Another Reason why the Lipid Hypothesis is Bunk

The lipid hypothesis, as evry fule kno, predicts that eating saturated fat causes elevation of serum cholesterol or LDL which then plays a causal role in cardiovascular heart disease. How or why no-one knows but the feeling out there is that saturated fat causes bad cholesterol and heart disease. The notion is, as they say, entrenched; it is a meme more widely believed now than any religious dogma.

Unlike the unknowable nature of God, the lipid hypothesis can be disproved by multiple lines of evidence. Here is one.

Animal fat is a blend of saturated fats, monounsaturated fats, and polyunsaturated fats. Polyunsaturated fats lower serum cholesterol, monounsaturated fats have no effect on serum cholesterol, and some saturated fats also have no effect on cholesterol. William Barendse describes the set-up eruditely and eloquently in his epic review “Should Animal Fats be Back on the Table? A critical review of the human health effects of animal fat” as follows;

“As an example from one of the hardest animal fats, approximately only 27% of tallow from pasture-fed beef is cholesterol-increasing saturated fatty acid (CISFA) (Yang et al. 1999b), i.e. chain length of 12–16 carbons, and which would raise serum cholesterol, 1% is polyunsaturated, ~4% is conjugated linoleic acid (CLA), and the rest is either MUFA or is the saturated fatty acid (SFA) stearic acid that causes the same effect on total serum cholesterol (TSC) as MUFA (Keys et al. 1965; Grande et al. 1970; Bonanome and Grundy 1988; Tholstrup et al. 1994a, 1994b; de Roos et al. 2001; Mensink et al. 2003). By comparison, in butter from pasture-fed cows, 42% of the fat is CISFA (Couvreur et al. 2006) and would raise serum cholesterol despite butter having a total of more than 60% SFA.”
(FYI, butter also supplies twice as much cholesterol as tallow.)

Therefore, if the lipid hypothesis were true, we would expect butter and other forms of dairy fat (of which butter is merely the concentrate) to cause, or at least be associated with, more heart disease than meat fat, especially considering that most meat fat is less saturated than tallow.

To the contrary, the 2012 epidemiological analysis, Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis, one of the few studies to separate saturated fats according to their dietary sources, found a strong protective (inverse) association between dairy fat and CVD, and a weaker positive association with the less saturated fat from meat, across a multi-ethnic population (this ruling out the possibility of the results being unduly influenced by genetic factors);

“When we evaluated risk across quintiles of SF consumption from each food source, a significant inverse association was seen for dairy SF [HR (95% CI) for extreme quintiles: 0.56 (0.38, 0.82); P-trend = 0.01], whereas meat SF was not statistically significantly associated with risk [HR (95% CI) for extreme quintiles: 1.40 (0.94, 2.08); P-trend = 0.12] (Figure 1). Butter and plant sources of SF were not associated with CVD risk, but ranges of SF consumption from these sources were quite narrow, which limited our ability to detect differences in risk across quintiles.”
“In sensitivity analyses in which angina was excluded from CVD endpoints, inverse associations of total, dairy, and plant SF with hard CVD were somewhat stronger, whereas the positive association of meat SF with hard CVD was slightly attenuated (data not shown).”

In case it is thought that the sample size in the MESA study (5,209) was too small, it is a common finding that dairy fat is either not, or is inversely, associated with CVD incidence.

An argument could be made that some factor associated with dairy fat, such as (hypothetically) calcium, reverses the harmful effect of saturated fat. If such were in fact the case, how nugatory would that harmfulness then need to be?

There may be things that raise cholesterol and that are associated with CVD. Industrial trans fatty acids seem to meet this case, as well as various organic toxins and heavy metals that are not fatty acids, and that are likely to be bad for you quite independently of any perturbations of your lipids. Sugar and high-GI starches are other potential candidates, which takes us into the intricacies of lipoprotein classes beyond the cartoon characters of cholesterol and LDL. There are also bound to be fatty acids, as well as other factors, which can increase CVD risk while lowering cholesterol. There have certainly been enough trials of cholesterol-lowering drugs, and cholesterol-lowering diets, where more people have died in the treated group, and sometimes died with lower cholesterol.

Yet people still believe this thing. It is nonsense. There are other things that better deserve the energy that has been poured into making people worry about saturated fat, and about the influence of dietary fats on cholesterol. The lipid hypothesis, and consequent pious attempts to respect or enforce the magical 10% saturated fat limit, have had a mischievous influence over the modern diet. Belief in it has not made us, in the majority, healthy, wealthy, or wise. It has made us saturate our bodies in polyunsaturated fats without considering whether they are omega 6 or omega 3, cis or trans, oxidised or unoxidised, or how far they are in fact necessary, or whether they bring anything in the way of nutrition to the diet to make up for the choline, carotenoids, cholesterol, retinol, menaquinone, and cholecalciferol we miss out on by not eating as much butter or fatty animal parts as our ancestors did. We have been fools, and we are making our society sick. It is time to stop.