Diet or Drugs to Prevent Heart Disease

2, Mar, 2013 by

Diet or Drugs to Prevent Heart DiseaseThe risk of heart disease has been associated with countless different things. Smoking, diabetes, high blood pressure, overweight, obesity, sitting and watching TV, eating too much fat, eating too much sugar, not eating certain fats, eating meat, not eating fish, eating too much animal fat, eating cholesterol, eating saturated fat, eating trans fats, high blood cholesterol, high LDL-cholesterol, inflammation, family history of heart disease…. The list is long. Is it really possible to avoid being hit by this dreadful disease, the most common cause of death and disability worldwide?

The risk of heart disease increases with age. So, if we become old enough, we will probably have heart disease sooner or later, and most likely die from it. But that is not necessarily a bad thing. We all have to die from something. Dying from something else is not a goal by itself. So maybe we would be more accurate if, instead of aiming at prevention, our goal was to delay the onset of heart disease. However, defining our goal is probably less important than defining the methods to achieve it.

A huge number of healthy adults will have heart disease in the next ten years. Many will be treated with drugs, some will have angioplasty  and stents, and some will have open heart surgery. Many will die from the disease. A substantial number will be left with severe disability.  Many will not be able to work, and many will not enjoy the quality of life they had before the disease hit them.  So, I presume we all agree that delaying the onset of heart disease is a worthwhile target.

Who should worry about getting heart disease? Probably everybody. But, who should worry the most? Who is most likely to be struck by heart disease in the next few years? This is where it comes to the so-called risk factors. If you have many risk factors, the risk of having a heart attack or stroke becomes higher. The strongest risk factors are smoking, diabetes, high blood pressure, high levels of LDL-cholesterol, low levels of HDL-cholesterol, overweight or obesity, and family history of premature coronary artery disease. If you don’t have any risk factors, your aim should be to avoid them at all costs. But, if you have some of these risk factors, what can you do?

Let’s assume you are a responsible person (you probably are by the way, because you are reading my blog), and you want to do everything you can to delay the onset of heart disease. Maybe your father had a heart attack in his fifties. Maybe you have gained a bit of weight and maybe your cholesterol level is a bit to high. So, you decide it´s time to have a chat with your general practitioner Dr. Oxenhaler, the family doctor. Last year he put you on a drug to lower your blood pressure. This time, you are better prepared for your visit because you have been reading my blog.

You are sitting in front of Dr. Oxenhaler in his office. He just finished measuring your blood pressure and now he is watching your blood work on his computer screen. This is how the conversation might evolve.

‘Is there a specific reason you decided to come to see me. Have you been having chest pain or discomfort of any kind?’
‘No Doctor Oxenhaler. I was just worried. I’ve been reading lots of stuff about heart disease on the internet. I was wondering what I should do to avoid having a heart attack.’
‘Well, I guess you should be a little bit worried, but I’m glad you care. That’s the first step. Your blood pressure is fine, thanks to the medication I prescribed for you last year. However, your cholesterol is 277 mg/dl (6.9 mmol/L), that’s way to high.’
‘How about my LDL cholesterol?’

Diet or drugs to prevent heart disease. A vist to Doctor Oxenhaler.

Doctor Oxenhaler watches you closely, his glasses gliding down on his nose. He takes a deep breath.
‘I see you’ve been reading. That’s good. Education is the key to a better health. Your LDL cholesterol is 182 mg/dL (4.7 mmol/L), that’s also way to high. HDL-C, the good cholesterol is 40 mg/dL (1.0 mmol/L) which is to low. Considering your family history and your history of high blood pressure, the risk is quite high. By using the Framingham risk calculator I can see that your risk of having a heart attack in the next ten years is about 17 percent.’

You feel a little numb, like the blood is draining from your face. Doctor Oxenhaler notices your paleness and becomes a bit more sympathetic.
‘Don’t be scared though. We can take care of this. Treatment is available. By putting you on a cholesterol lowering drug, we can lower your risk substantially. Your cholesterol will go down and so will LDL-cholesterol. Your risk of heart attack will be much less’.
‘But I read that the effects of statin drugs is very small when they’re used for prevention in people who don’t have heart disease’.
‘No. that’s a misinterpretation. The risk reduction in the clinical trials is about 30 percent among high risk individuals, which in my mind is quite substantial.’
‘You’re talking about relative reduction then Dr. Oxenhaler, aren’t you?´

There is a momentary pause. You catch a glimpse of surprise in his eyes. He looks at his watch and then back at you, a faint smile on his lips.
‘Yes, relative reduction, that’s correct’, he says.
‘I’ve read that statins have lots of side effects as well.’
‘Side effects are very uncommon. A small number of of people have muscle pain, but it’s rare. Most people do not have any problems with cholesterol lowering drugs.’
‘I read that some people have memory loss.’ 

He looks surprised.
‘I don’t recall any of my patients complaining of memory loss from statins.’
Now you can’t help wondering whether Doctor Oxenhaler is taking statins. You dismiss the thought immediately. You have to keep focus.
‘I’ve heard there is more risk of diabetes if you take statins.’
He losens his tie a bit, he has stopped smiling. You’re aware that you’re using up a lot of his time. There are more patients waiting for him.
‘Let me just tell you that the benefits of statins definitively outweigh the risks’, says Doctor Oxenhaler

But you’re not giving up.
‘Isn’t there something I can do by my self, change may diet or exercise more?, you ask.
‘Diet and exercise is fine. Cut down on fats, especially saturated fat and don’t eat too much cholesterol. That’s helpful. But it won’t replace statin treatment when it comes to reducing your risk.’
‘I heard about a study published recently in The New England Journal of Medicine showing that a Mediterranean diet could lower the risk of heart attack and stroke if you have risk factors like me’
‘You’re right indeed, but the effect is very small. Besides, diets are usually hard to stick with.’
‘I read that the relative risk reduction was about 30 percent on the Mediterranean diet compared to a low fat diet. Isn’t that about the same effect that statins have in a similar population?’ Could a Mediterranean diet be an alternative to statin therapy?

