The Diet-Heart Hypothesis: Stuck at the Starting Gate?

The diet-heart hypothesis is the idea that (1) dietary saturated fat, and in some versions, dietary cholesterol, raise blood cholesterol in humans and (2) therefore contribute to the risk of heart attack.

I'm not going to spend a lot of time on the theory in relation to dietary cholesterol because the evidence that typical dietary amounts cause heart disease in humans is weak.  Here's a graph from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.) to drive home the point. Eggs are the main source of cholesterol in the American diet. In this graph, the "low" group ate 0-2 eggs per week, the "medium" group ate 3-7, and the "high" group ate 7-14 eggs per week (click for larger image): The distribution of blood cholesterol levels between the three groups was virtually identical. The study also found no association between egg consumption and heart attack risk. Dietary cholesterol does not have a large impact on serum cholesterol in the long term, perhaps because humans are adapted to eating cholesterol. Most people are able to adjust their own cholesterol metabolism to compensate when the amount in the diet increases. Rabbits don't have that feedback mechanism because their natural diet doesn't include cholesterol, so feeding them dietary cholesterol increases blood cholesterol and causes vascular pathology.

The first half of the diet-heart hypothesis states that eating saturated fat raises blood cholesterol. This has been accepted without much challenge by diet-health authorities for nearly half a century. In 1957, Dr. Ancel Keys proposed a formula (Lancet 2:1959. 1957) to predict changes in total cholesterol based on the amount of saturated and polyunsaturated fat in the diet. This formula, based primarily on short-term trials from the 1950s, stated that saturated fat is the primary dietary influence on blood cholesterol.

According to Keys' interpretation of the trials, saturated fat raised, and to a lesser extent polyunsaturated fat lowered, blood cholesterol. But there were significant flaws in the data from the very beginning, which were pointed out in this critical 1973 literature review in the American Journal of Clinical Nutrition (free full text).

The main problem is that the controlled trials typically compared saturated fats to omega-6 linoleic acid (LA)-rich vegetable oils, and when serum cholesterol was higher in the saturated fat group, this was most often attributed to the saturated fat raising blood cholesterol rather than the LA lowering it. When a diet high in saturated fat was compared to the basal diet without changing LA, often no significant increase in blood cholesterol was observed. Studies claiming to show a cholesterol-raising effect of saturated fat often introduced it after an induction period rich in LA. Thus, the effect sometimes had more to do with LA lowering blood cholesterol than saturated fat raising it. This is not at all what I was expecting to find when I began looking through these trials.

Reading through the short-term controlled trials, I was surprised by the variability and lack of agreement between them. Some of this was probably due to a lack of control over variables and non-optimal study design. But if saturated fat has a dominant effect on serum cholesterol in the short term, it should be readily and consistently demonstrable.  

The long-term data are not kind to the diet-heart hypothesis. Reducing saturated fat while greatly increasing LA certainly does lower blood cholesterol substantially. This was the finding in the well-controlled Minnesota Coronary Survey trial, for example (14% reduction). But in other cases where LA intake changed less, such as MRFIT, the Women's Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).  The small changes that did occur could have been due to other factors, such as increased fiber and phytosterols, since these were multiple-factor interventions.

Another blow to the idea that saturated fat raises cholesterol in the long term comes from observational studies. Here's a graph of data from the Health Professionals Follow-up study, which followed 43,757 health professionals for 6 years (via the book Prevention of Coronary Heart Disease by Dr. Harumi Okuyama et al.): What this graph shows is that at a relatively constant LA intake, neither saturated fat intake nor the ratio of LA to saturated fat were related to blood cholesterol in freely living subjects. This was true across a wide range of saturated fat intakes (7-15%). 

There's more. If saturated fat were important in determining the amount of blood cholesterol in the long term, you'd expect populations who eat the most saturated fat to have high blood cholesterol levels. But that's not the case. The Masai traditionally get a high proportion of their calories from milk fat, half of which is saturated. In 1964, Dr. George V. Mann published a paper showing that traditional Masai warriors eating practically nothing but very fatty milk, blood and meat had an average cholesterol of 115 mg/dL in the 20-24 year age group. For comparison, he published values for American men in the same age range: 198 mg/dL (J. Atherosclerosis Res. 4:289. 1964). Apparently, eating three times the saturated animal fat and several times the cholesterol of the average American wasn't enough to elevate their blood cholesterol. What does elevate the cholesterol of a Masai man? Junk food.

