A Gluten-free January

Are You Gluten Sensitive?

Many people are totally unaware of the fact that they react poorly to gluten. Because they've been eating wheat, barley and/or rye products every day for virtually their entire lives, they don't know what their bodies feel like without gluten. In susceptible people, eating gluten is linked to a dizzying array of health problems that stem from an immune reaction to gliadins and other proteins in gluten (1). Are you a susceptible person? How do you know?

The gold standard way to detect a gluten sensitivity is to do a gluten "challenge" after a period of avoidance and see how you feel. People who react poorly to gluten may feel better after a period of avoidance. After a gluten challenge, symptoms can range from digestive upset, to skin symptoms, to fatigue or irritability within minutes to days of the gluten challenge.

With 2011 approaching, why not make your new year's resolution to go gluten-free for a month? A man named Matt Lentzner e-mailed me this week to ask if I would help with his (non-commercial) project, "A Gluten-free January". I said I'd be delighted. Although I don't typically eat much gluten, this January I'm going 100% gluten-free. Are you on board? Read on.

A Message from Matt Lentzner

Hi There.

My name is Matt Lentzner. I'm just some guy who lifts weights on his patio and tries to eat healthy. That's not important, but I have an idea that just might be.

I am trying to get as many people as possible to go gluten-free for one month - this January 2011.

I've considered this whole ancestral diet thing and I've come to a conclusion. If you could only do just one thing to improve your health then not eating gluten would be it. This is not to say that avoiding other nasty things like fructose or industrial vegetable oil is not important. They are, but you'd get the most bang for your buck from not eating gluten.

"Eat No Gluten" is simple and easy to remember. I think that sometimes the rules get so complicated and overwhelming and people just give up on it. We're keeping it simple here. Even at this simplified level I see that it's difficult for a lot of folks. I think people, Americans especially, tend not to pay much attention to what they're eating - what it is, where it came from, etc.

Getting people to get out of their eating ruts and think a little about what goes into their mouths is a valuable exercise. It sets the stage for better choices in the future. I hope that some success with the simple step will encourage people to further improve their diets.

I have a website at www.glutenfreejan.com. If you want to sign up just send an email with your first name, last initial, and town of residence to glutenfreejan@gmail.com. If you are on Facebook there's a community you can 'Like' called: Gluten Free January. So far I have over 120 people all over the world signed up. If you are already gluten-free then I still want you to sign up - the more the merrier. You can also use this opportunity to spread the word and sign up your family and friends.

Merry Christmas - Looking forward to a gluten-free New Year.

Matt

Potato Diet Interpretation

If you read my post on December 16th, you know that Chris Voigt saw remarkable fat loss and improvements in health markers as a result of two months of eating almost nothing but potatoes. This has left many people scratching their heads, because potatoes are not generally viewed as a healthy food. This is partially due to the fact that potatoes are very rich in carbohydrate, which also happens to be a quickly digested type, resulting in a high glycemic index. The glycemic index refers to the degree to which a particular food increases blood glucose when it's eaten, and I've questioned the relevance of this concept to health outcomes in the past (1, 2, 3). I think Mr. Voigt's results once again argue against the importance of the glycemic index as a diet-health concept.

It's often pointed out that potatoes are low in vitamins and minerals compared to vegetables on a per-calorie basis, but I think it's a misleading comparison because potatoes are much more calorie-dense than most vegetables. Potatoes compare favorably to other starchy staples such as bread, rice and taro.

Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).

On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But as Gary Taubes would say, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.

Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?

I believe Mr. Voigt's diet lowered his fat mass 'setpoint'. In other words, for whatever reason, the diet made his body 'want' to be leaner that it already was. His body began releasing stored fat that it considered excess, and therefore he had to eat less food to complete his energy needs. You see this same phenomenon very clearly in rodent feeding studies. Changes in diet composition/quality can cause dramatic shifts in the fat mass setpoint (5, 6). Mr. Voigt's appetite would eventually have returned to normal once he had stabilized at a lower body fat mass, just as rodents do.

Rodent studies have made it clear that diet composition has a massive effect on the level of fat mass that the body will 'defend' against changes in calorie intake (5, 6). Human studies have shown similar effects from changes in diet composition/quality. For example, in controlled diet trials, low-carbohydrate dieters spontaneously reduce their calorie intake quite significantly and lose body fat, without being asked to restrict calories (7). In Dr. Staffan Lindeberg's Paleolithic diet trials, participants lost a remarkable amount of fat, yet a recent publication from his group shows that the satiety (fullness) level of the Paleolithic group was not different from a non-Paleolithic comparison group despite a considerably lower calorie intake over 12 weeks (8, 9). I'll discuss this important new paper soon. Together, this suggests that diet composition/quality can have a dominant impact on the fat mass setpoint.