Doctor Oxenhaler does not answer right away. He stares at the computer screen.
‘Very well, why don’t you try the Mediterranean diet for six months and then come visit me again. We’ll measure your cholesterol and decide what to do. If it´s still high I definitively recommend statin treatment to cut your risk´, 
he says eventually, still watching the computer screen.
‘Isn’t it possible that the diet is helpful, although my cholesterol stays the same?’
Now he is looking at you again, more seriously than before. You can’t really tell whether he is annoyed or not.
‘If we are to succeed in lowering your risk of heart disease, we must lower your LDL-cholesterol. That’s a fact.’
‘But, I just read about the Women´s Health Initiative  where reducing the intake of fat lowered cholesterol, but did not cut the risk of heart disease’.
Now he is up on his feet and offering his hand. He shakes his head in disbelief, but he is smiling again.
Please come back to see me in six months. Good luck with the Mediterranean diet. Go easy on the wine though. And for God’s sake don’t believe everything you read on the internet…..

 

 

28 Comments

  1. Excellent piece Axel. Would that all patients were this well informed. As we know from the Lyon Diet Heart study, even in people who have survived a heart attack, adhering to the Mediterranean Diet lowers risk of death, cardiac death and recurrent heart attack, by even greater margins than that found in the recent primary prevention PREDIMED study, and without any significant lowering of LDL-cholesterol.

  2. The so-called Mediterranean diet is indeed healthy for the heart, but not for reasons most people visualize. Two studies suggest that inadvertently lowering omeg-6 is the key. Excerpts:

    The only striking difference between the two groups in the Lyon Diet Heart Study was the restriction of omega-6 fatty acids in the experimental group. You find omega-6 fatty acids in vegetable oils like corn, safflower, and sunflower oils. They accomplished this dietary change by giving the subjects in the experimental groups margarines rich in omega-3 fats and trans fats. Although there was a dramatic decrease in death between the two groups in the Lyon Diet Heart Study, there were no differences in weight, BMI, blood pressure, cholesterol (good and bad), and blood lipids between the two groups. In other words, all the usual suspects in heart disease were eliminated. The only differences between the two groups were in the fatty acids, both linoleic acid and the AA/EPA ratio…In the Lyon Diet Heart Study, the investigators were able to reduce the linoleic levels to 3.6%, which is similar to levels found in the Japanese (actually Okinawans), who have the lowest cardiovascular mortality in the developed world…Bottom line, unless you dramatically reduce omega-6 intake by reducing your consumption of vegetable oils (such as corn, soy and safflower oils), you will not get clear-cut clinical results (like reduction in death) no matter how much hype the media give to the research.” http://www.zonediet.com/blog/2013/02/good-diet-bad-study/

    “The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70%. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.” Google – PDF Dietary Fat Quality and Coronary Heart Disease

    Abstract from the study:
    In a prospective, randomised single-blinded secondary prevention trial we compared the effect of a Mediterranean alpha-linolenic acid-rich diet to the usual post-infarct prudent diet. After a first myocardial infarction, patients were randomly assigned to the experimental (n = 302) or control group (n = 303). Patients were seen again 8 weeks after randomisation, and each year for 5 years. The experimental group consumed significantly less lipids, saturated fat, cholesterol, and linoleic acid but more oleic and alpha-linolenic acids confirmed by measurements in plasma. Serum lipids, blood pressure, and body mass index remained similar in the 2 groups. In the experimental group, plasma levels of albumin, vitamin E, and vitamin C were increased, and granulocyte count decreased. After a mean follow up of 27 months, there were 16 cardiac deaths in the control and 3 in the experimental group; 17 non-fatal myocardial infarction in the control and 5 in the experimental groups: a risk ratio for these two main endpoints combined of 0.27 (95% CI 0.12-0.59, p = 0.001) after adjustment for prognostic variables. Overall mortality was 20 in the control, 8 in the experimental group, an adjusted risk ratio of 0.30 (95% CI 0.11-0.82, p = 0.02). An alpha-linolenic acid-rich Mediterranean diet seems to be more efficient than presently used diets in the secondary prevention of coronary events and death.” http://www.ncbi.nlm.nih.gov/pubmed/7911176

    Note: The researchers could have just as well characterized the experimental diet as lenoleic acid-restricted. But nobody worries about omega-6s, do they?

  3. Axel – I think that you coached the patient! Well done.

  4. Very politically correct and fun to read. Sadly very few patients challenge their doctor in this way. The doctor on the other hand does not need to provide any details on his CME to his patient base. Therefore the patients will never really be able to know whether or not the MD is current (up to date) in his practice. Quite an interesting aspect of the very unbalanced relationship between a doctor and a patient indeed! Thank god for the internet. Good article!

  5. Richard

    Sorry, Axel. I don’t really get this. What was the point of this article? The WHI-trial showed that when people consume 3/4 of their protein from animals together with daily intake of 16 grams of fiber per day, there is no substantial benefit of attempting to cut down on fats. The intervention arm, the ones who received their 20 min of counselling, did not increase their intake of whole-grains, legumes, fruits or vegetables. They kept tinkering on fat within the context of a diet high in animal products. The intervention arm did not show any difference in LDL cholesterol next to the controls.

