THE GREAT CAN-OLA
By Sally Fallon and Mary G. Enig, PhD
Says Wolke: ?I found no research studies indicating that today’s low-erucic-acid canola oil, as distinguished from ordinary rapeseed oil, is harmful to humans.? That’s because, even though canola oil now has Generally Recognized as Safe (GRAS) status, no long-term studies on humans have been done.
Animal studies on Low Erucic Acid Rapeseed oil were performed when the oil was first developed and have continued to the present. The results challenge not only the health claims made for canola oil, but also the theoretical underpinnings of the diet-heart hypothesis.
The first published studies on the new oil were performed in 1978 at the Unilever research facility in the Netherlands.11 The industry was naturally interested to know whether the new LEAR oil caused heart lesions in test animals. In earlier studies, animals fed high-erucic-acid rape seed oil showed growth retardation and undesirable changes in various organs, especially the heart, a discovery that touched off the so-called ?erucic acid crisis? and spurred plant geneticists to develop new versions of the seed.
The results of the LEAR study were mixed. Rats genetically selected to be prone to heart lesions developed more lesions on the LEAR oil and the flax oil, than those on olive oil or sunflower oil, leading researchers to speculate that the omega-3 fatty acids (not erucic acid) in LEAR and flax oil might be the culprit. But rats genetically selected to be resistant to heart lesions showed no significant difference between the four oils tested and LEAR oil did not cause heart problems in mice, in contrast to high-erucic oil which induced severe cardiac necrosis.
In 1979, researchers at the Canadian Institute for Food Science and Technology pooled the results of 23 experiments involving rats at four independent laboratories. All looked at the effects of LEAR and other oils on the incidence of heart lesions. They found that saturated fats (palmitic and stearic acids) were protective against heart lesions but that high levels of omega-3 fatty acids correlated with high levels of lesions. They found a lesser correlation with heart lesions and erucic acid.12
In 1982, the same research group published a paper that looked at the interaction of saturated fats with LEAR oil and soybean oil. When saturated fats in the form of cocoa butter were added to the diets, the rats in both groups had better growth and a significant lowering of heart lesions. Said the authors: ?These results support the hypothesis that myocardial lesions in male rats are related to the balance of dietary fatty acids and not to cardiotoxic contaminants in the oils.?13
Canadian researchers looked at LEAR oils again in 1997. They found that piglets fed milk replacement containing canola oil showed signs of vitamin E deficiency, even though the milk replacement contained adequate amounts of vitamin E.14 Piglets fed soybean oil-based milk replacement fortified with the same amount of vitamin E did not show an increased requirement for vitamin E. Vitamin E protects cell membranes against free radical damage and is vital to a healthy cardiovascular system.
In a 1998 paper, the same research group reported that piglets fed canola oil suffered from a decrease in platelet count and an increase in platelet size.15 Bleeding time was longer in piglets fed both canola oil and rapeseed oil. These changes were mitigated by the addition of saturated fatty acids from either cocoa butter or coconut oil to the piglets? diet. These results were confirmed in another study a year later. Canola oil was found to suppress the normal developmental increase in platelet count.16
Finally, studies carried out at the Health Research and Toxicology Research Divisions in Ottawa, Canada discovered that rats bred to have high blood pressure and proneness to stroke had shortened life-spans when fed canola oil as the sole source of fat.17 The results of a later study suggested that the culprit was the sterol compounds in the oil, which ?make the cell membrane more rigid? and contribute to the shortened life-span of the animals.18
These studies all point in the same direction — that canola oil is definitely not healthy for the cardiovascular system. Like rapeseed oil, its predecessor, canola oil is associated with fibrotic lesions of the heart. It also causes vitamin E deficiency, undesirable changes in the blood platelets and shortened life-span in stroke-prone rats when it was the only oil in the animals? diet. Furthermore, it seems to retard growth, which is why the FDA does not allow the use of canola oil in infant formula.19
When saturated fats are added to the diet, the undesirable effects of canola oil are mitigated. Most interesting of all is the fact that many studies show that the problems with canola oil are not related to the content of erucic acid, but more with the high levels of omega-3 fatty acids and low levels of saturated fats.
