The Modern-Day Heart Patient – From One Risk Profile to Another

Although the death rate from coronary heart disease (CHD) has declined rapidly during the last few decades, CHD remains the most common cause of death in most countries around the world. The reduction in death rate is partly due to fewer people being diagnosed with CHD and partly due to a better prognosis of those affected.

The Modern-Day Heart Patient - From One Risk Profile to Another

However, the tide may be turning and if we look closely we might see some dark clouds on the horizon. The recent obesity epidemic and the rapid increase in type 2 diabetes may have ignited a new pandemic of chronic disease. Obesity and diabetes are strong risk factors for heart disease, many cancers, and Alzheimer’s disease.

In order to understand where the winds are blowing it may be helpful to analyze the modern-day heart patient and compare him/her with the typical heart patient of the 1980’s.

What does the modern-day heart patient look like? Is he/she different from the typical heart patient of the 1980’s? If so, should we still give the same dietary and lifestyle recommendations as 30 years ago?

Official dietary guidelines tend to change very slowly. In order to catch up and be able to reverse the rapid rise in metabolic disorders associated with obesity and unhealthy dietary habits, we may have to react very quickly. We may also have to admit that we’ve made a number of mistakes along the way. Otherwise we may be facing problems of enormous proportions.

Of course, there is no typical heart patient. Heart patients are young and old, male and female, skinny and obese, lazy and active, there are all possible varieties. However, trying to define the typical heart patient may help us understand whether there is a pattern or not.

The Eighties

Looking 25 years back to the days when I was starting my training as a cardiologist I see the typical heart patient as a normal weight, middle aged, smoking man with family history of heart disease and sometimes raised LDL-cholesterol (LDL-C). At that time, therapy was relatively conservative compared with today, and prognosis was generally worse. Of course abstaining from smoking was a key issue for these patients. Other recommendations included a prudent low-fat diet, quite similar to the one still recommended by many medical professionals. Statins were not available at that time, but dietary recommendations were primarily aimed at reducing blood levels of cholesterol.

As a young doctor, my first scientific project was to collect data from patients younger than forty years old who suffered an acute heart attack (acute myocardial infarction) during the time period 1980-1984.

Fortunately, heart attack was fairly uncommon in this age group and most patients were men. Among those admitted to hospital, 97 percents were smokers and slightly more than 50 percent had a parent or sibling with a history of CHD.
The mean level of total cholesterol in these individuals was 244 mg/dL (6.32 mmol/L) which was the same as the mean cholesterol among healthy people in the same age group. However, triglyceride (TG) levels were higher among the heart attack patients than in the general population. Mean body mass index (BMI) was 26.1 which was not significantly different from the general population.

We generally consider the main risk factors for CHD to be smoking, high blood pressure, high blood levels of LDL-C, diabetes, obesity and emotional stress. Low levels of HDL-cholesterol (HDL-C) and high TG may also be important. In they eighties, obesity and diabetes were much less prevalent than today. Therefore our main emphasis was on controlling blood pressure, getting the patient to quit smoking, and urging him/her to lower cholesterol through dietary measures.

The Modern-Day Situation

Recently an analysis of patients 40 years and younger who suffered an acute heart attack during the time period 2005-2009 was performed at our institute. As in the 1980-1984 study, there was a high prevalence of smoking and family history was common. However, body mass index was 28.6 which is significantly higher than in the eighties study.

The mean level of total cholesterol was 197 mg/dL (5.1 mmol/L), significantly lower than in the eighties.Interestingly, this cholesterol level was also significantly lower than the total cholesterol of individuals of similar age in the general population. HDL-C was significantly lower among the patients than in the general population.

Thus, compared with the eighties, young heart attack victims today seem more overweight and have lower HDL-C than the general population. Interestingly, high LDL-C does not appear to be a problem among these patients. This pattern was also found in the large “Get With the Guidelines” study which showed that a large proportion of patients admitted to hospital in the U.S. in the years 2000-2006 because of CHD didn’t have elevated LDL-C. However, HDL-C was generally low among these patients.

