Omega-3 and omega-6: magic bullets for athletes

Nature or nurture? There is an age-old debate about whether performance is primarily ‘in your genes’ or develops in response to training. The common consensus is somewhere in between: that we inherit a set of genes which determine our potential, but it’s our training and nutrition that allow us to reach that potential. However, new evidence suggests this fatalistic approach to our genetic make-up is misplaced; fascinating research is emerging from the world of nutrition to suggest that essential fats in our diet can exert significant control over key metabolic genes in our cells, particularly those involved with fat storage, fat burning and glycogen synthesis. In plain English this means that, while you might not be born with the ideal genetic make-up for your chosen sport or event, correct fatty acid nutrition could help to ‘reprogramme’ your genetic code!

There are two principal essential fats: alpha-linolenic acid (sometimes called omega-3) and linoleic acid (omega-6). These two fats are essential because their chemical structure means that they can be used to make hormone-like substances called prostaglandins, which go on to regulate a host of other functions in the body. However, these fats cannot be synthesised by the body, which is why we rely on getting them ‘ready-made’ from the diet.

The complex structure of the fats also makes them very chemically reactive; put simply, they readily undergo chemical change and ‘fall apart’ when exposed to heat, light or air. This means that storing, cooking or processing foods rich in essential fatty acids (EFAs) inevitably leads to a loss in nutritional value. The problem is that we need more of these EFAs per day than any other single nutrient – measured in tablespoons, not milligrams! And the task of obtaining enough of them in unadulterated form in today’s world of tinned, dried, frozen, fast and processed food is a major challenge.

The best dietary sources of EFAs are nuts, seeds, fatty fish and unrefined whole grains. However, a glance at the table overleaf shows that, while the omega-6 fatty acid is quite abundant, omega-3 is more difficult to obtain. Unless your diet contains significant amounts of seeds and whole grains, it’s likely you’ll be falling short of your optimum omega-3 intake. And simply using more bottled oils, such as soy, rape and walnut oils, on salads and in cooking, may not be the answer either. Commercial oils are inevitably refined, processed and stored, which means that the essential fatty acid content will be partly degraded. Fatty fish, such as mackerel, herrings, sardines, trout and salmon, are rich in two different kinds of omega-3 fats – eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) – which can help to supplement the role of alpha linolenic acid in the body. Notice, though, that olive oil is devoid of omega-3 and very low in omega-6. Contrary to popular belief, olive oil is a very poor source of EFAs!

The role of EFAs in human nutrition has long been recognised; dietary omega-3 and omega-6 fats are needed for the synthesis of prostaglandins, which help regulate certain aspects of metabolism, such as blood viscosity, inflammatory processes, blood cholesterol and fat levels, and water balance. Additionally, it is now widely accepted that a low ratio of EFAs to saturated fatty acids is associated with an increased risk of coronary heart disease (CHD).

New findings on EFAs and obesity

However, more recent research on EFA nutrition has yielded some intriguing new findings. One of these is that increased intakes of these essential fats appear to reduce tissue levels of triglycerides (stored fats), which improves the sensitivity of insulin (the hormone that drives amino acids and glucose into muscle cells), so reducing the risk of obesity and CHD⁽¹⁾. Initially, these beneficial effects of EFAs were thought to be due to changes in the fatty acid composition of the cell membranes, leading to subsequent alterations in hormonal signalling. However, when researchers dug a little deeper it became apparent that something else was going on.

Dietary sources of EFAs

Food	Omega-3 (grams per100g)	Omega-6 (grams per 100g)
Flax	20.3	4.9
Hemp seeds	7.0	21.0
Pumpkin seeds	3.2	23.4
Salmon	3.2	0.7
Walnuts	3.0	30.6
Rape seed	2.1	9.0
Herring	2.0	0.4
Soybeans	1.2	8.6
Butter	1.2	1.8
Olive oil	0.6	7.9
Wheat germ	0.5	5.5
Sunflower seeds	0	30.7
Almond	0	9.2
Olives	0	1.6

They discovered that these fats, particularly those of the omega-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. In particular, they observed a phenomenon known as ‘fuel partitioning’, whereby dietary EFAs were able to direct glucose (from digested carbohydrates) towards glycogen storage while at the same time directing other fatty acids in the body away from triglyceride synthesis (ie fat storage) and towards fatty acid oxidation! In addition, these studies suggested that omega-3 fatty acids have the unique ability to enhance thermogenesis (the burning of excess fat to produce heat), thereby reducing the efficiency of body fat deposition^(2-7). In simple terms, this fuel partitioning phenomenon appears to conserve carbohydrate while simultaneously shedding fat – exactly what most athletes would give their right arm for!

Further study of this fuel partitioning effect led to the discovery that the EFAs were somehow boosting the production of enzymes involved with fatty acid oxidation (such as carnitine palmitoyltransferase, which helps transport fatty acids into the mitochondria of the cells for burning) while at the same time down-regulating the production of enzymes involved in fat synthesis, such as fatty acid synthase ^(8-12).

