Our response to a recent saturated fat study, in plain English

Dr. Sean Wheatley, PhD – Researcher and Trainer in Public Health/5 December 2016

Last week a research article was published in the British Medical Journal (BMJ) that concluded eating a lot of saturated fat (sat fat) makes it more likely that people will get coronary heart disease (CHD) (1). After reading this research we at X-PERT felt that there were a number of issues with the study that mean the conclusions weren’t justified, so we wrote a rapid response that was accepted by the BMJ for publication on their website (available here). We also published a longer version on our website as the BMJ limits responses to 1000 words.

We think it is important that everyone is able to engage with and understand new research and science relevant to them, and this isn’t always the case with academic writing. To try and counter this, this blog aims to provide a simplified, “plain English”, version of our response.

For those who read our blog on how to critique a research article, see how many of these limitations you recognise!

What did this research say?

As stated above, this research concluded that having a high intake of sat fat was associated with CHD. That is to say, the more sat fat they had in their diet the more likely they were to have, or die from, heart disease. They also concluded that if people swapped sat fat for “more healthy energy sources”, such as polyunsaturated fatty acids (PUFA) or wholegrains, this would result in less CHD.

Were there any strengths?

There were a lot of participants in the study- over 70,000 women and 40,000 men. This is a good thing! The study also went on for a long time, which is a benefit as it means there is plenty of time for any effects to happen. The use of hard-end points rather than surrogate markers is also a strength, as measuring how many people died and how many people were diagnosed with CHD is more useful to us than knowing secondary markers, like blood cholesterol, which might never actually lead to adverse effects.

So what’s the problem?

Conflict of Interest

Where the people writing the study stand to benefit from a certain outcome it is important to consider their conclusions carefully. In this case, half of the authors were associated with Unilever; who are the world’s largest producer of margarine. Unilever therefore benefit massively if people swap saturated fat (the kind butter has a lot of) for PUFA (the kind margarine has a lot of), which is exactly what the study says we should do! Although a conflict of interest in itself does not prove a study’s outcomes are wrong, there is research that has found studies funded by industry sources are more likely to reach a favourable outcome then studies that aren’t (2, 3). An independent meta-analysis of observational studies notably didn’t produce findings supporting Zong et al’s conclusions (4). Either way, a conflict this big starts alarm bells ringing!

Research Progress

Observational studies are useful tools for identifying things that might be related, but have limitations which mean they cannot prove any links (discussed in the next section). What this means practically is that experimental trials are normally carried out to try and confirm any trends seen in observational research. In the case of sat fats there have been a number of randomised controlled trials (RCT’s), and even a number of meta-analyses carried out to try and combine the results of these studies (e.g. 4-9). RCT’s and meta-analyses are better sources of evidence than observational research, so it is questionable why more observational studies are being carried out trying to answer the same question. This study by Zong et al is also the third study (References 1, 10 and 11) published by the same research group in the last 18 months asking essentially the same question, and using the same data to try and answer it. This would be unusual in itself, even disregarding the fact better evidence exists.

Observational Study

The limitations of observational studies were discussed in our “ask for evidence” blogs. One of the main limitations is that there are too many different factors involved to be able to isolate the effect of one thing on another. In the case of this study for example they tried to establish the effect of eating sat fat on CHD, but there are a lot of other factors that can also have an effect on CHD that aren’t fully accounted for (for example people’s fitness levels, their levels of stress, or their body composition). They tried to account for a lot of factors that might have played a role but even this is difficult to do. For example they tried to account for the effect of physical activity, but this is very difficult to measure accurately. As a results it is very unlikely they fully isolated the effects of SFA.

Another of the major issues is that correlation does not prove causation. That is to say, just because two things are related that doesn’t mean that one causes the other (I suggest having a look at some of these to see this in action). These limitations are why it is usual to try and test any observations through experiments, where: a) we can see if changing one things does effect another, and b) we can better control for other things that might have an influence.

The methods themselves

It is important to consider that all studies have limitations. There is no such thing as a perfect study, and as such it is easy for people to try and discredit research they don’t agree with by highlighting its flaws. Sometimes the limitations are acceptable though, and the study still provides some useful information. It is debatable though whether the limitations with Zong et al’s research fall into this category.

One of the major issues with the methods was the use of food frequency questionnaires to assess peoples’ diets. Essentially what this involves is providing the participants with a list of foods, and they make a note of how many times each day/week they eat each one. Some of the major flaws with this include issues with people remembering what they’ve actually eaten, whether people are entirely honest even where they do remember, and the fact that the list of foods would have to be incredibly long to include all the possible food stuffs people might consume. One of the other responses online to this research goes as far to say that using food frequency questionnaires means the paper should be retracted, because “their methods are pseudo-scientific and their data and results are inadmissible as scientific evidence”. There are a number of other limitations, such as the large number of assumptions made and some issues with the statistical analyses; but there isn’t time to fully discuss them here.

Not all saturated fats are the same

The last thing I want to talk about is the fact that not all sat fats are the same. The study sets out to see if different sat fats have different associations with CHD, but it doesn’t really achieve this. People who had more of one type of sat fat tended to have more of other types as well, which makes it difficult to isolate the individual effects of each. This could be an important limitation as there is evidence that different sat fats do indeed effect the body in different ways.

The main difference in sat fats is their length. Some come in short chains, which have been suggested to be beneficial for the bacteria in our gut (13). Some have medium length chains, which are broken down quickly in the liver and seem to be related to gaining less weight and having smaller fat deposits (14). Longer chains meanwhile seem be associated with having a lower risk of Type 2 diabetes (15). Whether there are an odd or even number of molecules also seems to be important, and Zong et al didn’t consider odd chain sat fats at all. Odd chain sat fats seem to be related to having less chance of Type 2 diabetes, whilst even chains are possibly linked to increased risk (15). Complicating things further, the presence of even chain sat fats in the blood may be a reflection of the carbohydrate we eat rather than dietary fat, as excess carbohydrate can be turned into sat fat in the liver! This means that even some of the relationships seen between even chain sat fats in the blood with poor health outcomes do not necessarily mean we should be scared of eating sat fat.

