of 5:1-10:117, Sweden recommends a ratio of 5:118, Canada recommends 4:1-10:114, and Japan recently changed its recommendation from 4:1 to 2:119. Based on the proposed AI’s, the NIH suggests a ratio of 2:1-3:113. One study found that a ratio of 4:1 allows for adequate conversion to DHA in healthy vegetarians.20 Another research group suggested that the optimal ratio to maximize the conversion of ALA to DHA is 2.3:121. Given the rate of conversion of ALA to EPA and DHA, it has been suggested that a safe and adequate ratio for the vegetarian and vegan populations would be in the range of 2:1-4:122. This can best be achieved by increasing ALA in the diet and decreasing LA, if indicated (see below).
EFA Intake and Status of Vegetarians
Total omega-3 fatty acid intakes are similar for vegans, vegetarians and omnivores (approximately 1-3 gms/day, with the current average being about 1.1-1.6 grams/day)2, 18. However, the intakes of very long-chain omega-3 fatty acids (EPA and DHA) vary appreciably. Vegans consume negligible amounts of EPA and DHA, while vegetarians consume minimal EPA (less than 5 mg/day) and varying amounts of DHA depending on egg consumption (a source of DHA, averaging approximately 33 mg/day)7. Consumption of EPA and DHA in omnivores varies according to fish and egg intake, with average intakes in the 100-150 mg/day range. Omega-6 intakes are significantly higher in vegan and vegetarian populations than in omnivorous populations, ranging from a low of about 5-7% of calories in omnivores to a high of about 10-12% of calories in vegans. As a result, the n-6:n-3 ratio is generally considered to be elevated in vegans (approximately 14:1-20:1) and lacto-ovo vegetarians (approximately 10:1-16:1) compared with omnivores (approximately 10:1).
Because the consumption of long-chain n-3 fatty acids is low in vegetarian populations, and LA intakes are relatively high, one would expect decreased levels of EPA and DHA in body stores. Reports to date suggest that this is indeed the case, but that it is significantly more pronounced in vegans than in vegetarians. In 1978 Sanders et al. first noted that the plasma and total erythrocyte lipid levels of vegans were significantly decreased. EPA levels were only 12-15% nonvegetarians and DHA levels were 32-35% that of nonvegetarians. 23. Sanders and Roshanai (1992) found that vegan EPA plasma levels were only 22% that of omnivores and DHA levels were 38% of omnivores, although AA levels were similar 24. In 1994, Reddy et al. again demonstrated that vegetarians (who appeared to be vegan, based on a zero intake of EPA and DHA) had reduced EPA in plasma phospholipids (37% of nonvegetarians), and DHA (52% of nonvegetarians).25. Krajcovicova et al. (1995) compared the fatty acid status of vegans, lacto-ovo vegetarians, semi-vegetarians and omnivores between the ages of 11-15 years. While the levels of EPA and DHA were similar in vegetarians and nonvegetarians, they were significantly lower in vegans (62-65% of nonvegetarians). Interestingly, while long-chain omega-3 fatty acids were reduced in vegan children, they were not as severely decreased as reported in vegan adults. The higher EPA and DHA levels in vegan children may be the result of reserves from extended breastfeeding, or from better conversion in this age group26. Ågren et al. (1995) compared serum lipid levels of vegans eating uncooked food and nonvegetarians. The proportions of EPA and DHA in vegans were only 29-36% and 49-52% that of nonvegetarian controls, respectively, while the levels of AA were similar, indicating no difficulty with the n-6 conversion27. Sanders and Reddy (1992) compared the essential fatty acid content of vegan, vegetarian and nonvegetarian human milk. Milk from vegan mothers had over double the LA and LNA of the nonvegetarian mothers, but less than half of the DHA. The EFA status of the infants (as determined by erythrocyte lipids) reflected the levels in the milk they received. Vegan infants had less than 30% of the EPA and DHA of omnivorous infants28. Melchert et al. (1987) examined the fatty acid levels in the serum of vegetarians and nonvegetarians and found that DHA levels were approximately 40% lower in vegetarians than nonvegetarians29. Two other groups comparing EPA and DHA status of vegetarians and nonvegetarians found little difference in their levels [Kirkeby and Bjerkedal (1968)30 and Holub and Conquer (1997)31]. Holub and Conquer suggest that it is possible that Canadian vegetarians have elevated LNA intakes due to the high consumption of canola oil in their diets and, thus, better DHA status. These studies did not assess EFA status in vegans.