The Modern Day Heart Patient

These data suggest that metabolic syndrome is becoming more prevalent among individuals with CHD. Metabolic syndrome is characterized by a large waistline, high blood levels of TG, low HDL-C, and sometimes diabetes.

High TG/HDL-C ratio generally reflects insulin resistance and is often associates with preponderance of small LDL-particles. This pattern is associated with increased risk of cardiovascular events. The metabolic syndrome is strongly associated with the risk of heart attack and stroke.

A recent EAS (European Atherosclerotic Society) Consensus Panel paper has highlighted a lipid pattern that is likely to cause atherosclerosis and thereby increase the risk of CHD. The combination of elevated triglyceride-rich lipoproteins and low HDL cholesterol are key factors driving risk in individuals with the metabolic syndrome.

An analysis of a large international registry showed that individuals with increased body mass index (BMI)  had a more severe coronary artery disease than could be explained by the presence of traditional risk factors. Another study showed that waist-to-hip ratio was significantly associated with the risk of heart attack, highlighting the risk of abdominal obesity.

Researchers from the University of Oxford recently followed the health of 1.2 million women from England and Scotland for  almost a decade. Analysis of the data showed that the occurrence of CHD increased with BMI.  Every 5 unit increase in BMI, increases the risk of coronary artery disease by 23 percent.

report from a French registry showed recent increase in the number of younger patients with heart attack, particularly women. The proportion of women with heart attack, younger than 60 years increased from 12 to 26 percent within fifteen years. The prevalence of risk factors among these women is worth thinking about. In fifteen years, smoking increased from 37 percent to 73 percent, and obesity from 18 percent to 27 percent among women younger than 60 years who had a heart attack. The proportion of young patients not having high blood pressure, diabetes, or high blood levels of cholesterol also increased markedly.

Is the Prudent Low Fat Diet Outdated?

Two-thirds of U.S. adults are overweight or obese. Obesity rates have more than doubled in adults and children since the 1970’s. The same trend is seen in many countries around the world making obesity a worldwide problem. Such an enormous change in such a short time is both astounding and frightening, considering the strong relationship between heart disease, stroke, diabetes and certain types of cancer.

So, obviously we will see a new wave of chronic diseases, it’s only a question of time. However, everything indicates that this is a man-made pandemic. But, therein lies the solution. Obesity is a preventable disorder. It’s a lifestyle issue. However, that doesn’t mean the solution is simple, only that it is potentially preventable.

Today preventing heart disease should aim at preventing obesity and the metabolic syndrome. It’s not about choosing low-fat and prescribing cholesterol-lowering drugs (statins) anymore.  Although preventing obesity is not a simple task, some of the targets are obvious. If the over-consumption of refined sugars doesn’t stop, we don’t stand a chance.

Keep in mind Dr. John Yudkin’s word from his great book Pure, White and Deadly“There is no physiological requirement for sugar, all human nutritional need can be met in full without having to take a single spoon of white or brown or raw sugar, on it’s own or in any food or drink”.

But, how do we deal with the modern-day heart patient? Does a prudent low-fat diet still apply? Probably not. A lot of evidence indicates that carbohydrate restriction with a relatively high consumption of fats is more likely to reduce insulin resistance, decrease TG, increase HDL-C and improve LDL-particle size and number.

The changing risk profile of patients with coronary heart disease illustrates the need for re-evaluation of our dietary recommendations. Albert Einstein’s is believed to have said: “Insanity is doing the same thing over and over again and expecting a different result.”

25 thoughts on “The Modern-Day Heart Patient – From One Risk Profile to Another”

  1. Another great article Axel. From one who has adopted the LCHF lifestyle (12 months now) I can attest to lowered TG’s and other lipid markers normalising. A1c’s back in the ‘normal’ non diabetic range….. post meal BGL’s in the low range…… this way of living works!

  2. Doc,

    according to IMPACT models, depending the country in question, plummeting TC cholesterol levels explain around 25-85% of the decreased CHD mortality (Capewell et al). This drop in TC cholesterol took place much before the wide-scale use of statin and is almost completely explained by the changes in the intake of saturated fats. In US f.ex, the mean TC dropped from 240s to 200s followed by the changes in the intake of eggs and butter.

    Moreover, I have somewhat problems with your integrity, or rather, the lack of it. You often misuse the data from WHI and MRFIT trials to show that therapies aiming to reduce the intake of SFA and dietary cholesterol is useless, without providing a larger picture for you audience. In addition, if you are as serious with diet as you claim to be, why don’t you promote the work of Dean Ornish. What’s wrong with you? The participants in the Ornish study did not use drugs, not even aspirin.

    The relative failure of these smoking cessations trials can be considered a very good example of why all forms of evidence need to be considered when evaluating a hypothesis, not just a few data points from randomized controlled trials or prospective cohorts from homogeneous populations. The lack of statistically significant favourable findings in the group that received counselling on smoking cessation has been explained by a lack of follow-up time sufficient to achieve the maximum benefits of smoking cessation (which is believed to be more than 2 decades), lack of participant size, a smaller than anticipated number of participants in the group that received counselling that quit smoking, and a greater than anticipated number in the group that did not receive counselling that quit smoking. These limitations are very similar to those that plague the trails that attempted to test the diet-heart hypothesis.

    Moreover, recent reanalysis of MRFIT demonstrated a significant decreased risk of CHD and CVD events during the trial and that the non-fatal events during the trial were strongly associated with CVD mortality during the 20 years after the trial ended. This demonstrates that the trial was too short to demonstrate a significant benefit for the degree of change made between the intervention and control groups (it was observed that the participants of the control group also made an effort to improve risk factors).

    PrimitiveNutrion is out with a new serie and shows that the intervention arm in MRFIT used a drug which elevated the LDL is the patients and increased the risk of cardiovascular abnormalities, moreover, once the doctors of the control arm heard that their patients were on a trial, the care for controls was intensified, the control arm was NOT a non-treated group but was actually treated in terms of cholesterol and blood-pressure alike, almost to an equal extent as the intervention arm was treated.

    • Richard. You’re probably right that cutting saturated fat lowers LDL- cholesterol. But, because of their high-carb content, low fat diets also decrease HDL-cholesterol and increase triglycerides, well established independent risk factors for coronary heart disease. In fact, in the metabolic syndrome low HDL-C and high triglycerides associated with insulin resistance may be more of a concern than LDL-cholesterol.

      Also keep in mind that low fat diets, in reality often become high carb diets. Real life people usually have a problem sticking with a low fat Ornish type diet.

      The current epidemic of obesity, type II diabetes, and the metabolic syndrome in retrospect seems to be, at least partly, the result of our efforts to promote low fat products and not warning against unlimited carb intake.

      Finally, there is evidence that saturated fats, which represent the smallest proportion of calories by the currently recommended food pyramid, carry no more risk than carbs, which represent the highest proportion of calories according to the same food pyramid.

      • Axel, aren’t you ignoring the fact that there’s consistent evidence from epidemiological studies that the recommended sources for carbs (veggies, fruit & berries, whole grain) are associated with smaller CHD risk whereas safa as such intake isn’t?

        I agree with you on that there’s no need to oversimplify things an’ continue the “safa, safa, it’s always just safa” mantra of Richard’s, but as far as recommendable choices go, the comparison of “carbs vs safa” is misleading in the way you chose to make it above.

  3. In addition to what I wrote, I’d like to clarity this one:

    “you wrote: We generally consider the main risk factors for CHD to be smoking, high blood pressure, high blood levels of LDL-C, diabetes, obesity and emotional stress. Low levels of HDL-cholesterol (HDL-C) and high TG may also be important”.

