The first Dietary Goals for the United States (DGUS) were released in 1977 to not a lot of fanfare.  At that time, the great unwashed masses hadn’t really heard much about the word cholesterol, a substance the DGUS recommended that we should limit to 300 mg per day.  Doctors didn’t routinely screen for it, and if they did, they didn’t pay much attention to it.  In fact, at that time – as I recall, anyway – the upper limit of normal for total cholesterol was 240 mg/dl.  I was in medical school back then, and I don’t really remember any emphasis on cholesterol or blood lipids.  I think we had one lecture on it in biochemistry, given by a nebbish little professor we called Mighty Manford (his first name was Manford), who labored away in the obscurity of the biochemistry department. It’s hard to believe in today’s world of lipophobia that as little as 30 years ago, no one much cared about cholesterol.

One of the major players in bringing cholesterol to the public’s awareness was Time magazine. Its piece on cholesterol in the March 26, 1984 issue was a devastating hit piece on both dietary cholesterol and dietary fat.  Both – the article explained – were a main driving force behind the development of heart disease.

Reading this article today, it’s amazing how it drips with misinformation.  At the time, however, most people – physicians included – accepted it as gospel.  Sadly, even today, many physicians who should know better believe in and act in accordance to the bountiful misinformation contained in this piece.

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A study appeared this week sure to drive members of the low-fat and vegan tribes sprinting for their Protexid.

Ron Krauss and his group published a paper in the Articles in Press section of the American Journal of Clinical Nutrition (AJCN) stating there is no evidence that saturated fat intake increases the risk for heart disease.  The paper, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, is not a study per se, but is a meta-analysis, a compilation of numerous studies looking at the relationship between saturated fat intake and the risk for developing heart disease.

As I’ve discussed before on these pages, meta-analyses are not my favorite types of studies.  I’ve attacked them when they’ve been used to ‘prove’ the low-fat diets are better, so I can’t very well embrace meta-analyses when they present a conclusion I agree with.  And I really can’t embrace meta-analyses when they are compilations of observational studies, which are themselves next to worthless.

For those who don’t know, meta-analyses are compilation studies in which researchers comb the medical literature for papers on a particular subject and then combine all the data  from the individual studies together into one large study.  This combining is often done to bring together a collection of studies, none of which contain data that has reached statistical significance, to see if the aggregate of all the data in the studies reaches statistical significance.  I think these types of meta-analyses are highly suspect, because they can lead to conclusions not warranted by the actual data.

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Synchronicity strikes again.  The seeds of this post were sown when Gary Taubes emailed me about a study published in early 2009 in the New England Journal of Medicine (NEJM) that I had seen at the time, briefly skimmed and tossed aside as worthless.  Gary agreed that the study was of little value, but notice that it contained a peculiar statement by the authors, an interesting admission about HDL, the lipophobe’s favorite lipoprotein.  And not only had the authors made this strange admission, but so had another prominent lipophobe who wrote the accompanying editorial.

I pulled the study, read it more thoroughly and still found it mediocre at best.  But I did come across the strange HDL statements that Gary had mentioned. (More about which later.)

As I was shaking my head over the amount of money spent on what was a truly abominable study, the synchronicity occurred.  I got a ding that I had a new email.  It was a notice from the American Heart Association telling me that this august body had deemed the very study I was holding in my hands as one of the ten most important papers published in 2009.  The sheer stupidity of it nearly took my breath away.

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In the early 1980s MD and I were laboring away in anonymity in our clinics in Little Rock, Arkansas.  By that time I had gone through my thin-to fat-to thin again metamorphosis, and I was starting to treat patients for obesity.  My own transformation had been fairly striking, a fact not lost on many of my overweight patients, a number of whom were seeking my professional advice on treating their own weight problems.  I was still doing a fair amount of general primary care medicine, but more and more of my time was being diverted to helping people lose weight.

When I, myself, had gotten fat, I had tried a few diets that were then being extolled (including the Pritikin diet) and had experienced pretty much the same thing most people did with these diets:  I lost a few pounds, drifted from the diet, and regained the lost weight plus a little.  I then started thinking seriously about obesity as a medical problem, and, in an effort to learn all I could about it, I turned to the medical textbooks on my shelves.  Unfortunately, none of them contained any information I found particularly enlightening.  The texts went into great detail about the risks associated with obesity and the many diseases that it either caused or made worse, but, other than recommending caloric restriction, none really discussed the treatment.  None really discussed (at least not to my satisfaction) what happens metabolically that makes people store excess fat.

I next turned to physiology texts, which didn’t help a lot, either.  I then grabbed my old medical school biochemistry textbook (I hadn’t been out of med school all that long at the time, so it was fairly current) and struck gold.  I started tracing out all the pathways for fat storage and noticed that in virtually every one insulin turned up somewhere.  Then I started reading about all the pathways involving insulin and realized that excess insulin had to be the agent driving the storage of excess fat.  I then went back to the physiology texts, reread them in light of my new found knowledge, and discovered that they reinforced what I had learned from the biochemistry text. I just hadn’t realized it, until I had made the insulin connection. (I drew out all the different pathways insulin worked through on piece of paper that we’ve saved, but I can’t lay my hands on it right now.  If I find it, I’ll post it.)

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Pity the poor lipophobes and statinators.  They’ve just taken another grievous wound to their favorite theory and haven’t even got sense enough to know it.  In fact, not only do they not have sense enough to realize they’ve taken the hit, they’re actually crowing about it.

The current issue of the Journal of the American Medical Association (JAMA) has an article titled Trends in High Levels of Low-Density Lipoprotein Cholesterol in the United States, 1999-2006 that puts another major dent in whatever validity remains of the lipid hypothesis of heart disease.

I’m going to start categorizing the types of findings published in this paper under the rubric of The Statinator Paradox.  I find it interesting that whenever scientists discover data that shows the opposite of what their hypotheses predict, they don’t conclude that their hypotheses might be wrong; instead they deem the contradiction a ‘paradox’ and bumble on ahead with their hypotheses intact.

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