Implications of Reduced EFA Status
Highly unsaturated fatty acids are essential for health. Arachidonic acid, dihommo-gamma-linolenic acid (DGLA) and eicosapentaenoic acid all serve as precursors for eicosanoids. Those formed from AA are very potent, increasing blood pressure, inflammation, platelet aggregation, thrombosis, vasospasm and cell proliferation, while those formed from EPA and DGLA are less potent in protecting against these responses. While the eicosanoids formed from AA are important, their over- production relative to eicosanoids formed from EPA, has been associated with elevated risk for numerous disease states including heart disease, cancer, diabetes, osteoporosis, and many numerous immune/inflammatory disorders.
Docosahexaenoic is not a precursor for eicosanoids, but is an important structural component of the gray matter of the brain, the retina of the eye and specific cell membranes, and is found in high levels in the testes and sperm. Low levels of DHA have been associated with several neurological and behavioral disorders such as depression, schizophrenia, Alzheimer’s disease and Attention Deficit Hyperactivity Disorder (ADHD)7. In addition, low levels of DHA are also linked to sub-optimal visual acuity and reduced brain development in infants32. Thus, while these long chain fatty acids are not technically “essential” nutrients, it is important to assure sufficient levels by relying on conversion from “parent” fatty acids or by direct consumption.
Scientific Evidence for Increasing N-3 Fatty Acids in Vegetarian Diets
There is a rapidly expanding data base that demonstrates remarkable effects of n-3 fatty acids on primary and secondary prevention of cardiovascular disease (CVD). Both epidemiologic and randomized controlled clinical studies have evaluated the effects of marine and plant sources of n-3 fatty acids from food sources as well as supplements. These studies have established that both marine and plant-derived n-3 fatty acids have cardioprotective effects. These findings have prompted great interest in unraveling the biological mechanisms that explain these benefits reported in epidemiologic studies and clinical trials. It is apparent that there are multiple mechanisms of action that mediate the effects of n-3 fatty acids. Collectively, advances from epidemiologic, clinical and biochemistry/molecular biology research will be useful in refining dietary guidance to further decrease risk of CVD.
Epidemiologic Studies
a-Linolenic Acid
Recent epidemiologic studies have shown that dietary a-linolenic acid (ALA) is associated with a lower risk of CVD in men and women. In the EURAMIC Study, the relative risk for myocardial infarction was 0.42 (P for trend = 0.02) in individuals with the highest quintile of adipose tissue ALA, a long term measure of ALA intake.33 However, after adjusting for other CVD risk factors, this association was non-significant. In a 10-year follow-up of the Nurses’ Health Study, Hu et al.34 reported a dose-response relationship between ALA intake and relative risk of fatal ischemic heart disease. Risk was reduced by 45% in the highest quintile of ALA intake (P for trend = 0.01). However, ALA was not related to non-fatal myocardial infarction. In the Health Professionals’ Follow-up Study, conducted with men, a 1% increase in ALA was associated with a 0.41 relative risk for acute MI (P for trend = 0.01), however, there was no association with fatal CHD.35 The highest quintile of ALA intake was 1.4-1.5 g/day. In a recent cross-sectional study (the National Heart, Lung, and Blood Institute Family Heart Study) with 4584 men and women, ALA was inversely related to coronary artery disease.36 ALA intake in the top three quintiles was 0.65, 0.76 and 0.96 g/day; the prevalence odds ratio of coronary artery disease in these three quintiles was reduced approximately 40% for men and 50 to 70% for women.