Rapeseed Oil In Traditional Diets
Rapeseed oil has been used in China, Japan and India for thousands of years. In areas where there is a selenium deficiency, use of rapeseed oil has been associated with a high incidence of fibrotic lesions of the heart, called Keshan’s disease.20 The animal studies carried out over the past twenty years suggest that when rapeseed oil is used in impoverished human diets, without adequately saturated fats from ghee, coconut oil or lard, then the deleterious effects are magnified.
In the context of healthy traditional diets that include saturated fats, rapeseed oil, and in particular erucic acid in rapeseed oil, does not pose a problem. In fact, erucic acid is helpful in the treatment of the wasting disease adrenoleukodystrophy and was the magic ingredient in Lorenzo’s oil.
High levels of omega-3 fatty acids, present in unprocessed rapeseed oil, don’t pose a problem either when the diet is high in saturates. A 1998 study indicates that diets with adequate saturated fats help the body convert omega-3 fatty acids into the long-chain versions EPA and DHA, which is what the body wants to do with most of the 18-carbon omega-3s.21
Conversion is reduced by 40-50 percent in diets lacking in saturated fats and high in omega-6 fatty acids from commercial vegetable oils (particularly soybean oil). In the animal studies on canola oil, dietary saturated fats mitigated the harmful effects of omega-3s.
A 1995 Wall Street Journal article reported that use of rapeseed oil in cooking was associated with greatly increased rates of lung cancer in the women breathing the fumes.22 Once again, a lack of saturates in the diet may explain the association, because the lungs can’t work without adequate saturated fats.23 In India, rapeseed oil has been used as a cooking oil for thousands of years, but only recently have Indian housewives been cajoled into the belief that saturated butter and ghee should be avoided. Many now use vanispati, an imitation ghee made of partially hydrogenated soybean oil.
Rapeseed has been used as a source of oil since ancient times because it is easily extracted from the seed. Interestingly, the seeds were first cooked before the oil is extracted. In China and India, rapeseed oil was provided by thousands of peddlers operating small stone presses that press out the oil at low temperatures. What the merchant then sells to the housewife is absolutely fresh.
Modern oil processing is a different thing entirely. The oil is removed by a combination of high temperature mechanical pressing and solvent extraction. Traces of the solvent (usually hexane) remain in the oil, even after considerable refining. Like all modern vegetable oils, canola oil goes through the process of caustic refining, bleaching and degumming — all of which involve high temperatures or chemicals of questionable safety.
And because canola oil is high in omega-3 fatty acids, which easily become rancid and foul-smelling when subjected to oxygen and high temperatures, it must be deodorized. The standard deodorization process removes a large portion of the omega-3 fatty acids by turning them into trans fatty acids. Although the Canadian government lists the trans content of canola at a minimal 0.2 percent, research at the University of Florida at Gainesville, found trans levels as high as 4.6 percent in commercial liquid oil.24 The consumer has no clue about the presence of trans fatty acids in canola oil because they are not listed on the label.
A large portion of canola oil used in processed food has been hardened through the hydrogenation process, which introduces levels of trans fatty acids into the final product as high as 40 percent.25 In fact, canola oil hydrogenates beautifully, better than corn oil or soybean oil, because modern hydrogenation methods hydrogenate omega-3 fatty acids preferentially and canola oil is very high in omega-3s. Higher levels of trans mean longer shelf life for processed foods, a crisper texture in cookies and crackers — and more dangers of chronic disease for the consumer.26
The Myth Of Monounsaturated
Consumer acceptance of canola oil represents one in a series of victories for the food processing industry, which has as its goal the replacement of all traditional foods with imitation foods made out of products derived from corn, wheat, soybeans and oil seeds. Canola oil came to the rescue when the promotion of polyunsaturated corn and soybean oils had become more and more untenable. Scientists could endorse canola oil in good conscience because it was a ?heart-healthy? oil, low in saturated fat, high in monounsaturates and a good source of omega-3 fatty acids.
But most of the omega-3s in canola oil are transformed into trans fats during the deodorization process; and research continues to prove that the saturates are necessary and highly protective.
At least it can be said that canola oil is a good source of monounsaturated fat — like olive oil — and therefore not harmful. . . Or is it? Obviously monounsaturated fatty acids are not harmful in moderate amounts in the context of a traditional diet, but what about in the context of the modern diet, where the health-conscious community is relying on monounsaturated fats almost exclusively?