It’s also important to consider that we don’t eat fat in isolation, we eat foods. No food contains just fat, or even just one type of fat. Extra virgin olive oil for example, which is hailed as healthy due to the high monounsaturated fat content, also has ~15% sat fat and ~10% polyunsaturated fat. The different fats in different foods are also accompanied by a variety of different combinations of other macronutrients (carbohydrates and proteins), vitamins and minerals. These things further complicate the issue of what effect the sat fat itself has. Dairy products for example are suggested to be good for our health (16-18); but whether this is down to the odd chain sat fats found in dairy fats, the other vitamins and minerals (such as calcium or vitamin d), or something else entirely is hard to tell. It is even possible the only reason we see these relationships is due to flaws in the studies that concluded this!

The role of different types of sat fat are not well understood, and some of the evidence we do have is only observational (and we know the limitations of that!). Nevertheless, there is enough evidence to suggest the type of sat fat may be important, so any research that vilifies total sat fat intake without considering this properly probably isn’t telling us the whole story.

Conclusion

By its nature nutrition research is difficult. Carrying out a study that fully controls everything that might have an effect on the outcome is almost impossible, so sometimes we need to accept the limitations of studies and make the best use of the evidence that is available. Despite this, there comes a point where the repetition of the same old studies doesn’t add any value to the field. In an area like sat fat research where there are already a number of RCT’s, meta-analyses, and an abundance of observational data available the publication of another observational study does nothing to clear the confusion. Particularly when this new study has so many flaws!

As with all our blogs and other work we’d love to hear your thoughts and feedback, so feel free to comment below, drop me an e-mail at sean.wheatley@xperthealth.org.uk or tweet us/me at @XPERTHealth or @SWheatley88.

Research

1. Zong G, Li Y, Wanders AJ, Alssema M, Zock PL, Willett WC, et al. Intake of individual saturated fatty acids and risk of coronary heart disease in US men and women: two prospective longitudinal cohort studies. Bmj. 2016:i5796.

2. Lexchin J, Bero LA, Djulbegovic B, Clark O. Pharmaceutical industry sponsorship and research outcome and quality: systematic review. BMJ : British Medical Journal. 2003;326(7400):1167-.

3. Chartres N, Fabbri A, Bero LA. Association of Industry Sponsorship With Outcomes of Nutrition Studies: A Systemtic Review and Meta-analysis. JAMA Internal Medicine. 2016.

4. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med. 2014;160(6):398-406.

5. Schwingshackl L, Hoffmann G. Comparison of long-term low-fat versus high-fat diets on blood lipids: a systematic review and meta-analysis. Proceedings of the Nutrition Society. 2012;71(OCE3):doi:10.1017/S0029665112003114.

6. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Archives of internal medicine. 2009;169(7):659-69.

7. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. The American Journal of Clinical Nutrition. 2010;91(3):502-9.

8. Schwingshackl L, Hoffmann G. Comparison of the long-term effects of high-fat v. low-fat diet consumption on cardiometabolic risk factors in subjects with abnormal glucose metabolism: a systematic review and meta-analysis. The British journal of nutrition. 2014;111(12):2047-58.

9. Harcombe Z, Baker JS, DiNicolantonio JJ, Grace F, Davies B. Evidence from randomised controlled trials does not support current dietary fat guidelines: a systematic review and meta-analysis. Open Heart. 2016;3(2).

10. Wang DD, Li Y, Chiuve SE, et al. Association of specific dietary fats with total and cause-specific mortality. JAMA Internal Medicine. 2016.

11. Li Y, Hruby A, Bernstein AM, Ley SH, Wang DD, Chiuve SE, et al. Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study. J Am Coll Cardiol. 2015;66(14):1538-48.

12. Bradford Hill A. The Environment and Disease: Association or Causation? Proceedings of the Royal Society of Medicine. 1965;58(5):295-300.

13. Bugaut M. Occurrence, absorption and metabolism of short chain fatty acids in the digestive tract of mammals. Comparative biochemistry and physiology B, Comparative biochemistry. 1987;86(3):439-72.

14. St-Onge MP, Jones PJ. Physiological effects of medium-chain triglycerides: potential agents in the prevention of obesity. The Journal of nutrition. 2002;132(3):329-32.

15. Forouhi NG, Koulman A, Sharp SJ, Imamura F, Kröger J, Schulze MB, et al. Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study. The Lancet Diabetes & Endocrinology. 2014;Oct;2(10):810-8. doi: 10.1016/S2213-8587(14)70146-9. Epub 2014 Aug 5.

16. Alexander DD, Bylsma LC, Vargas AJ, Cohen SS, Doucette A, Mohamed M, et al. Dairy consumption and CVD: a systematic review and meta-analysis. The British journal of nutrition. 2016;115(4):737-50.

17. Drehmer M, Pereira MA, Schmidt MI, Alvim S, Lotufo PA, Luft VC, et al. Total and Full-Fat, but Not Low-Fat, Dairy Product Intakes are Inversely Associated with Metabolic Syndrome in Adults. The Journal of nutrition. 2016;146(1):81-9.

18. Santiago S, Sayón-Orea C, Babio N, Ruiz-Canela M, Martí A, Corella D, et al. Yogurt consumption and abdominal obesity reversion in the PREDIMED study. Nutrition, Metabolism and Cardiovascular Diseases. 2015.

 

 

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