At first it was assumed that this ‘up-regulation’ of fat burning/glycogen synthesising enzymes and ‘down-regulation’ of fat storage enzymes occurred through hormonal signalling; in other words that the EFAs were somehow altering the cell membranes, causing a change in chemistry and leading to altered enzyme production by the genes responsible. However, these changes in gene transcription occur too quickly to be explained in this way; there seemed to be a much more direct effect. And eventually researchers discovered, to their amazement, that these EFAs were able to control gene expression directly via a steroid-like substance called PPARα ^(13,14).

PPARα is known as a ‘lipid-activated transcription factor’. This means it switches on key genes by binding to DNA, but only when it has been activated itself by binding to lipids such as EFAs. And it turns out that the genes it switches on are precisely those which code for enzymes involved in fat burning! Not only was this a remarkable discovery in itself, it was also the first time science had clearly demonstrated that nutritional components of the diet can exert direct control over the function of genes.

Although PPARα was believed to act as a ‘master switch’, helping to switch on genes involved in fatty acid oxidation and switch off those involved in fat storage, more recent research^(15,16) has demonstrated that the down-regulation of fat storage enzymes occurs because EFAs impair the release of another group of steroid-like substances called ‘sterol response element binding proteins’, or SREBPs for short!^(15,16). One of these (SREBP-1) helps to switch on the gene that codes for a fat synthesis enzyme called fatty acid synthase. However, a different type (SREBP-2) is a regulator of genes coding for proteins involved in cholesterol synthesis, which probably explains why healthy intakes of the EFAs reduce cholesterol ^{(17, 18)}.

The thermogenesis effect of omega-3 fats mentioned earlier is now believed to occur as a result of their ability to activate a gene that codes for a protein called ‘uncoupling protein-3’ ⁽¹³⁾; this protein allows the energy derived from the oxidation of fatty acids to be dissipated as heat, rather than coupled to the metabolic processes in order to do work.

EFAs and athletic performance

The role of EFAs in modifying gene expression and stimulating the phenomenon of fuel partitioning now appears to be scientifically beyond doubt. But how does this translate into athletic performance? Can athletes expect to benefit from metabolic changes brought about by higher intakes of EFAs? Anecdotal reports of increased human performance on high EFA diets abound, but this is a relatively new area of research and hard scientific evidence is thin on the ground.

In 2001 Dr Udo Erasmus (considered by many to be a crusader for the health benefits of EFAs) carried out a study with 61 Danish athletes. After eight weeks of supplementation with a 2:1 blend of omega-3/omega-6 oil, the athletes (selected from a wide variety of sports) showed a significant increase in HDL (healthy) cholesterol levels, a more favourable ratio of HDL to LDL (unhealthy) cholesterol and lower levels of fasting triglycerides. A large percentage of the group also reported subjective improvements in endurance and recovery. However, subjective measurements are notoriously prone to the placebo effect, which means that the results should be interpreted with caution.

Meanwhile, a well-controlled study carried out on football players in 1997 showed no increase in VO2max or anaerobic threshold when diets were supplemented with 2.5 grams per day of omega-3 from fish oils ⁽¹⁹⁾. However, the dose of omega-3 used was very small, and the fuel partitioning effects of EFAs described above could only be expected to improve endurance and reduce body fat – parameters which were not assessed in this study.

Turn to animal and ‘in vitro’ studies, though, and things begin to look much more promising. In a study carried out last year, scientists studied the effects of omega-3 fat supplementation on swimming performance in rats ⁽²⁰⁾. By comparison with a control group of unsupplemented rats, there was a 300% rise in the ‘swimming muscle’ levels of FABP, a protein that binds fatty acids and transports them to the mitochondria for oxidation, but no increase in muscle triglycerides. The researchers concluded that this effect was probably due to an up-regulation of the fatty acid metabolism genes via the PPARα mechanism discussed earlier.

In a study on rat muscle fibres, high omega-3 and omega-6 diets produced 16-21% more muscle tension and up to 32% greater endurance during high frequency stimulation⁽²¹⁾. Moreover, when these rats resumed their standard diets for a period of six weeks, their muscle function returned to the level of un-supplemented rats.

Rat studies on EFAs and body composition also look promising. In a Japanese study, very young rats were fed for four months on a diet containing one of the following ⁽²²⁾:

• 12% perilla oil (very rich in omega-3);
• safflower oil (very rich in omega-6);
• olive oil (rich in mono-unsaturates);
• beef fat (rich in saturated fats).