In contrast to epidemiologic studies that have demonstrated a beneficial association between ALA intake and CVD there is some evidence to the contrary. In the Zutphen Elderly Study, a prospective epidemiologic study with 667 men, ages 64-84 years, there was no beneficial effect of ALA intake and incidence of 10-year coronary artery disease.37 The results of this study, however, were complicated by an association between ALA and trans-fatty acid intake36 as well as limitations in the collection of the dietary data (estimated only on the basis of food tables and dietary recollection data).38 ALA intake still had no effect on coronary artery disease risk even when foods that did not contain trans fatty acids were evaluated.
Based on available epidemiologic evidence from within population studies, ALA has been shown to have a protective effect on coronary disease. These findings provide strong support for conducting well controlled intervention trials to assess the cause and effect relationship between ALA and incidence of CVD.
Marine-Derived n-3 Fatty Acids
There has been controversy in the literature about whether fish consumption decreases CHD mortality. To resolve this controversy, Marckmann and Gronbaek39 systematically reviewed studies of fish or n-3 polyunsaturated fatty acid intake and CHD death (n = 11 with 116,764 subjects). This study found that individuals at high risk for CHD appeared to benefit in a dose responsive manner from increased fish consumption. The optimum dose for fatal CHD prevention in high risk populations is 40-60 g/day. In contrast, increased fish consumption does not appear to protect against CHD in individuals at low risk of CHD and with healthy lifestyles.
There have been various explanations for the conflicting data from epidemiologic studies of fish consumption and CVD risk. These reflect many differences in the experimental designs employed including definitions of sudden death,40 variability in the endpoints studied, experimental design or how fish intake was estimated, different study populations.41 Another consideration relates to the type of fish consumed where fatty fish but not lean fish consumption was associated with a lower CHD mortality.42 In addition, possible adverse effects of methylmercury content of fish may attenuate the health benefits of n-3 fatty acids.43
The available evidence supports a conclusion that fish consumption is protective against coronary disease. Because of this, the American Heart Association Dietary Guidelines recommend two servings of fish per week to reduce risk of coronary disease.44
Randomized Controlled Clinical Trials
The effects of n-3 fatty acids have been evaluated in clinical trials with subjects either with existing CVD or at high risk for CVD using both marine-derived EPA and DHA and plant-derived ALA. Collectively, these studies have shown a beneficial effect of both sources of n-3 fatty acids.
The Diet And Reinfarction Trial (DART) reported a 29% reduction in all-cause mortality after two years in male MI survivors who counseled to increase their intake of oily fish (200-400 g of fatty fish per week that provided an additional 500-800 mg/day of omega-3 fatty acids).45 A fish oil supplement (900 mg of EPA + DHA/day) was given to patients who would not eat fish and a subsequent analysis demonstrated that n-3 fatty acids accounted for the protective effect.46 Singh et al.47 studied patients with suspected acute myocardial infarction who were randomized to either fish oil capsules (containing 1.8 g of EPA+DHA/day), mustard oil (20 g/day providing 2.9 g a-linolenic acid) or placebo. Total cardiac events were lower in the fish oil and mustard oil groups (25%, and 28%, respectively) compared with the placebo group (i.e., 35%; P < 0.01). In the GISSI-Prevention Study48, 11,324 patients with pre-existing CHD (who were receiving conventional cardiac pharmacotherapy) were randomized to 850 mg of omega-3 fatty acid ethyl esters (as EPA and DHA), 300 mg of vitamin E, both or neither. The n-3 fatty acid intervention group experienced a 20% reduction in all-cause mortality (p=0.01) and a 45% reduction in sudden death (p<0.001) compared to the control group. There was no additional benefit conferred by vitamin E.
In contrast, a recent study did not find an effect of 3.5 g of DHA + EPA per day compared with corn oil on cardiac events in post-MI patients (n = 300) after 1.5 years of intervention.49 The lack of response to marine-derived n-3 fatty acids may have been due to the high habitual fish intake in western Norway, beyond which supplemental n-3 fatty acids would not be of benefit.