There are indications that monounsaturated fats in excess and as the major type of fat can be a problem. Overabundance of oleic acid (the type of monounsaturated fatty acid in olive and canola oil) creates imbalances on the cellular level that can inhibit prostaglandin production.27 In one study, higher monounsaturated fat consumption was associated with an increased risk of breast cancer.28
Even the dogma that monounsaturated fatty acids are good for the heart is at risk. According to a 1998 report, mice fed a diet containing monounsaturated fats were more likely to develop atherosclerosis than mice fed a diet containing saturated fat.29 In fact, the mice fed monounsaturated fats were even more prone to heart disease than those fed polyunsaturated fatty acids.
This means that the type of diet recommended in books like The Omega Diet — low in protective saturates, bolstered with high levels of omega-3 fatty acids and relying on monounsaturated fatty acids, whether from olive or canola oil, for the majority of fat calories — may actually contribute to heart disease. Such diets have been presented with great marketing finesse, but we need to recognize them for what they are — payola for the food companies and con-ola for the public.
11. RO Vles and others. Nutritional Evaluation of Low-Erucic-Acid Rapeseed Oils. Toxicological Aspects of Food Safety, Archives of Toxicology, Supplement 1, 1978:23-32
12. HL Trenholm and others. An Evaluation of the Relationship of Deitary Fatty Acids to Incidence of Myocardial Lesions in Male Rats. Canadian Institute of Food Science Technology Journal, October 1979;12(4):189-193
13. JKG Kramer and others. Reduction of Myocardial Necrosis in Male Albino Rats by Manipulation of Dietary Fatty Acid Levels. Lipids, 1982;17(5):372-382.
14. FD Sauer and others. Additional vitamin E required in milk replacer diets that contain canola oil. Nutrition Research, 1997;17(2):259-269.
15. JK Kramer and others. Hematological and lipid changes in newborn piglets fed milk-replacer diets containing erucic acid. Lipids, January 1998;33(1):1-10.
16. SM Iunis and RA Dyer. Dietary canola oil alters hematological indices and blood lipids in neonatal piglets fed formula. Journal of Nutrition, July 1999;129(7):1261-8.
17. WMN Ratnayake and others. Influence of Sources of Dietary Oils on the Life Span of Stroke-Prone Spontaneously Hypertensive Rats. Lipids, 2000;35(4):409-420.
18. MN Wallsundera and others. Vegetable Oils High in Phytosterols Make Erythrocytes Less Deformable and Shorten the Life Span of Stroke-Prone Spontaneously Hypertensive Rats. Journal of the American Society for Nutritional Sciences, May, 2000;130(5):1166-78
19. Federal Register, 1985.
20. OA Levander and MA Beck. Selenium and viral virulence. British Medical Bulletin, 1999;55(3):528-33.
21. H Gerster. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? International Journal of Vitamin and Nutrition Research 1998;68(3):159-73.
22. Wall Street Journal, June 7, 1995, p. B6.
23. MG Enig. Benefits of Saturated Fats. Wise Traditions, Summer 2000;1(2):49.
24. S O’Keefe and others. Levels of Trans Geometrical Isomers of Essential Fatty Acids in Some Unhydrogenated US Vegetable Oils. Journal of Food Lipids 1994;1:165-176.
25. JL Sebedio and WW Christie, eds. Trans Fatty Acids in Human Nutrition, The Oily Press, Dundee, Scotland, 1998, pp 49-50.
26. MG Enig, Trans Fatty Acids in the Food Supply: A Comprehensive Report Covering 60 Years of Research, 2nd Edition, Enig Associates, Inc., Silver Spring, MD, 1995.
27. Horrobin, David F, Prostaglandins: Physiology, Pharmacology and Clinical Significance The Book Press, Brattleboro, Vermont, 1978, p 20, 35
28. V Pala and others. Erythrocyte membrane fatty acids and subsequent breast cancer: a prospective Italian study. Journal of the National Cancer Institute, July 18, 2001;93(14):1088-95.
29. LL Rudel and others. Dietary monounsaturated fatty acids promote aortic atherosclerosis in LDL-receptor-null, human ApoB100-overexpressing transgenic mice. Arteriosclerosis, Thrombosis and Vascular Biology, November 1998;18(11):1818-27.