The amount of food consumed and the weight gained was the same in all four groups, but the amount of fat stored, the number of fat cells and fat cell volume were all significantly lower in the omega-3 and -6 groups. Furthermore, the genes involved in fat cell differentiation were significantly down-regulated in the omega-3 group by comparison with the olive oil and beef fat groups! Intriguingly, some human research points to a synergistic effect between endurance training and EFA metabolism. Earlier this year, scientists studying the phenomenon of ‘uncoupling’ in human muscle mitochondria found (as expected) that the genes coding for uncoupling proteins (the ones that stimulate thermogenesis via uncoupled respiration) were activated by omega-3 fats. What surprised them, however, was that after endurance training the stimulating effect of omega-3 fats was even stronger. In other words, omega-3 oils seem to stimulate thermogenesis most effectively in muscles that are endurance-trained!

So where does all this leave athletes? Although there’s a dearth of well-controlled double-blind studies on the interaction of EFA and genes in humans, there’s no doubting the weight of evidence accumulating from animal and in-vitro studies. Numerous studies have demonstrated that western diets containing significant amounts of processed foods and saturated or chemically-altered fats are very low in EFAs, particularly omega-3 fats, creating an unbalanced ratio of dietary omega-6:omega-3 ⁽²³⁾. Typically, this ratio in modern diets is between 10:1 and 25:1, although the World Health Organisation recommends a ratio of between 5 and 10:1. Some nutritional researchers recommend an even higher proportion of omega-3, with as much as a third of total EFA intake from omega-3.

UK dietary advice is conservative

Current UK dietary recommendations are for around 6% of calorie intake to come from polyunsaturated (essential) fats, with around 0.2g per day of omega-3 fats⁽²⁴⁾. However, this figure seems extremely conservative; assuming a total calorie intake of around 2,000 per day, it would equate to 13g of omega-6, giving an omega-6:omega-3 ratio of over 60:1!

The simple fact is that there is very little consensus among nutritionists about how much omega-3 and omega-6 oils are needed in total for optimum health and about the ideal ratio between the two. Pioneers in the field of fatty acid nutrition, such as Dr Erasmus, recommend around 9g per day of omega-6 and 6g per day of omega-3 oils for general health (1.5:1 omega-6:omega-3). This sits well with recommendations from the US National Cholesterol Education Program Diet and American Heart Association that no more than 30% of total calorie intake should come from fat, of which polyunsaturates (omega-3 and 6) should constitute 10% – ie around 20g per day in total.

On the available evidence, this would seem a very good place to start. For the fuel-partitioning effects mentioned earlier, higher intakes of EFA might be required; the animal studies demonstrating this effect supplied EFAs at between 10 and 20% of total calorie intake (22-44g per day in a 2,000 calorie/day diet). The studies on Danish athletes carried out by Dr Erasmus supplemented around 20g of omega-3 and 10g of omega-6 per day.

It’s all too easy to fall short of even the minimum intakes of EFAs required to maintain optimum health, let alone to produce any of the potential benefits discussed here. And this is not just down to the popularity of processed and refined foods. In their efforts to follow a healthy ‘low-fat’ lifestyle, many people, including athletes, have thrown out the ‘EFA baby’ with the bathwater! Below are some dietary tips which can help to boost your EFA intake.

• Use fresh seeds sprinkled on salads, especially hemp, pumpkin and sunflower;
• Use nuts in salads or mixed with raisins as snacks, especially walnuts, pecans and hazelnuts;
• Switch to wholemeal bread – the wheatgerm in whole wheat is a good source of EFAs;
• Eat whole grain breakfast cereals, such as Shredded Wheat, Weetabix and oat flakes, rather than refined cereal, such as cornflakes;
• Use brown rice and wholemeal pasta instead of white varieties;
• Use a cold-pressed seed oil in salad dressings, but make sure that it is fresh and has been packaged in an oxygen-free container that is also opaque to light;
• Eat fatty fish at least once a week. If you can get fresh mackerel, herring or unfarmed salmon and trout, so much the better;
• Don’t rely too heavily on low fat/diet foods and shakes for your calories – these are nearly all devoid of EFAs;
• Choose free range chicken and wild meats where possible – these generally contain higher amounts of EFAs than their intensively-reared counterparts;
• Choose organic free-range eggs if you can get them. Free foraging hens fed on natural foods lay eggs containing up to 30% of the fat as EFAs.

If you choose to supplement EFAs additionally, the best way to do this is with a bottle of proprietary seed oil blend. These tend to contain around two thirds omega-3 to one third omega-6. This is the reverse of the recommended dietary ratio, the idea being that you need extra omega-3 because it’s harder to obtain from normal dietary sources than omega-6. Flax seed oil is also an excellent source of omega-3 but contains very little omega-6. Whatever you choose, it should be fresh and packaged in an oxygen-free container that is also opaque to light. Ideally, the oil should have been kept refrigerated since production and should be stored in your fridge and used within four weeks of opening. Remember that EFAs (especially omega-3) are chemically very fragile and spoil rapidly if not stored correctly. For this reason you would be wise to avoid seed oil or fish oil capsules, which will almost certainly have been processed and stored at room temperatures for long periods of time!

Andrew Hamilton

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