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Saturated Fat Intake Associated with Coronary Disease

Published 3.22.2017
Coronary disease or heart disease is a topic of ongoing interest for me, as I attempt to avoid ever crossing paths with cardiologists (for treatment, I'm sure are lovely people would be fun to chat with at the pub or at a party).

Another study shows that high saturated fat intake is associated with increased heart disease. Association of course, is not causation. Here is the results from the abstract:

Mean intake of SFAs accounted for 9.0-11.3% energy intake over time, and was mainly composed of lauric acid (12:0), myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0; 8.8-10.7% energy). Intake of 12:0, 14:0, 16:0 and 18:0 were highly correlated, with Spearman correlation coefficients between 0.38 and 0.93 (all P<0.001). Comparing the highest to the lowest groups of individual SFA intakes, hazard ratios of coronary heart disease were 1.07 (95% confidence interval 0.99 to 1.15; Ptrend=0.05) for 12:0, 1.13 (1.05 to 1.22; Ptrend<0.001) for 14:0, 1.18 (1.09 to 1.27; Ptrend<0.001) for 16:0, 1.18 (1.09 to 1.28; Ptrend<0.001) for 18:0, and 1.18 (1.09 to 1.28; Ptrend<0.001) for all four SFAs combined (12:0-18:0), after multivariate adjustment of lifestyle factors and total energy intake. Hazard ratios of coronary heart disease for isocaloric replacement of 1% energy from 12:0-18:0 were 0.92 (95% confidence interval 0.89 to 0.96; P<0.001) for polyunsaturated fat, 0.95 (0.90 to 1.01; P=0.08) for monounsaturated fat, 0.94 (0.91 to 0.97; P<0.001) for whole grain carbohydrates, and 0.93 (0.89 to 0.97; P=0.001) for plant proteins. For individual SFAs, the lowest risk of coronary heart disease was observed when the most abundant SFA, 16:0, was replaced. Hazard ratios of coronary heart disease for replacing 1% energy from 16:0 were 0.88 (95% confidence interval 0.81 to 0.96; P=0.002) for polyunsaturated fat, 0.92 (0.83 to 1.02; P=0.10) for monounsaturated fat, 0.90 (0.83 to 0.97; P=0.01) for whole grain carbohydrates, and 0.89 (0.82 to 0.97; P=0.01) for plant proteins.

This is why the conversation about removing fat from diets is so confusing. There is more than one type of saturated fat. Chain length of the molecule matters. Replacing animal derived sat fat with poly or mono unsaturated fats (plant based) has been shown to be protective, but most saturated fat is replaced with refined carbs (in other words with sugar and grains not fruits and vegetables). Grains are carbs, but not all carbs are grains, despite what reading the low carb blogosphere would suggest.

Results showed an association between heart disease and higher sat fat intake, but the only replacement that made a significant improvement in risk was PUFAs Indeed, if you look at the plot of the risk hazard ratios, the only result is for the replacement of sat fat with PUFA. No other result is significant.

These data are again based on food survey of recalled ingestion, which is always and ever problematic. So, if you take the stance that studies based on food surveys are garbage, then this is not a result to pay attention to. However, if you eliminate studies based on food surveys, then you are stuck with the metabolic ward studies, such as those directed by Kevin Hall, which are devastating to low car dogmatists. That fact is why they try so very, very hard to discredit Hall’s work.

Free living studies by design have to rely on subjects honesty in reporting intake. There is good historical evidence to denounce this practice as bunk. Free living studies give low carb dogmatists their best evidence for their diet. In metabolic wards, low carb diets, at best, are no better or worse than low fat diets, and at worst, result in metabolic disadvantages compared to a low fat diet.

And all that is before you start to subjectively compare the relative health, BMI, and longevity of low carb gurus to their low fat counterparts. I’ll leave the googling to the curious, but low carbers do not fare well in such a comparison. They tend to have more health issues, be fatter (which ought to be disqualifying for a weight loss guru), and they die younger. There are many factors to health beyond diet of course, but if you are touting a way of eating as the elixir of life, then you ought to look and act the part. Too many low carb proponents do not.

Evolocumab may be the answer to CVD? Haven’t we heard this before? The drug works by altering how the liver functions— what could possibly go wrong?

Evolocumab is an antibody just like the weapons used by the immune system to fight infection.However, it has been designed to target a protein in the liver with the name PCSK9.

And ultimately it makes the organ better at whipping bad cholesterol out of the blood and breaking it down.

Other trials have shown such antibodies have cut bad cholesterol levels by 60% and Amgen is not the only company looking at this approach.

Here is a skeptical view.

We can't afford PCSK9 inhibitors at their current price. By we, I mean either individuals or our healthcare system. If our model of healthcare is pay for value, 1% to 2% reductions in nonfatal events are worth something. But they are not worth many thousands of dollars per year. And no, we don't need a complex modeling study to tell us the cost of this drug will have to come down.

Cranky Scottish doctor Malcom Kendrick offers an even more skeptical view. Kendrick doesn't think that cholesterol causes cardio-vascular disease (CVD) so a drug that lowers cholesterol will not lower CVD. Kendrick also notes that Pfizer abruptly ended its PCSK9 inhibitor development.

Pulling the plug when 27,000 patients had been fully enrolled. What on earth did they see. Something more than slightly worrying. I guess we will never really know, but that is one hell of a write off.

There are many reasons to dump a project and cut your losses, of course, but it does charge the imagination with speculation of possible answer.


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