Monday, May 10, 2010

When the cure is worse than the disease


In a letter–to-the-editor of the Lancet (1983) Dr. Wayne Martin wrote: “In early 20th century Britain and the United States everyone cooked and baked with butter or lard, and death from what we now call myocardial infarction was so rare that it had no name or medical recognition. The oilseed industry was founded shortly before 1920 and by 1926 was injecting into the national diet trainloads of new vegetable fats which, in the concept of the ‘prudent’ diet are now the ‘good’ fats… I suggest that the introduction of trans-trans linoleic acid in the 1920s in margarines and refined vegetable oils was the main cause of the pandemic of myocardial infarction and that since 1960 orthodox medicine has been fostering a cause of this disease as the cure”. Powerful words…and subsequent research has shown that Dr. Martin was indeed right. So right that food processors and manufacturers are now tripping over themselves in their haste to remove trans fats from their products…which they, of course, should do. If fat is removed, however, then something must replace it. In some cases the replacement might be sugar or other refined carbohydrate (a bad choice and subject for another discussion). In other cases, where a carb replacement won’t work, the replacement ingredient is usually a non-hydrogenated vegetable oil, and most often a vegetable oil rich in linoleic acid, otherwise termed omega-6 fatty acid. Today’s blog might be a bit more technical than usual, but I think it’s important for you to be at least exposed to this view-point.
My goal is to draw your attention to the real threat posed by excessive intake of omega-6 fatty acids, especially when that intake further skews an already inappropriate ratio of omega-6:omega-3 (fish oils). The importance of omega-3s in the diet won’t be discussed here, since I’m pretty sure that most are already aware of this fact.
It’s been shown by various western countries that the average person consumes roughly ten times more vegetable oil than was the case fifty years ago. I would go so far as to suggest that we’re consuming roughly 1000 times more than we did a century ago. After all…who could squeeze a corn cob? Expressed oil simply wasn’t available, although those lucky enough to live around the Mediterranean did have olive oil with its relatively low level of linoleic acid. In fact, one could make a good case for the reason behind the benefits of the “Mediterranean Diet” being that the intake of linoleic acid is so low.
The problem with excessive omega-6 is that it can interfere with omega-3 uptake (already in short supply), resulting in serious potential for conditions including inflammation, platelet aggregation, reduced HDL cholesterol levels, increased gallstone formation, predisposition to lipid peroxidation, hypertension, depressed immune function, cancer, abdominal weight gain and age-related macular degeneration.
As far back as 1994 studies were being published that warned about possible adverse effects of polyunsaturated fats in the development of CHD. Writing in the Lancet, J. L. Witztum found a positive association between omega-6 fatty acids in adipose tissue and plaque…and no association between saturated fats and plaque. The conclusion was that “ …current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered”…and that was in 1994, long before the rush to replace trans fats with vegetable oil. A study by Felton found that the adipose tissue concentration of linoleic acid was positively associated with the degree of CHD, as was Omega-6 and cancer.

Linoleic acid is the only fatty acid to exhibit an unequivocal cancer-enhancing effect in rodents, impacting mammary, pancreatic and colon cancer. A number of nutrients exhibit tumour-enhancing properties, but excessive levels of intake are usually required. This is not the case, however, with linoleic acid of which, based on the work of Michael Pariza, only five times the amount needed for optimal growth will bring about mammary tumour development in rats. The effect of “fat type” on cancer development has been the subject of a great deal of research, but the effects are almost always related to linoleic acid intake. The more linoleic acid in a product (corn oil for example), the more carcinogenesis enhancement compared to low linoleic acid foods like dairy fat, beef tallow and fish oils.

In 1997 Rose examined the effect of dietary fatty acids on breast and prostate cancers and concluded that “omega-6 fatty acids perform functions in experimental prostate cancer progression similar to those described for breast cancer” and that saturated fats have no effect on breast carcinogenesis or progression. Goodstine’s research indicated that a higher omega-3:omega-6 ratio (or conversely, the opposite) would reduce the risk of breast cancer, especially in pre-menopausal women. Other researchers looked at the influence of maternal diet on breast cancer risk among female offspring and determined that “a high dietary linoleic acid intake can elevate pregnancy estrogen levels and this, possibly by altering mammary gland morphology and expression of fat-and/or estrogen-regulated genes, can increase breast cancer risk in the offspring. It’s not a great stretch to speculate that the same may be true regarding prostate cancer risk in male offspring of mothers on diets rich in linoleic acid. Results from the EURAMIC (European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Cancer) breast cancer study also provide evidence for the hypothesis that the balance between omega-6 and omega-3 may play a role in breast cancer. Spanish researchers found that an excess of omega-6 fats in the diet accelerates breast cancer by altering the activity of a group of genes.
Looking specifically at prostate cancer Godley researched biomarkers of essential fatty acid consumption and found that “linoleic acid consumption was positively associated with prostate cancer risk, which is consistent with results from animal experiments”. Wang investigated the impact of a high versus low-fat diet on risk of prostate cancer and found that fat reduction was definitely positive. The reporting of that study, however, generally failed to mention that the source of fat in the high-fat diet was linoleic-rich corn oil. A 2006 study by Brown found that a diet rich in omega-6 fatty acids appeared to promote the spread of prostate cancer, while a diet rich in omega-3s impeded the spread. Hughes-Fulford, in 2006, found a significant link between the ratio of omga-6:omega-3 and prostate cancer and was quoted as saying she would never use any of the high-linoleic acid oils.
Among several other conditions laid at the foot of excessive linoleic acid intake are asthma, eczema, allergic rhinitis, and hay fever. It has also been proposed that unnoticed changes in fatty acid composition of ingested fats over the last decades have been important determinants in the increasing prevalence of childhood overweight and obesity. Unscientific though it may seem, one can’t help but pause while considering the concomitant rise in cancers of the breast, prostate and colon along with a rise in linoleic acid consumption. While vegetable oil intake was on the dramatic increase, consumers were urged (and heeded the call) to sharply reduce the amount of cancer-fighting, CLA-rich animal fats in their diet.
Thomas Edison once said “The doctor of the future will give no medicine, but will interest his patients in the care of the human body, in diet, and in the cause of prevention of disease”. Though Edison was no nutritionist, I think he was on to something. This blog is not to suggest that you should avoid linoleic acid in your diet…it’s essential! What we should avoid are diets that are excessive…in anything.

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