Let's put to bed, once and for all, dietary advice to avoid full-fat dairy products
In the very same week it is reported that medication used in the treatment of diabetes now accounts for some 10 per cent of spending by the National Health Service here in the UK, I am somewhat baffled that the media – in reporting a study containing the most convincing evidence to date that saturated fats are not harmful to health – have largely overlooked what is perhaps the most significant conclusion in this study (1): namely that trans-palmitoleic acid, which is present in dairy products, offers protection from type 2 diabetes, the form of the disease responsible for the relentless increase in the incidence of diabetes in the UK and other westernised societies.
For years, misguided ‘experts’ have advised the public to reduce their consumption of saturated fats, so much so that dairy products have been all but demonised. It is now high time the record was set straight. The shift to vegetable oils in place of dairy products has caused a massive increase in the ratio of omega-6 to omega-3 polyunsaturates in western diets. This shift is associated with pro-inflammatory conditions and it is no coincidence that it has been accompanied by an equally alarming increase in the incidence of our major inflammatory diseases, namely type 2 diabetes and cardiovascular disease (2,3).
Evidence for the beneficial effects of particular trans-fats of endogenous origin, as opposed to those of industrial origin, is widely documented in the literature (4-6). In addition to trans-palmitoleic acid (5), cis-9, trans-11 conjugated linoleic acid, the main isomer of CLA present in dairy products, is also believed to be protective against diabetes (6). Now that the health benefits of these trans-fats have been ‘demonstrated’ using statistics (the ‘blind’ method, so favoured by those forever offering inconsistent dietary advice), will the experts please come clean and admit to the wider public that they were wrong to demonise dairy products? I quote a statement from a 2010 paper by Mozaffarian and colleagues (5):
‘Our results suggest that efforts to promote exclusive consumption of low-fat and nonfat dairy products, that would lower population exposure to trans-palmitoleate, may be premature until the mediators of health benefits of dairy consumption are better established.’
It is due to such efforts to reduce saturated fat intake that the typical low-fat ‘healthy’ yoghurt contains some 16 grams of sugar, which is certainly not conducive to good health! In the intervening years, since the 2010 paper, studies have been published which support the assertion that the consumption of dairy products is associated with a lowered risk of type 2 diabetes (7, 8).
The public have not been credited with the ability to handle anything more than health messages that are so uncomplicated – so simple – as to be useless, if not outright counterproductive. Why did all trans-fats have to be demonised just because the artificial, industrial varieties are harmful? Many people still fret unnecessarily about the presence of trans-fats in their food, but the food industry has gone to considerable lengths to reduce these to amounts that are insignificant to those consuming a sensible, balanced diet. Foods containing fats of animal origin will always contain very small amounts of trans-fats, but these are a completely different kettle of fish to those that were once introduced in large quantities by artificial means.
Those who recommend the replacement of dietary animal fats with vegetable oils usually base their reasoning on the observation that this leads to a reduction in plasma low density lipoprotein (LDL), which – the argument goes – lowers the risk of cardiovascular disease. This reasoning is based, however, almost entirely on statistical ‘risk factors’ and fails to take proper account of the underlying biochemical mechanisms of atherosclerosis.
Whilst it is unclear precisely how atherosclerosis is initiated, it is evident that the ongoing process comprises a vicious cycle of inflammation and self-amplifying free-radical chain reactions, culminating in the modification of LDL to an oxidised form (‘oxLDL’) that is avidly taken up via the scavenger receptor pathway. The basic chemistry of LDL modification is ‘screaming out loud’ to us that polyunsaturated fatty acids, being far more susceptible to lipid peroxidation than their saturated relatives, should promote the process (9).
If we accept that a certain fraction of LDL in the bloodstream is going to be converted to oxLDL, then of course lowering total LDL will lower the absolute level of the modified lipoprotein. It is an unfortunate coincidence, then, that the dietary measures commonly recommended to lower total LDL (‘high in polyunsaturates/low in saturates’) can logically be assumed to promote oxLDL formation. Rather than intervening downstream to the LDL oxidation step, after the damage has been done, it would surely make more sense to consume diets which minimise LDL modification in the first place. Raised LDL per se is not the problem: prevent its oxidation and elevated levels should not be atherogenic.
Unfortunately such nuances will never be revealed by the adoption of a mechanism-blind statistical approach to the investigation of the links between diet and cardiovascular disease. No matter how ‘significant’ the statistics, how perfectly ‘controlled’ the sample, number crunching should always be subservient to mechanism-based biological chemistry. If we are to break free from this perpetual cycle of conflicting dietary advice, a major rethink is required as to what constitutes evidence worthy of forming the basis of dietary guidelines. Blind statistics it is not.
1. De Souza, R. J. et al. (2015) Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta analysis of observational studies. BMJ 351:h3978
2. Simopoulos, A. P. (1999) Essential fatty acids in health and chronic disease. Am. J. Clin. Nutr. 70 (suppl.), 560S – 569S
3. Blasbalg, T. L. et al. (2011) Changes in consumption of omega 3 and omega 6 fatty acids in the United States during the 20th century. Am. J. Clin. Nutr. 93, 950 – 962
4. Pariza, M. W. (2004) Perspective on the safety and effectiveness of conjugated linoleic acid. Am. J. Clin. Nutr. 79 (suppl.), 1132S – 1136S
5. Mozaffarian, D. et al. (2010) Trans-palmitoleic acid, metabolic risk factors, and new-onset diabetes in US adults. Ann Intern. Med. 153, 790 – 799
6. Castro-Webb, N., Ruiz-Narváez, E. A. and Campos, H. (2012). Cross-sectional study of conjugated linoleic acid in adipose tissue and risk of diabetes. Am. J. Clin. Nutr. 96, 175 – 181
7. O’Connor, L. M. et al. (2014) Dietary dairy product intake and incident type 2 diabetes: a prospective study using dietary data from a 7-day food diary. Diabetologia DOI 10.1007/s00125-014-3176-1
8. Zong, G. et al. (2014) Dairy consumption, type 2 diabetes, and changes in cardiometabolic traits: a prospective cohort study of middle-aged and older Chinese in Beijing and Shanghai. Diabetes Care 37, 56 – 63
9. Burkitt, M. J. (2001) A critical overview of the chemistry of copper-dependent low density lipoprotein oxidation: roles of lipid hydroperoxides, -tocopherol, thiols, and ceruloplasmin. Arch. Biochem. Biophys. 394, 117 –135
Competing interests: No competing interests