    Providing insights from global epidemiology would have been helpful for your audience. Pritikin wrote already in 1978 that atherosclerosis cannot develop when patients maintain their cholesterol around 130mg/dl*. This is achieved by high-starch, whole-food, plant-based diets. Similar to those used by Dean Ornish and Caldwell Esselstyn. Daniel Steinberg noted how the Japanese were relatively immune to heart disease in 1958 even though their blood-pressure was higher than observed in Western societies; smoking prevalence n Japan was also higher comprared to West. The Framingham study shows that durinng the last 40-years only 5-6 people have got a heart-attack out of those who have maintained their TC Cholesterol < 150mg/dl (3,88mmol/l) consistently. We see absence of CHD among populations who maintain their TC cholesterol < 150 throughout their lives. This isn't rocket science. We shouldn't pretend global epidemiology and Dean Ornish did not exist. But then again, plant-based diets promoted by Ornish and others do nothing for the fragile male-ego. Perhaps, that’s the core of the problem. It’s the cholesterol, stupid

    “One important line of evidence comes from a consideration of the Japanese experience. In 1952, mortality from CHD among Japanese men 55 to 64 years of age was <10% of what it was in the United States.15,16 Their total cholesterol levels at the time averaged ≈160 mg/dL (estimated LDL, ≈80 mg/dL). It is noteworthy that the Japanese enjoyed this relative immunity to CHD despite the fact that the prevalence of one of the major risk factors—cigarette smoking—was much higher in Japan than in Western countries,17 and another—-hypertension—was just as high.18 Even the diabetic population in Japan fares better than the diabetic population in Western countries. In 1985, almost 30% of British male diabetics but only ≈15% of the Japanese male diabetics had CHD.19 The implication is that if blood cholesterol levels are sufficiently low, the other dominant risk factors, including cigarette smoking, hypertension, and diabetes mellitus, constitute much less of a threat”

    –Steinberg, 2008

    *Pritikin’s landmark article: “High-Carbohydrate Diets: maligned and misunderstood”.
    http://www.drmcdougall.com/misc/2013nl/feb/pritikinpdf3.pdf

  6. @ Richard,

    Quote: Firstly, the idea that ‘lower is better’ has not been formally tested. It’s actually based on assumptions. And these assumptions come from studies that were never able to determine whether getting cholesterol levels down to a certain level is better for patients than other levels. In fact, it’s been previously noted in the scientific literature that the idea of treating people according to predetermined cholesterol levels is not founded in science at all. http://www.drbriffa.com/2013/02/28/are-we-soon-to-see-a-relaxing-in-cholesterol-guidelines/

  7. Richard

    ^I feel I need to clarity myself. This was excellent piece and illustrated very well the new kind of problems doctors face with patients these days. But I wasn’t too enthusiastic about these little, subtle enunciations in the text in regards to statin therapy and dietary interventions.

  8. Doc´s opinion

    I get your point Richard. I wanted to reflect on the doctor-patient relationship in the age of information and internet. A doctor has to follow scientific results and clinical guidelines delivered to him by the medical and scientific community. By doing that he is practicing evidence base medicine which in my mind he definitively should. However, he also has to deal with pressure from other informative sources which are good or bad, true or false, or somewhere in between. This isn´t always an easy task. Therefore, I think we have to show Doctor Oxenhaler some sympathy.

    Another thing I wanted to bring forward is the fact that the efficacy of drugs is usually tested by comparing them with placebo. Patients however often wonder whether a change in lifestyle may be an alternative to drug therapy. Therefore, it would certainly be interesting if the effect of statin therapy for example was compared to lifestyle change or a diet intervention. Such studies, unfortunately are not available.

  9. Richard

    Yes, Doc. You are absolutely right. However, in regards to your last argument. The drug-free Ornish program is known to lead in ~40% reduction in LDL cholesterol in 12-weeks. This is equal to high-dose statin therapy and verified in multiple sites (more information, see Ornish’s own website) Ofcourse this kind of program is hard to replicate in hospitals and clinics which have not “installed” the Ornish program. However the large reduction in LDL ought to be mediated pretty much by the diet alone. I think patients should be informed about this kind of powerful, drug-free, evidenced based therapy. It has no side-effects. Although, it can be discussed whether it is entirely in accordance with good medical practice to treat high-risk patients without statins these days. I am thinking this from an ethical perspective.

    http://www.ornishspectrum.com/

    BTW, Axel, did you pay attention that this new PREDIMED study completely failed in terms of weight-management. The intervention arm did not loose any weight, and stayed in statins and diuretics throughout the whole trial. Eventhough, it was an event-free group at the baseline. I am pretty scared if the mainstream considers the results from PREDIMED as something to tout about. The mediterranean diet used by the intervention arm was slightly better than the horrible diet consumed by the controls, and that explained the small differences in outcomes. However we must keep in mind that the mediterranean diet promoted CHD in people who did not have CHD. Moreover, the controls were worse off in terms of BMI and waist circumference at the base-line. I’m waiting the new, pending study by Dr. Esselstyn that should include 200 patients. I hear the results are staggering.

  10. Richard, I would encourage you to investigate the omega-6 hazard. Among the advantages of the Ornish program is that it drastically reduces over all fat intake inadvertently lowering omega-6 intake. Unfortunately, the low-fat approach is not appropriate for that portion of the population that is carbohydrate resistant(1).

    Dr. Barry Dears critiqued the PREDIMED study. His comment:

    In contrast to this poorly executed study, there exists a far more powerful study conducted nearly 20 years ago on the benefits of a stricter Mediterranean diet. This is was the Lyon Diet Heart Study. The primary clinical difference between this new study and older Lyon Diet Heart Study is that the Lyon Diet Heart Study generated a 65% reduction in overall cardiovascular mortality, a complete reduction in cardiac sudden death, and 44% reduction in all-cause mortality. Those are clinical end points to get excited about. On the other hand, this New England Journal of Medicine article showed no impact on mortality. The only striking difference between the two groups in the Lyon Diet Heart Study was the restriction of omega-6 fatty acids in the experimental group. You find omega-6 fatty acids in vegetable oils like corn, safflower, and sunflower oils. They accomplished this dietary change by giving the subjects in the experimental groups margarines rich in omega-3 fats and trans fats. Although there was a dramatic decrease in death between the two groups in the Lyon Diet Heart Study, there were no differences in weight, BMI, blood pressure, cholesterol (good and bad), and blood lipids between the two groups. In other words, all the usual suspects in heart disease were eliminated. The only differences between the two groups were in the fatty acids, both linoleic acid and the AA/EPA ratio(2).

    Where overall health is concerned, visceral fat is important. Excerpt:

    “It is well established that some people are heavy but metabolically healthy. It’s also well established that some whole population groups, such as ethnic Indians, are especially prone to accumulate the most dangerous kind of fat- visceral fat. With even very modest weight gain, some people are genetically predisposed to put that extra fat right where it does the most damage. The result is that some people are ‘thin’ in their dimensions, but metabolically obese. This weakens the apparent association between obesity and diabetes, but that’s misleading. The reality is that in general, gaining body fat increases diabetes risk- and the results reported by Basu et al. corroborate this. But weight, per se, does not account for all of the variation in diabetes risk, nor should we expect it to(3).”

    References
    1. http://www.samj.org.za/index.php/samj/article/view/5627/4216
    2. http://www.zonediet.com/blog/2013/02/good-diet-bad-study/
    3. http://www.linkedin.com/today/post/article/20130302143554-23027997-sweet-nothings-bitter-truth

  11. Richard

    David Brown,

    see the article by Pritikin. Pritikin refers to studies which have put diabetics in a diet where 80% of the calories have come in the form of pure table sugar. Such diets have improved the glucose tolerance of diabetics. No one is advocating sugar to diabetics but it ought to put things into perspective. Diabetics have got their diabetes thanks to high-fat diets, and studies show that diabetics are off the medicine in few weeks after adhering some exercise and complex carbohydrate feeding. Ornish diet works very well on diabetics. In fact, you can see it in Forks over Knives movie yourself.

  12. Richard,

    I’m reading the article. Quote from page 9: “Can a diet restricting fat to 10% produce deficiencies? The only fat the body cannot manufacture is lenoleic acid. Winitz(24) has shown the daily requirement for lenoleic acid to be only two grams. Recent findings by Press(27) demonstrate that only .1% of total calories as lenoleic acid as a therapeutic dose is required to correct essential fatty acid deficiency: that is only 1/300th of an ounce per day.”

    Seems like the Pritikin article supports my position. Omega-6s are a novel addition to the modern human dietary(1,2). Yet, there is very little interest in researching the effects of high omega-6 intake(3). For example:

    “As far as I know, to date, no one besides Susan Alport has experimented with omega-6 intake to determine it’s effects on visceral fat. (Google – “omega-6 me” to locate information about her experiment.) Yes indeed. Sugar alone is not the problem. And omega-6 alone is not the problem. Together, however, they make a deadly duo. Since 2004 there has been lots of sugar research. Why isn’t there a similar interest in testing the effects of excessive omega-6 intake? Perhaps it’s because of the prejudice against saturated fat. Or perhaps it’s just prejudice. Negative findings from omega-6 research are difficult to get published. Excerpt from article about Sanjoy Ghosh’s research: “This is not the first time that Ghosh has produced findings that turned popular notions about nutrition and health on their head. As a graduate student Ghosh discovered by accident that so-called “heart healthy” oils rich in Omega-6 polyunsaturated fatty acids inflicted damage to the hearts of rats and neo-natal pigs. The result was so shocking that Ghosh was turned down for publication by all the major scientific journals(4).”

    References
    1. http://www.psychologytoday.com/blog/evolutionary-psychiatry/201103/your-brain-omega-3
    2. http://articles.orlandosentinel.com/2003-09-28/news/0309270148_1_overweight-or-obese-women-were-overweight-south-africa?pagewanted=all
    3. http://www.linkedin.com/today/post/article/20130302143554-23027997-sweet-nothings-bitter-truth (see comments section)
    4. http://life.nationalpost.com/2013/01/23/excessive-omega-fatty-acids-may-make-heart-health-worse-not-better-b-c-researchers/

  13. Mie

    “In fact, it’s been previously noted in the scientific literature that the idea of treating people according to predetermined cholesterol levels is not founded in science at all. http://www.drbriffa.com/2013/02/28/are-we-soon-to-see-a-relaxing-in-cholesterol-guidelines/

    Briffa’s piece is based on a review by Hayward et al (2006) which is outdated. According to the recent Joint ESC Guidelines, more recent meta-analyses have examined the same issue and confirmed the treatment goals for high-risk patients:

    http://www.ncbi.nlm.nih.gov/pubmed/21067804

    http://www.bmj.com/content/338/bmj.b2376

    http://www.ncbi.nlm.nih.gov/pubmed/19022156

    Concerning the “n-6 & inflammation” -case: much ado about nothing. According to NHANES 2009-10, a regular American gets about 6,5% of total energy intake from n-6 fatty acids. If we compare this to e.g. Sydney Diet Heart (which, according to some, offered further proof of the detrimental effects of n-6 fatty acids) where the amount of n-6 was about 12+ % of total energy intake, you’ll see that there’s little reason to be alarmed. Even less reason if we consider that current dietary recommendations argue for adequate n-3 intake.

