Statistics and fat
Both point out the problems with this whole “saturated fat is going to give you heart disease” thing. The data on inspection just don’t add up.
Not only do they not add up, they sometimes show the opposite of what is claimed. But, after statistical adjustment for possible confounders we see something.
Here’s what I mean – the big combined cohort paper from Yanping et al (including Walter Willett as senior last author) claims that saturated fat is still the bad guy and replacing it with either good quality carbs or polyunsaturated fat will reduce the risk of heart disease.
In the blog Doc’s Opinion Dr Sigurdsson combines data in Yapping et al’s Table 2 from the two cohorts used in this study. The numbers below show the combined number of fatal Coronary Heart Disease events and non-fatal MIs (heart attacks) in both cohorts. One after 24 years of follow up the HPFS cohort, and a second after 30 years of follow up – the NHS cohort.
What’s shown here are the combined number of CHD events for the highest and lowest 20% of intakes of various types of nutrients.
You’ll see the actual combined raw data run contrary to their final conclusions on a number of key nutrients.
I especially draw you attention (see table below) to the LOWER CHD in people who ate more fat (1420 v 1641 events), more saturated fat (1434 v 1599), and less total carbs (1378 v 1717).
The thing is these are the actual number of people who had actual heart disease (death or non-fatal heart attack).
But the dietary differences were confounded at baseline. That is, multiple differences co-occurred… “At baseline (Table 1), men and women with a high intake of SFAs as a percentage of energy were slightly younger, had a higher body mass index, had a lower prevalence of physical activity and multivitamin use, and consumed more cholesterol. Participants with higher energy intake from SFAs also tended to have higher energy intake from MUFAs and trans fats and lower energy intake from carbohydrates (Table 1). ”
So they used some statistical techniques to adjust for these differences.
“To obtain overall estimates for both sexes and to increase statistical power, the HRs [Hazard ratios] from the age- and multivariable-adjusted models from the 2 cohorts were combined with the use of a fixed-effects inverse variance-weighted meta-analysis because no significant heterogeneity between the cohorts was observed.”
What this means in the end is that they claim that saturated fat causes heart disease. When in reality these effects never occurred. In fact, you’d have to say that the unadjusted data supports the idea that we should eat more total fats including SFA and PUFA, less carbs and sugar, and if you are eating carbs eat good quality (unprocessed) ones. Yet these raw effects are never dealt with.
Remember these raw data are actual people suffering actual heart disease. The rest of the adjusted models are only theoretical, allowing for the confounders as they choose. I’m all for statistical adjustment, but not when you end up making claims that seem to bear no resemblance to reality, because the original association has somehow been reversed.
What I’d take from this paper – there is evidence that what we eat affects our health. One indicator is heart disease. Several things seem to interact, which isn’t surprising because when you reduce energy from one nutrient you generally will replace it with another. Likely issues in these two cohorts are too much carbohydrate (and low carbohydrate quality) and not enough fat.
Why can’t there be some agreement on this part? Why do we revert back to “dietary guidelines are still right and we should avoid saturated fat”? Defence of the status quo under such conditions depends on tolerating the dissonance that this generates. This “vision of the anointed”, or rather lack of vision, is still a major issue for public health nutrition.
Whatever the adjustment and statistical techniques, these data don’t show causation. We need experiments for that. Such dietary experiments are hard (and expensive) to do. In the past, several such trials were done for disease prevention (heart disease or cancer) which involved various versions of the low-fat diet, with mediocre results and no effect on mortality from either disease. Any of these longer term preventive trials could have included a low carbohydrate arm, but none did. However, we do see medium term effects of exactly what the raw epidemiological data in Yanping et al shows – that eating more fat, less and better quality carbs is generally a good thing.
Bottom line: Saturated fats as they occur in whole plant and animal foods represent no serious public health risk worth making recommendations about.