The world of dietary fats is a complicated alphabet soup of names and numbers, and our understanding of how each type of fat works in the body – for good or ill – is far from complete.
To aid our understanding, we tend to reduce the issue to its most basic equation. For a long time, this has translated into ‘fat is bad’. The official advice from medical circles – both conventional and alternative – has been to cut out all ‘unnecessary’ fat from your diet.
Nevertheless, fats are important in nutrition. They provide a concentrated source of energy for the body, constitute a form of insulation for body tissues, and aid the absorption of the fat-soluble vitamins A, D, E and K.
They are also important in food preparation, enhancing its flavour and its ‘feel’ in the mouth. Fats tenderise meat products, and conduct heat during cooking. Some nutritionists even believe that fats are important for feelings of satiety. So, in slavishly following a low-fat diet, we could be condemning ourselves to life-long feelings of hunger as well as a range of debilitating diseases.
The question is: how much fat do we need? This question is particularly pertinent to the essential fatty acids (EFAs) known as omega-6 and omega-3. The body cannot make these fats and must obtain them from dietary sources. Yet, no single authority can agree on the quantities we need or the correct proportions of these important dietary fats in relation to each other. Even the recommendations of ‘experts’ are mostly guesswork pieced together from information on traditional diets and the official guidelines of various authorities.
Inuits (Eskimos) eating a traditional diet may consume approximately 5 g of omega-3 fatty acids daily, equivalent to the EFAs in about a pound of salmon. But most of us don’t need this much to benefit from the omega-3s.
Researchers in Sweden tell us that fish has a ‘dose-dependent’ effect – that is, the more fish in your diet, the healthier your heart (BMJ, 1986; 293: 426). In one study, men who included as little as half a pound of fatty fish in their diet every week had healthier cardiovascular systems than non-fish eaters (N Engl J Med, 1985; 312: 1205).
Nutritionists do not know the optimal intake of omega-6 fatty acids. It is generally believed that, to prevent a deficiency in adults, about 2 per cent of daily calories should be derived from omega-6 fatty acids. This is equivalent to approximately 4.5 g of omega-6 fatty acids per day.
The ideal intake of omega-3s is also unknown, though some researchers recommend a general daily intake of 3 g (Arch Intern Med, 1993; 153: 1429-38; Arthritis Rheum, 1994; 37: 824-9).
Taking these recommendations on board means that the average person would be getting a ratio of 1.5:1 of omega-6 to omega-3.
Yet, this ratio is not reflected in official recommendations and is certainly not reflected in our normal eating habits. The current dietary omega-6 to omega-3 ratio in the West ranges from about 10:1 to 25:1, indicating that the typical diet is very low in omega-3 fatty acids compared with the Paleolithic diet on which humans evolved (Am J Clin Nutr, 1991; 54: 438-63).
After ignoring the problem for years, the US Institute of Medicine finally set recommended daily intakes for omega-6 and omega-3 at a ratio of around 10:1 (IOM, National Academy of Sciences Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids, National Academy Press, 2002).
In the UK, the official Reference Nutrient Intake tables, issued by the Department of Health, suggest a range of anywhere from 1:1 to 3:1 of omega-6 to omega-3.
In Canada, daily intake ratios range from 4:1 to 10:1 (Scientific Review Committee, Nutrition Recommendations, Ottawa: Minister of National Health and Welfare Canada, 1990). The joint committee of the Food Agriculture Organization/World Health Organization recommends a ratio between 5:1 and 10:1 (Nutr Rev, 1995; 53: 202-5).
The problem of determining sensible recommendations is, of course, further confounded by the fact that essential fatty acid needs may vary according to lifestyle as well as climate. A physically active person in a cold climate may require more fats of all kinds than a sedentary person living in a warmer climate.
Nevertheless, what is clear is that our diets are dangerously overbalanced towards omega-6, a problem that sets up a vicious cycle. Omega-6 and omega-3 fatty acids compete in the body for the same binding sites. The more omega-6, the less of the already meagre omega-3 in the diet will be absorbed (Am J Clin Nutr, 2000; 71: 179-88).
Problems of overabundance
There is good evidence to suggest that EFAs are important for heart health, relief from allergies, optimal immunity and even protection from cancer. But equally good evidence links diets containing an excess of omega-6 in relation to omega-3 not only to heart disease, but also cancer and autoimmune disorders (Lancet, 1989; ii: 757-61; Nutr Cancer, 1987; 9: 205-16; Br J Rheumatol, 1997; 36: 513-5). A relative excess of omega-6 has also been linked to depression (Lipids, 1996; 31: S157-61).
