Seth’s blog

Here are the details of my two heart scan scores, one recent, the other one and a half years ago.

February 2009:

August 2010:

To give some context, this group of patients given a whole bunch of treatments (”statin therapy, niacin, the American Heart Association Therapeutic Lifestyle Changes (TLC) diet, omega-3 fatty acids and vitamin D-3 supplementation”) meant to improve these scores managed, on average, about a 0% change in scores after 1-2 years of the treatments. Which is better than the usual 25%/year increase, but not as good as what happened to me.

My recent heart scan results were 50% lower (= better) than predicted. Apparently I am doing something right.
You might think that my lipid values would reflect that. Not quite. They were measured twice in the last two weeks, first with a Cholestech LDX machine (instant results); second, ordinary lab tests.
Here are the scores (first test, second test). Total Cholesterol: 210, 214, which is “borderline high” (borderline bad) according to the Cholestech LDX quick reference sheet. HDL = 17, 36, which is “low” (bad). TRG = 62, 75, which is “normal”. LDL = 180, 163, which is “high” (bad).

There is no hint in these numbers that I am doing the right thing! If anything, they imply the opposite, that I’m doing the wrong thing. This supports all those people, such as Uffe Ravnskov, who say the connection between cholesterol and heart disease is badly overstated.

In The New Yorker (25 January 2010), David Owen wrote about his father’s mother:

Gaga lived to be ninety-two, despite never having had much conventional health care. . . . She made foul-smelling yogurt . . .

My recent heart scan score was about 50% less than you’d expect from an earlier score. Why the improvement?

During the year between the two tests, I’d made one big change: eat much more animal fat. That’s the obvious explanation. Three things support it:

1. Mozaffarian et al., as I blogged, found a similar result.

2. The animal fat (pork fat and butter) had both produced large immediate improvements when I began to eat them. The pork fat had improved my sleep; the butter, my arithmetic scores. This sort of large immediate effect we associate with the supply of a missing necessary nutrient — giving Vitamin C to someone with scurvy, for example. My brain, at least, needed much more animal fat than I’d been eating. Different parts of the body need different nutrients, sure, but they all must work well with the same set of nutrients. If Nutrient X helps one part of the body, it is more likely to help another part.

3. My initial score put me at the 50th percentile for my age. I’d had an unusual diet for a long time. I stopped eating bread, potatoes, rice, pasta, and dessert 13 years ago. I’d started consuming lots of omega-3 and fermented foods a few years earlier. It was possible that those other changes produced improvement but if so it was a strange coincidence that, as my score got better and better over the years, I happened to measure it for the first time just when it crossed the 50th percentile.

This explanation makes a prediction: If you greatly increase your animal-fat intake, your heart scan score should improve. A commenter said what he’d read on paleo-diet forums supported this prediction: “If you hang out in the paleo/low carb forums, you see this kind of thing a lot.”

I posted yesterday that a recent heart scan found my arteries about 50% less calcified than a previous scan predicted. Apparently the improvement was due to eating much more animal fat (pork fat and butter).

In 2004, an American Journal of Clinical Nutrition article found something similar: heart disease progressed less in women who ate more saturated fat. “In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis,” the authors wrote. Here’s how they saw this finding:

The inverse association between saturated fat intake and atherosclerotic progression was unexpected. However, this finding should perhaps be less surprising. Ecologic and animal experimental studies showed positive relations between saturated fat intake and CHD risk (8). However, cohort studies and clinical trials in humans have been far less consistent (9 –12). Furthermore, most studies of dietary fat and CHD risk have been performed in men (15, 16). The relations in women—particularly postmenopausal women—are much less well-established, and evidence from dietary intervention trials suggests that diets low in saturated fat may have different effects on CHD risk factors in women (15, 17–22).

In their study, women with the highest intake of saturated fat did not get worse during the study period, whereas women with lower intakes did get worse.

An editorial about this study described some of the evidence that supports the “article of faith” that “saturated fat . . . accelerates coronary artery disease”:

One of the earliest and most convincing studies of the better efficacy of unsaturated than of saturated fat in reducing cholesterol and heart disease is the Finnish Mental Hospital Study conducted in the 12 y between 1959 and 1971. In this study, the usual high-saturated-fat institutional diet was compared with an equally high-fat diet in which the saturated fat in dairy products was replaced with soybean oil and soft margarine and polyunsaturated fats were used in cooking. Each diet was provided for 6 y and then the alternate diet was provided for the next 6 y. After a comparison of the effects of the 2 diets in both men and women, the incidence of coronary artery disease was lower by 50% and 65% after the consumption of polyunsaturated fat in the 2 hospitals.

My results make the results of that earlier study exceedingly puzzling. I found a large change in one direction; the Finnish study found a large effect in the opposite direction. Given the huge effect (50% or 65% reduction) observed in the Finnish study, it is hard to understand why “cohort studies and clinical trials in humans have been far less consistent”.