One possibility is that cutting the wheat, sugar, most vegetable oil and other processed food out of Mr. Voigt's diet was responsible for the fat loss. I think that's likely to have contributed. Many people find, for example, that they lose fat simply by eliminating wheat from their diet.

Another possibility that I've been exploring recently is that changes in palatability (pleasantness of flavor) influence the fat mass setpoint. There is evidence in rodents that it does, although it's not entirely consistent. For example, rats will become massively obese if you provide them with chocolate flavored Ensure (a meal replacement drink), but not with vanilla or strawberry Ensure (10). They will defend their elevated fat mass against calorie restriction (i.e. they show a physiological starvation response when you try to bring them down to a lower weight by feeding them less chocolate Ensure) while they're eating chocolate Ensure, but as soon as you put them back on unpurified rodent pellets, they will lose fat and defend the lower fat mass. Giving them food in liquid or paste form often causes obesity, while the same food in solid pellet form will not. Eating nothing but potatoes is obviously a diet with a low overall palatability.

So I think that both a change in diet composition/quality and a decrease in palatability probably contributed to a decrease in Mr. Voigt's fat mass setpoint, which allowed him to lose fat mass without triggering a starvation response (hunger, fatigue).

The rest of his improvements in health markers were partially due to the fat loss, including his decreased fasting glucose, decreased triglycerides, and presumably increased insulin sensitivity. They may also have been partially due to a lack of industrial food and increased intake of certain micronutrients such as magnesium.

One of the most striking changes was in his calculated LDL cholesterol ("bad" cholesterol), which decreased by 41%, putting him in a range that's more typical of healthy non-industrial cultures including hunter-gatherers. Yet hunter-gatherers didn't eat nothing but potatoes, often didn't eat much starch, and in some cases had a high intake of fat and saturated fat, so what gives? It's possible that a reduced saturated fat intake had an impact on his LDL, given the relatively short timescale of the diet. But I think there's something mysterious about this setpoint mechanism that has a much broader impact on metabolism than is generally appreciated. For example, calorie restriction in humans has a massive impact on LDL, much larger than the impact of saturated fat (11). And in any case, the latter appears to be a short-term phenomenon (12). It's just beginning to be appreciated that energy balance control systems in the brain influence cholesterol metabolism.

Mr. Voigt's digestion appeared to be just fine on his potato diet, even though he generally ate the skins. This makes me even more skeptical of the idea that potato glycoalkaloids in common potato varieties are a health concern, especially if you were to eliminate most of the glycoalkaloids by peeling.

I asked Mr. Voigt about what foods he was craving during the diet to get an idea of whether he was experiencing any major deficiencies. The fact that Mr. Voigt did not mention craving meat or other high-protein foods reinforces the fact that potatoes are a reasonable source of complete protein. The only thing he craved was crunchy/juicy food, which I'm not sure how to interpret.

He also stopped snoring during the diet, and began again immediately upon resuming his normal diet, perhaps indicating that his potato diet reduced airway inflammation. This could be due to avoiding food allergies and irritants (wheat anyone?) and also fat loss.

Overall, a very informative experiment! Enjoy your potatoes.


*Until the last 5.5 weeks, when he deliberately stuffed himself beyond his appetite because his rapid weight loss worried him. Yet, even with deliberate overfeeding up to his estimated calorie requirement of 2,200 calories per day, he continued to lose weight. He probably was not quite reaching his calorie goal, or his requirement is higher than he thought.

Trouble With RSS Feed?

I've received several comments that my blog posts are no longer showing up in peoples' RSS feeds. I've gone into my settings, and the blog is still set to full feed mode, so I don't know why that would be. I'm trying to understand if the problem is widespread or only affects a few people. Please let me know in the comments section if new posts (since the potatoes and human health series) are not showing up in your reader. Also, please let me know if new posts are showing up. Thanks!

Dr. Mellanby's Tooth Decay Reversal Diet

I have a lot of admiration for Drs. Edward and May Mellanby. A husband-and-wife team, they discovered vitamin D, and determined that rickets is caused by poor calcium (or phosphorus) status, typically due to vitamin D deficiency. They believed that an ideal diet is omnivorous, based on whole foods, and offers an adequate supply of fat-soluble vitamins and easily absorbed minerals. They also felt that grain intake should be modest, as their research showed that unsoaked whole grains antagonize the effect of vitamins D and A.

