Commenter Kiwi Geoff kindly wrote a program that calculates LDL using the Friedewald equation and the equation from this paper, which may be more accurate for people with a total cholesterol over 250 and triglycerides under 100. For people whose triglycerides are over 100, the Friedewald equation should be relatively accurate. You can plug your total cholesterol, HDL and triglycerides into the program (in mg/dL), and it gives you both LDL values side-by side. Here it is:
LDL Cholesterol Calculator
Thanks, Geoff.
Another Fatty Liver Reversal
Just to show it wasn't a fluke, reader "Steve" replicates the experiment:
The liver is a remarkable organ. Besides being your "metabolic grand central station", it's the only organ in the human body that can regenerate almost completely. It can be 75% obliterated, and it will grow back over time. Fatty liver and NASH are largely reversible.
I had a similar problem as what Sam described, and it just happened to coincide with my discovery of and commitment to a new eating plan (based on low/good carb, high in good fat and omega 3, and good protein--basically a mix of paleo, primal, low carb, whatever they call it). I consider myself lucky to have had great fortune in my timing of finding out about my fatty liver.And a later comment:
My ALT and AST [markers of liver damage] had been at 124 and 43 respectively, and then still at 80 and 30 in a follow up a few months later. I weighed in at about 205 (I'm 6'1.5" on a slimmish frame), which was my heaviest. I had been on a basic American (bad) diet. The whole thing shocked me, especially after a CT with contrast showed the fatty deposits on my liver (and prior to that, when the muddy ultrasound revealed a fatty liver and a possible pancreatic mass, later ruled out by the CT). Like Sam, though I was surely overweight, I was not fat or heavy. (Most people have noticed I look leaner, but are shocked when I disclose how much weight I have lost since they say "I cannot believe you had that much to lose.")
At about the same time I found out about my liver issue, I had been getting into reading about diet and health (something I had done once when I read the Zone stuff from Sears many years ago). I practically dove through Taubes, Eades, Cordain, and a bunch of blogs (including yours), and I made a commitment to fix my problem.
I started a pretty severe regimen at first, which included only protein and good fats with a minimal amount of non-starchy fruits and vegetables. Almost immediately, I started losing weight and body fat (as measured by an electrical impedance scale). I have always supplemented with fish oil, but I added krill oil and I also started eating grass-fed beef and pastured eggs and pastured pork as much as possible. I have added some coconut oil and pastured butter to my diet as well. I have dropped almost 40 pounds, I am down to about 10-11% body fat (from 24%), and my ALT/AST on my last test was 24/14 [normal]. I am getting another test soon, and I expect similar results.
I can add to the story that I first found out about the fatty liver on a routine new patient blood screening when I moved to a new town. I can also add that it took a bit of initiative on my part to get to the right diagnosis. The first doctor suspected hepatitis, but when blood work ruled that out, he ordered the imagining tests. Once I was referred to a GI specialist, it was a quick diagnosis. Still, I had to undertake myself to figure out the best diet. The GI recommended eliminating white bread, rice, pasta, starches, etc. but also recommended lowering fat intake. Having done some of my reading on diet and health, I knew to follow the former advice and to modify the latter to be "get plenty of fat, but make sure its the right kind."Steve took the initiative and fixed his damaged liver. He modified his GI doctor's advice based on what he had read about nutrition, with excellent results. I suspect his doctor will be all ears next time Steve comes into his office.
The liver is a remarkable organ. Besides being your "metabolic grand central station", it's the only organ in the human body that can regenerate almost completely. It can be 75% obliterated, and it will grow back over time. Fatty liver and NASH are largely reversible.
When Friedewald Attacks
I don't get very excited about nitpicking blood lipids. That's not to say they're not useful. There's definitely an association between blood lipids and certain health outcomes such as cardiovascular disease. The thing that tires me is when people uncritically interpret those associations as evidence that lipids are actually causing the problem.
Low-density lipoprotein, or LDL, is the cholesterol fraction that typically gets the most attention. High LDL associates with heart attack risk in Americans and some other groups. Statins reduce LDL and reduce heart attack risk in a subset of the population, and this has been used to support the idea that elevated LDL causes heart attacks. This is despite the fact that lowering LDL via diet doesn't seem to reduce heart attack risk (typically by reducing total fat and/or saturated fat). Statins may in fact work because they're anti-inflammatory, rather than because they reduce LDL. But both explanations are speculative at this point.
The fact remains that if you want to know if Mr. Jones is going to have a heart attack in the next five years, measuring his LDL will give you more information than not measuring his LDL. This association doesn't seem to apply to all cultures or to Americans eating atypical diets. Then you can get into the fractions that associate more tightly with heart attack risk, such as low HDL, high triglycerides, small dense LDL, etc. Triglycerides vary with HDL (that is, when trigs go up, HDL generally goes down) and the ratio also happens to be a predictor of insulin sensitivity. Total cholesterol is virtually useless for predicting heart attack risk in the general population. This is something I'll discuss in more detail at another time.
