Of all nutrients deficient in a bodybuilder’s diet, the most likely are the essential fatty acids, or EFAs. Experts dubbed them essential around 1930, when they realized that two in particular must be supplied through the diet: linoleic acid (LA) and alpha-linoleic acid (ALA). They’re often lacking in athletes’ diets because they show up in the higher-calorie foods that dieters try to avoid.

The odd aspect of the avoidance, however, is that essential fats not only are vital for good health but can promote fat loss as well. They modify the activity of eicosanoids, which control myriad body reactions, from heart function to blood pressure, and also appear to promote fat loss.

The fat-burning property of fat was first popularized in bodybuilding by the great trainer and gym owner Vince Gironda. Vince often implored those he trained to eat fatty foods because ‘fat burned fat’; he was speaking from observation and experience. Although he wasn’t aware of the technical reasons for the seemingly paradoxical behavior of some dietary fats, scientific studies confirm that essential fats appear to suppress fatty acid synthetase, the main enzyme the body requires for fat synthesis.

Saturated fat, the type the body stores, isn’t essential; if anything, most people eat far too much of it, and it’s associated with a number of adverse health effects. In the liver saturated fat is the primary precursor of cholesterol synthesis, which explains why saturated fat intake is so strongly linked to cardiovascular disease. Saturated fat also adversely changes the composition of cellular membranes, making them ‘harder’ and less able to process various hormones.

Monounsaturated fat, found in olive oil, for example, is considered a neutral fat, although recent studies show that it’s more of a ‘good’ fat. Unlike other fats, such as the polyunsaturated kind found in many vegetable oils, monounsaturated fats don’t lower protective high-density lipoprotein (HDL) or have any inflammatory effects in the body. That’s key because out-of-control inflammation in the body is now known to be the cornerstone of many major diseases, including cardiovascular disease and cancer.

Despite the beneficial effects of monounsaturated fats, they’re not considered essential. Only linoleic acid (omega-6) and alpha-linoleic acid (omega-3) are because they’re the direct precursors of other fatty acids that play vital roles in the body. Omega-6 fats, primarily derived from vegetable oils, are converted into arachidonic acid. While vital for many reactions in the body, arachidonic acid is also a major player in the body’s inflammatory processes.

Omega-6 fats should be balanced with omega-3 fats. Prehistoric diets naturally balanced the essential fats for ancient humankind because of their natural abundance in unprocessed foods. Meats in those days were far higher in omega-3 fats than modern versions are. Today, research shows, most people get about 10 times more omega-6 than omega-3 fats, and many are outright deficient in the latter.

Alpha-linoleic acid (ALA) is considered essential because it’s converted by enzymes into two other fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These so-called fish-oil fatty acids are present in fattier fish’salmon, halibut, mackerel and sardines, for instance. Although ALA is listed as essential, the real players in human physiology are EPA and DHA.

Scientists initially noted the beneficial health effects of EPA and DHA after studying the eating habits of Greenland Inuits, whose diets contained large amounts of fatty fish known to be rich in EPA and DHA. Despite eating other types of fat, such as saturated fat, considered dangerous for cardiovascular health, the Inuits showed low incidence of cardiovascular disease, a fact traced to their intake of fatty fish.

Subsequent studies revealed that EPA and DHA offer cardiovascular protection. They help maintain proper heart rhythm; cardiac arrhythmia can result in sudden death. Most studies show that omega-3 fats can lower the risk of such a death by at least 50 percent.

Omega-3 fats also lower blood triglyceride, or fat; inhibit formation of platelets’elements in the blood that lead to clotting’a major immediate cause of heart attacks; and suppress the inflammatory chemicals that are thought to cause most forms of cardiovascular disease. Omega-3s oppose the inflammatory effects of omega-6 fats. ALL ALA = EPA + DHA’or No?

The jury is still out on whether you can effectively derive the health benefits of EPA and DHA from a dietary precursor, such as alpha-linoleic acid. The best dietary sources of ALA are flaxseed, canola and soybean oils. Flaxseed is by far the richest source, containing about 57 percent ALA. English walnuts are another natural source but don’t have as much ALA as flaxseed oil.

Many bodybuilders take flaxseed oil because of its generally favorable fatty-acid profile. Others use it because they’ve been told that it’s a good source of omega-3s. Flaxseed oil, however, contains no preformed omega-3, such as EPA and DHA. It contains only a high content of ALA. The question is just how useful flaxseed oil is as a dietary supplement.

