What is omega 6?

All fats – animal or vegetable – are made up of building blocks called fatty acids which generally fall into three main groups called saturated, monounsaturated and polyunsaturated. There are two classes of polyunsaturated fatty acids – omega 6 and omega 3. The omega 3 in vegetable oils is called α-linolenic acid and the omega 6 is linoleic acid. The concern about omega 6 relates to linoleic acid which is the most common polyunsaturated fatty acid in the diet.

Do omega 6 fats cause cancer?

In the early 1980s it was thought that fat intake may affect the risk for cancer of the breast and bowel. This hypothesis was based on very basic evidence i.e. different cancer incidence in countries with differing fat intakes, but worth investigating nevertheless.

Several prospective cohort studies were commenced around this time. Data from seven of these studies were pooled in the definitive breast cancer study by Hunter and colleagues. Breast cancer risk was not associated with intake of total fat, animal fat, vegetable fat or polyunsaturated fat. Another pooled analysis of cohort studies published five years later confirmed that polyunsaturated fat was not associated with breast cancer. So omega 6 was off the hook.

When the early results of studies into fats and bowel cancer were published there were hints that animal fat or saturated fat may increase risk, but not polyunsaturated fats or omega 6. Soon it became clear that the problem wasn’t even animal fat; it was red meat. In their review Giovannucci and Goldin concluded:

Intake of red meat or beef has been related to colon cancer risk in most case-control and cohort studies, whereas dietary fat from sources other than red meat, including dairy, poultry, and vegetable oils, does not increase risk of colon cancer.

No smoking gun for omega 6 there.

In fact, there is simply negligible evidence that omega 6 increases cancer risk in humans. Today no credible scientific organisation anywhere in the world recommends restricting omega 6 intake to lower cancer risk.

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Do omega 6 fats cause macular degeneration?

Over a decade ago a case-control study suggested that different types of fatty acids may be linked to the risk for age-related macular degeneration, a condition that can lead to loss of clear vision in older people. A small cohort study (261 subjects) then found that total fat and all major classes of fatty acids were linked to progression of the disease.

However, these findings were not confirmed by two larger cohort studies conducted in Australia. The Melbourne Collaborative Cohort Study and the Blue Mountains Eye Study found no associations between macular degeneration and intakes of total fat, total polyunsaturated fats or omega 6.

Do omega 6 fats cause Parkinson’s disease?

There is a hypothesis that eating lots of omega 6 leads to lots of these polyunsaturated fats in the membranes of brain cells, which in turn leads to oxidative stress, which may then lead to Parkinson’s disease. Okay, it’s a long shot but does the evidence support it?

The question was addressed by Harvard researchers using data from two large cohorts. This study found that replacing saturated fat with polyunsaturated fat was associated with lower risk of Parkinson’s disease. In the Rotterdam Study, intake of polyunsaturated was associated with lower risk for Parkinson’s disease. And that’s all the cohort data we have to go on. Neither of these studies supports the hypothesis that high omega 6 intake increases the risk for Parkinson’s disease.

Do omega 6 fats cause inflammation?

It is often said that too much omega 6 in the diet causes inflammation and therefore may worsen inflammatory conditions, such as rheumatoid arthritis, ulcerative colitis and asthma. However, epidemiological studies do not find higher omega 6 intakes to be associated with higher levels of inflammatory markers. In fact, studies in the United States and Japan find the opposite.

Let’s dig into this. It’s complicated so stay with me.

Inflammation is not a bad thing per se as it is part of the body’s response to infection or injury. But when it occurs in an uncontrolled way the body’s tissues may be damaged. At the cellular level inflammation is governed by long-chain omega 6 and omega 3 fatty acids in cell membranes. The more potent of these is the long-chain omega 6 which is called arachidonic acid (AA). AA can be made in the body from the common omega 6 in the diet, linoleic acid. So the argument is that too much omega 6 in the diet leads to too much AA in the cell membranes, which in turn leads to too much inflammation.

It makes sense, so why doesn’t it happen in real life?

Just because the body can turn omega 6 from the diet into AA doesn’t mean that it automatically happens. The rate of conversion of omega 6 to AA varies depending on the circumstances. If the amount of AA in cell membranes is too low (essential fatty acid deficiency), the rate of conversion of omega 6 to AA is very high. However, if AA in cell membranes is normal the rate of conversion of omega 6 to AA is tiny, about 0.2%. Once the desirable level of AA in cell membranes is achieved it is tightly controlled and stays constant even if omega 6 intake is increased to high levels. Rather than feeding the inflammation process most of the excess omega 6 is burned off for energy.

For a good review on omega 6 and inflammation take a look at the American Heart Association’s Science Advisory on omega 6.

