DHA (short for docosahexaenoic acid) is a long chain omega-3 fatty acid with 22 carbon atoms that is absolutely essential for life and health. DHA is incorporated into cell walls or membranes, where it serves to enable nutrient transport into and out of the cells.

Health Benefits of DHA

People with higher levels of cell membrane DHA in their systems are proven to have lower levels of circulating small-dense LDL and lower circulating triglycerides, lower insulin resistance, improved blood pressure control, improved immune response, and higher rates of fat metabolism or 'fat burning.' DHA is vitally important as we age and in the management of many degenerative diseases including cardiovascular disease, strokes, diabetes, hypertension, cancer, depression, bipolar, ADHD or ADD, arthritis, and Alzheimer's, among many others.

Poor Conversion into DHA from Plant Derived Omega-3 Oils

New radioactive tagging or tracing techniques have consistently revealed the actual levels of DHA being converted in human subjects from various dietary animal vs. plant sources.This new technology has vastly improved our knowledge about omega-3 and 6 fats, and the degree to which each type of fat is converted and utilized by specific tissues in the body. This is revolutionary information.

While the human body can manufacture very small quantities of DHA from the shorter, intermediate-chain 18 carbon molecules of omega-3 oils or 'essential fatty acids' taken from plants, seeds and nuts, it has extreme difficulty making more than microscopic amounts.

This is especially true for adult males who manage to convert only a fraction of 1% (actually ranging from 0.1% to 0.5%) of plant derived, 18 carbon omega-3 (called alpha-linolenic acid, ALA) into the longer-chain DHA form of 22 carbon omega-3 that is used by the body in cell membranes.

Adult females during their estrogen producing child-bearing years do slightly better at DHA conversion from plant omega-3 sources, at least until menopause. This fact alone may account for the greater longevity for females compared to men across all cultures.

Best DHA Sources

The best source of DHA is from marine animals, including most fatty or oil fish varieties, and many shellfish including clams, oysters, muscles and other bivalves. Common fish oil from mackerel, salmon and herring contains about 12% pure DHA. Fish oil from anchovies and sardines may contain up to 20% or more of pure DHA. Blue algae is another source, but is less common in the marketplace and contains much less DHA by weight than fish oils.

If you are a vegan, you may want to try marine DHA from algae, which has no animal products. One such 100% vegetarian DHA product is:

Deva Vegan Omega-3 DHA, Derived from Algae, 90 Vcaps, which sells for $25.99 per 90 capsule bottle. Each capsule contains 200mg DHA and no EPA. Vegans can get their EPA from taking flaxseed oil supplements. The final cost of DHA per gram for this product is $1.44 per gram of DHA.

For people who don't mind taking fish oil (non-vegetarians, or the rest of us), we recommend this pharmaceutical grade, concentrated fish oil product:

Super Omega-3 EPA/DHA with Sesame Lignans & Olive Fruit Extract, 120 softgels, which sells for $21.28 per 120 capsule bottle. Each capsule contains 250mg DHA and 350mg EPA, plus sesamin and olive extracts. The final cost of DHA per gram for this product is $0.71 per gram of DHA. This high quality fish oil is half the price per dose of DHA as the vegan algae DHA above, plus you get the EPA, sesamin and olive extracts as 'free bonuses'.

Diet Changes

Vegetarians who exclude fish and fish oil products from their diet should reconsider this practice in light of recent human research that consistently demonstrates extremely inefficient production of DHA from all plant sources. If they insist on making NO EXCEPTIONS then we suggest the 100% vegan DHA product above, even though it costs twice as much as fish oil does and does not contain the EPA we need to control inflammation.

Even non-vegetarians are advised to include enough fish and/or fish oil supplements in their diet to ensure sufficient consumption of this vital nutrient. "The rest of us" who are non-vegans should take the recommended Super Omega-3 fish oil product above. It is far superior in our opinion due to the lower cost per gram of DHA, plus its combined sesamin and olive extracts, which help reduce inflammation more than merely DHA and EPA alone.

How Much Fish or Fish Oil Do We Need?

This varies depending on the amount of omega-6 vegetable oils and saturated fats in our diet. Each of these oils compete with DHA for inclusion into cell membranes. The more of them we eat, the more DHA we need to win its share of the competition.

Latest cell wall or membrane inclusion studies in adult humans reveal that limiting the portion of omega-6 tends to have greater effect in raising levels of membrane DHA than limiting the same portion of saturated fats. In scientific jargon, comparing the same moeities or concentrations, omega-6 plant oil is almost twice as likely to be included in cell membrane tissue as is saturated fat from animals. The amount of DHA inclusion is indirectly proportional to either of those competitive fats, but to varying degrees. So, although controlling both is important, restricting omega-6 from vegetable oils is the first priority to maximize your DHA inclusion into cell membranes.

These restricted 'high omega-6' oils would include those made from seeds and nuts, including safflower oil, peanut, corn, soybean, sunflower, cottonseed and other common cooking or salad oils other than olive or canola oils. Olive and canola oils are mainly omega-9 oils and do not contain much omega-6. The next target for restriction is saturated animal fats from meats, skins, dairy products, etc.

Here is our suggested diet using the recommended low-sat-fat, low-omega-6 and high marine omega-3 dietary approach. Advantages of that diet also include high levels of fiber, antioxidants, polyphenols, catechins, low sugar levels, and resulting lower levels of inflammation and insulin resistance.

How much FISH OIL would we need to take every day?

Studies of people on a 'typical American diet' tend to support taking up to 12 grams of common fish oil per day to ensure adequate DHA inclusion into cell walls. That provides an approximate total DHA of about 1,440mg/day. If you think you are consuming only 1/2 of the omega-6 and saturated fats that an average American does, then divide the amount of fish oil by 2, and so on. It is possible that people with very little saturated fat or omega-6 may only need to take 1 or 2 grams of fish oil per day to achieve and maintain the optimum DHA levels.

How much FISH per day would that be?

If you were trying to offset the typical American's consumption of omega-6 and saturated fats by eating fish, you would have a very difficult time of it.

In order to get the equivalent of 12 grams of fish oil in terms of its DHA content, you would have to eat about 22 pounds per day of salmon, and even more of most fish varieties. Clearly this is not possible.

So you must decrease your sat-fat and omega-6 vegetable oil consumption to very low levels. Assuming you are eating about 5-10% of the average American's consumption of those fats, then you could just barely get by with a 4-ounce serving of oily fish like herring, salmon, mackerel, sardines or anchovies, eaten 3 times per week.

Do you think you've controlled your diet so well that you are 10-20 times better than the 'average American'? If you're confident of that, then rely on eating fish. Otherwise, take several fish oil capsules per day.

References

1. "Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements." Plourde M, Cunnane SC. Research Center on Aging, Departments of Medicine, and Physiology and Biophysics, Université de Sherbrooke, 1036 Belvedere St, South, Sherbrooke, QC J1H 4C4, Canada. Appl Physiol Nutr Metab. 2007 Aug;32(4):619-34.

Abstract: "There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent PUFA, linoleic acid or alpha-linolenic acid (ALA), to their respective long-chain PUFA products. As a result, there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that asymptotically equal to 5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary ALA have a negligible effect on plasma DHA, an effect paralleled in the omega6 PUFA by a negligible effect of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the desaturation - chain elongation pathway."

2. "Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)?"

Gerster H. Vitamin Research Department, F. Hoffman-Roche Ltd, Basel, Switzerland. Int J Vitam Nutr Res. 1998;68(3):159-73.

Abstract: "A diet including 2-3 portions of fatty fish per week, which corresponds to the intake of 1.25 g EPA (20:5n-3) + DHA (22:6n-3) per day, has been officially recommended on the basis of epidemiological findings showing a beneficial role of these n-3 long-chain PUFA in the prevention of cardiovascular and inflammatory diseases. The parent fatty acid ALA (18:3n-3), found in vegetable oils such as flaxseed or rapeseed oil, is used by the human organism partly as a source of energy, partly as a precursor of the metabolites, but the degree of conversion appears to be unreliable and restricted. More specifically, most studies in humans have shown that whereas a certain, though restricted, conversion of high doses of ALA to EPA occurs, conversion to DHA is severely restricted. The use of ALA labelled with radioisotopes suggested that with a background diet high in saturated fat conversion to long-chain metabolites is approximately 6% for EPA and 3.8% for DHA. With a diet rich in n-6 PUFA, conversion is reduced by 40 to 50%. It is thus reasonable to observe an n-6/n-3 PUFA ratio not exceeding 4-6. Restricted conversion to DHA may be critical since evidence has been increasing that this long-chain metabolite has an autonomous function, e.g. in the brain, retina and spermatozoa where it is the most prominent fatty acid. In neonates deficiency is associated with visual impairment, abnormalities in the electroretinogram and delayed cognitive development. In adults the potential role of DHA in neurological function still needs to be investigated in depth. Regarding cardiovascular risk factors DHA has been shown to reduce triglyceride concentrations. These findings indicate that future attention will have to focus on the adequate provision of DHA which can reliably be achieved only with the supply of the preformed long-chain metabolite."

3. "Compartmental modeling to quantify alpha-linolenic acid conversion after longer term intake of multiple tracer boluses." Goyens PL, Spilker ME, Zock PL, Katan MB, Mensink RP. Department of Human Biology, Maastricht University, Maastricht, The Netherlands. J Lipid Res. 2005 Jul;46(7):1474-83. Epub 2005 Apr 16.