    Let see, the 7CS with its 25-year follow-up showed that the Japanese had a higher blood-pressure (due to excessive salt intake), and cigarette smoking was more prevalent than in the West. HDLC, although not separately measured, was most likely significantly lower than in the West as well. Yet, the prevalence of atherosclerotic CHD was near-non-existent in the 1960s. What could be explain this, if not the cumulative exposure to low-fat diet induced low cholesterol levels? This is not just Japan. In South-Korea, the mean TC of rural farmers was 117mg/dl, which is much lower than most western diabetic have their LDL-C alone at. The food balance sheets show that the consumption of animal products in South-Korea was 3% as late as 1969.

    The atherosclerosis scholars throughout the word know that cholesterol (LDL) is pretty much the whole CHD story. Any thoughts, Axel?

    • Richard. I’m not sure which scholars you are citing. Of course I know that some people believe that LDL-cholesterol is pretty much the whole CHD story. However I don’t believe in such a naive oversimplification. So, don’t waste more efforts in trying to change my mind – you won’t succeed.

  4. You said “A lot of evidence indicates that carbohydrate restriction with a relatively high consumption of fats is more likely to reduce insulin resistance, decrease TG, increase HDL-C and improve LDL-particle size and number.”

    Again – it comes back to LDL-P. If yoyr particle number goes up are you willing to bet your life that none of the particles will penetrate the endothelium and become oxidized.

    You’re assuming that a person’s markers of inflammation will always be low – well what happens in the case of infection that raises systemsic inflammation, WBC, etc?

    If you have high LDL-P, high ApoB, high LDL-C what would happen then?

    • Markers of inflammation such as hs-CRP are often elevated in individuals with the metabolic syndrome. That may add further to their risk, independent of LDL-C.

      We still have a lot to learn about the effects of diet on LDL-P and ApoB. However, there is eveidence that LDL-P and LDL-C may be differently affected by diets. In addition the size of LDL particles could be important as well. Although saturated fats may raise LDL-C they also appear to decrease the number of small LDL-particles which may positively affect risk.

      • Err, I thought that studies like EPIC and MESA have shown that after adjusting for confounders, LDL particle size doesn’t really matter. Once you account for LDL-P, the case for particle size is pretty much abolished

        In addition, if you still want to continue putting your money on particle sizes, I thought that ALL fats (except for trans fats) increase LDL particle sizes in relation to e.g. refined carbs – but that safa also e.g. increases LDL-C and impairs HDL activity?

      • Mie. Some authors still highlight the importance of small particles, among them are Ronald M Krauss. This is from a 2010 paper from his group: “However, replacement of saturated fat by carbohydrates, particularly refined carbohydrates and added sugars, increases levels of triglyceride and small LDL particles and reduces high-density lipoprotein cholesterol, effects that are of particular concern in the context of the increased prevalence of obesity and insulin resistance“.

      • Krauss is a prominent advocate of sdLDL, but that doesn’t change the abovementioned findings which account for the issue with particle size. Besides, the 2010 article doesn’t even discuss EPIC or MESA or the issue of confounding factors in the case of particle sizes & CHD – which would of course be relevant if you wanted to use to argue for your case.

        As for carbs & fats, here’s the final line from the abstract (capital letters by yours truly):

        “Therefore, dietary recommendations should emphasize substitution of polyunsaturated fat AND minimally processed grains for saturated fat.”

        Now, this kinda hints that Krauss doesn’t consider safa to be relevant and/or beneficial even when talking about particle sizes.

      • That’s the problem doc, A 2010 paper. We are currently in 2014. Particle size was a risk factor low carbers jumped on, thinking that it excuse’s their high LDL. People were and still are, being told that their high LDL is no problem because their triglycerides are low and that therefore their large LDL phenotype is “non-atherogenic”.

        Even Krauss has started to conclude that particle size is doesn’t account for anything when LDL-p is measured.

  5. Doc,

    yes, Axel, I know, I cannot persuade you, although, I see this around 180-degree the opposite 🙂

    However, I’d like to point you what Jeremiah Stamler did (2010); nearly any diet that result in weight-loss will result in decrease of triglycerides and elevation of HDL-C, shift from small dense to less atherogenic particle, etc. This is not about sugar, but about excess calories. You make it seem that people got ill because they ate too much potatoes and rye bread. People got fat, because they ate too much and that’s why their HDL went down and triglycerides up. Don’t make things more complicated than they are.