ALA is a shorter-chain omega-3, containing 18 carbon atoms. EPA and DHA have longer chains, containing 22 and 23 carbon atoms, respectively. To convert ALA into the other fatty acids, the body employs enzymes called elongases and desaturases. Delta-6 desaturase is the rate-limiting enzyme that determines how effectively ALA converts to the longer-chain EPA and DHA.

That enzyme, however, presents a problem. It turns out that omega-6 fats, such as linoleic acid, also use it, actually competing with ALA for it. Since most people take in far more omega-6 fats than omega-3s, omega-6 usually gets more delta-6 desaturase. When that happens, ALA just doesn’t convert into EPA and DHA effectively.

For a supplement such as flaxseed oil to supply any EPA and DHA, your body’s omega-6 levels must be low. That’s rare; studies show that the body’s capacity to convert ALA to EPA and DHA is lower than previously thought. Scientists have discovered that most ALA enters the beta-oxidation, or fat-oxidation, pathway, leaving only up to 9 percent to be converted into EPA or DHA. Nor does ALA raise blood levels of DHA. Preformed EPA and DHA do not go into the energy pathway.

Women appear to more readily convert ALA into DHA than men,1 apparently because of interaction with estrogen. DHA forms about 40 to 60 percent of the fat in the brain and in the retina of the eye. It’s also essential for the normal development of babies, whose EPA and DHA come from Mom.

In young men, conversion of ALA to DHA is either very low or completely absent,2 though they can convert some ALA to EPA. Whether that presents a problem is debatable. While DHA forms a large part of the structure of cellular membranes in the brain and retina, it tends to accumulate in the brain. A feedback mechanism may prevent the conversion of DHA in men simply because their bodies often have it in sufficient levels. On the other hand, low-level DHA is consistent with certain pathologies, including Alzheimer’s disease. Those who avoid all fish are likely to have low or deficient body stores of both DHA and EPA. If you’re taking a preformed omega-3 fatty acid supplement, such as some type of fish oil, your body doesn’t have to convert ALA into EPA and DHA.

The Prostate-Cancer Connection

Several studies published in the early ’90s suggested that ALA may promote prostate cancer. That was a curious finding; omega-3 fatty acids like those in fish inhibit prostate cancer, most likely because they foster a favorable balance of eicosanoids. Early studies linking ALA to prostate cancer often suggested that its content in red meat was the culprit. An immediate problem with that hypothesis, however, is that red meat is a poor source of ALA. Other research suggests that the iron content in meat may lead to ALA oxidation and thus promote cancer. Even more confusing are findings that men with prostate cancer have subnormal levels of ALA in their bodies, as opposed to findings that ALA appears to cause apoptosis, or cancer-cell suicide. Moreover, why, as some studies show, would ALA promote prostate cancer in men yet prevent breast cancer in women? The most up-to-date ALA research suggests that there is no clear-cut connection between prostate cancer and ALA intake.3 One caveat: ALA can become rancid and convert to free radicals, which are linked to cancer. What you need to do is avoid rancid oil supplements: Refrigerate them. Another good idea is to take antioxidant nutrients that stabilize oils and neutralize free radicals, such as vitamin E.

Numerous studies show that ALA offers many of the same cardiovascular-protective effects as the preformed omega-3s, such as those derived from fish oil. Given the abundance of omega-6 in the vast majority of American diets, a supplement such as flaxseed oil can only help.

Even so, flaxseed oil may be a better supplement for women than men because of women’s more efficient conversion of ALA into EPA and DHA. Women also burn less ALA for energy than men, leaving more to convert into EPA and DHA. The best way to absorb an EFA supplement based on ALA is to avoid the omega-6 variety, which practically ensures no conversion.

The most reliable way to ensure an adequate intake of EPA and DHA is to either eat fatty fish or take them in supplement form’which, by the way, avoids the problems linked to contamination of fish. Commercial fish-oil supplements are derived from fish muscle, not liver, and don’t accumulate toxins.

Food Sources of ALA

Grams of ALA per tablespoon
Flaxseed oil 8.5
Flaxseed 2.2
Canola oil 1.3
Soybean oil 0.9
English walnuts 0.7
Olive oil 0.1

References

1 Burdge, G.C., et al. (2002). Conversion of a-linoleic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic in young women. Br J Nutr. 88:411-20.
2 Burdge, G.C., et al. (2002). Eicosapentaenoic and docosapentaenoic acids are the principal products of a-linoleic acid metabolism in young men. Br J Nutr. 88:355-63. 3 Attar-Bashi, N.M., et al. (2004). A-linoleic acid and the risk of prostate cancer: what is the evidence? J Urology. 171:1402-1407. IM