Abstract: "To estimate in vivo alpha-linolenic acid (ALA; C18:3n-3) conversion, 29 healthy subjects consumed for 28 days a diet providing 7% of energy from linoleic acid (C18:2n-6) and 0.4% from ALA. On day 19, subjects received a single bolus of 30 mg of uniformly labeled [(13)C]ALA and for the next 8 days 10 mg twice daily. Fasting plasma phospholipid concentrations of (12)C- and (13)C-labeled ALA, eicosapentaenoic acid (EPA; C20:5n-3), docosapentaenoic acid (DPA; C22:5n-3), and docosahexaenoic acid (DHA; C22:6n-3) were determined on days 19, 21, 23, 26, 27, and 28. To estimate hepatic conversion of n-3 fatty acids, a tracer model was developed based on the averaged (13)C data of the participants. A similar tracee model was solved using the averaged (12)C values, the kinetic parameters derived from the tracer model, and mean ALA consumption. ALA incorporation into plasma phospholipids was estimated by solving both models simultaneously. It was found that nearly 7% of dietary ALA was incorporated into plasma phospholipids. From this pool, 99.8% was converted into EPA and 1% was converted into DPA and subsequently into DHA. The limited incorporation of dietary ALA into the hepatic phospholipid pool contributes to the low hepatic conversion of ALA into EPA. A low conversion of ALA-derived EPA into DPA might be an additional obstacle for DHA synthesis."

4. "Long-chain conversion of [13C]linoleic acid and alpha-linolenic acid in response to marked changes in their dietary intake in men." Hussein N, Ah-Sing E, Wilkinson P, Leach C, Griffin BA, Millward DJ. Centre for Nutrition and Food Safety, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey GU2 7XH, United Kingdom. J Lipid Res. 2005 Feb;46(2):269-80. Epub 2004 Dec 1.

Abstract: "We studied the long-chain conversion of [U-13C]alpha-linolenic acid (ALA) and linoleic acid (LA) and responses of erythrocyte phospholipid composition to variation in the dietary ratios of 18:3n-3 (ALA) and 18:2n-6 (LA) for 12 weeks in 38 moderately hyperlipidemic men. Diets were enriched with either flaxseed oil (FXO; 17 g/day ALA, n=21) or sunflower oil (SO; 17 g/day LA, n=17). The FXO diet induced increases in phospholipid ALA (>3-fold), 20:5n-3 [eicosapentaenoic acid (EPA), >2-fold], and 22:5n-3 [docosapentaenoic acid (DPA), 50%] but no change in 22:6n-3 [docosahexanoic acid (DHA)], LA, or 20:4n-6 [arachidonic acid (AA)]. The increases in EPA and DPA but not DHA were similar to those in subjects given the SO diet enriched with 3 g of EPA plus DHA from fish oil (n=19). The SO diet induced a small increase in LA but no change in AA. Long-chain conversion of [U-13C]ALA and [U-13C]LA, calculated from peak plasma 13C concentrations after simple modeling for tracer dilution in subsets from the FXO (n=6) and SO (n=5) diets, was similar but low for the two tracers (i.e., AA, 0.2%; EPA, 0.3%; and DPA, 0.02%) and varied directly with precursor concentrations and inversely with concentrations of fatty acids of the alternative series. [13C]DHA formation was very low (<0.01%) with no dietary influences."

5. "Influence of alpha-linolenic acid and fish-oil on markers of cardiovascular risk in subjects with an atherogenic lipoprotein phenotype." Wilkinson P, Leach C, Ah-Sing EE, Hussain N, Miller GJ, Millward DJ, Griffin BA. Centre for Nutrition and Food Safety, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, UK. Atherosclerosis. 2005 Jul;181(1):115-24.

Abstract: "We tested the hypothesis that dietary alpha-linolenic acid (ALA) can exert effects on markers of cardiovascular risk similar to that produced by its longer chain counterparts in fish-oil. A dietary intervention study was undertaken to examine the effects of an ALA-enriched diet in 57 men expressing an atherogenic lipoprotein phenotype (ALP). Subjects were randomly assigned to one of three diets enriched either with flaxseed oil (FXO: high ALA, n = 21), sunflower oil (SO: high linoleic acid, n = 17), or SO with fish-oil (SOF n = 19) for 12 weeks, resulting in dietary intake ratios of n-6:n-3 PUFA of 0.5, 27.9 and 5.2, respectively. The relative abundance of ALA and EPA in erythrocyte membranes increased on the FXO diet (p < 0.001), whereas both EPA and DHA increased after fish-oil (p < 0.001). There were significant decreases in total plasma cholesterol within (FXO -12.3%, p = 0.001; SOF -7.6%, p = 0.014; SO -7.3%, p = 0.033) and between diets (p = 0.019), and decreases within diets after 12 weeks for HDL cholesterol on flaxseed oil (FXO -10%, p=0.009), plasma TG (-23%, p < 0.001) and small, dense LDL (-22% p = 0.003) in fish-oil. Membrane DHA levels were inversely associated with the changes in plasma TG ( p= 0.001) and small, dense LDL (p<0.05) after fish-oil. In conclusion, fish-oil produced predictable changes in plasma lipids and small, dense LDL (sdLDL) that were not reproduced by the ALA-enriched diet. Membrane DHA levels appeared to be an important determinant of these fish-oil-induced effects."