    A highly recommended Slideshare on the issue of fats & inflammation:

    http://www.slideshare.net/pronutritionist/fats-and-inflammation

  14. Mie

    Richard stated:

    “Pritikin refers to studies which have put diabetics in a diet where 80% of the calories have come in the form of pure table sugar. Such diets have improved the glucose tolerance of diabetics.”

    As far as I can see, there is only one such study mentioned in the article you linked.

    http://ajcn.nutrition.org/content/26/6/600.full.pdf+html

    Both the glucose and the sucrose groups had significantly worse triglyseride values and the former gained weight (on a diet with the same energy intake as the control group!). Hurrah??

  15. Richard

    “Both the glucose and the sucrose groups had significantly worse triglyseride values and the former gained weight (on a diet with the same energy intake as the control group!). Hurrah??”

    Yes, this was the observed downside, and no one has insisted that sugar ought to fed to diabetics. Patients in Ornish’s (1990) intervention arm showed mild elevation in triglyceride levels as well, simultaneously as their plaques were regressing. Complex carbohydrate feeding usually result in lower triglycerides as multiple studies have indicated. Hence, I am entirely sure what happened with Ornish’s patients. Nevertheless, elevation of triglycerides, a second-tier risk-marker, was trivial to plaque regression. Anyways, I consider the results of the study which Pritikin referred to as very illustrative. Sugar is not the fundamental problem for a diabetics. Furthermore, Smith (1994) used a diet consisting 85% of refined carbohydrates, yet the condition of diabetic patients improved on almost every measurable parameter. High-carb diets are not a problem for diabetics, especially if complex carbohydrates are preferred. This was my main argument.

    Are there any low-carb studies that have managed to improve the glucose tolerance on patients adhering to such diets? I am not sure. However, I am sure that there are well-controlled and rigorously done studies showing that LC diets have the potential to jeopardize the sugar metabolism on healthy individuals within few days.

  16. Excerpt: “Sugar feeding markedly exaggerated the hyperglyceridemia in all of the patients studied. Equicaloric substitution of starch for sugar in the diet resulted in lowering of the elevated serum lipids toward normal. It was necessary to raise the daily carbohydrate intake to 85-90% of the total daily caloric intake in order to induce hyperglyceridemia in normolipemic subjects.” http://ajcn.nutrition.org/content/20/2/116.abstract

    The lesson here is that people vary in their metabolic makeup which modulates their response to macronutrient configuration. Some do not tolerate high-fat intake well. Others thrive on high-fat. Ditto for carbohydrates. Richard says, “Complex carbohydrate feeding usually results in lower triglycerides as multiple studies have indicated.” What does “usually results” mean? To me it suggests that complex carbohydrates, with the attendant supportive nutrition (vitamins and minerals) and, hopefully, fiber slows absorption of glucose. It also means that the liver does not have to deal with fructose molecules, many of which get converted to triglycerides.

    On the other hand, high saturated fat intake doesn’t necessarily result in high triglyceride levels when carbohydrate is restricted(1). It is likely the best and safest way to treat carbohydrate resistant diabetics(2). Quotes:

    “Contrary to stereotypes, low-carbohydrate dieters do not substantially increase either fat or protein consumption. Whereas per cent fat may increase, the absolute amount of fat does not change much before and after a carbohydrate-restricted diet. Low-carbohydrate diets are high in vegetables and, in practice, are not particularly iconoclastic. Such diets are relatively low in fruits but researchers emphasize that fruits and vegetables are nutritionally different: per gram, fruits have, on average, more calories, more carbohydrates, more sugar, fewer antioxidants and lower potassium.”

    “At the end of our clinic day, we go home thinking, ‘The clinical improvements are so large and obvious, why don’t other doctors understand?’ Carbohydrate-restriction is easily grasped by patients: because carbohydrates in the diet raise the blood glucose, and as diabetes is defined by high blood glucose, it makes sense to lower the carbohydrate in the diet. By reducing the carbohydrate in the diet, we have been able to taper patients off as much as 150 units of insulin per day in 8 days, with marked improvement in glycemic control-even normalization of glycemic parameters.”
    — Eric Westman, MD, MHS (Nutr Metab (Lond) 2008, 5:10).

    References
    1. http://rdfeinman.wordpress.com/2012/02/22/saturated-fat-on-your-plate-or-in-your-blood/
    2. http://rdfeinman.wordpress.com/2012/03/26/dietary-carbohydrate-restriction-in-the-management-of-diabetes-the-15-theses/

  17. Mark

    A high fat, low carbo (Paleo) diet has virtually eliminated my diabetes, so not sure I follow. High sugar,high carbs and my readings are off the chart

  18. Mark

    Just take a look at Dr Bernstein’s success with low carbing and diabetes. This is pretty much a no-brainer for us diabetics.

  19. Dear Doc Sigurdsson

    At least one such study (actually, series of studies) IS available: the work by Dr David Jenkins on the Portfolio Diet compared to first-generation statins:

    Sample quote:

    “We conclude that acceptable diets of foods from supermarkets and health food stores that contain recognized cholesterol-lowering dietary components in combination (a dietary portfolio) may be as effective as the starting dose of older first-line drugs in managing hypercholesterolemia.”