Omega-6 fatty acids contribute to the production of prostaglandins, which can contribute to, among other conditions, inflammation of the airways. Indeed, a recent study showed that toddlers who consume large quantities of margarine and fried foods may be twice as likely to develop asthma as their peers who eat less of these foods (Thorax, 2001; 56: 589-95).
While we think of saturated fats as killers, a recent Swedish study involving 60,000 participants found that it was the consumption of vegetable oil, not saturated fat, that was most strongly linked with the development of breast cancer (Arch Intern Med, 1998; 158: 41).
Even more disturbing, given the myth of heart protection that has sprung up for polyunsaturated oils, atheromas – the first step toward atherosclerotic plaques – have been found to be made up of 74 per cent polyunsaturated fats and only 26 per cent saturated fats (Lancet, 1994; 344: 1195-6).
Omega-3s are generally considered more healthful; supplementation can benefit a range of inflammatory conditions such as Crohn’s, rheumatoid arthritis, kidney diseases and chronic obstructive pulmonary diseases (Gastroenterology, 1991; 100: A228; Arthritis Rheum, 1995; 38: 1107-14; J Am Soc Nephrol; 1999; 10: 1772-7; N Engl J Med, 1994; 331: 228-33). Omega-3s can also help Raynaud’s disease, immune function and cardiac arrhythmias (Am J Med, 1989; 86: 158-64; Nutrition, 1998; 14: 627-33; J Nutr, 1997; 127: 383-93). Fish oil can prevent cancer (Nutr Cancer, 1995; 24: 151-60), and low blood levels of omega-3 have been found in people with depression (Psychiatry Res, 1999; 85: 275-91).
But while fish oils may appear beneficial over the short term, longer-term studies have revealed a possible paradoxical effect.
In a small-scale study of 40 people given either placebo or increasing doses of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), early results showed the expected healthful effects – a rise in blood and red-blood-cell levels of both these fatty acids, and a decline in the more harmful arachidonic and linoleic acids (see box above).
After a month, the participants were exposed to an oxidising agent. Again, as expected, there was significantly less fatty-acid oxidation with the highest doses of EPA and DHA compared with the sugar placebo pills.
But, in contrast to the earlier benefits, after six months, the oxidative damage in red blood cells was significantly greater with the highest doses of EPA and DHA. The authors concluded that long-term megadosing with these omega-3s could actually lead to atherosclerosis (Am J Clin Nutr, 1996; 64: 297-304).
High levels of the omega-3 alpha-linolenic acid (LNA) have also been implicated in an increased risk of heart attack. LNA is less effective than fish oil at reducing triglyceride fats (Am J Clin Nutr, 1997; 66: 591-8). In one study, fatty tissue taken from heart-attack victims was found to be high not only in trans fatty acids, but also in linoleic acid (LA, an omega-6) and LNA (Eur J Clin Nutr, 2000; 54: 618-25). Other data show an increase in atherosclerosis over the long term with omega-3s (Arterioscler Thromb Vasc Biol, 1996; 16: 1197-202).
Similarly, when the Nurses Health Study of 88,795 healthy women compared breast cancer rates in those who derived more than 30 per cent of their calories from fat with those who derived less than 20 per cent of their calories from fat, it found that women on the low-fat diet had the higher rates of breast cancer (JAMA, 1999; 281: 914). Closer examination of the findings revealed that all types of fats, except omega-3s, were protective. In fact, omega-3s derived from fish oil actually increased the risk of breast cancer.
Animal, vegetable, or what?
Such findings only add fuel to the debate over not just optimal amounts, but optimal sources of essential fats. For years, fish and fish oils have been the preferred source of omega-3s. But most recently, with the increasing pollution of marine life, the pendulum has swung in favour of vegetable sources such as flaxseed (linseed) and hempseed oils.
But accumulating evidence suggests that replacing fish oils (which contain easily assimilated EPA and DHA omega-3s) with flaxseed oil, which has relatively high amounts of LNA (but is an earlier form or precursor to EPA and DHA) may not be as sound as we thought.
Although LNA can be converted in the body into EPA and DHA, in some people, particularly the elderly, this process may be inefficient (Am J Clin Nutr, 1991; 54: 438-63). Other studies have found that, even in healthy individuals, the amount of LNA converted into EPA in the body may be very low (Prostagl Leukotr Essential Fatty Acids, 2000; 63: 287-92).
It is generally believed that around 14 per cent of LNA is converted to EPA. But in one (albeit small) study, only 0.2 per cent of the LNA in a flaxseed oil supplement was available for conversion to the final omega-3 fatty acid – compared with the 23 per cent of EPA already present in fish oil (J Lipid Res, 2001; 42: 157-65).