Not only did the Mellanbys discover vitamin D and end the rickets epidemic that was devastating Western cities at the time, they also discovered a cure for early-stage tooth decay that has been gathering dust in medical libraries throughout the world since 1924.

It was in that year that Dr. May Mellanby published a summary of the results of the Mellanby tooth decay reversal studies in the British Medical Journal, titled "Remarks on the Influence of a Cereal-free Diet Rich in Vitamin D and Calcium on Dental Caries in Children". Last year, I had to specially request this article from the basement of the University of Washington medical library (1). Thanks to the magic of the internet, the full version of the paper is now freely available online (2).

You don't need my help to read the study, but in this post I offer a little background, a summary and my interpretation.

In previous studies, the Mellanbys used dogs to define the dietary factors that influence tooth development and repair. They identified three, which together made the difference between excellent and poor dental health (from Nutrition and Disease):

1. The diet's mineral content, particularly calcium and phosphorus
2. The diet's fat-soluble vitamin content, chiefly vitamin D
3. The diet's content of inhibitors of mineral absorption, primarily phytic acid

Once they had defined these factors, they set about testing their hypotheses in humans. They performed eight trials, each one in children in an institutionalized setting where diet could be completely controlled. The number of cavities in each child's mouth was noted at the beginning and end of the period. I'll only discuss the three most informative, and only the most successful in detail. First, the results:

I'll start with diet 1. Children on this diet ate the typical fare, plus extra oatmeal. Oatmeal is typically eaten as an unsoaked whole grain (and soaking it isn't very effective in any case), and so it is high in phytic acid, which effectively inhibits the absorption of a number of minerals including calcium. These children formed 5.8 cavities each and healed virtually none-- not good!

Diet number 2 was similar to diet 1, except there was no extra oatmeal and the children received a large supplemental dose of vitamin D. Over 28 weeks, only 1 cavity per child developed or worsened, while 3.9 healed. Thus, simply adding vitamin D to a reasonable diet allowed most of their cavities to heal.

Diet number 3 was the most effective. This was a grain-free diet plus supplemental vitamin D. Over 26 weeks, children in this group saw an average of only 0.4 cavities form or worsen, while 4.7 healed. The Mellanbys considered that they had essentially found a cure for this disorder in its early stages.

What exactly was this diet? Here's how it was described in the paper (note: cereals = grains):

...instead of cereals- for example, bread, oatmeal, rice, and tapioca- an increased allowance of potatoes and other vegetables, milk, fat, meat, and eggs was given. The total sugar, jam, and syrup intake was the same as before. Vitamin D was present in abundance in either cod-liver oil or irradiated ergosterol, and in egg yolk, butter, milk, etc. The diet of these children was thus rich in those factors, especially vitamin D and calcium, which experimental evidence has shown to assist calcification, and was devoid of those factors- namely, cereals- which interfere with the process.

Carbohydrate intake was reduced by almost half. Bread and oatmeal were replaced by potatoes, milk, meat, fish, eggs, butter and vegetables. The diet is reminiscent of what Dr. Weston Price used to reverse tooth decay in his dental clinic in Cleveland, although Price's diet did include rolls made from freshly ground whole wheat. Price also identified the fat-soluble vitamin K2 MK-4 as another important factor in tooth decay reversal, which would have been abundant in Mellanby's studies due to the dairy. The Mellanbys and Price were contemporaries and had parallel and complementary findings. The Mellanbys did not understand the role of vitamin K2 in mineral metabolism, and Price did not seem to appreciate the role of phytic acid from unsoaked whole grains in preventing mineral absorption.

Here are two sample meals provided in Dr. Mellanby's paper. I believe the word "dinner" refers to the noon meal, and "supper" refers to the evening meal:

Breakfast- Omelette, cocoa, with milk.
Lunch- Milk.
Dinner- Potatoes, steamed minced meat, carrots, stewed fruit, milk.
Tea- Fresh fruit salad, cocoa made with milk.
Supper- Fish and potatoes fried in dripping, milk.

Breakfast- Scrambled egg, milk, fresh salad.
Dinner- Irish stew, potatoes, cabbage, stewed fruit, milk.
Tea- Minced meat warmed with bovril, green salad, milk.
Supper- Thick potato soup made with milk.

