A question I often get is: “Why do I need to take fish oil when I can get Omega 3s from flax oil or other vegetarian oils?” Well in light of our recent “Get Healthy” series, I think it’s important to follow it up with some relevant information for you, the reader to use in making your decisions. I profess to be “mostly vegan” which simply means that I eat a vegan diet 95% of the time, supplementing with fish oil and maybe having a little fish once a month. Without further adieu…
Fish Oil vs. Flax Oil
There is a large and growing body of research suggesting that increasing omega-3 consumption is beneficial for health from birth through old age, and many health care practitioners and patients alike recognize its potential for clinical use. However, most studies showing the benefits of omega-3s have used fish oil-based supplements, and flaxseed oil is not generally considered to be an effective alternative by the medical community. The reason is that the specific omega-3 fatty acids provided by flaxseed oil are different from those provided by fish oils, and these different fatty acids do not have the same effects upon health.
Fish oil is an excellent source of long-chain omega-3 fatty acids, most notably eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Flaxseed oil, by contrast, is rich in alpha-linolenic acid (ALA), the parent omega-3 essential fatty acid. Although it is an omega-3 essential fatty acid, ALA has not been shown to possess the same benefits as with EPA and DHA. Research has shown that increasing the ratio of omega-3 to omega-6 fatty acids in the diet with ALA may not enhance neuronal DHA levels in infants (Bowen, et al. 1999), and some epidemiological studies even indicate an increased risk of prostate cancer associated with flaxseed oil consumption1.
Most studies indicate that the human conversion of ALA to EPA is inefficient, with only about 15% of ALA converting to EPA, and that the conversion of ALA to DHA is even less efficient, with only about 5% of ALA converting to DHA, if any at all2,3. The conversion of ALA to EPA and DHA is described in Sprecher’s Pathway (back).
The first study examined the capacity for conversion of ALA to EPA and DHA in young men4. Emulsified ALA tagged with the radioactive isotope carbon 13 was given in addition to a habitual diet. Approximately 33% of administered radio labeled ALA was recovered as CO2 on breath over the first 24 hours. The time scale of conversion of ALA to EPA indicated that the liver was the main site of desaturation and elongation, which has been shown previously in animals. However, there was no enrichment of DHA in total plasma to be recorded at any time point up to 21 days. The distribution of total plasma omega-3 fatty acids over this time period was 84% ALA, 7.9% EPA and 0% DHA.
The authors concluded that even if some ALA seems to be converted into EPA, the extent of DHA synthesis is likely to be of negligible biological significance. A conversion of ALA to DHA in tissues where the fatty acid was not released into plasma could, however, not be excluded. The nutritional
demands for DHA in healthy adults are likely to be modest, and the need for DHA may be satisfied by existing pools of DHA within the body or preferably by eating fatty fish. Since, however, elderly people with cognition defects have low levels of DHA in red blood cell membranes, it seems that these pools will have to be continuously replenished in order to counteract a negative balance.
The second study was performed in women of reproductive age with the same methodological setup as in the previous study. The results were slightly different compared to what was found in men since the extent of ALA conversion to DHA was greater in the women5. A direct comparison is difficult due to methodological reasons, but in this study the fractional excursions of labeled fatty acids in total plasma lipids was 21% for EPA and 9.2% for DHA. These data suggest greater synthesis of both EPA and DHA in women compared with men. It has been shown previously that estrogens used for anticonception increase the conversion of ALA to DHA6. The capacity to regulate ALA conversion by the action of sex hormones may contribute to the higher DHA concentration in women. This may be important during pregnancy and lactation in order to provide the fetus with sufficient DHA for brain development and maturation.
However, a third study could not find any increase of DHA in lactating women given flaxseed oil, which is rich in ALA7. Seven lactating women were given this oil, providing a daily intake of 10.7 g ALA. Breast milk and plasma ALA and EPA increased significantly, but no increase was observed for DHA. The authors concluded that flaxseed oil supplementation would not be an adequate method of increasing the availability of DHA for the developing infant.
A 2002 consensus report issued by the UK Food Standard Agency confirms these findings. After reviewing current research to investigate whether ALA was as beneficial to cardiovascular health as the omega-3 fatty acids from marine sources, the report concluded that ALA supplementation either as flaxseed oil or as fortified food such as margarine could increase the levels of ALA and EPA, but hardly any DHA, if at all8. The studies presented suggested little, if any, benefit of ALA on risk factors for cardiovascular disease. The effects previously observed with supplementation of marine omega-3 fatty acids were not replicated by ALA supplementation. The report had reservations about the evidence suggesting beneficial effect of ALA on the secondary prevention of coronary heart disease, and felt it still needed to be established.
The promotion of the use of ALA as a source for the marine omega-3 fatty acids has been based on data from studies on EPA and DHA. It now seems that this argument is not valid, based on recent studies in humans. The claimed benefits of providing ALA on primary prevention and secondary prevention seems to be non-existing, and further large clinical studies will have to be presented before health claims of flaxseed and linseed oils can be warranted.
The biological effects of very long-chain omega-3 fatty acids are much stronger than those of ALA on parameters related to specific health concerns such as cardiovascular health (Harris W. 1997), and preformed dietary DHA is 7-fold more effective than dietary ALA at increasing DHA levels in the brain (Su, et al. 1999; Abedin, et al. 1999).
Fish oil is a reliable, direct source of EPA and DHA, providing the optimal means of enhancing EPA and DHA in the body and targeting specific health concerns related to omega-3 fatty acid deficiencies.
If you made it to the end of the scientific jargon, congratulations! Thanks for reading and I hope to hear from you soon. Please subscribe so that you can have a new blog delivered to your email whenever I post.
References
1 Myers CE. Alpha-linolenic acid. Prostate Forum 2000 Aug;V5:2,7–8. 2 Brenna JT. Efficiency of conversion of alpha-linolenic acid to long chain n-3 fatty acids in
man. Curr Opin Clin Nutr Metab Care 2002 Mar;5(2):127–32.
3 Gerster H. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? Int J Vitam Nutr Res 1998;68(3):159–73.
4 Burdge GC, Jones AE, Wooton SA. Eicosapentaenoic and docosapentaenoic acids are the principal products of alfa-linolenic acid metabolism in young men. Br J of Nutr 2002;88:355–363.
5 Burdge GC, Wooton SA. Conversion of alfa-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J of Nutr 2002;88:411–420.
6 Silfverstolpe G, Johnson P, Samsice G, et al. Effects induced by two different estrogens on serum individual phospholipid and serum lecitin fatty acid composition. Hormone and Metabol Res 1981;13:141–145.
7 Francois CA, Connor SL, Bolewicz LC, et al. Supplementing lactating women with flaxseed oil does not increase docosahexaenoic acid in their milk. Am J Clin Nutr 2003;77:226–233.
8 Sanderson P, Finnegan YE, Williams CM, et al. UK Food Standards Agency alfa-linolenic acid workshop report. Br J of Nutr 2002;88:573–579.
Silfverstolpe G, Johnson P, Samsice G, et al. Effects induced by two different estrogens on serum individual phospholipid and serum lecitin fatty acid composition. Hormone and Metabol Res 1981;13:141–145.
Sprecher’s pathway
The rate-limiting step is the delta-6 desaturation activity. This step can also be further inhibited by several factors, including:
n A diet high in linoleic acid (common in the U.S.), which can inhibit conversion by as much as 40% (Emken, 1995).
n Certain health conditions, such as diabetes, and drugs inhibit delta-6-desaturase activity (Horrobin, 1981).
n A deficiency of any of the vitamin and mineral cofactors (vitamins B3, B6, C, zinc, and magnesium) required by elongase and delta-6-desaturase may inhibit conversion (Mahfous, et al. 1989).
n A loss of delta-6-desaturase activity occurs during normal aging (Hrelia, 1989). n A high maternal intake of linoleic acid (omega-6 from corn, safflower oil, etc.) inhibits conversion to EPA and DHA
and reduces omega-3 availability to the developing fetus (Al, 1996).
n Saturated and trans fatty acids inhibit ALA desaturation and elongation (Packman & Cunnane, 1992; Houwelingen & Hornstra, 1994).
n Ethanol inhibits conversion of ALA to EPA and DHA (Salem, et al. 1996). n Certain populations, such as North American natives, Inuits, Orientals, Norwegians, and Welsh-Irish, may not
effectively convert ALA to EPA.
This research confirms that the de facto conversion from ALA to EPA and DHA is likely very low for most Americans. There have also been three more recently published studies addressing this issue in humans.
