In his terrific book The Great Cholesterol Con, Dr. Malcolm Kendrick describes how the Lipid Hypothesis, despite the mounting evidence against it, is kept alive by ad-hoc hypotheses:
Ad-hoc hypotheses are devices scientists use to explain away apparent contradictions to much-loved hypotheses. Ad-hoc hypotheses work along the following lines: you find a population with a low saturated fat intake — yet, annoyingly, they still have a very high rate of heart disease. Once such population would be emigrant Indians in the U.K. The ad-hoc hypothesis used to explain away their very high rate of heart disease is as follows: Emigrant Indians are genetically pre-disposed to develop heart disease, which then leads to heart disease. Alakazoom! The paradox disappears.
On the other hand, if you find a population with high saturated fat intake but a low rate of heart disease, such as the Inuits, you can always find something they do that explains why they are protected. In their case it was the high consumption of Omega 3 fatty acids from fish.
This particular game has no end. There is no evidence that cannot be dismissed one way or another. And there is also no end to the development of new ad-hoc hypotheses. You can just keep plucking them out of the air endlessly… There is no end, ever, to the ability of researchers to come up with a reason that every single paradox is not really a paradox at all.
We saw some of that recently when autopsies on ancient Egyptian mummies indicated a high rate heart disease. You could almost imagine the researchers stammering.
“This can’t be right! Their diets were full of fruits and vegetables and healthy whole grains.”
Maybe grains aren’t actually the health food we thought they were, professor.
“They were physically active, and they didn’t eat much saturated fat.”
Professor, can I interrupt? Maybe saturated fat has nothing to do with heart disease.
“And yet look at all these clogged arteries. You know what this means, don’t you?”
Yes, professor. It means the Lipid Hypothesis is a load of bologna.
“It means we’d better warn people to eat even less saturated fat than the Egyptians if they want to avoid heart disease. That’s the only possible conclusion.”
Professor, may I borrow your desk? I need to bang my head on it.
Now a new study has been reported on the Medical News Today website under the headline:
Heart Attack Risk Not Elevated By Dairy Consumption
Dairy products can be high in harmful saturated fat but not necessarily in risk to the heart. A newly published analysis of thousands of adults in Costa Rica found that their levels of dairy consumption had nothing to do statistically with their risk of a heart attack.
Read that first sentence again and try to make sense of it. I dare ya.
To conduct the study, [researchers] analyzed data on 3,630 middle-aged Costa Rican men and women who participated in an epidemiological study between 1994 and 2004 by co-author Hannia Campos of the Harvard School of Public Health.
They split the study population between two equal groups: 1,815 “cases” who had non-fatal heart attacks and 1,815 comparable “controls” who did not. The researchers looked not only at the subjects’ self-reported dairy intake, but also at measurements of dairy fat biomarkers, namely 15:0 and 17:0, in their bodies.
I’m not sure why Medical News Today felt the need to put “cases” and “controls” in “quotes.” I guess they assume “readers” are too “stupid” to figure out what those terms “mean.” Anyway …
The dairy biomarkers mentioned in the article are pentadecanoic and heptadecanoic fatty acids removed from the subjects’ fat tissues, according to the study abstract. From what I read elsewhere online, concentrations of those acids in our fat tissues provide an accurate measurement of long-term dairy-fat intake … which makes me wonder why the researchers also had the subjects fill out food-intake questionnaires.
“Thank you for turning in your diet log, Mr. Rodriquez. Now if you’ll just step over here, we’d like to insert this needle and suck some fat from your belly.”
“Because everybody lies on food questionnaires.”
So for once, we apparently have an observational study with reliable data for dairy-fat intake. But it’s still an observational study, and I’ve said many times that observational studies don’t prove cause and effect, right?
Right. Just because two traits are correlated, it doesn’t mean one of them is causing the other. However, if two traits are not correlated, the odds are overwhelming that there’s no cause and effect going on.
For example: if I prove that people with yellow-brown stains on their teeth are more likely to develop lung cancer, that correlation doesn’t prove that yellow-brown teeth cause lung cancer. It could simply mean that both are caused by something else, such as smoking. But if I look for a correlation between yellow teeth and lung cancer and don’t find one, you can bet your bottom dollar yellow teeth don’t cause lung cancer. If they did, we’d see a correlation.
With that in mind, here’s what the researchers found — or didn’t find, to be more accurate:
What they found is that the dairy intake of people who had heart attacks was not statistically different than the intake of people who did not. After breaking people into quintiles, based on their dairy consumption amount, there was no significant linear relationship between consumption and heart risk, even among the most voracious consumers. The highest consumption quintile consumed an average of 593 grams of dairy foods a day.
When the researchers controlled for such risk factors as smoking, waist-to-hip ratio, alcohol intake, and physical activity, the lack of a statistically significant association between dairy intake and heart attack risk remained.
The study abstract also mentioned that the researchers found a “protective association” in all but the highest quintile of dairy-fat intake. In other words, within the other four quintiles, people who consumed more dairy fat had a slightly lower rate of heart attacks. People who consumed the most dairy fat merely had the same rate of heart attacks.
So … you’re a researcher crunching these numbers. You’ve been told for your entire academic career that saturated fat causes heart disease, which is why we urge people to cut back on butter, cheese and whole milk. Then your own research shows that full-fat dairy products, if anything, may slightly lower the risk for heart disease. What should you conclude? How about something like this:
Rather than suggesting that the saturated fats in dairy products are harmless, Aslibekyan and co-author Ana Baylin, an adjunct assistant professor of community health at Brown, hypothesize that other nutrients in dairy products are protective against heart disease, for all but perhaps the highest dairy consumption quintile in their study. The potentially beneficial nutrients include calcium, vitamin D, potassium, magnesium and conjugated linoleic acid (CLA).
Got that? Saturated fat is bad, and dairy products are full of saturated fat, but dairy products don’t cause heart disease because … uh … because you’re so protected by the calcium, vitamin D, potassium, magnesium and CLA that you end up with a lower rate of heart disease than people who don’t consume all that artery-clogging saturated fat … uh … unless you consume a whole lot of these protective nutrients, in which case they stop protecting you, and then consuming lots of artery-clogging saturated fat merely means you have the same risk for heart disease as people who don’t. So saturated fat is still bad, you see.
Head. Bang. On. Desk.
I keep wondering how this kind of nonsense can continue. The Lipid Hypothesis fails over and over in research and ought to be long dead by now. But then I noticed this study was funded by the NIH. So here’s my ad-hoc theory: when it comes to bad science, government exerts a protective effect.