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Summing up

None of these arguments against omega 6 stacks up which is why we hear most of them via the internet and social media rather than from expert scientific organisations.

In my next post I’ll consider omega 6 and coronary heart disease, a topic that is actively debated in the scientific literature.

In 1981 the eminent epidemiologists Richard Doll and Richard Peto wrote a famous paper in which they argued that many cases of cancer were due to environmental factors and were therefore potentially preventable. It was suggested that poor diet was second only to smoking as a cause of cancer and could account for 35% of cases. Based on the evidence available at the time, Doll and Peto suggested that increased intakes of fruits and vegetables may prevent cancer. A generation of nutritionists and dietitians embraced the idea with a passion and started communicating the good news.

Better evidence now available

The early evidence suggesting protective effects of fruits and vegetables against cancer came primarily from case-control studies, with all their well-documented bias. Over the last two decades much better evidence in relation to fruits, vegetables and cancer has become available as large prospective studies and in some cases pooled analyses of these studies have been conducted. Most of the results are negative.

The effect of fruits and vegetables on colon cancer risk was assessed in a pooled analysis of 14 cohort studies, with three quarters of a million subjects. The results – no statistically significant effect for fruits alone, vegetables alone, or fruits and vegetables combined. It was the same story in a pooled analysis of eight cohort studies of fruits, vegetables and breast cancer. And no association was found with prostate cancer or lung cancer.

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Dietary fibre and colon cancer

A recent meta-analysis appeared to provide a glimmer of hope finding that dietary fibre was protective against colorectal cancer. However, when individual sources of dietary fibre were considered only cereal fibre was associated with protection. No significant associations were observed with intake of fibre from fruit, vegetables or legumes. Wholegrains were found to be protective in the same study suggesting that the emphasis of food-based recommendations for the prevention of colorectal cancer should be on grains rather than fruits and vegetables.

Overall cancer risk: the EPIC Study

The European Prospective Investigation into Cancer and Nutrition (EPIC) is the largest study of diet and health ever undertaken, with over half a million subjects from ten countries. The very different dietary patterns between these European countries provided a good opportunity to assess the role of various foods in cancer prevention. A paper from EPIC on the role of fruit and vegetable consumption in relation to overall cancer risk was recently published. Inverse associations between intake of fruits, vegetables, and fruits plus vegetables combined and cancer risk were observed in this study but in each case the magnitude was tiny, just 1-3% reductions. Both the researchers and commentators noted that these results may be due to residual confounding rather than any real effect of fruits and vegetables.

In the accompanying editorial Harvard researcher Walter Willett concluded In summary, the findings from the EPIC cohort add further evidence that a broad effort to increase consumption of fruits and vegetables will not have a major effect on cancer incidence. Willett’s view is particularly relevant as not only he is eminent in the field, he is also a vegetarian.

In a recent review another prominent vegetarian cancer researcher, Tim Key from Oxford University, concluded For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk.

Tim Key and Walter Willett agree that obesity and high alcohol intakes are associated with increased cancer risk and that these should be the focus of efforts to prevent cancer by dietary means.

Response by health authorities

It is interesting to compare and contrast how various health authorities have responded to these developments. In its extensive 2007 report the World Cancer Research Fund downgraded the evidence of a link between the consumption of fruits and vegetables and the risk for cancer. In the Dietary Guidelines for Americans (2010) the whole section on fruits, vegetables and cancer was removed and the topic is now addressed in a single sentence. This is science in action – the evidence changes, so the advice to the general public changes.

And in Australia?

We do things differently in Australia: witness the draft Australian Dietary Guidelines. There was obviously plenty of interest in whether fruits and vegetables may protect against cancer – no fewer than 21 systematic reviews were commissioned. (You may recall that no systematic reviews were conducted in relation to saturated fat, trans fat, glycaemic index or vitamin D). None of the 21 reviews found more than C Grade evidence of a link between fruits, vegetables and cancer.

However, why let a lack of evidence stand in the way of a good yarn? In the draft Australian Dietary Guidelines the section devoted to fruit, vegetables and cancer has doubled in size since the previous edition. Using terms such as ‘evidence suggests’ and ‘emerging evidence’ the Guidelines paint a misleading picture suggesting that scientific support for a protective effect of fruits and vegetables against cancer is actually building, contrary to the findings of the Guidelines’ own literature reviews. Over a page of text is dedicated to mechanisms explaining the protective effect of vegetables, legumes/beans and fruit for some cancers. What protective effect do you imagine the authors are talking about? Truly bizarre.

So in Australia the science may have changed but the message stays the same. Why are our national nutrition authorities attempting to perpetuate a myth rather than distilling the evidence and giving us the facts? If this section is not aligned with the evidence in the final version of the Dietary Guidelines it will mislead all who read it.