On causes, Noakes, and making prudent claims related to diet

Three pieces related to diet and the low-carb high-fat fad are worthy of highlighting this week, because all of them are a counterpoint to the “sugar is addictive and you’re a victim of a conspiracy” seam that continues to be mined by the likes of Professor Tim Noakes. The first is by Gary Taubes, who Noakes cites as being responsible for removing the scales from his own eyes, and the second is a response to Taubes by Dr David Katz, who says that Taubes is asking the wrong questions.

You can read those pieces yourself – the only aspect I want to highlight here is how moderate Taubes’ tone is. He acknowledges that the science isn’t settled, but that he’s biased in favour of “sugars and refined grains” being the problem. He even includes the rider that “we all have our biases”. Indeed we do. But on that minimal (and yes, selective) quote, Taubes could be saying the same thing that mainstream nutrition science is – which is at a significant remove from the claims made by Noakes, who speaks as if there’s no doubt that carbohydrates are the cause of most of our ills, and that most of our ills can be eliminated (or at least managed) by eliminating the majority of carbs from our diets.

In other words, Taubes at least speaks as if he acknowledges the possibility of being wrong. Noakes, by contrast, leaps straight to rather humorous epithets when people disagree with him, calling them victims of “Group Think”, “statinators”, or “The Anointed”. Alternatively, he’ll poison the well by making very generalised aspersions about funding, as if to pre-emptively taint any claims that are being made. It’s tinfoil-hat territory, and in short, in no way confidence-inspiring, at least not for those of us who want to resist signing up to a cult.

And it’s the third piece that merits your careful attention, if you care for holding science and scientists up to rigorous and principled scrutiny. Not because it says anything new, but because it quite clearly articulates a very essential, and simple, principle of scientific reasoning. Namely: what question is being asked, and what sort of an answer will we be willing to accept as legitimate? The key passage for me – at least in terms of highlighting how Noakes is compromising critical thinking – is this one:

It seems likely that we were seduced by the early successes of epidemiology with point-causes with large effects — infectious diseases — and we were similarly seduced by Mendel’s carefully engineered successes with similar point causes — single genes — for carefully chosen traits, but these are paradigms that don’t fit the complex world we’re now in. What Mendel showed was that causal elements were inherited with some specifiable probability, and he did that in a well-posed setting (selective choice of traits and highly systematized breeding experiments). But Mendel’s ideas rested on the notion that while the causal elements (we now call them alleles) were transmitted in a probabilistic way, once inherited they acted deterministically. Every pea plant with the same genotype had the same color peas, etc. We now know that that’s an approximation for some simple situations, but not really applicable generally.

This passage reminds me of the dispute between Humean accounts of causation and what I’ll call the “causal powers” account, described very usefully in Harre and Madden’s 1975 book, Causal Powers: A Theory of Natural Necessity. In short, the distinction could be captured in discriminating between the fact that high carbs typically mean high quantities of refined foods, sugars, a sedentary lifestyle etc. and the fact that neither does it need to mean that, nor that those causal factors exist in isolation.

By way of example: To say that aspirins relieve headaches is to say that, because of its nature, an aspirin can relieve a headache while a laxative cannot. The means by which it achieves this are neither occult nor unfathomable – it does not have this power in spite of its nature; it is rather because of its nature that this is possible.

In cases like these, scientists are able to investigate the chemical composition of an aspirin, and then to figure out why it has the effect it has on the body, describable in terms of chemical reactions within the body. An aspirin’s power to relieve headaches is furthermore something which exists even when the tablet is not being used to relieve a headache. When we say that aspirins relieve headaches, we are saying that in a particular situation (essentially, a person having a headache), aspirins will be more effective than other things, because they by nature have the power to relieve headaches.

When we open the medicine cupboard, looking for something to relieve our headache, we choose aspirin over a laxative because we think or indeed know that it currently has such and such powers. The difference between a placebo and an aspirin is not that the aspirin will relieve the headache and the placebo will not, as there will be situations in which the aspirin is ineffective or the placebo effective, the difference is in the natures of the two substances, and that, by nature, aspirins generally behave in such a way as to exhibit the power to relieve headaches.

Harre and Madden go on to draw a distinction between enabling conditions and stimulus conditions, where enabling conditions are those that ensure that a thing is in a state of readiness to create a certain effect, and stimulus conditions which actually bring about an effect, assuming that the enabling conditions have been fulfilled. In other words, we’re talking about potential causal factors rather than absolute causes.

Enabling conditions for an aspirin would be that the aspirin is in a state whereby it could possibly alleviate pain – if an aspirin is consumed after its sell-by date, the possibility exists that certain changes have taken place in its chemical structure, resulting in that aspirin not being able to relieve pains. So, assuming that the aspirin is enabled in this way (this is not to say that this is the sole enabling condition), what are the stimulus conditions which actually bring about the response from the aspirin that causes the headache to be relieved?