When you walk into the doctor's office and ask him to measure your cholesterol, the numbers you get back will generally be total cholesterol, LDL, HDL and triglycerides. All of those except LDL are measured directly. LDL is calculated using the Friedewald equation, which is (in mg/dL):
I had a lipid panel done a while back, just for kicks. My LDL, calculated by the Friedewald equation, was 131 mg/dL. Over 130 is considered high. Pass the statins! But wait, my triglycerides were 48 mg/dL, which is quite low. I found a paper through Dr. Eades' post that contains an equation for accurately calculating LDL in people whose triglycerides are below 100 mg/dL*. Here it is (mg/dL):
*This equation was designed for individuals with a total cholesterol over 250 mg/dL.
Low-density lipoprotein, or LDL, is the cholesterol fraction that typically gets the most attention. High LDL associates with heart attack risk in Americans and some other groups. Statins reduce LDL and reduce heart attack risk in a subset of the population, and this has been used to support the idea that elevated LDL causes heart attacks. This is despite the fact that lowering LDL via diet doesn't seem to reduce heart attack risk (typically by reducing total fat and/or saturated fat). Statins may in fact work because they're anti-inflammatory, rather than because they reduce LDL. But both explanations are speculative at this point.
The fact remains that if you want to know if Mr. Jones is going to have a heart attack in the next five years, measuring his LDL will give you more information than not measuring his LDL. This association doesn't seem to apply to all cultures or to Americans eating atypical diets. Then you can get into the fractions that associate more tightly with heart attack risk, such as low HDL, high triglycerides, small dense LDL, etc. Triglycerides vary with HDL (that is, when trigs go up, HDL generally goes down) and the ratio also happens to be a predictor of insulin sensitivity. Total cholesterol is virtually useless for predicting heart attack risk in the general population. This is something I'll discuss in more detail at another time.
When you walk into the doctor's office and ask him to measure your cholesterol, the numbers you get back will generally be total cholesterol, LDL, HDL and triglycerides. All of those except LDL are measured directly. LDL is calculated using the Friedewald equation, which is (in mg/dL):
LDL = TC - HDL - (TG/5)Low-carb advocates have known for quite some time that this equation fails to accurately predict LDL concentration outside certain triglyceride ranges. Dr. Michael Eades put up a post about this recently, and Richard Nikoley has written about it before as well. The reason low-carb advocates know this is that reducing carbohydrate generally reduces triglycerides, often below 100 mg/dL. This is the range at which the Friedewald equation becomes unreliable, resulting in artificially inflated LDL numbers that make you have a heart attack just by reading them.
I had a lipid panel done a while back, just for kicks. My LDL, calculated by the Friedewald equation, was 131 mg/dL. Over 130 is considered high. Pass the statins! But wait, my triglycerides were 48 mg/dL, which is quite low. I found a paper through Dr. Eades' post that contains an equation for accurately calculating LDL in people whose triglycerides are below 100 mg/dL*. Here it is (mg/dL):
LDL = TC/1.19 + TG/1.9 - HDL/1.1 - 38I ran my numbers through this equation. My new, accurate calculated LDL? 98 mg/dL. Even the U.S. National Cholesterol Education Panel wouldn't put me on statins with an LDL like that. I managed to shave 33 mg/dL off my LDL in 2 minutes. Isn't math fun?
*This equation was designed for individuals with a total cholesterol over 250 mg/dL.
Letter to the Editor
I just got a letter to the editor published in the journal Obesity. It's a comment on an article published in October titled "Efficiency of Intermittent Exercise on Adiposity and Fatty Liver in Rats Fed With High-fat Diet."
In the study, they placed rats on a diet composed of "commercial rat chow plus peanuts, milk chocolate, and sweet biscuit in a proportion of 3:2:2:1," and then proceeded to simply call it a "high-fat diet" in the title and text body, with no reference to its actual composition outside the methods section. We can't tolerate this kind of fudging if we want real answers from nutrition science. Rats eating the "high-fat diet" developed abdominal obesity, fatty liver and hyperphagia, but this was attenuated by exercise.
As I like to say, the problem isn't usually in the data, it's in the interpretation of the data. The result is interesting and highly relevant. But you can't use terminology that tars and feathers all fat when your diet was in fact high in linoleic acid (omega-6), low in omega-3 and high in sugar and refined grains. Especially when butter and coconut oil don't cause the same pathology. I pointed out in the letter that we need to be more precise about how we define "high-fat diets". I also pointed out that the study is highly relevant to the modern U.S., because it supports the hypothesis that a junk food diet high in linoleic acid and sugar causes metabolic disturbances and fatty liver, and exercise may be protective.
In the study, they placed rats on a diet composed of "commercial rat chow plus peanuts, milk chocolate, and sweet biscuit in a proportion of 3:2:2:1," and then proceeded to simply call it a "high-fat diet" in the title and text body, with no reference to its actual composition outside the methods section. We can't tolerate this kind of fudging if we want real answers from nutrition science. Rats eating the "high-fat diet" developed abdominal obesity, fatty liver and hyperphagia, but this was attenuated by exercise.