Poorly metabolised oils may increase free-radical damage. The inability of some individuals to metabolise LNA may be one reason why its supplementation has been linked to higher rates of prostate cancer (J Natl Cancer Inst, 1994; 86: 281-6; Int J Cancer, 1997; 71: 545-51). LNA has been touted as a potent inhibitor of other types of cancer cells, but the evidence is inconclusive (Am J Clin Nutr, 1997; 66 [Suppl]: 998S-1003S).
Proponents of flaxseed oil claim that the improvement in skin condition often noted with supplementation is a sign that it’s working to improve the whole body. But this could simply be a result of the high phytoestrogen content of the oil rather a reflection of LNA action – and if this is the case, are these phytoestrogens doing harm or good?
At the moment, there is no evidence either way as researchers aren’t exploring these questions.
Saturated fat to the rescue
The current received wisdom accepts that fat intake is associated with obesity, heart disease and cancer. But the data are far from unequivocal. As one review of the evidence into dietary fat and heart health concluded: ‘Despite decades of effort and many thousands of people randomised, there is still only limited and inconclusive evidence of the effects of modification of total, saturated, monosaturated or polyunsaturated fats on cardiovascular morbidity and mortality’ (BMJ, 2001; 322: 757-63).
In fact, evidence continues to show that saturated fats are not the poisons we think they are. All fats – with the exception of man-made trans fats – have something positive to offer the body. The current trend is toward a moderate intake of saturated fats rather than its wholesale elimination from the diet.
We now know, for instance, that fatty acids such as those found in butter are more easily metabolised for energy. The body also needs saturated fats to absorb EFAs, to take up calcium in the bones, to stimulate the immune system, and to add (along with cholesterol) structure and stability to cell walls.
Saturated fats are also more stable than polyunsaturates. They don’t turn rancid as quickly and are more stable when heated (making them more suitable for cooking). This means they are less likely to produce heart-damaging and cancer-causing free radicals.
Polyunsaturated fatty acids have been associated with a range of adverse effects on the thyroid, resulting in hypothyroid-like symptoms. Saturated fats, on the other hand, increase tissue sensitivity to thyroid hormone T3 (J Biol Chem, 1986; 261: 13997-4004).
While we associate tropical oils, such as coconut and palm oils, with poor health, they have evidence of as yet unexplored promise. For example, lauric acid, prominent in coconut oil, has potent antiviral, antibacterial, and antiprotozoal properties (J Gen Virol, 1994; 75: 353-61). Until recently, no one in the mainstream nutrition community has made the link between this and the treatment of many serious viral infections, yet the potential is there.
Tropical oils may also benefit heart health. A review of the literature on coconut oil’s effect on cholesterol and atherogenesis concluded that ‘coconut oil is a neutral fat in terms of atherogenicity’ (J Philippine Med Assoc, 1989; 65: 144-52).
Other studies comparing the effect of coconut and soy oils in healthy young men found that coconut oil increased (good) HDL cholesterol while soy oil reduced it (Br J Nutr, 1990; 63: 547-52). Where intake of tropical oils is traditionally high, heart disease is rare. But when these people moved to places where the typical Western diet is consumed, their total and (bad) LDL cholesterol increased while HDL cholesterol was decreased (Am J Clin Nutr, 1981; 34: 1552-61).
Good, bad and ugly?
These days, we make what we believe are subtle distinctions between different types of fats. They can, for instance, be good fats – like the monounsaturates found in olive and canola oils, cashews, peanuts, macadamia nuts, almonds and avocados, and the polyunsaturates found in salmon, mackerel, herring, sardines, hemp, sunflowerseeds and flaxseeds, and flax, corn, safflower, sunflower, soybean and sesame oils.
Fats can also be bad, like the saturated fats in meat, butter, cheese, egg yolks, whole milk, and coconut and palm oils.
Or they can be just plain ugly, like the trans fatty acids in partially hydrogenated vegetable oils, margarine, deep-fried foods, doughnuts, and commercial snack products such as crackers, cookies and pastries.
In truth, most fats are a mixture of all three – what makes them ‘good’ or ‘bad’ may largely be a matter of quantity or quality. The highly successful marketing of polyunsaturated fats and low-fat diets have made it acceptable for all of us to include far more processed oils and spreads in our diets than have earlier generations – to our detriment. With the exception of man-made trans fats, there may be no such thing as ‘bad’ fat – there may be only ‘too much’ fat.
The surest path through this thicket of contradictory information is to let common sense and your body’s innate wisdom prevail. Avoid megadosing on supplements and eat the widest variety of organic, unprocessed food, particularly the kind that has stood the test of the ages.