To relate that to diet, what are the conditions under which carbohydrates cause obesity, or type 2 diabetes, or whatever? Noakes would respond to say that the conditions are quite clear – namely that they obtain when one is insulin-resistant. But he only mentions this qualification when challenged to do so. Page 22 of the Real Meal Revolution states quite plainly – without any qualifications – that “fat does not make you fat. Carbs do”.

The very next page introduced insulin, but without any suggestion that we might have variable insulin reactions to carbohydrates. And the page ends with a generalised warning of a “near-perpetual cycle of weight gain. Unless, of course, you break the addiction…”. Never mind, of course, that the word and concept of “addiction” is being used in a rather quackish sense here.

In other words, the qualification that this only applies to some is introduced grudgingly, under duress, whereas his generalised opposition to what he dubs the ‘prudent diet’ recommendations gives the clear signal that he’d prefer for dietary guidelines to suggest a low-carb high-fat approach, for everyone. As he says in an interview in early February 2014, he’s calling for a “return to your dietary roots, bringing you back to the way humans are meant to eat and returning your body and mind back to the trim, happy, energised state our ancestors experienced thousands of years ago. They didn’t get fat or suffer from obesity, diabetes or other lifestyle illnesses” – and as he’s pointed out in every talk I’ve heard and read, those dietary roots (allegedly) involved high fat diets and low carbohydrate intake.

Yes, he does allow for wiggle-room, with some of us allowed to eat “a maximum of 200 grams of carbohydrates a day, depending on your insulin resistance”. But he’s also claimed that 60% or more of us would benefit from the LCHF diet, so it seems clear that – unless you prove yourself carb-worthy by whatever standard he sets – the presumption is that you, like him, should avoid carbs.

Here’s the thing: dieticians already know that excessive consumption of carbs is a bad thing, especially when they come in super-refined forms, and especially in the form of sugar. If that were all Noakes were saying, nobody would care. He’s saying something more, which is that we don’t need to fear saturated fat, and that the proportions of proteins and saturated fat we consume should increase, at the expense of the proportions of carbs.

When making these sorts of claims, he cites sources like the Harvard School of Public Health, even though they include the (standard) cautions against saturated fats. Just as he and his followers have been claiming that Sweden has “officially” adopted LCHF, even though they’ve done no such thing. And when faced with challenge, the retort is that you’re indulging in “Group Think”, as though conspiracy theory isn’t a perfect example of exactly that.

Take the example of that tweet, pasted above. In Noakes-science, that’s evidence (or so it seems). For the rest of us, we might say a) that’s a post-hoc (ergo fallacious) argument; or b) that it seems fairly straightforward to intuit that high cholesterol is sometimes a potential causal factor, but never a necessary one, in causing heart attacks; and c) what about the other 50% – does their elevated cholesterol not mean anything, on this model?

As I’ve said before, I really hope he’s right (leaving aside the fact that non-human animals will be killed in even higher numbers if his diet takes off). But damn, I wish he could try sounding like a scientist for a change.

  • GerritTonder

    Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD
    Jacques, please comment on this meta study n= 350 000
    Until proven wrong, I believe Tim Noakes. And the chance is small

    © 2010 American Society for Nutrition

    Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease1,2,3,4,5

    Authors

    Abstract

    Background: A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.Objective: The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.Design: Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.Results: During 5–23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.Received March 6, 2009.Accepted November 25, 2009.

    • Gerrit, why in the world should I satisfy a demand for comment on something unrelated to the topic of this post? Believe Noakes if you like, and if you want to comment on the philosophy of science, do so. Otherwise, go comment somewhere where the actual dietary issues are on the table, so to speak?

      • GerritTonder

        Jammer Jacques. My Engels is nie so goed nie en as ek lees dat die LCHF a fad dieet is en dat jy alweer vir Noakes bykom, vind ek dit vreemd. Bring die bewyse dat Noakes verkeerd is, dan sal ek jou glo

  • Shaun Wewege

    Bruce Fordyce tweeted that since he’d “gone Paleo” two years ago, he’d lost weight and was in top running form. Of course this has been used as evidence (by Noakes and others) of effectiveness. Why does nobody focus on the fact that for his 9 consecutive Comrades wins, Fordyce was not a Paleo eater?

    • Indeed. It’s perfectly understandable – we all suffer from confirmation bias – but it’s nevertheless a problem to see such proud & oblivious cherry-picking in matters of science.

  • Harris Steinman

    “Sweden does not have any guidelines on low-carb-high-fat diets. The information that Sweden has guidelines on low-carb-high-fat diets is based on incorrect information circulating on the Internet.” Anna Karin Lindroos, PhD, a nutritionist at Sweden’s National Food Agency. http://experiencelife.com/newsflashes/debunking-news-of-swedens-low-carb-high-fat-guidelines/

    • Yep, it’s a ‘zombie fact’ that LCHF proponents keep recycling as if it’s true. The worry is how easily simply making the claim persuades some folk – you might almost call it “Group Think”…