As I like to say, the problem isn't usually in the data, it's in the interpretation of the data. The result is interesting and highly relevant. But you can't use terminology that tars and feathers all fat when your diet was in fact high in linoleic acid (omega-6), low in omega-3 and high in sugar and refined grains. Especially when butter and coconut oil don't cause the same pathology. I pointed out in the letter that we need to be more precise about how we define "high-fat diets". I also pointed out that the study is highly relevant to the modern U.S., because it supports the hypothesis that a junk food diet high in linoleic acid and sugar causes metabolic disturbances and fatty liver, and exercise may be protective.
Fatty Liver Reversal
On April 15th, I received an e-mail from a reader who I'll call Sam. Sam told me that he had elevated levels of the liver enzyme ALT (alanine transaminase) in his blood, which indicates liver damage. ALT is an enzyme contained in liver cells that's released into the bloodstream when they rupture. Sam also had fatty liver confirmed by biopsy.
Liver damage with fat accumulation is very common in the United States. According to the NHANES health and nutrition surveys, in the time period 1999-2002, 8.9% of Americans had elevated ALT. Just 10 years earlier (1988-1994), the number was 4.0%. Fatty liver is a growing epidemic that currently affects roughly a quarter of Americans. Sam told me he had been trying to reverse his fatty liver for nearly a decade without success, and asked if I had any thoughts. He was not overweight, and from what I could gather, his diet was already better than most. I believe Sam knew intuitively that the right diet would improve his condition. With the usual caveats that this is not advice and I'm not a doctor, here's what I told him:
The latest test was 52, just on the cusp of normal. That's nearly 50% lower than his next lowest result over the past 7 years, in less than one month of eating well. I suspect that his next ALT test will be well within the normal range, and the fat in his liver will gradually disappear, if he continues this diet. When I asked him how he was feeling, he said:
How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
Liver damage with fat accumulation is very common in the United States. According to the NHANES health and nutrition surveys, in the time period 1999-2002, 8.9% of Americans had elevated ALT. Just 10 years earlier (1988-1994), the number was 4.0%. Fatty liver is a growing epidemic that currently affects roughly a quarter of Americans. Sam told me he had been trying to reverse his fatty liver for nearly a decade without success, and asked if I had any thoughts. He was not overweight, and from what I could gather, his diet was already better than most. I believe Sam knew intuitively that the right diet would improve his condition. With the usual caveats that this is not advice and I'm not a doctor, here's what I told him:
The quality of fat you eat has a very large influence on health, and especially on the liver. Excess omega-6 is damaging to the liver. This type of fat is found primarily in refined seed oils such as corn oil, soybean oil, and safflower oil... Sugar is also a primary contributor to fatty liver. Reducing your sugar intake will go a long way toward reversing it. Omega-3 fats also help reverse fatty liver if an excess of omega-6 is present. There was a clinical trial using fish oil that was quite effective. You might try taking 1/2 teaspoon of fish oil per day.On May 11, I received another e-mail from him:
The day after your recommendations, less than a month ago, I started a regimen of 1200 mg/day of fish oil concentrate.In the same e-mail, he sent me his new ALT test results. He had been getting tested since 2002. The latest result, reflecting his progress since adopting the new diet, followed the previous test by less than a month. Here's a graph of his ALT levels. Below 50 is considered normal:
At the same time, I significantly reduced or even eliminated all forms of sugar from my diet. I did have a half glass of orange juice for breakfast every few days or so, and some fruits, and maybe a taste of dessert or a small candy bar here and there. I never exceeded the 30 g/day sugar limit you suggested.
I completely eliminated any and all fried foods and avoided most oils. I also avoided high glycemic index foods to some degree, e.g. white bread and potatoes. I did eat quite a bit more protein, including red meat, eggs, fish, chicken, and pork.
The balance of my diet and lifestyle was largely unchanged. I do drink a couple of beers every two to three weeks, but never more than three drinks in day. I have been doing more yard work, simply because of the season. Other than that, I don't get much more exercise than a typical inactive office worker.
The latest test was 52, just on the cusp of normal. That's nearly 50% lower than his next lowest result over the past 7 years, in less than one month of eating well. I suspect that his next ALT test will be well within the normal range, and the fat in his liver will gradually disappear, if he continues this diet. When I asked him how he was feeling, he said: I did feel different after adjusting my diet. It's hard to describe, but overall I just felt better. I wasn't as tired when I woke up in the morning and I became a little slimmer, not a lot, maybe 3-5 pounds [note: he was not overweight to begin with]. I figured it was a placebo effect, but I think the fish oil has made a real difference.Fatty liver is a serious problem that responds readily to diet. I believe the main culprits are excess omega-6 from industrial vegetable oils; insufficient omega-3 from seafood, leafy greens and pastured animal foods; and excess sugar. The liver is your "metabolic gatekeeper", so it pays to take care of it.
Yesterday I had a few potato chips, corn chips, and some others. I didn't like it at all. Today I had half of a brownie for an afternoon snack and I completely crashed after an hour or so. I had a hard time keeping my eyes open. I no longer have much of a craving for snack food, I prefer to eat a full meal with more protein, e.g. beans, meat etc.