    Some references (not exhaustive):

    A dietary portfolio approach to cholesterol reduction: Combined effects of plant sterols, vegetable proteins, and viscous fibers in hypercholesterolemia [vs control diet using lovastatin]

    http://www.metabolismjournal.com/article/S0026-0495%2802%2900166-X/abstract

    Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin [lovastatin] in hypercholesterolemic participants

    http://ajcn.nutrition.org/content/81/2/380.full

    Direct comparison of dietary portfolio vs statin [lovastatin] on C-reactive protein

    http://www.nature.com/ejcn/journal/v59/n7/full/1602152a.html

    Comparison of a dietary portfolio diet of cholesterol-lowering foods and a
    statin [lovastatin] on LDL particle size phenotype in hypercholesterolaemic participants

    http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN98_06%2FS0007114507781461a.pdf&code=2384f78b240dacee79829c68c457666d

    The one hitch is that the diet, strictly followed, is vegan, and therefore even harder to switch to or stick with than the Med Diet for most folks.

    But I can personally confirm that I followed a modified non-vegan version including eg mackerel and based on the same sum-is-more-than-the-parts food combining principle and cut my total cholesterol by 54% and LDL-C by 69% – even more dramatic results than in Jenkins’ studies.

    In just FOUR weeks.

    So if you ask me (n=1, of course), diet works.

    And even in cases where it doesn’t do the whole job, it may be worth considering before, or in addition to, drug therapy:

    Diet First, Then Medication for Hypercholesterolemia

    http://jama.jamanetwork.com/article.aspx?articleid=196974

    Finally, you may be interested in this article confirming your view that even the longest-lived of us will likely die of heart disease, not “old age”:

    http://www.sagecrossroads.net/node/299

    Perhaps the most accurate statement of our goal is not even to “delay onset” of heart disease, but to ensure that we remain asymptomatic until we succumb to, eg pneumonia.

    Assuming, of course, we are interested in living so long in the first place.

    Wishing you enduring health

    Ivor

  20. “It would certainly be interesting if the effect of statin therapy for example was compared to lifestyle change or a diet intervention. Such studies, unfortunately are not available.”

    Oh yes they are! For the Portfolio Diet devised by Dr Jenkins. He’s done a whole series of studies. I’ll cite just two:

    Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin [lovastatin] in hypercholesterolemic participants

    http://ajcn.nutrition.org/content/81/2/380.full

    A Dietary portfolio: Maximal reduction of low-density lipoprotein cholesterol with diet

    http://link.springer.com/article/10.1007/s11883-004-0091-9

    The catch: the diet is harder both to switch to and stick with for regular eaters than the Med Diet, since it’s vegan.

    But I can personally confirm that I cut my own total cholesterol by 54% and my LDL-C by 69% in just 4 weeks on a modified version of this diet that used the same “sum-is-more-than-the-parts” principle but included proven cholesterol lowering ANIMAL protein eg mackerel and phytosterol-fortified plain yogurt.

    Those are more dramatic results than were found even by Jenkins.

    So if you ask me (n=1), of course, diet is a better idea than drugs.

    But then again, it’s not necessarily either/or, is it?

    Diet First, Then Medication for Hypercholesterolemia

    http://jama.jamanetwork.com/article.aspx?articleid=196974

    And in support of your view we die of something (usually heart disease) and not “old age”

    Dying of Old Age: An Old Wives’ Tale?

    http://www.sagecrossroads.net/node/299

    Assuming we want to live so long in the first place, naturally.

    Wishing you enduring health

    Ivor

  21. Doc´s opinion

    Thanks Ivor. I appreciate your comments. I agree with you on diets vs. drugs. It does not need to be either or, and it should’nt be. However, it is often easier for doctors, and other health professionals to prescribe a drug than to inform about lifestyle alternatives. My article was supposed to underscore the importance of lifestyle measures when it comes to cardiovascular prevention, and that they should not be ignored although we have drugs. I also wanted to highlight some of the issues that may surface regarding the doctor-patient relationship when dealing with these matters. The doctor’s and the patient’s ecpectations don’t always match.

  22. Mie

    “The catch: the diet is harder both to switch to and stick with for regular eaters than the Med Diet, since it’s vegan.”

    Indeed. And the results in triglyserides and HDL are less impressive than with statins. However, Portfolio does seem to beat regular low-fat diet hands down, so at the very least it seems a feasible (short-term) clinical solution in a situation where you need to address LDL levels quickly. In terms of regular diet and/or weight management: not so.

  23. Doc´s opinion

    Although we have studies comparing the effects on lipid parameters of diet vs. cholestereol lowering drugs, we still don’t haves any studies available comparing the effects of these two treatment options on clinical endpoints such as mortality and cardiovascular events.

  24. As important (more important?) than the question of proven efficacy of statins vs diet may be the question: which are patients most likely to comply with enough to make a worthwhile difference?

    Here again, diet seems to be the clear winner on current evidence.

    http://ajcn.nutrition.org/content/83/3/582.full

    Jenkins found 79% of Portfolio Dieters in a 1-year study stuck successfully to almonds, and 67% to sterol-enriched margarine. By contrast, compliance for either viscous fibre or soy protein was little better than 50-50. Even so, overall 32% of subjects reduced LDL-C by >20%.

    Those higher figures – and the outcomes – look very much better than the results of prescribing statins most patients don’t stick with, according to this summary:

    http://www.medicine.ox.ac.uk/bandolier/booth/cardiac/patcomp.html

    “The majority of patients for whom statins are prescribed in clinical practice either stop taking the drug altogether or take less than the prescribed dose within a year. This is likely to reduce or remove any benefit, and may even cause harm.”