The effects of ALA on coronary events has been evaluated in four studies. Three reported beneficial effects of ALA, whereas one did not. The Indian Experiment of Infarct Survival47 (see above) reported a significant decrease in total cardiac events in the mustard seed oil (a source of ALA) group that was quite comparable to the EPA and DHA treatment group. The Lyon Heart Trial, a seminal study, was designed to evaluate the effects of a blood cholesterol-lowering, Mediterranean-type diet (including increased amounts of ALA; 1.5 g/day versus 0.5 g/day for the control group) on reoccurrence rates of cardiac events compared with a prudent Western diet.50,51 Subjects in the experimental group were instructed to adopt a Mediterranean-type diet that contained more bread, more root vegetables and green vegetables, more fish, fruit at least once daily, less red meat (replaced with poultry) and margarine high in alpha-linolenic acid (ALA) supplied by the study to replace butter and cream. This diet provided 30% of calories from fat, 8% from saturated fat, 13% from monounsaturated fat, 4.6% from polyunsaturated fat (0.84% ALA) and 203 mg/day of cholesterol. Despite a similar coronary risk factor profile (plasma lipids and lipoproteins, systolic and diastolic blood pressure, BMI and smoking status), subjects following the Mediterranean-Style diet had a 50-70% lower risk of recurrent heart disease. The Mediterranean Alpha-Linolenic Enriched Groningen Dietary Intervention (MARGARIN) Study reported a trend towards fewer CVD events in subjects (n = 124 men and 158 women) with multiple CVD risk factors who used a margarine high in ALA versus linoleic acid (1.8% vs. 5.7%, p=0.20).52 However, the 10-year estimated ischemic heart disease risk decreased similarly in both groups (2.1% and 2.5%, respectively).
The Norwegian Vegetable Oil Experiment53 did not report a beneficial effect of ALA. In this study, 0ver 13,000 men age 50-59 with no history of myocardial infarction were randomized to consume 5.5 g of a-linolenic acid per day (from 10 mL of linseed oil) or 10 mL of sunflower seed oil for one year. In each treatment group there were 27 cases of new CHD or sudden death and 40 vs. 43 deaths from any cause in the control compared with the linseed oil group.
In summary, evidence from RCTs show a beneficial effect of dietary and supplemental n-3 fatty acids, including both EPA + DHA and ALA, on coronary heart disease.54 Thus, there is scientific evidence that an adequate intake of n-3 fatty acids will elicit cardioprotective effects. From this, it follows that n-3 fatty acids are an integral component of a diet designed to maximally reduce risk of CVD.
Achieving Optimal EFA Intake and Status in Vegetarians
There are two important steps vegetarians can take to improve their essential fatty acid intake and status:
1. Maximize the conversion of alpha-linolenic acid conversion to EPA and DHA.
2. Provide a direct source of DHA.
For those with increased needs for EPA/DHA (e.g. pregnant and lactating women), or at greater risk for poor conversion (diabetics, those with neurological disorders, premature infants and the elderly), it may be prudent to assure a direct source of EPA/DHA. While it is not common, it is possible to over-consume n-3 fatty acids. If a person minimizes n-6 fatty acids and uses large amounts of n-3 fatty acids (i.e. over 2 Tbsp. flax oil/day), resulting in a ratio of n-6: n-3 of less than 1:1, insufficient LA conversion to HUFA can occur. Elongase and desaturase enzymes preferentially convert omega-3 fatty acids, when compared to omega-6 fatty acids. A balance of 2:1-4:1 (n-6:n-3) appears optimal for vegetarians, and others who do not receive preformed EPA/DHA.
Maximizing Conversion of Omega-3 Fatty Acids
While conversion of essential fatty acids to longer chain fatty acids is, at least in part, dependent on genetics, age and overall health, several dietary factors also have a significant impact on the conversion process. First, it is important to assure that the diet is nutritionally adequate, as poorly designed diets can impair the conversion process. Insufficient energy or protein decreases the activity of conversion enzymes, as can deficiencies of pyridoxine, biotin, calcium, copper, magnesium and zinc55,56. Excessive intakes trans fatty acids can also depress conversion enzymes. In addition, alcohol inhibits the activity of delta-5 and delta-6 desaturase and depletes tissues of long-chain omega-3 fatty acids56. High omega-6 fatty acid content can have a profound effect on omega-3 fatty acid conversion, reducing it as much as 40%58.
In the context of current guidance, total PUFA intake should be approximately 7% of calories with 10% being the maximum. Vegetarians currently consume about 8-12% of their calories from PUFA. Given a total PUFA intake of 7% to 10% of calories, to achieve a n-6:n-3 ratio of 4:1, approximately 1.5 to 2% of calories should be obtained from n-3 fatty acids and, as a result, 5.5 to 8% of calories from n-6 fatty acids. Alternatively, LA can be decreased, however, given the recognized health benefits of LA, a marked reduction is not recommended. Nonetheless, to achieve reduced omega-6 intakes, oils rich in omega-6 fatty acids should not be used as primary cooking oils. Cooking oils with the greatest omega-6 fatty acid content include safflower oil (75% n-6), grapeseed oil (70% n-6), sunflower oil (65% n-6), corn oil (57% n-6), cottonseed oil (52% n-6), and soybean oil (51% n-6). Processed foods, convenience foods and snack foods also are significant contributors to n-6 intake, thus their use should be moderated. Omega-6-rich whole foods such as sunflower seeds, pumpkin seeds, sesame seeds, walnuts, wheat germ and soy foods need not be avoided, as they tend to be relatively minor contributors to overall omega-6 intake. These foods also provide a myriad of beneficial dietary components, including phytochemicals, fiber, B-vitamins, vitamin E and trace minerals.
The primary fat in the diet should come from foods and oils rich in monounsaturated fat. When monounsaturated fats predominate, saturated fats, trans fatty acids and omega-6 fatty acids are kept in check, and the balance of omega-6 to omega-3 fatty acids improves. Monounsaturated fats are high in nuts (except for walnuts and butternuts), peanuts (a legume) olive oil, olives, avocados, canola oil, high-oleic sunflower and high-oleic safflower oils. Whole foods rather than oils are better sources of monounsaturated fats because they contribute many other nutrients to the diet.
Finally, it is important to assure sufficient amounts of alpha-linolenic acid, which are necessary for the production of EPA and DHA. Most healthy vegetarians would be well advised to double their intake of alpha-linolenic acid, providing at least 1% of energy from omega-3 fatty acids or 1.1 grams per 1000 calories. For those with increased needs or decreased capacity to convert, an intake of 2% of energy or 2.2 grams per 1000 calories may be necessary. The primary sources of alpha-linolenic acid are selected seeds, nuts and legumes (flaxseed, hempseed, canola, walnuts and soy) and the green leaves of plants, including phytoplankton and algae. Table 1 provides a list of common ALA-rich plant foods, the percent of fat as ALA, the n-6:n-3 ratio of the fat and the total grams ALA per serving.
Table 1: ALA Content Selected Plant Foods
|
FOOD/serving size |
ALA % |
LA % |
n-6:n-3 Ratio |
ALA Gm/serving |
Comments |
|
Flaxseed oil, 1 Tbsp. |
57% |
16% |
0.28:1 |
8.0 |
Richest known source of ALA. Highly unstable.
Should not be heated. |
|
Flaxseed, whole, 2 Tbsp. |
57% |
16% |
0.28:1 |
5.2 |
Keep well at room
temperature. |
|
Flaxseed, ground, 2 Tbsp. |
57% |
16% |
0.28:1 |
3.8 |
Best kept refrigerated or
frozen. |
|
Greens (mixed), 1 c |
56% |
11% |
0.19:1 |
0.1 |
Fat in greens is over 50% ALA, however total fat is so low, they are not
significant contributors to intake for most people. |
|
Hempseed oil, 1 Tbsp. |
19% |
57% |
3:1 |
2.7 |
One of the few foods that contains GLA – 1.7% GLA |
|
Walnuts, 1 oz (1/4 c) |
14% |
58% |
4:1 |
2.6 |
Highest n-3 content of any common nut – only the candlenut has more (30% |
|
Canola oil, 1 Tbsp. |
11% |
21% |
2:1 |
1.6 |
Excellent n-6:n-3 ratio. To avoid the genetically engineered canola, buy certified organic.
|
|
Soybean oil, 1 Tbsp. |
7% |
51% |
7:1 |
0.9 |
Not the best choice for general use due to high n-6 content.
|
|
Soybeans, 1 c cooked |
7% |
50% |
7:1 |
1.0 |
Can make a significant contribution to total |
|
Tofu, firm ½ c (4.5 oz) |
7% |
50% |
7:1 |
0.7 |
|
Provide a Direct Source of EPA/DHA
The primary sources of EPA and DHA are fish and seafood. Thus, for vegetarians, increasing consumption of these long-chain omega-3 fatty acids can be a challenge. For lacto-ovo vegetarians, eggs provide a reasonable amount of DHA (approximately 50 mg/egg), though very little EPA. Most supermarkets also sell DHA-rich eggs, providing 2-3 times the DHA of conventional eggs. Eggs from chickens fed flax generally provide 60-100 mg DHA per egg, while those from chickens fed microalgae contain 100-150 mg DHA per egg.
The only plant sources of long-chain omega-3 fatty acids are plants of the sea – microalgae and seaweed. There is a great deal of confusion about the essential fatty acid content of plants. While they are the original sources of EPA and DHA (fish do not produce long-chain omega-3 fatty acids), most are not concentrated sources due to their extremely low total fat content. An important exception is a DHA-rich microalgae, which provides 10-40% DHA by dry weight and is currently available in supplement form. See Table 2 for a list of microalgae-based supplements. When supplementing with a direct DHA source, 100-300 mg/day is recommended. Blue-green algae (spirulina and aphanizomenon flos aquae) are low in long-chain omega-3 fatty acids. Spirulina is rich in gamma-linolenic acid (GLA - omega-6), while aphanizomenon flos aquae is more concentrated in ALA. While blue-green algae is not a significant source of EPA or DHA, some research indicates that it has a very high conversion rate in comparison to other plants59. Macroalgae, otherwise known as seaweed, is even lower in fat than most vegetables (<1-14% of calorie s from fat), although it does contain small amounts of long chain fatty acids. A 100 gm serving provides, on average, about 100 mg of EPA, but little DHA. Seaweeds do not contribute significantly to EPA intakes in the Western world, but are important sources where people use large quantities of seaweed on a daily basis (e.g. Japan and other parts of Asia). Thus, while vegetarians can rely on eggs and/or microalgae supplements for DHA, most consume little, if any EPA. However, approximately 10-11% of DHA is retroconverted back to EPA, thus if sufficient ALA and DHA are consumed, total EPA production would be expected to be adequate60.
Table 2: Microalgae-based DHA Supplements
|
Company |
Supplement Names |
DHA/cap |
Type of Caps |
Comments |
| NuTru | O-Mega-Zen3 |
300 mg |
Veggie caps |
Excellent value. |
| Seroyal | Neurogen |
100 mg |
Veggie caps |
Not available in retail stores (Sold through alternative care health practitioners.) |
| Martek |
Neuromins |
100 mg 200 mg |
Gel Caps |
Not completely vegetarian due to use of gel caps. |
| OmegaTech |
Gold Mines |
100 mg 200 mg |
Gel Caps |
Not completely vegetarian due to use of gel caps. |
Practical Guidelines: Achieving Optimal EFA Intake and Status in Vegetarians
-
Make a wide variety of whole plant foods the foundation of the diet.
-
Get most of your fat from whole foods – nuts, seeds, olives, avocados and soyfoods.
-
If using concentrated fats and oils, select those rich in monounsaturated fats, such as olive, canola, or nut oils. Omega-3-rich oils can also be used, but should not be heated. Moderate use of omega-6-rich oils is recommended.
-
Limit intake of processed foods and deep-fried foods rich in trans and omega-6 fatty acids.
-
Reduce intake of foods rich in saturated fat and cholesterol.
-
Include foods rich in omega-3 fatty acids in the daily diet. Aim for a total of about 2-4 grams of ALA per day.
-
Consider using a direct source of DHA. Aim for 100-300 mg/day.
References
Conquer JA, Holub BJ. Supplementation with an algae source of docosahexanoic acid increases (n-3) fatty acid status and alters selected risk factors for heart disease in vegetarian subjects. J Nutr 1996;126:3032-3039.