How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
A Little Tidbit
I'm gearing up for a new series of posts based on some fascinating reading I've been doing lately. I'm not going to spill the beans, but I will give you a little hint, from a paper written by Dr. Robert S. Corruccini, professor of anthropology at Southern Illinois university. I just came across this quote and it blew me away. It's so full of wisdom I can't even believe I just read it. The term "occlusion" refers to the way the upper and lower teeth come together, as in overbite or underbite.
That's why you have to study modernizing populations that are transitioning from good to poor health, which is exactly what Dr. Weston Price and many others have done. Only then can you see the true, non-genetic, nature of the problem.
Similar to heart disease and diabetes which are "diseases of civilization" or "Western diseases" (Trowell and Burkitt, 1981) that have attained high prevalence in urban society because of environmental factors rather than "genetic deterioration," an epidemiological transition (Omran, 1971) in occlusal health accompanies urbanization.In other words, the reason observational studies in affluent nations haven't been able to get to the bottom of dental/orthodontic problems and chronic disease is that everyone in their study population is doing the same thing! There isn't enough variability in the diets and lifestyles of modern populations to be able to determine what's causing the problem. So we study the genetics of problems that are not genetic in origin, and overestimate genetic contributions because we're studying populations whose diet and lifestyle are homogeneous. It's a wild goose chase.
Western society has completely crossed this transition and now exists in a state of industrially buffered environmental homogeneity. The relatively constant environment both raises genetic variance estimates (since environmental variance is lessened) and renders epidemiological surveys largely meaningless because etiological factors are largely uniform. Nevertheless most occlusal epidemiology and heritability surveys are conducted in this population rather than in developing countries currently traversing the epidemiological transition.
That's why you have to study modernizing populations that are transitioning from good to poor health, which is exactly what Dr. Weston Price and many others have done. Only then can you see the true, non-genetic, nature of the problem.
The Lyon Diet-Heart Study: A Few More Thoughts
Although the degree of atherosclerosis (hardening/narrowing of the arteries) correlates with the risk of heat attack, the correlation isn't perfect. In fact, if you read my previous post on 20th century coronary heart disease trends in the U.K., you know that the frequency of heart attacks rose dramatically during the first half of the century, while the prevalence of severe atherosclerosis stayed the same or even declined.
If you accept the standard idea of how a heart attack occurs, first the coronary arteries become narrowed due to atherosclerosis. Then a clot forms, which lodges itself in a narrowed artery, blocking it and cutting off the blood supply to part of the heart muscle. The clot may be the result of a ruptured atherosclerotic plaque.
If you're unlucky, the loss of blood to your heart causes arrhythmia, or a loss of coordination of the heart muscle. This can cause it to pump blood inefficiently, sometimes resulting in death. Arrhythmias are estimated to account for about half of all heart attack deaths in the U.S. Sometimes they occur without a coronary blockage as well.
Omega-3 fatty acids seem to affect all three parts of the process: the atherosclerosis, the clot formation and the arrhythmia. Supplementing fish oil, even in the absence of reduced omega-6, may slow the progression of atherosclerosis according to a controlled trial.
Where omega-3 really shines is its ability to prevent clots and arrhythmias. In the DART and Lyon trials, the benefits of improving omega-6:3 balance appeared much more quickly than would be possible if it were acting by reversing atherosclerosis. This may have involved the blood-thinning properties of omega-3. The most dramatic effects were on sudden cardiac death, often the result of arrhythmia. Omega-3 fatty acids potently suppress arrhythmias in animal models.
You can have severely narrowed and calcified arteries, but if a clot never shows up, you may never actually have a heart attack. The modern industrial diet is extremely thrombotic (clot-promoting), probably in large part due to the combination of excessive omega-6 and insufficient omega-3. If the artery blockage doesn't cause an arrhythmia, the heart attack may not be fatal.
Omega-3 fats seem to prevent heart attacks on multiple levels.
The Lyon Diet-Heart Study: Background
The Lyon Diet-Heart Study
The Lyon Diet-Heart Study: Implications
Polyunsaturated Fat Intake: What About Humans?
If you accept the standard idea of how a heart attack occurs, first the coronary arteries become narrowed due to atherosclerosis. Then a clot forms, which lodges itself in a narrowed artery, blocking it and cutting off the blood supply to part of the heart muscle. The clot may be the result of a ruptured atherosclerotic plaque.
If you're unlucky, the loss of blood to your heart causes arrhythmia, or a loss of coordination of the heart muscle. This can cause it to pump blood inefficiently, sometimes resulting in death. Arrhythmias are estimated to account for about half of all heart attack deaths in the U.S. Sometimes they occur without a coronary blockage as well.
Omega-3 fatty acids seem to affect all three parts of the process: the atherosclerosis, the clot formation and the arrhythmia. Supplementing fish oil, even in the absence of reduced omega-6, may slow the progression of atherosclerosis according to a controlled trial.