In addition, children received vitamin D daily. Here's Dr. Mellanby's summary of their findings:

The tests do not indicate that in order to prevent dental caries children must live on a cereal-free diet, but in association with the results of the other investigations on animals and children they do indicate that the amount of cereal eaten should be reduced, particularly during infancy and in the earlier years of life, and should be replaced by an increased consumption of milk, eggs, butter, potatoes, and other vegetables. They also indicate that a sufficiency of vitamin D and calcium should be given from birth, and before birth, by supplying a suitable diet to the pregnant mother. The teeth of the children would be well formed and more resistant to dental caries instead of being hypoplastic and badly calcified, as were those in this investigation.

If I could add something to this program, I would recommend daily tooth brushing and flossing, avoiding sugar, and rinsing the mouth with water after each meal.

This diet is capable of reversing early stage tooth decay. It will not reverse advanced decay, which requires professional dental treatment as soon as possible. It is not a substitute for dental care in general, and if you try using diet to reverse your own tooth decay, please do it under the supervision of a dentist. And while you're there, tell her about Edward and May Mellanby!

Preventing Tooth Decay
Reversing Tooth Decay
Images of Tooth Decay Healing due to an Improved Diet
Dental Anecdotes

Interview with a Kitavan

Kitava is a Melanesian island that has maintained an almost entirely traditional, non-industrial diet until very recently. It was the subject of a study by Dr. Staffan Lindeberg and colleagues, which I have written about many times, in which they demonstrated that Kitavans have a very low (undetectable) rate of heart attack, stroke, diabetes and overweight. Dr. Lindeberg described their diet as consisting mostly of yam, sweet potato, taro, cassava, coconut, fruit, fish and vegetables. Over the seven days that Dr. Lindeberg measured food intake, they ate 69% of their calories as carbohydrate, 21% as fat (mostly from coconut) and 10% as protein.

I recently received an e-mail from a Kitavan by the name of Job Daniel. He's working at the Papua New Guinea Institute of Medical Research in Madang, studying the social and economic impacts of malaria and related health issues in Papua New Guinea. He recalls many details of Dr. Lindeberg's visit to Kitava, which Dr. Lindeberg has confirmed are correct. Job generously offered to answer some of my questions about the traditional Kitavan diet. My questions are in bold, and his responses are below.

How many meals a day do Kitavans eat?
People on the island eat mostly two meals a day. But nowadays, breakfast is mainly comprised of tubers (yam and sweet potato and greens all cooked in coconut cream and salt) and dinner is the same with the inclusion of fish as protein most often. In between these two meals, lunch is seen as a light refreshment with fruits or young coconut only to mention these two popular ones. In between the morning and the evening, we mostly eat fruits as snack or lunch. Generally speaking, there are only two main meals per day, i.e breakfast and dinner.

Do Kitavans eat any fermented food?
There are fermented fruits and nuts like you've said for breadfruit, nuts, yams and not forgetting fish. We ferment them by using the traditional method of drying them over the fire for months. And this fermented foods last for almost one to two years without getting stale or spoiled. Food preservation is a skill inherited from our great grand fathers taking into consideration the island's location and availability of food. Foods such as bread fruit and fish are fermented and preserved to serve as substitutes to fresh food in times of trouble or shortage. Otherwise, they're eaten along the way.

Is this really fermentation or simply drying?
To your query about the fermentation methods we use, apart from drying food over the fire, we also use this method like the Hawaiians do with taro [poi- SJG]. For our case we bury a special kind of fruit collected from the tree and buried in the ground to ripen, which takes about 2 - 3 days. I don't really know the English name, but we call it 'Natu' in vernecular. There's also a certain nut when it falls from the tree, women collect them and peel off the rotten skin, then mumu [earth oven- SJG] them in the ground covered with leaves to protect them from burning from the extreme heat of the fire, both from the open fire on top and hot stones underneath. After a day, the nuts are removed from the mumu and loaded into very big baskets which are then shifted to the sea for fermentation. This takes a week (minimum) to ferment or be ready for consumption at last. After the fermentation period is over, i.e one week some days or two
weeks to be exact, then the nuts are finally ready for eating. The length of time it takes before the nuts are no longer edible is roughly one week.

What parts of the fish are eaten?
As islanders, we eat almost every creature and body part of a sea creature. Especially fish eggs, it is one of the favorites of children. They always prefer it burnt on the fire and consumed greedily. Every part of the fish is eaten except for the feces, gall bladder, bones and the scales.

Is food shortage really rare on Kitava?
Generally speaking it is rare. BUT sometimes we run out of food only if there is a drought and the sea is useless. Otherwise, we tend to use the preserved or fermented foods on the dryer in the kitchen. As you would understand, we have seasons and they affect the type and availability of food on the island. In the beginning of the year, we eat sweet potato, cassava and mostly tuna for protein. During mid year, before yam comes in to replace sweet potato and cassava, taro is then ready for harvest. And then yams are ready for harvesting so the food supply is continued on. OK when yams are harvested, some are eaten, some are stored away for reserve and seedlings. In this way, we don't run out food towards the end of the year before sweet potato would be ready for harvest. So as you can see, the food supply on the island is somewhat planned by our ancestral economists where it continues throughout the year without stopping.

Do Kitavans traditionally eat pork, and if so, how often?
We do eat pork but not that often because pork meat is chiefly regarded important on the island. We only eat pork on special occasions so I'd rather say that pork is only eaten occasionally. In most cases in the middle of the year when the yams are harvested (yam harvest celebrations and towards the end of the year for certain rites and activities). Otherwise the everyday meal is always topped with fish.

How long are infants breast fed on Kitava?
Women breast feed for a minimum of 2 years. But breast feeding is again determined by the size and health situation of the baby. If the baby is looking healthy and big, it is most likely that this baby would be adopted temporarily by someone else so as to be removed from breast milk after two years of age minimum. Child care nowadays is paramount as people start to realize the importance of health and hygiene in general. But Kitavans are well known in that part of the country for their hygiene practices. They also got the provincial and district awards for a 'clean community' in early 90s and right now, they still maintain their hygiene level and awareness.

Are there any other foods that are commonly eaten on Kitava that I might not be aware of?
Bananas, pineapple, corn and watermelons. For watermelon and corn, they are plentiful especially at this time of the year.

Thanks for your help, Job! I know many people will appreciate reading these responses.

Diet-Heart Controlled Trials: a New Literature Review

Many controlled studies have measured the cardiovascular effects of replacing animal ("saturated") fats with seed oils (predominantly the omega-6 polyunsaturated fat linoleic acid) in humans. A number of these studies recorded heart attacks and total mortality during the following 1-8 years. Several investigators have done meta-analyses (literature reviews) to try to tease out overall conclusions from these studies.

I'm pleased to point out a new meta-analysis of these controlled trials by Dr. Christopher Ramsden and colleagues (1). This paper finally cleans up the mess that previous meta-analyses have made of the diet-heart literature. One recent paper in particular by Dr. Dariush Mozaffarian and colleagues concluded that overall, the controlled trials show that replacing animal fat with linoleic acid (LA)-rich seed oils reduces heart attack risk (2). I disagreed strongly with their conclusion because I felt their methods were faulty (3).

Dr. Ramsden and colleagues pointed out several fundamental flaws in the review paper by Dr. Mozaffarian and colleagues, as well as in the prevailing interpretation of these studies in the scientific literature in general. These overlap with the concerns that I voiced in my post (4):

1. Omission of unfavorable studies, including the Rose corn oil trial and the Sydney diet-heart trial.
2. Inclusion of weak trials with major confounding variables, such as the Finnish mental hospital trial.
3. Failure to distinguish between omega-6 and omega-3 fatty acids.
4. Failure to acknowledge that seed oils often replaced large quantities of industrial trans fats in addition to animal fat in these trials.
   

Dr. Ramsden and colleagues accounted for all of these factors in their analysis, which has never been done before. They chose inclusion criteria* that made sense, and stuck with them. In addition, they did an impressive amount of historical work, digging up old unpublished data from these trials to determine the exact composition of the control and experimental diets. The paper is published in the British Journal of Nutrition, an excellent journal, and overall is written in a scientific and professional manner.

What did they find?

• Interventions that replaced animal and trans fat with seed oils that were rich in LA but low in omega-3 caused a non-significant trend toward increased heart attacks (13% increase) and overall mortality.
  
• Interventions that replaced animal and trans fat with a combination of LA and omega-3 fats significantly reduced heart attacks (by 22%). The numbers for total mortality followed a similar trend.

In other words, LA-rich seed oils do not prevent heart attacks (and may actually promote them), but correcting an omega-3 deficiency and reducing industrial trans fat intake may be protective. This is similar to what I've been saying for a while now, based on my own interpretation of the same studies and others. However, Dr. Ramsden and colleagues have taken the idea to a new level by their thorough and sophisticated detective work and analysis. For example, I didn't realize that in virtually all of these controlled trials, the intervention group reduced its trans fat intake substantially in addition to reducing animal fat. From the paper:

...experimental diets replaced common �hard� margarines, industrial shortenings and other sources of [trans fat] in all seven of the [controlled trials] included in the meta-analysis by Mozaffarian et al. The mean estimated [trans fat] content of the seven control diets was 3�0 [% of calories] (range 1�5�9�6 [%]).
...the displacement of [trans fat], rather than the substitution of mixed n-3/n-6 [polyunsaturated fat] for [saturated fat], may account for some or all of the 22% reduction in non-fatal [heart attacks and heart attack] death in our meta-analysis. By contrast, the increased [heart attack] risks from n-6 specific [polyunsaturated fat] diets in our meta-analysis may be underestimated as n-6 [polyunsaturated fat] also replaced substantial quantities of [trans fat] (Table 3). The consistent trends towards increased [heart attack] risk of n-6 specific [polyunsaturated fat] diets may have become significant if the n-6 [polyunsaturated fat] replaced only [saturated fat], instead of a combination of [saturated fat] and [trans fat].

In other words, it looks like trans fat is probably the issue, not animal fat, but these trials replaced both simultaneously so we can't know for sure. I will note here that trans fat does not generally promote atherosclerosis (thickening and hardening of arteries) in animal models, so if it does truly increase heart attack risk as many studies suggest, it's probably through a mechanism that is independent of atherosclerosis.

The article also contains an excellent discussion of the Finnish mental hospital trial (5, 6) and why it was excluded from the meta-analysis, in which Dr. Ramsden and colleagues point out major design flaws, some of which I was not aware of. For example, trans fat intake was on average 13 times higher in the control groups than in the experimental groups. In addition, one of the control groups received more than twice as much of the antipsychotic drug thioridazine, which is known to be highly toxic to the heart, as any other group. Ouch. I'm glad to see this study finally discussed in an open and honest manner. I discussed my own problems with the Finnish trial in an earlier post (7).

I was also glad to see an open discussion of the Oslo Diet-heart study (8), in which diet changes led to a reduction in heart attack risk over five years. Dr. Mozaffarian and colleagues included it in their analysis as if it were a controlled trial in which animal fat was replaced by seed oils only. In reality, the investigators changed many variables at once, which I had also pointed out in my critique of Dr. Mozaffarian's meta-analysis (9). Here's what Dr. Ramsden and colleagues had to say about it:

First, experimental dieters were instructed to substitute fish, shellfish and �whale beef� for meats and eggs, and were actually supplied with �considerable quantities of Norwegian sardines canned in cod liver oil, which proved to be popular as a bread spread�(32)... Second, the experimental group consumed massive amounts of soybean oil, which provided large quantities of both LA (15�6 en %) and ALA (2�7 en %). ALA consumption was about 4�5 times average US intake(42), or about twelve typical flax oil pills (1 g pill � 560 mg ALA) per d. In addition, the fish and cod liver oil consumption provided Oslo (598N latitude) dieters with 610 IU (15�25 mg) of daily vitamin D3, recently linked to lower blood pressure, plaque stabilisation, and reduced [heart attack risk] (64). Furthermore, experimental dieters were encouraged to eat more nuts, fruits, and vegetables; to limit animal fats; and to restrict their intake of refined grains and sugar.

trans fat intake was also reduced substantially by excluding margarine in the experimental group. Other review papers have used this trial as a justification to replace animal fat with seed oils. Hmm... The only reason they get away with this is because the trial was published in 1966 and almost no one today has actually read it.

One criticism I have of Dr. Ramsden's paper is that they used the Oslo trial in their analysis, despite the major limitation described above. However, they were extremely open about it and discussed the problem in detail. Furthermore, the overall result would have been essentially the same even if they had excluded the Oslo trial from the analysis.

Overall, the paper is an excellent addition to the literature, and I hope it will bring a new level of sophistication to the dialogue on dietary prevention of cardiovascular disease. In the meantime, brace yourselves for an avalanche of criticism from the seed oil brigade.


* Guidelines that determine which studies to include in the analysis. For example, you want to exclude any study that wasn't randomized, because it will not be interpretable from a statistical standpoint. You also want to exclude trials where major variables differ between groups besides the specific variable you're trying to test. The Finnish mental hospital trial fails by both criteria.