Now let's swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I'm aware of. How's their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s).  Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Does dietary saturated fat influence total cholesterol and LDL over the long term?  I don't have the answers, but I do think it's interesting that the evidence is much less consistent than it's made out to be.  It may be that if dietary saturated fat influences total cholesterol or LDL concentration in the long term, the effect is is secondary to other factors.  That being said, it's clear that linoleic acid, in large amount, reduces circulating total cholesterol and LDL.

Dog Park

My attempt at getting some action pictures of Max at the dog park. I am fortunate that he gets along with most all dogs, even large ones! Even thought the tennis ball is about the size of his head, he still enjoys fetching it. He's been a good dog, still getting used to his name. I am the lucky one.

American Life Today

Wouldn't it be nice to meet an American, everyday?

As I traveled on my road trip last year, I expected to see some amazing places. I didn't expect to meet some of the most fascinating people along the way.

As I listened to their stories, I thought that there needs to be a way where people could learn about their life! Who is going to tell their story? How about them! I found it exhilarating to listen to personal stories from all walks of life in campgrounds, restaurants, parks, and truck stops.

That's how American Life Today.com came about. I wanted to capture the "everyday" American life asking them 5 questions, to keep it simple. Because you know how it is when granddad dips into the "juice" at the campsite...he can go on and on. I wanted to share just enough to keep you interested and awake, as well as promote a favorite charity.

Some of your stories have moved me to tears.

As sad as it is, the site will come to a close soon. I am going to start another journey in the next few weeks so I will schedule all of the remaining profiles that are waiting to post. After that, I will post as they come in but I will no longer beg you to answer the questions. You know I did!

A big THANK YOU to those of you who took the time to share your life. I know that people have enjoyed reading them, especially me.

Until the next adventure...

The Finnish Mental Hospital Trial

This diet trial was conducted between 1959 and 1971 in two psychiatric hospitals near Helsinki, Finland. One hospital served typical fare, including full-fat milk and butter, while the other served "filled milk", margarine and polyunsaturated vegetable oils. Filled milk has had its fat removed and replaced by an emulsion of vegetable oil. As a result, the diet of the patients in the latter hospital was low in saturated fat and cholesterol, and high in polyunsaturated fat compared to the former hospital. At the end of six years, the hospitals switched diets. This is known as a "crossover" design.

The results were originally published in 1972 in the Lancet (ref), and a subset of the data were re-published in 1979 in the International Journal of Epidemiology (ref). They found that during the periods that patients were eating the diet low in saturated fat and cholesterol, and high in vegetable oil, male participants (but not females) had roughly half the incidence of heart attack deaths. There were no significant differences in total mortality in either men or women. The female data were omitted in the 1979 report.

This study is often cited as support for the idea that saturated fat increases the risk of heart attack. The reason it's cited so often is it's one of a minority of trials that came to that conclusion. The only other controlled trial I'm aware of that replaced animal fat with polyunsaturated vegetable oil (without changing other variables at the same time) and found a statistically significant decrease in cardiovascular deaths was the Los Angeles Veterans' Administration study. However, there was no difference in total mortality, and there were significantly more heavy smokers in the control group. The difference in heart attack deaths in the V.A. trial was 18%, far less than the difference seen in the Finnish trial.

I can cite three controlled trials that came to the opposite conclusion, that switching saturated fat for vegetable oil increases cardiovascular mortality and/or total mortality: the Anti-Coronary Club Trial (4 years), the Rose et al. corn oil trial (2 years), and the Sydney Diet-Heart trial (5 years). Other controlled trials found no difference in total mortality or heart attack mortality from this intervention, including the National Diet-Heart Study (2 years) and the Medical Research Council study (7 years). Thus, the Finnish trial is an outlier whose findings have never been replicated by better-conducted trials.

I have three main bones to pick with the Finnish trial. The first two are pretty bad, but the third is simply fatal to its use as support for the idea that saturated fat contributes to cardiovascular risk:

1) A "crossover" study design is not an appropriate way to study a disease with a long incubation period. How do you know that the heart attacks you're observing came from the present diet and not the one the patients were eating for the six years before that? The Finnish trial was the only trial of its nature ever to use a crossover design.

2) The study wasn't blinded. When one wants to eliminate bias in diagnosis for these types of studies, one designs the study so that the physician doesn't know which group the patients came from. That way he can't influence the results, consciously or unconsciously. Obviously there was no way to blind the physicians in this study, because they knew what the patients in each hospital were eating. I think it's interesting that the only outcome not susceptible to diagnostic bias, total mortality, showed no significant changes in either men or women.