    There’s not a single trial which would indicate that modulation of triglycerides or HDL from the baseline would be beneficial, perhaps because there biomarkers are markers of abdominal obesity, among other things. Triglycerides cannot even penetrate the arterial wall, and hence not directly related to atherosclerosis. If these things were crucial, then we’d find atherosclerosis in find people with heterozygous knock-out PCSK9 mutation with their life-long LDLS around 50-60s, so far not a single case identified.

    The scholars I referred are basically the most cutting-edge researchers in the face of this planet, including Brown & Goldstein and the whole campus of UT South Western Medical Center in Dallas. Are these people naive? From AHA meeting, starting after 7minutes.

    Anyways, I am happy you willing to at least consider differing opinion.

    • Richard. I find your argumentation a bit odd: “Triglycerides cannot even penetrate the arterial wall”? Cholesterol can’t either! I thought you knew that it’s indeed lipoproteins that penetrate the arterial wall, not the lipids themselves. Certain triglyceride rich lipoproteins, such as small VLDL’s and IDL do penetrate the arterial wall. These lipoproteins are atherogenic. Indeed, we don’t have any proof that they are less atherogenic than cholesterol containing lipoproteins.

      You provided a video-clip on the role of PCSK-9 inhibition and the importance of lowering LDL-C . I think that’s a bit of topic. Of course these are important issues as well, although they weren’t the topic of my article. Actually I’ve written a piece on PCSK-9 and it’s role as a possible treatment target. I bet you’ll love reading it.

  6. Doc,

    my previous post suddenly disappeared, why? I am not a lipid expert, but you probably can show us or at least refer to us to an experimental model in which elevation of triglycerides induces atherosclerosis in the context of low LDL. Would be interesting to see such study. People who maintain elevated triglycerides throughout the life since birth are not in greater risk of CHD.

    If you think that it’s difficult to get people to follow Ornish diet even though Ornish himself have never had any problems with this (he gets excellent adherence consistently), I am fine with that, just don’t give us BS about low-fat being the cause of obesity and CHD. That’s ridiculous. You confuse the alleged dangers of “carbs” to excess calories. The root cause for CHD is saturated animal fats, dietary cholesterol and excess calories. Sugar plays marginal role. People who have traditionally shown the highest intake of sugars (Cuba, Costa Rice, Venezuela) have traditionally had very low rates of CHD, high carb diet does not induce CHD in the context of low animal fat diet and low LDL. Whereas, the opposite does not hold the truth (low sugar intake, high animal fat intake).

    Causal Relevance of Blood Lipid Fractions in the Development of Carotid Atherosclerosis: Mendelian Randomization Analysis.

    “Conclusion: Our findings confirm a causal relationship between LDL-C and CIMT but not with HDL-C and triglycerides. At present, the suitability of CIMT as a surrogate marker in trials of cardiovascular therapies targeting HDL-C and triglycerides is questionable and requires further study”

    Doc, it’s rather clear to me that you are a pathological denialist and any rational attempt to demonstrate the futility of your reasoning is meaningless.

    • Richard. Your comment didn’t disappear. I just didn’t approve it, because sometimes you repeat yourself over and over and do a lot of copy/pasting. However, I decided to accept the one above and we’ll let the matter rest for the time being. Thanks for contributing 🙂

  7. Doc

    You said

    “Atherosclerotic clinical events are uncommon among individuals with lifelong very low plasma cholesterol levels. It must be emphasized however, that it is lipoprotein that interact with the arterial wall and initiate the cascade of events that leads to atherosclerosis. Cholesterol is only one of many components of lipoproteins. A causative role for cholesterol in itself has never been proven, although it appears that atherosclerosis will not occur without this compound.”