    Even if the Portfolio Diet may be hard to swallow whole, one commentator concludes:

    http://www.ncbi.nlm.nih.gov/pubmed/23069003

    “By careful food component selection, appropriate to the individual, the effect of including ONLY TWO components in the diet with good compliance could be a sustainable 10% reduction in LDL-cholesterol; this is sufficient to make a substantial impact on cholesterol management and reduce the need for pharmaceutical intervention.” [Emphasis added]

    Almonds or other nuts palatable to particular patients are the obvious #1 recommendation (allergics aside). I guess sterol-enriched margarine would get Jenkins’ vote for runner-up, but not mine, due to issues of heart risk and trans fats, o-6 fatty acids etc. Personally, I’d propose sterol-enriched yogurts. Better yet, a study could be done to draw up a compliance league table for common and affordable foods.

    Wishing you enduring health

    Ivor

  25. Mie

    Ivor, your reasoning here is flawed (and I wouldn’t let Jenkins et al. off the hook either…)

    First, this:

    “As important (more important?) than the question of proven efficacy of statins vs diet may be the question: which are patients most likely to comply with enough to make a worthwhile difference?

    Here again, diet seems to be the clear winner on current evidence.
    http://ajcn.nutrition.org/content/83/3/582.full

    You cannot possibly compare a 12-month-long small RCT (55 participants completing the study) which didn’t even look at CV endpoints to large statin trials with a) tens of thousands of patients going on for b) several years and expect to be able to say anything on the efficacy of these two options that isn’t … well, pure speculation!!

    Yes, this study shows that the portfolio diet can be effective in modifying CVD risk with those who can comply to it. But that’s just looking at risk factors on a short-term scale. In no way does it challenge statin treatment – nor can you say that dietary approaches such as the portfolio diet are superior. There simply is no evidence to back this claim up.

    As for this

    “http://www.medicine.ox.ac.uk/bandolier/booth/cardiac/patcomp.html

    notice that you’re creating an unfair comparison between two DIFFERENT things: compliance in clinical setting and compliance in trial setting. It’s a well-known fact that dietary approaches in CVD risk modification show much better benefit when the trials are short (less than a year or so), but as time passes on … Heck, if dietary approaches were the best available solution, why do you think we have lipid-lowering medication in the first place???

    Notice that I’m not arguing that dietary approaches to preventing CVD be discontinued. No, I’m just stating the “ugly truth”: as far as evidence is concerned, in secondary prevention and with high risk patients in primary prevention, they simply ARE NOT ENOUGH.

  26. 1. “You cannot possibly compare a 12-month-long small RCT (55 participants completing the study) which didn’t even look at CV endpoints to large statin trials with a) tens of thousands of patients going on for b) several years and expect to be able to say anything on the efficacy of these two options that isn’t … well, pure speculation!!”

    I used the word “seems” advisedly. Of course the evidence as it currently stands isn’t anywhere near enough to prove the superiority of this (or any other) diet to statins.

    But the larger point is that it doesn’t matter how efficacious statins or any other drugs are in studies if you can’t get patients to take them in efficacious doses in the real world, or perhaps just can’t get patients to comply nearly as well with them as they might with some diet or food that is equally efficacious when consumed in the recommended amounts.

    To get some proper answers here, “more research is needed” (indeed, when is it not, LOL).

    2. “In no way does it challenge statin treatment – nor can you say that dietary approaches such as the portfolio diet are superior.”

    As I made quite clear, I don’t regard it as an either/or choice. I even cited a study to that effect. I imagine many sensible physicians would recommend some combination of drugs, diet and exercise for hypercholesterolemia. Who am I to disagree with them?

    But supposing diet turns out, after further, and much more comprehensive, research to be the adjustment patients find easiest to make in their lives, physicians might at least consider whether to give it much greater WEIGHT among treatment options than they do now. Indeed, the current alternative mindset (instinctively reaching for the drug cabinet before and/or instead of the larder) is what Jenkins is trying to argue against.

    But as you point out, his studies are small, while those of the pharmaceutical companies (with gargantuan research budgets and billions of dollars of revenue at stake) are large and currently far more persuasive.

    I guess more (dietary) research is needed.

    3. “Heck, if dietary approaches were the best available solution, why do you think we have lipid-lowering medication in the first place???”

    The situation, as I think all of us are underlining with different emphases, is that we just don’t KNOW whether dietary approaches are the best available solution. The research hasn’t been done to determine the issue, and many interrelated issues, either way.

    More, I suggest, is needed.

    A more cynical person than myself might also theorize that a class of patentable pharmaceuticals that includes the single most revenue-generating drug in history may, just possibly, be more likely to have attracted more marketing, R&D and lobbying support than age-old, unpatentable, low-margin foodstuffs, without overmuch care, thought or attention first being given to the relative efficacy of the two.

    4. “As for this

    “http://www.medicine.ox.ac.uk/bandolier/booth/cardiac/patcomp.html

    notice that you’re creating an unfair comparison between two DIFFERENT things: compliance in clinical setting and compliance in trial setting. It’s a well-known fact that dietary approaches in CVD risk modification show much better benefit when the trials are short (less than a year or so), but as time passes on …”

    Well, yes and no.

    (a) Yes, Jenkins’ study was a trial setting, the statin-compliance study above looked at clinical settings, but

    (b) both addressed real-world settings in which patients were, in the jargon, “free living”. In neither case were they confined to artificial settings such as hospital wards.

    In Jenkins’ words: “Our aims were to determine the effectiveness of consuming a combination of cholesterol-lowering foods (dietary portfolio) UNDER REAL-WORLD CONDITIONS [emphasis added] and to compare these results with published data from the same participants who had undergone 4-wk metabolic studies to compare the same dietary portfolio with the effects of a statin.”

    (c) the time-frame the clinical study zeroed in on was the same as in Jenkins’ study (12 months): “Clinical bottom line: The majority of patients for whom statins are prescribed in clinical practice either stop taking the drug altogether or take less than the prescribed dose WITHIN A YEAR” (Emphasis added)

    (d) Yes, quite possibly compliance with the almonds and margarine in Jenkins’ Portfolio Diet might have dropped as time went on. But then, so did compliance with statins in the longer timeframes considered in the clinical practice study. In one table they show, full compliance dropped from 43% at 6 months to 26% at 60 months and 32% at 120 months.

    So it might quite conceivably be the case that certain foodstuffs would keep their compliance advantage over statins in the longer term too.

    I suppose we can’t really tell without more research.

    (e) On the whole, I’d imagine patients might more easily be persuaded almonds (i) are tasty (ii) are good for them and (iii) don’t carry the risk unacceptable side effects, than they ever will be that the same is true of statins.

    But really, we need more research on this.

    5. “Notice that I’m not arguing that dietary approaches to preventing CVD be discontinued. No, I’m just stating the “ugly truth”: as far as evidence is concerned, in secondary prevention and with high risk patients in primary prevention, they simply ARE NOT ENOUGH.”

    I’m not aware of anyone who claims that they are. Least of all, my unqualified self. Only that they may help, and should be considered far more seriously than they currently appear to be, especially of course in NOT-so-high risk cases.

    At the rather high risk of repeating myself, may I again cite:

    http://jama.jamanetwork.com/article.aspx?articleid=196974

    Diet First, Then Drugs for Hypercholesterolemia

    Wishing you enduring health

    Ivor

  27. Mie

    Ivor,

    “But the larger point is that it doesn’t matter how efficacious statins or any other drugs are in studies if you can’t get patients to take them in efficacious doses in the real world, or perhaps just can’t get patients to comply nearly as well with them as they might with some diet or food that is equally efficacious when
    consumed in the recommended amounts.”

    Perhaps. However, with the patients to whom statins are recommended from the start, there’s no evidence to suggest that the latter (lifestyle intervention getting better compliance than medication) is the case. Unfortunately so. It’d be great if we could do without drugs, but …

    “As I made quite clear, I don’t regard it as an either/or choice. I even cited a study to that effect. I imagine many sensible physicians would recommend some combination of drugs, diet and exercise for hypercholesterolemia. Who am I to disagree with them?
    But supposing diet turns out, after further, and much more comprehensive, research to be the adjustment patients find easiest to make in their lives, physicians might at least consider whether to give it much greater WEIGHT among treatment options than they do now. Indeed, the current alternative mindset (instinctively reaching for the drug cabinet before and/or instead of the larder) is what Jenkins is trying to argue against.
    But as you point out, his studies are small, while those of the pharmaceutical companies (with gargantuan research budgets and billions of dollars of revenue at stake) are large and currently far more persuasive.
    I guess more (dietary) research is needed.”

    Now Ivor, you’re not being entirely honest here, are you? :-) The ol’ strategy of “yes, I agree BUT …” isn’t very productive. You’re speculating. That’s fine as such, but you can’t really push forth speculative thoughts to counter evidence, can you?

    “The situation, as I think all of us are underlining with different emphases, is that we just don’t KNOW whether dietary approaches are the best available solution. The research hasn’t been done to determine the issue, and many interrelated issues, either way.”

    Philosophy of science? We have thousands and thousands of studies in which lifestyle interventions (including different types of diet) have been tested in both primary and secondary prevention setting. Considering that cardiovascular diseases are the leading cause of death in the developed world, this is no surprise.

    Now, you can always argue that we simply have missed something or that the trials/studies/data are woefully inadequate etc. etc. but … Well, did I already mention the words “speculation” and “real life”?

    “Well, yes and no.
    (a) Yes, Jenkins’ study was a trial setting, the statin-compliance study above looked at clinical settings, but
    (b) both addressed real-world settings in which patients were, in the jargon, “free living”. In neither case were they confined to artificial settings such as hospital wards.”

    Which doesn’t change the fact that you cannot compare an on-going trial to non-trial setting. Did you know that simply being a part of a trial has beneficial effects (ever heard of plasebo)?

    “I suppose we can’t really tell without more research.”

    Bingo.

    “At the rather high risk of repeating myself, may I again cite:
    http://jama.jamanetwork.com/article.aspx?articleid=196974
    Diet First, Then Drugs for Hypercholesterolemia”

    And at the rather high risk of repeating myself, may I again point out that when it comes to treating patients with CVD and/or people with high risk of developing CVD, guidelines both in the US and in the EU etc. etc. – which are based on high quality epidemiological & trial evidence and their meta-analyses & systematic reviews – state … well, you know what they state. If there are fundamental flaws in these guidelines, I’d sure like to hear about them.

  28. Only one point worth replying to explicitly, I think.

    I must confess I HAVEN’T heard of “plasebo” no :-) I HAVE heard of the placebo effect. But it’s a spurious reason for drawing a distinction between Jenkins’ trials and clinical studies of statins.

    Why? Because objective outcomes such as blood lipid levels have been used to measure efficacy in both cases. In general, placebos have been found to have “no significant effects on objective…outcomes [and only] possible small benefits in studies with continuous subjective outcomes” http://www.ncbi.nlm.nih.gov/pubmed/11372012

    There is certainly an interesting philosophical debate to be had (and no, I am NOT going to get into it on this thread!) about whether, even so, some kind of placebo effect underlies all medicine. See, eg, http://www.sciencedaily.com/releases/2010/12/101222173033.htm where one doctor comments: “these findings suggest that rather than mere positive thinking, there may be significant benefit to the very performance of medical ritual.”

    But, so far as that goes, there’s no reason to distinguish between a kindly authority figure in a white coat handing out almonds and one handing out statins.

    Wishing you enduring health

    Ivor

Let me know what you think!