Where omega-3 really shines is its ability to prevent clots and arrhythmias. In the DART and Lyon trials, the benefits of improving omega-6:3 balance appeared much more quickly than would be possible if it were acting by reversing atherosclerosis. This may have involved the blood-thinning properties of omega-3. The most dramatic effects were on sudden cardiac death, often the result of arrhythmia. Omega-3 fatty acids potently suppress arrhythmias in animal models.
You can have severely narrowed and calcified arteries, but if a clot never shows up, you may never actually have a heart attack. The modern industrial diet is extremely thrombotic (clot-promoting), probably in large part due to the combination of excessive omega-6 and insufficient omega-3. If the artery blockage doesn't cause an arrhythmia, the heart attack may not be fatal.
Omega-3 fats seem to prevent heart attacks on multiple levels.
The Lyon Diet-Heart Study: Background
The Lyon Diet-Heart Study
The Lyon Diet-Heart Study: Implications
Polyunsaturated Fat Intake: What About Humans?
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The Lyon Diet-Heart Study: Implications
There's something ironic about the Mediterranean diet used in the Lyon diet heart study, the one that dramatically reduced participants' risk of heart attack and all-cause mortality relative to the prudent diet control group: it wasn't actually a Mediterranean diet.
The concept of the Mediterranean diet as protective against heart disease may have originated in Dr. Ancel Keys' Seven Countries study, in which he compared the food habits and cardiovascular mortality statistics both between and within seven European countries. Countries surrounding the Mediterranean, and in particular the Greek island of Crete, had the lowest cardiovascular death rates. The Cretan diet is high in monounsaturated fat, relatively low in saturated fat, low in omega-6, and high in omega-3 fatty acids, including fat from seafood and the plant omega-3 alpha-linolenic acid. It also includes abundant green vegetables. This became the inspiration for the modern American concept of the "Mediterranean diet". The part about low omega-6 tends to be omitted.
Of course, if you look at modern heart attack mortality statistics by country, France is the lowest in Europe. France is a Mediterranean country, yet happens to have a very high intake of saturated fat per capita. So the cardiologist-approved version of the Mediterranean diet isn't exactly accurate.
The Lyon study departs even further from the traditional Mediterranean diet. Neither the Cretan nor the French diet are low in fat, yet participants were encouraged to reduce their fat intake. The Cretan diet includes some animal fat and eggs, while Lyon participants were encouraged to avoid these. And finally, the margarine. You could be guillotined for using margarine instead of butter in France, and I'm sure the Cretans aren't too fond of it either. Yet the margarine used in the Lyon study was rich in omega-3 alpha-linolenic acid, a critical factor.
Previous intervention trials such as MRFIT, the Women's Health Initiative (WHI) dietary modification trial, and others, exhaustively tested the hypothesis that reducing total fat intake reduces cardiovascular mortality. It doesn't. A dozen trials have also tested the idea that reducing saturated fat reduces cardiovascular mortality. It doesn't. Increasing fiber doesn't, according to the DART trial. Increasing fruit and vegetables modestly doesn't, according to WHI.
So what's left that's unique about the Lyon trial? It was the only trial to dramatically reduce omega-6 consumption, to below 4% of calories, while increasing omega-3 consumption from plant and seafood sources. In my opinion, that combination is the only plausible explanation for the large reduction in heart attacks and total mortality. That combination also happens to be a consistent feature of the real Mediterranean diet. In both Crete and France, omega-6 intake is relatively low, and omega-3 intake is relatively high. They also eat more real food than processed food in general, a factor that I don't underestimate.
Where do we go from here? Obviously I'm not going to recommend eating omega-3 enriched margarine. Mediterranean countries don't need industrial goop to avoid a heart attack, and neither do you. Anyone who's been to France knows they don't deprive themselves over there. They eat real food and they enjoy it.
The way to preserve the essential elements of the Mediterranean diet without becoming an ascetic is to eat fats that are low in omega-6, and find a modest source of omega-3. That means eating full-fat dairy if you tolerate it, fatty meat if you enjoy it, organs, seafood, olive oil in moderation, coconut oil, butter, lard, and tallow. Along with a diet that is dominated by real, homemade food rather than processed food. Some people may also wish to supplement with small doses of high-vitamin cod liver oil, fish oil or flax. I consider the latter to be inferior to animal sources of omega-3, but it can be useful for vegetarians.
The concept of the Mediterranean diet as protective against heart disease may have originated in Dr. Ancel Keys' Seven Countries study, in which he compared the food habits and cardiovascular mortality statistics both between and within seven European countries. Countries surrounding the Mediterranean, and in particular the Greek island of Crete, had the lowest cardiovascular death rates. The Cretan diet is high in monounsaturated fat, relatively low in saturated fat, low in omega-6, and high in omega-3 fatty acids, including fat from seafood and the plant omega-3 alpha-linolenic acid. It also includes abundant green vegetables. This became the inspiration for the modern American concept of the "Mediterranean diet". The part about low omega-6 tends to be omitted.
Of course, if you look at modern heart attack mortality statistics by country, France is the lowest in Europe. France is a Mediterranean country, yet happens to have a very high intake of saturated fat per capita. So the cardiologist-approved version of the Mediterranean diet isn't exactly accurate.
The Lyon study departs even further from the traditional Mediterranean diet. Neither the Cretan nor the French diet are low in fat, yet participants were encouraged to reduce their fat intake. The Cretan diet includes some animal fat and eggs, while Lyon participants were encouraged to avoid these. And finally, the margarine. You could be guillotined for using margarine instead of butter in France, and I'm sure the Cretans aren't too fond of it either. Yet the margarine used in the Lyon study was rich in omega-3 alpha-linolenic acid, a critical factor.
Previous intervention trials such as MRFIT, the Women's Health Initiative (WHI) dietary modification trial, and others, exhaustively tested the hypothesis that reducing total fat intake reduces cardiovascular mortality. It doesn't. A dozen trials have also tested the idea that reducing saturated fat reduces cardiovascular mortality. It doesn't. Increasing fiber doesn't, according to the DART trial. Increasing fruit and vegetables modestly doesn't, according to WHI.
So what's left that's unique about the Lyon trial? It was the only trial to dramatically reduce omega-6 consumption, to below 4% of calories, while increasing omega-3 consumption from plant and seafood sources. In my opinion, that combination is the only plausible explanation for the large reduction in heart attacks and total mortality. That combination also happens to be a consistent feature of the real Mediterranean diet. In both Crete and France, omega-6 intake is relatively low, and omega-3 intake is relatively high. They also eat more real food than processed food in general, a factor that I don't underestimate.
Where do we go from here? Obviously I'm not going to recommend eating omega-3 enriched margarine. Mediterranean countries don't need industrial goop to avoid a heart attack, and neither do you. Anyone who's been to France knows they don't deprive themselves over there. They eat real food and they enjoy it.
The way to preserve the essential elements of the Mediterranean diet without becoming an ascetic is to eat fats that are low in omega-6, and find a modest source of omega-3. That means eating full-fat dairy if you tolerate it, fatty meat if you enjoy it, organs, seafood, olive oil in moderation, coconut oil, butter, lard, and tallow. Along with a diet that is dominated by real, homemade food rather than processed food. Some people may also wish to supplement with small doses of high-vitamin cod liver oil, fish oil or flax. I consider the latter to be inferior to animal sources of omega-3, but it can be useful for vegetarians.
The Lyon Diet-Heart Study
Now that we have the proper context, it's time to dig into the Lyon Diet-Heart trial, one of the most important and misunderstood diet trials of all time.
The trial enrolled 605 middle-aged French men and women who had previously suffered a heart attack. This is called a "secondary prevention" trial because it's designed to prevent a second heart attack. The advantage of secondary prevention trials is that they can be smaller, because men who have already had a heart attack are at a much higher risk of having another. This increases your statistical power. The disadvantage is that the participants aren't necessarily representative of the population at large.
Participants were divided into a control group and an intervention group. The control group "received no dietary advice from the investigators but nonetheless were advised to follow a prudent diet by their attending physicians". Ah, the prudent diet rears its ugly head once again. In a later paper, they describe the prudent diet they used in a bit more detail:
So far, these changes are not unique. They're similar to the interventions in the ineffective MRFIT and WHI trials in the last post. Here's where it gets interesting. The intervention group ate three times as much omega-3 alpha-linolenic acid as the control group, and 32% less omega-6 linoleic acid. The ratio was 20 : 1 linoleic acid : alpha-linoleic acid in the control group, and 4.4 : 1 in the intervention group. This was due to the combination of a low-fat diet and the canola oil goop they were provided free of charge.
But it gets even better. The intervention group reduced their omega-6 linoleic acid intake to 3.6% of calories, below the critical threshold of 4%. As I described in my recent post on eicosanoid signaling, reducing linoleic acid to below 4% of calories inhibits inflammation, while increasing it more after it has already exceeded 4% has very little effect if omega-3 is kept low*. This is a very important point: the intervention group didn't just increase omega-3. They decreased omega-6 to below 4% of calories. That's what sets the Lyon Diet-Heart trial apart from all the other failed diet trials.
After five years on their respective diets, 3.4% of the control (prudent diet) group and 1.3% of the intervention ("Mediterranean") group had died, a 70% reduction in deaths. Cardiovascular deaths were reduced by 76%. Stroke, angina, pulmonary embolism and heart failure were also much lower in the intervention group. A stunning victory for this Mediterranean-inspired diet, and a crushing defeat for the prudent diet!
There's a little gem buried in this study that I believe is the other reason it didn't get accepted to the New England Journal of Medicine: there was no difference in total cholesterol or LDL values between the control and experimental groups. The American scientific consensus was so cholesterol-centric that it couldn't accept the possibility that an intervention had reduced heart attack mortality without reducing LDL. The paper was accepted to the British journal The Lancet, another well-respected medical journal.
In the next post, I'll describe how we can benefit from the findings of the Lyon trial, and even surpass it, without having to resort to canola oil margarine.
*I admit 4% is somewhat arbitrary, but I think it's a good reference point based on the shape of the HUFA curve in this post.
The trial enrolled 605 middle-aged French men and women who had previously suffered a heart attack. This is called a "secondary prevention" trial because it's designed to prevent a second heart attack. The advantage of secondary prevention trials is that they can be smaller, because men who have already had a heart attack are at a much higher risk of having another. This increases your statistical power. The disadvantage is that the participants aren't necessarily representative of the population at large.
Participants were divided into a control group and an intervention group. The control group "received no dietary advice from the investigators but nonetheless were advised to follow a prudent diet by their attending physicians". Ah, the prudent diet rears its ugly head once again. In a later paper, they describe the prudent diet they used in a bit more detail:
[The control subjects] were expected to follow the dietary advice given by their attending physicians, similar to that of step I of the prudent diet of the American Heart Association.And what exactly is this prudent diet? It was created by the National Cholesterol Education Panel, that very conflicted organization I've written about before. Step I is now defunct, having given way to the next generation of NCEP guidelines in 2000. Here's a summary of the old Step I from the American Heart Association's website:
The Step I diet restricted total fat to no more than 30 percent of total calories, saturated fat to no more than 10 percent of total calories, and cholesterol to less than 300 mg/day. It was intended as the starting point for patients who had high cholesterol levels.This is an important point: the Lyon Diet-Heart trial wasn't an ordinary trial comparing the average person's diet to a different diet. It was a bare-knuckle showdown between the prudent diet and a modified version of the Mediterranean diet! I believe that's part of the reason it was rejected by the prestigious New England Journal of Medicine, although there's another reason I'll get to later. The intervention group received different advice:
Patients in the experimental group were advised by the research cardiologist and dietician, during a one-hour-long session, to adopt a Mediterranean-type diet: more bread, more root vegetables and green vegetables, more fish, less meat (beef, lamb, and pork to be replaced with poultry), no day without fruit, and butter and cream to be replaced with margarine supplied by the study.After five long years of these brutal diets, participants in the intervention ("Mediterranean") group were eating slightly less total fat, 29% less saturated fat, 32% less cholesterol, a bit more bread, legumes, fruit, vegetables and fish, compared to the control (prudent diet) group. They were also eating less meat and much less butter and cream, although cheese consumption was the same between groups. French people know better than to give up their cheese!
Because the patients would not accept olive oil- traditional to the Mediterranean diet- as the only fat [because French people use more butter than olive oil- SG], a rapeseed (canola) oil-based margarine (Astra-Calve, Paris, France) was supplied free for the whole family to experimental subjects. This margarine had a composition comparable to olive oil [mon oeil- SG] with 15% saturated fatty acids, 48% oleic acid but 5.4% 18:1 trans. However, it was slightly higher in linoleic [omega-6- SG] (16.4 vs 8.6%) and more so in alpha-linolenic acid [omega-3- SG] (4.8 vs 0.6%), a fatty acid markedly higher (3 fold) in the plasma of the Cretan cohort in the Seven Country study compared to that of Zutphen (Netherlands).
The oils recommended for salads and food preparation were rapeseed and olive oils exclusively. Moderate alcohol consumption in the form of wine was allowed at meals. At each subsequent visit of the experimental patients, a dietary survey and further counseling were done by the research dietician.
So far, these changes are not unique. They're similar to the interventions in the ineffective MRFIT and WHI trials in the last post. Here's where it gets interesting. The intervention group ate three times as much omega-3 alpha-linolenic acid as the control group, and 32% less omega-6 linoleic acid. The ratio was 20 : 1 linoleic acid : alpha-linoleic acid in the control group, and 4.4 : 1 in the intervention group. This was due to the combination of a low-fat diet and the canola oil goop they were provided free of charge.
But it gets even better. The intervention group reduced their omega-6 linoleic acid intake to 3.6% of calories, below the critical threshold of 4%. As I described in my recent post on eicosanoid signaling, reducing linoleic acid to below 4% of calories inhibits inflammation, while increasing it more after it has already exceeded 4% has very little effect if omega-3 is kept low*. This is a very important point: the intervention group didn't just increase omega-3. They decreased omega-6 to below 4% of calories. That's what sets the Lyon Diet-Heart trial apart from all the other failed diet trials.
After five years on their respective diets, 3.4% of the control (prudent diet) group and 1.3% of the intervention ("Mediterranean") group had died, a 70% reduction in deaths. Cardiovascular deaths were reduced by 76%. Stroke, angina, pulmonary embolism and heart failure were also much lower in the intervention group. A stunning victory for this Mediterranean-inspired diet, and a crushing defeat for the prudent diet!
There's a little gem buried in this study that I believe is the other reason it didn't get accepted to the New England Journal of Medicine: there was no difference in total cholesterol or LDL values between the control and experimental groups. The American scientific consensus was so cholesterol-centric that it couldn't accept the possibility that an intervention had reduced heart attack mortality without reducing LDL. The paper was accepted to the British journal The Lancet, another well-respected medical journal.
In the next post, I'll describe how we can benefit from the findings of the Lyon trial, and even surpass it, without having to resort to canola oil margarine.
*I admit 4% is somewhat arbitrary, but I think it's a good reference point based on the shape of the HUFA curve in this post.
The Lyon Diet-Heart Study: Background
To appreciate the full significance of the Lyon diet-heart study, we have to go back in time a bit. We're off to 1982, the year the U.S. National Heart, Lung and Blood Institute published the results of their massive study, the Multiple Risk Factor Intervention Trail (MRFIT).
By 1982, the idea of the "prudent diet" was well ingrained in American medicine, despite a lack of direct evidence to support it, and even a certain amount of evidence at odds with it (such as the ill-fated Anti-Coronary Club trial). The prudent diet was designed to reduce the risk of heart attack, and suggests reducing total fat, saturated fat and cholesterol intake, while increasing consumption of vegetables, whole grains, fruit and fiber. Some versions of the diet replace saturated fat with polyunsaturated vegetable oils.
MRFIT involved 12,866 men at high risk of heart attack, making it one of the largest controlled trials of all time. Half of the group were told to keep doing what they were doing, under medical supervision, and the other half were given intense diet and lifestyle counseling. The intervention group was counseled to quit smoking and reduce their consumption of saturated fat and cholesterol, and increase polyunsaturated vegetable oil consumption.
After 6 years, 46% of the intervention group had quit smoking, compared to 29% in the control group. The intervention group reduced their cholesterol intake by 40% and their saturated fat intake by more than one-fourth, and increased their consumption of polyunsaturated fat (omega-6) by one third relative to the control group (source).
The results? After seven years, total mortality was 41.2 per 1,000 in the intervention group and 40.4 in the control group, a difference that was not even close to statistically significant. There were also no significant differences in heart attack rate or heart attack death rate. The authors and their apologists tried to wiggle out of the obvious conclusion through an avalanche of slippery math and editorials.
The results were mirrored by a later intervention trial published in 2006, the Women's Health Initiative dietary modification trial. This one was even larger, involving 48,835 postmenopausal women! This was another test of the prudent diet, in which participants were intensively counseled to
I think you know what's coming...
There was one interesting finding that came out of MRFIT, which foreshadowed the result of the Lyon trial. MRFIT participants eating the most omega-3 from fish were at a 40% lower risk of coronary heart disease and a 22% lower risk of dying of any cause. This was not part of the intervention, so it doesn't necessarily reflect cause and effect. For that, we'll have to look at the Lyon trial.
By 1982, the idea of the "prudent diet" was well ingrained in American medicine, despite a lack of direct evidence to support it, and even a certain amount of evidence at odds with it (such as the ill-fated Anti-Coronary Club trial). The prudent diet was designed to reduce the risk of heart attack, and suggests reducing total fat, saturated fat and cholesterol intake, while increasing consumption of vegetables, whole grains, fruit and fiber. Some versions of the diet replace saturated fat with polyunsaturated vegetable oils.
MRFIT involved 12,866 men at high risk of heart attack, making it one of the largest controlled trials of all time. Half of the group were told to keep doing what they were doing, under medical supervision, and the other half were given intense diet and lifestyle counseling. The intervention group was counseled to quit smoking and reduce their consumption of saturated fat and cholesterol, and increase polyunsaturated vegetable oil consumption.
After 6 years, 46% of the intervention group had quit smoking, compared to 29% in the control group. The intervention group reduced their cholesterol intake by 40% and their saturated fat intake by more than one-fourth, and increased their consumption of polyunsaturated fat (omega-6) by one third relative to the control group (source).
The results? After seven years, total mortality was 41.2 per 1,000 in the intervention group and 40.4 in the control group, a difference that was not even close to statistically significant. There were also no significant differences in heart attack rate or heart attack death rate. The authors and their apologists tried to wiggle out of the obvious conclusion through an avalanche of slippery math and editorials.
The results were mirrored by a later intervention trial published in 2006, the Women's Health Initiative dietary modification trial. This one was even larger, involving 48,835 postmenopausal women! This was another test of the prudent diet, in which participants were intensively counseled to
reduce total fat intake to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and grains to at least 6 servings/d.After 6 years, the intervention group was eating 22% less fat, 23% less saturated fat, 20% less cholesterol, 15% more carbohydrate, 22% more fruits and vegetables, and slightly more fiber and whole grains than the control group. LDL dropped a bit in the intervention group.
I think you know what's coming...
Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women...Oh and you forgot to mention, 4.9% of women died in the intervention group as opposed to 5.0% in the control group. A "minor detail" that I couldn't find in the paper so I had to look up elsewhere. The study also showed that the diet modifications didn't reduce the incidence of breast or colorectal cancer, two of the most common cancers. RIP, prudent diet. Although it still seems to be struggling along, despite the beating. Another set of editorials appeared claiming that the diet didn't work because it wasn't extreme enough. How far do we have to move the goalposts before we give up?
There was one interesting finding that came out of MRFIT, which foreshadowed the result of the Lyon trial. MRFIT participants eating the most omega-3 from fish were at a 40% lower risk of coronary heart disease and a 22% lower risk of dying of any cause. This was not part of the intervention, so it doesn't necessarily reflect cause and effect. For that, we'll have to look at the Lyon trial.
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