    SO – if it appears that atherosclerosis will NOT occur without cholesterol wouldn’t a diet that raises TC, LDL, ApoB, LDL-P be a bad thing?

    It appears that the VLCHF diet crowd are betting that low markers of inflammation will somehow prevent the particles from penetrating the endothelium and becoming oxidized.

    It seems to me that it’s a numbers game. The higher the particle count the greater the chance of endothelium penetration.

    SO – If you want to stop atherosclerosis, you must lower the LDL particle number!

    • Charles. In my opinion, an LCHF diet is a treatment option for overweight/metabolic syndrome and obesity. There appear to be some positive effects on lipids and metabolism in general, not least glucose metabolism. In some cases there may be a substantial elevation of LDL-C and LDL-P on such diets, in particular if the consumption of SFA is very high. We don’t really know what this means in terms of risk, but we can’t rule out the possibility that it may be harmful. Others will say that the increase in LDL-C is mainly due to an increase in large LDL-particles and thus not necessarily harmful.

      If your primary aim is to lower LDL-C, you should probably not adopt an LCHF diet, unless you believe that weight loss and other positive metabolic effects of such diets weigh more than the raised LDL-C. Of course I agree with you that particle number is important as well, and maybe more so than LDL-C.

      Indeed, I don’t believe it’s a numbers game. It’s about people. Some are lean, some are obese. Some have genetically elevated LDL-C and others don’t. Some are smokers, some are not. Some are pre-diabetic. Some have the metabolic syndrome. Some are dealing with huge stress, some are not. There are also individual preferences, and family and social issues that have to be taken care of. Therefore, it’s about people, not numbers. There is no diet formula that applies to everybody.

      • Axel, a dietary intervention that WORSENS a well-known indicator of CHD risk is hardly ideal. If the patient has no problems in this particular sense (that is, ok LDL levels already), then maybe yes, especially if there are other risk markers which need improvement, for instance, low HDL, high triglyserides, overweight. And the talk about fluffy LDL particles not being harmful is simply not true. When looking at the issue in terms of particle numbers per se, all LDL subtypes are clearly atherogenic. Increase in LDL-C (or LDL-P) is not desirable.

        But yes, in the end the idea is of course to treat the person, not risk markers. Therefore you just need to recommend a diet that the patient can comply with and follow the progress.

      • Mie. There are situations where you would accept a slight elevation of LDL-C, for example if the tradeoff is weight loss, improved HDL-C, improved triglycerides, improved blood sugar and better quality of life. This may indeed sometimes be the case in individuals with obesity and/or the metabolic syndrome.

  8. @Doc

    SO – assume you go on a LC diet and lose all of the weight you want to lose BUT your LDL-C rises, your HDL rises, your ApoB rises and your TC rises.

    What would you suggest the person focus on?

    Should they get a CT Heart Calcium Scoring test, a Carotid Duplex Bilateral ultrasound test, etc?

    If the CAC shows a value >0 does that indicate that the person has atherosclerosis?

    If yes what should that person do to stabilize or regress the plaque? Continue with the same diet that apparently caused the problem? Go on an Ornish type, plant-based diet? Start taking a statin?

    Your thoughts

  9. “There is no physiological requirement for sugar, all human nutritional need can be met in full without having to take a single spoon of white or brown or raw sugar, on it’s own or in any food or drink”

    This a phrase that is being underlined and repated so often. Do we have physiological requirement for butter, or saturated fatty acids per se? No, we dont. All human nutritional need can be met in full without haven to take a single spoon of butter or coconut oil, on it’s own or in any food or drink. 🙂

    • You’re absolutely right Reijo. However I think Yudkin’s words are important because they underline the fact that sugar, so often over-consumed, is basically unnecessary. The consumption of saturated fat is hardly a problem today. When it comes to the metabolic syndrome and modern day obesity the overuse of refined sugars, not least beverages, has to be highlighted as a problem rather than anything else.

    • Indeed. Avoiding saturated fats may be helpful for those with hypercholesterolemia, particularly high levels of LDL-cholesterol.


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