3) The Finnish Mental Hospital trial was not actually a controlled trial. In an editorial in the November 1972 issue of the Lancet, Drs. John Rivers and John Yudkin pointed out, among other things, that the amount of sugar varied by almost 50% between diet periods. In the December 30th issue, the lead author of the study responded:

In view of the design of the experiment the variations in sugar intake were, of course, regrettable. They were due to the fact that, aside from the fatty-acid composition and the cholesterol content of the diets, the hospitals, for practical reasons, had to be granted certain freedom in dietary matters.

In other words, the diets of the two hospitals differed significantly in ways other than their fat composition. Sugar was one difference. Carbohydrate intake varied by as much as 17% and total fat intake by as much as 26% between diet periods (on average, carbohydrate was lower and total fat was higher in the polyunsaturated fat group). The use of psychiatric drugs with known cardiovascular side effects differed substantially between groups and could have accounted for some of the difference in cardiovascular events.  

The definition of a controlled trial is an experiment in which all variables are kept reasonably constant except the one being evaluated. Therefore, the Finnish trial cannot rightfully be called a controlled trial. The fact that the result has never been replicated casts further doubt on the study.
I could continue listing other problems with the study, such as the fact that the hospital population included in the analysis had a high turnover rate (variable, but as high as 40%), and patients were included in the analysis even if they were at the hospital for as little as 50% of the time between first admission and final discharge (i.e., they came and went). But what's the use in beating a dead horse?

Planning his Escape

It's been a while since I've painted so I decided to give it a shot. Here is Max in the gate which should be called "Heeeeeere's MAX." He's a bit of a devil I am finding. I know this is nothing like what Kellie Straw does with her dogs, but it sorta looks like Max so that is success to me.

Travels with Max

I am about to begin another cross country road trip. The past few weeks I’ve been preparing to leave and this time, I am renting my home. I am lucky enough to be able to have a nice young couple and their chocolate lab stay here while Max and I embark on our adventure.

This time, it’s going to be different.

“Trailie” is staying home, Max and I are going to camp with a tent, I am going to read more, journal more and paint a little. I have a general timeline but I don’t know what path we will take yet. I have two weeks to decide which roads we will embark on, or perhaps we will leave and decide as we go.

Renting out your home is a journey in itself. I’ve lived here for 7 years and when you settle in a place, you usually don’t take the time to see what you have. I am going through and cleaning all cupboards, drawers, closets…everything. It’s a lot of “stuff.” Doing this cleanses the soul in a way. I am not attached to things as I once was. As time consuming and exhausting as it is, it brings a sense of relief to find homes for unwanted items and to purge the things I haven’t looked at or missed in years.

Max is settling in just fine. He is now guarding the house and is used to our little routine we have around here. It’s nice. We are bonding. I introduced him to “trailie” the other day and told him about the adventure Maggie and I had last summer. I broke down and cried. He slept at my feet.

Max and I will document our journey here so you can see what we are up to. I would love to hear of a destination that holds a special place with you.

Max

I can't imagine my life without a pet. I've had cats, dogs, guinea pigs, turtles, and fish as pets growing up. As you know from my travels, Maggie and I had the trip of a lifetime last summer. The past few months have been incredibly hard not having her around. She was with me for 10 years. Moved with me 4 times. Visited 26 States together.

Last Sunday, I went to the Farmer's market to pick up some strawberries and came home with a new family member. His name is Max. His time was up at a local shelter and a rescue group saved him on his last day. I took him out of the group cage to spend some time together and he didn't leave my side. I didn't want him to. I was instantly smitten.

I haven't had a small dog in the house for 23 years. My last 2 dogs were both larger so it's an adjustment. For instance, you need to bend lower to the ground to pet them, watch where you step so you don't crush them, buy smaller toys, less food, softer play and it's harder to hide your "does my butt look big in these jeans?" days with a smaller dog in a picture. Now there is nowhere to hide. Your butt looks even bigger. Not that you turn around and squat with pictures with your dog. Never mind. Anyway...

No, I am not going to carry him in a purse.

One of the things we are enjoying is going to the dog park and the dog beach. This was something I could never enjoy with Maggie since she would try to attack anything that wasn't a human. A bit of a buzz kill.

I look forward to this new chapter. I am excited about taking Max on new adventures. I think another trip is in order. Soon.

Here are some pictures from his week of making friends at the park and playing at the beach: