Category: Cholesterol

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The Year of the Fat

Estimated reading time: 9 minutes

During the first few months of this year, we’ve seen at least three strong signs suggesting that health authorities have misled the public for several decades about dietary fats. This finding is of particular interest because later this year the 2015 Dietary Guidelines for Americans will be published.

Ever since the beginning of the 1960s, “eat less fat, in particular, less saturated fat and cholesterol” has been repeatedly emphasized by medical professionals and other experts.

Food manufacturers have played along by emphasizing low-fat food varieties of all possible kinds, whether it’s dairy products or something else. Butter consumption has decreased, and cooking oils have become very popular, all according to public health advice with the aim to eliminate cholesterol and saturated fat from our dishes.

What started all this was observational data showing an association between blood cholesterol and the risk of cardiovascular disease. Many health experts assumed that by reducing cholesterol and saturated fat in our diet the epidemic of heart disease might be stopped because these interventions would lower blood cholesterol. However, this was an untested hypothesis.

Nobody knew what would happen after the first US dietary recommendations were launched in 1980 because the implications of such an advice had never been tested in a scientific study.

Today, these guidelines may be regarded as a research protocol for the biggest dietary intervention trial so far performed. The trial was designed without a control group; everybody had the same advice. There was no informed consent and the trial wasn’t performed according to defined ethical principles for medical research involving human subjects (1).

However, to be fair, the death rated from coronary heart disease has dropped dramatically in most western countries for the past 30 years. Of course, this achievement is due both to modification of risk factors and improved treatment. Data from the US and many other countries suggest that lowering of cholesterol in the population may have contributed to this benefit (2).

On the other hand, since the introduction of the dietary guidelines, rates of obesity and diabetes have risen dramatically.

In fact, questions have repeatedly been asked about the Dietary Guidelines for Americans. It has been pointed out that the guidelines were implemented despite lack of supportive evidence and in the face of contradictory evidence (3).

Recently, the Dietary Guidelines Advisory Committee published its Scientific Report (4) preparing for the upcoming 2015 edition of the Dietary Guidelines for Americans. The U.S. Department of Health and Human Services (HHS) and the U.S. Department of Agriculture (USDA) jointly publish the Dietary Guidelines every five years.

The Scientific Report reflects important changes regarding dietary fats compared with previous guidelines. At the same time, two recent scientific publications suggest that our basic assumptions on dietary fats may have been wrong from the beginning.

Dietary Cholesterol

Recommendations to reduce dietary cholesterol were initiated by the American Heart Association (AHA) in the 1960s and have been a mainstay of the USDA and other public health guidelines for many years. All this time, excess dietary cholesterol has been regarded as a public health concern.

According to the Recent Scientific Report from the Dietary Guidelines Advisory Committee (4), ”Cholesterol is not considered a nutrient of concern for overconsumption.” It is assumed that this change of direction will make it to the final guidelines that will be published later this year.

Although blood levels of cholesterol are still considered an important risk factor for cardiovascular disease, the abrupt change of direction reflects scientific data suggesting that cholesterol consumed in food appears to play a minor role in determining the blood levels of this substance.

So apparently, the guidelines have been wrong for decades. There is no reason anymore to believe that eating eggs or other food rich in cholesterol will cause heart disease.

It will be interesting to see how the AHA will approach this recent change of heart.

Saturated Fat and Heart Disease

From the beginning, dietary guidelines have underscored the importance of limiting the amount of saturated fat in our diet. This advice was based on observational data showing an association between the intake of saturated fats and death rate from heart disease.

It is well known that although observational studies may show an association between two variables, they can very rarely prove a causative relationship. Although dietary guideline committees have always been aware of this fact, they have been determined to stick with their initial approach regarding saturated fat, most likely because of their immense respect for blood levels of LDL cholesterol (5).

For decades, LDL cholesterol has been regarded as an important target when it comes to reducing the risk of heart disease. It’s often assumed the almost every measure able to lower LDL cholesterol will be beneficial.

There is some evidence linking the consumption of some types of saturated fat with raised LDL cholesterol. Accordingly, these fats will increase risk. But, using surrogate markers like LDL cholesterol to determine risk may be misleading (6).

Only randomized clinical trials can prove that the intake of saturated fats will increase the risk of heart disease. Interestingly, results from such trials were available the time of the publication of the first dietary guidelines

Last month, British investigators published a systematic review and meta-analysis of results from randomized clinical trials that were available when the first US and UK dietary guidelines were published in the late 1970s and early 1980s (7).

The authors found six dietary trials, including a total of 2.467 male participants. The intervention differed somewhat between studies but all aimed at reducing total fat and/or saturated fat consumption in the intervention group.

There were no differences in all-cause mortality and non-significant differences in mortality from heart disease, resulting from the dietary interventions. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups.

So despite lowering cholesterol, interventions aimed at reducing saturated fat intake did not lower mortality nor decrease death rate from heart disease.

The authors arrived at three pretty sobering conclusions:

Government dietary fat recommendations were untested in any trial prior to being introduced

Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from randomized clinical trials

The present review concludes that dietary advice not merely needs review; it should not have been introduced

Macronutrient Consumption Data

In 1977 the U.S. Senate Selection Committee on Nutrition and Human Needs issued Dietary Goals for the United States, which recommends that fat consumption be reduced to 30% of energy intake, and that carbohydrate consumption be increased to account for 55-60% of energy intake (8).

The focus on the relative contribution of different macronutrients was maintained by the first Dietary Guidelines for Americans that were launched by the USDA in 1980 and have remained largely unchanged since then.

There were two reasons experts believed reducing fats and increasing carbohydrates would be beneficial. Firstly, this would lower blood cholesterol and thereby the risk of heart disease. Secondly, because one gram of fat contains more calories than one gram of carbohydrates, the intervention would reduce the risk of obesity.

A recently published U.S. paper addresses the long-term dietary consumption of the U.S. population from 1965-2011 based on NHANES (National Health and Nutrition Examination Survey) data focusing on Americans aged 18-64 (9).

The main goal of the study was to address whether Americans have been following dietary guidelines with regards to the macronutrient composition of the diet.

Cohen et al, Statistical review of U.S. macronutrient consumption data, 1965–2011 Americans have been following dietary guidelines, coincident with the rise in obesity doi:10.1016/j.nut.2015.02.007

In 1965, fat consumption comprised 44.7% of calories of adult Americans’ diets, compared with 39% for carbohydrate. By 1999, fat consumption reached a through of 32.4% while carbohydrate consumption hit its peak at 52.1%. Protein consumption remained relatively constant throughout the period.

In 1971, saturated fat comprised 13.5% of total calories. By 2011, Americans were eating 10.7% of their calories as saturated fat (a 20.5% reduction since 1971).

Per capita cholesterol consumption decreased down below 300 mg/day, from over 400 mg/day in 1971.

The study also confirms a clear shift towards more obesity during the study period.

The authors underscore that there is a strong correlation between the increase in carbohydrate share of total intake and obesity.

They also address the question whether the increased prevalence of obesity can be explained by an increase in overall calorie intake by conducting their tests over two subsamples of participants who consumed similar calories over time. They conclude “the increase in calorie consumption since 1971 is not likely to offer any significant explanation for the increase in BMI (body mass index) over the last four decades.”

The main findings of the study were

  • Americans have been adhering to federal dietary guidelines for the past 40 years
  • Fat consumption by U.S. adults has decreased from 45% to 34% between 1965 and 2011
  • Carbohydrate consumption has increased from 39% to 51% over this same period
  • There is a high correlation between the change in diet and the rise of obesity
  • The percentage of overweight adults has increased from 42% to 66% since 1971

The Bottom Line

Recently we have seen important evidence suggesting that the fear of dietary fats, in particular, the fear of saturated fats and cholesterol is not based on reliable scientific data.

This evidence adds further to the belief that we have been misinformed for decades by public authorities about dietary fat intake.

Although authors of dietary guidelines seem to have admitted that there is no reason to avoid dietary cholesterol, I’m still afraid they haven’t got it right. For example, the advice to avoid saturated fats was never based on evidence from randomized clinical trials.

It is hard to accept that public health recommendations are not based on solid scientific evidence.

A  part of the problem is that the guideline process is too complicated, and recommendations are often hard to change.

The dietary fat history is a tragic example of how easy it is to mess things up for years when you get it wrong from the beginning.

Guideline writers should acknowledge the lack of evidence for most recommendations and write shorter guidelines. They should stick to hard evidence. Who needs hundreds of pages of expert consensus? The public deserves to be guided by real science.

Finally, despite the forthcoming 2015 Dietary Guidelines for Americans, this could be the year of the fat.

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What About Saturated Fats if You Already Have Heart Disease?

Estimated reading time: 7 minutes

We’re all aware of the aggressive campaign driven by public health authorities and medical professionals to decrease blood cholesterol.

It all started more than fifty years ago when the Framingham Heart Study reported that high blood cholesterol was a major risk factor for coronary heart disease (1).  

 

Central to the dogma was the belief that lowering blood cholesterol would lower the risk of heart disease.

At the same time, it was assumed that dietary saturated fats and dietary cholesterol caused an increase in blood levels of total cholesterol as well as LDL cholesterol (the “bad” cholesterol).

So, it was a foregone conclusion that dietary saturated fats and dietary cholesterol would cause heart disease because they supposedly raised blood cholesterol.

However, recently evidence questioning a lack of a causal relationship between the intake of saturated fats and heart disease has accumulated (3). Even so, restriction of dietary saturated fats is still included in most current dietary guidelines and recommendations on cardiovascular prevention (4,5).

Although some recent studies have suggested that replacing saturated fatty acids with monounsaturated or polyunsaturated fatty acids may be beneficial, replacing saturated fats with carbohydrates may increase risk (6).

Before I go further, keep in mind that the lack of evidence for a causal relationship between the intake of saturated fats and heart disease doesn’t necessarily defy or contradict the lipid hypothesis.

Although high intake of saturated fats may raise total cholesterol and LDL cholesterol, it also tends to elevate HDL cholesterol (the “good” cholesterol).

In addition, high intake of saturated fats is associated with a higher concentration of large cholesterol-enriched LDL particles and lower concentration of small, dense LDL particles (7). The presence of small, dense LDL particles is associated with an increased risk of subsequently developing heart disease (8), and appears a strong predictor of blockage in the coronary arteries (9).

So, a lack of relationship between high intake of saturated fats and the occurrence of heart disease may indeed fit quite well with the lipid hypothesis. However, it suggests that the simplified version of this hypothesis, the one that only targets LDL cholesterol may be misleading (10).

What About Saturated Fats if You Already Have Heart Disease?

The public recommendation to restrict the intake of saturated fats has been primarily targeted at healthy people in order to reduce the risk of heart disease. However, the same advice has been given extensively to patients diagnosed with cardiovascular disease, whether it be coronary heart disease or stroke.

Very few studies have investigated the impact of saturated fat intake in patients already diagnosed with heart disease. For this reason, I became quite interested to find a scientific paper on the issue published very recently in the Journal of Nutrition (11).

The study included 2,412 patients who underwent coronary angiography because of coronary artery disease or aortic valve stenosis between 1994 and 2004 at two university hospitals in Norway (Haukeland University Hospital, Bergen and Stavanger University Hospital, Stavanger).

Information on dietary intake was obtained at baseline by an FFQ (Food Frequency Questionnaire) developed at the Department of Nutrition, University of Oslo.

The patients were divided into quartiles based on the amount of saturated fat consumed (percentage of energy consumed). In group 1, the amount of saturated fat intake was between 3.9-9.8%, in group 2 it was between 9.8-11.5%, in group 3 between 11.5-13.2 and group 4 between 13.2-28.7.

There were some quite interesting findings at baseline. For example, patients with a higher intake of saturated fats were less likely to have a history of heart attack, prior coronary artery bypass surgery or to have triple heart disease (blockages of all three main coronary arteries) at baseline.

Increased intake of saturated fatty acids corresponded to an increased intake of both total energy and total fat. Participants with the highest saturated fatty acid intake also had higher consumption of mono-and polyunsaturated fat and dietary cholesterol.

High intake of saturated fats was associated with lower consumption of total carbohydrates, dietary fibre and alcohol. Patients with higher intake of saturated fats had higher intakes of meat, cheese, butter, milk, eggs, cakes, sugar and sweets.

Interestingly, despite higher calorie consumption among those with the highest saturated fatty acid intake, body mass index (BMI) was similar in all four groups.

Patients with higher intake of saturated fats were less likely to have high blood pressure but more likely to smoke. Their blood levels of total and LDL cholesterol tended to be higher but triglycerides lower compared to those with lower intake of saturated fats. There were no significant differences in the blood levels of HDL cholesterol between the groups.

The prevalence of diabetes was similar in all four groups.

During a median follow-up of 4.8 years, a total of 292 (12%) patients experienced a coronary event (heart attack, unstable angina or coronary death), and 137 patients died from any cause.

During follow-up, most of the patients were on conventional medication such as aspirin (90%), statins (89%) and beta-blockers (78%).

There were no significant associations between the intake of saturated fatty acids and coronary events or death from any cause. In other words, patients with high intake of saturated fats did not do worse than those with lower intake of saturated fatty acids. This was true also after multivariate adjustments for possible confounding factors.

Of course, this study has several strength and limitations. For example, it is important to understand that dietary intake was estimated at baseline only. No such information was collected during follow-up. For this reason, it is not possible to account for changes in dietary habits during the study period.

However, the authors point out that the majority of patients selected for participation in the study had known coronary heart disease at baseline. Thus, it may be assumed that most patients willing to change their dietary habits towards less SFA intake had already done so before inclusion in the study.

The Bottom Line

For decades, cardiologists have advised patients with heart disease to restrict the intake of saturated fats and dietary cholesterol. Many patients still believe this to be the cornerstone of their lifestyle modification.

The main reason for avoiding saturated fats is the assumption that they adversely affect the lipid profile of our patients.

Public authorities and medical societies usually recommend restricting the intake of saturated fats to less than 10 percent of total energy consumption. In the above study, only 27% of the patients met these dietary recommendations.

The American Heart Association goes even further by recommending a dietary pattern that achieves 5% to 6% of calories from saturated fat. That means, for example, if you need about 2,000 calories a day, no more than 120 of them should come from saturated fats. That’s about 13 grams of saturated fats a day (12). That equals two slices of cheddar cheese.

Recent studies suggest that the recommendation to avoid saturated fats may have been premature and not based on solid scientific evidence.

Now, a recently published Norwegian study shows that dietary intake of saturated fatty acids was not associated with risk of future events or death among patients with established coronary artery disease.

It is important to keep in mind that most of the patients were receiving secondary prevention drug therapy including aspirin, beta blockers and statins.

Anyhow, the results of the study certainly suggest that high intake of saturated fats is not a risk factor among patients with coronary heart disease receiving modern-day treatment.

These recent scientific data don’t imply hat we should urge our patients to consume high amounts of saturated fats. They only tell us that there is no association and accordingly, restriction won’t help.

So, it’s certainly a lifeline for those who believe red meat, whole-fat milk, cheese, cream, butter and eggs can be a part of a healthy diet.

On the other hand, we must realise that scientific studies often provide contradictory results. A US study published last year suggested that greater adherence to a low carbohydrate diet high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality following acute heart attack (13).

It appears the jury is still out…



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HDL Cholesterol – The “Good” Cholesterol Explained

Estimated reading time: 8 minutes

High-density lipoprotein cholesterol (HDL cholesterol) is commonly measured to assess the risk of heart disease.

If you’ve had a blood sample drawn for assessment of lipid panel you probably already know if your cholesterol level is acceptable or not. You might also recall something about good and bad cholesterol and the ratio between these two.

Of course, there is only one type of cholesterol. The “good” and “bad” has to do with the lipoproteins that carry cholesterol molecules in our blood stream.

A standard lipid panel provides information about total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL cholesterol) and HDL cholesterol.

LDL cholesterol is often termed “the bad cholesterol” because high levels are associated with increased risk of heart disease.
On the other hand, HDL cholesterol is usually nicknamed “the good cholesterol” because high blood levels are associated with less risk of heart disease whereas low concentrations are correlated with increased risk.

In other words; there is an inverse relationship between HDL cholesterol and the risk of heart disease. It is believed that HDL’s act as scavengers, picking up excess cholesterol in the blood and transporting it to the liver where it’s broken down.

Atherosclerosis and Heart Disease

Atherosclerosis is the hallmark of coronary artery disease. It may be described as a chronic inflammation of the arterial wall.

Atherosclerosis leads to the formation of lesions or plaques that protrude into the lumen of the artery causing arterial narrowing, which can disturb blood flow. If this occurs in the coronary arteries, it may cause chest pain often termed angina pectoris.

The coronary arteries supply blood to the heart muscle. Acute heart attack (myocardial infarction) occurs when there is a sudden disruption of blood flow in a coronary artery. A sudden blockage is usually caused by a rupture of an atherosclerotic plaque in the vessel wall, with subsequent formation of a blood clot (thrombosis) at the rupture site. The sudden disruption of blood flow causes the death of heart muscle cells (infarction) and may impair the function of the heart muscle.

In 1961, the Framingham Study reported that high blood levels of cholesterol and high blood pressure were associated with increased risk of coronary artery disease and acute heart attack. This lead to the term “coronary risk factors” being defined.

Cigarette smoking, various fractions of cholesterol, insulin resistance, diabetes, obesity, physical activity, mental stress and depression are all examples of modifiable risk factors which, if present increase the risk of heart attack. However, although many risk factors have been identified, coronary heart disease remains a common disorder. Despite extensive research, our understanding of the mechanisms behind this disease is incomplete.

Lipids and Lipoproteins

Lipids, like cholesterol and triglycerides, are essential substances for the human body. They are used by cells for energy utilization, hormone production, bile acid formation and much more.

Because lipids are insoluble in blood, they are carried by lipoproteins that transport them to various tissues and organs. Lipoproteins consist of cholesterol, triglycerides, phospholipids and protein. The lipoproteins act as carriers transporting essential fat substances to the organs of the body.

There are five major types of lipoproteins; chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

HDL and LDL lipoprotein particles have very different roles. Therefore, measuring the amount of cholesterol within these particles tells two different stories.

Elevated levels of LDL cholesterol are associated with increased risk of heart disease, but high levels of HDL cholesterol are associated with low risk. HDL particles seem to be involved in clearing and removing cholesterol from arteries and atherosclerotic plaques while LDL particles appear directly involved in the atherosclerotic process.

HDL Particles

It is important to understand that measurements of HDL cholesterol only provide information about the amount of cholesterol carried by HDL particles. HDL particles differ in size and function, and there are many types, both small and large.

HDL particle number can be measured by NMR (Nuclear Magnetic Resonance). Studies have shown that such measurements are more strongly associated with atherosclerosis than measurements of HDL cholesterol.

Recent studies have shown that simple measurements of HDL cholesterol may not always reflect HDL function. Thus, there is growing evidence that HDL function may sometimes be impaired although measurements of HDL cholesterol are normal. Therefore, measuring HDL cholesterol may not be the best method to assess HDL function.

Although incomplete, HDL cholesterol is still the most widely used measurement to assess HDL.

Other metrics that are currently being tested include HDL particle number, average HDL size, specific HDL subclasses, and HDL functional properties.

HDL Cholesterol and Heart Disease

An inverse relationship exists between HDL cholesterol and the development of coronary artery disease. In other words, high levels are associated with low risk of heart disease, and low levels are linked to high risk.

Based on data from the Framingham Heart Study the risk of heart attack increases about 25 percent for every 5 mg/dl (0.13 mmol/L) decrement in blood levels of HDL cholesterol. However, whether HDL cholesterol is a causal risk factor or merely a marker of risk is still intensely debated.

The most widely accepted hypothesis regarding the protective properties of HDL when it comes to atherosclerosis is that it promotes the uptake of cholesterol from tissues, including the vascular wall, and returns the cholesterol to the liver from where it is excreted. This process is often termed “reverse cholesterol transport.”

It has also been postulated that HDL’s may promote normal function of the endothelium, the innermost layer of the arteries. Furthermore, HDL’s may reduce inflammation, protect against oxidation of LDL, and positively affect blood clotting (thrombosis).

HDL Cholesterol Range

The table below shows the reference values;

HDL cholesterol (mg/dL)
(U.S. and some other countries)		 HDL cholesterol (mmol/L
(Canada and most of Europe)		  
Below 40 mg/dL (men)
Below 50 mg/dL (women)		 Below 1.0 mmol/L (men)
Below 1.3 mmol/L (women)		 Too Low
40-49 mg/dL (men)
50-59 mg/dL (women)		 1-1.3 mmol/L (men)
1.3-1.5 mmol/L (women)		 Acceptable
60 mg/dL and above 1.6 mmol/L and above Very good

 

Levels above 60 mg/dl (1.6 mmol/L) are associated with low risk of coronary heart disease. This is more likely to be seen among women than men.

HDL cholesterol below 40 mg/dL (1.0 mmol/L) is considered too low and appears to be an independent risk factor for coronary artery disease. Furthermore, the definition of metabolic syndrome includes low HDL cholesterol as one of the five criteria for classification. Low HDL cholesterol is one of the most common phenotypes seen in persons with premature heart disease.

HDL cholesterol in the range of 20-40 (0.5-1.0 mmol/L) may appear in isolation but is often associated with high triglyceride concentration, insulin resistance and increased risk of type 2 diabetes. Furthermore, some drugs, such as beta-blockers may lower HDL cholesterol. Anabolic steroids can markedly reduce HDL cholesterol and should be suspected particularly in healthy young men with unexpectedly low HDL cholesterol levels.

Levels of less than 20 mg/dL (0.5 mmol/L) are uncommon and can sometimes be attributed to very high triglycerides. It may also be due to rare genetic mutations, such as Tangier disease and fish-eye disease.

Individuals with high HDL cholesterol often have large LDL particles. They are also likely to have low LDL particle number (LDL-P). LDL-P is a reliable marker of risk for coronary artery disease.

Measuring apolipoprotein B or LDL-P may help to estimate risk among individuals with high levels of both LDL-and HDL cholesterol. Calculating non-HDL cholesterol may also be useful to assess risk under these circumstances. Determining the triglyceride/HDL cholesterol ratio may provide further information.

How Can HDL Cholesterol Be Influenced?

HDL cholesterol can be influenced by lifestyle modification.

Smoking reduces HDL cholesterol, and smoking cessation is associated with moderately increased levels.

Regular aerobic exercise can modestly increase HDL cholesterol. This increase is related to the frequency and intensity of physical activity, with greatest increases occurring with frequent, low-intensity exercise, such as five 30-minute sessions per week.

Obesity is associated with low HDL cholesterol levels and high triglyceride levels. A negative correlation exists between HDL cholesterol and body mass index (BMI), meaning that HDL cholesterol tends to be lower with increasing BMI. Weight loss usually raises HDL cholesterol.

Dietary choices affect HDL cholesterol. If the intake of fat is reduced, levels of LDL- and HDL cholesterol both decline. In one study comparing calorically balanced diets, those who consumed a low-fat diet had lower HDL-cholesterol than those who were fed a high-fat diet.

Intake of saturated fats usually increases both LDL- and HDL cholesterol. Substituting monounsaturated fat for saturated fatty acids may improve the ratio between these two subfractions of cholesterol.

Limiting intake of simple carbohydrates is usually helpful, in particular, if triglycerides are elevated. This is often the case in obese people and those with metabolic syndrome.

A diet rich in n–3 polyunsaturated fatty acids (omega-3) – sources include oils (olive, canola, soy, flaxseed), nuts (almonds, peanuts, walnuts, pecans), cold-water fish (salmon, mackerel), and shellfish — with limited carbohydrates, such as those found in ready-to-eat cereals, potatoes, white bread, and snack foods, is often recommended.

Moderate alcohol consumption raises HDL cholesterol but is usually not recommended for that purpose.

Several classes of medications increase HDL cholesterol levels; these include niacin and fibrates, and, to a lesser degree, statins. With the exception of statins, drug therapy that elevates HDL cholesterol has not been shown to improve outcome or reduce the risk of coronary events.

The 2013 American College of Cardiology/American Heart Association Guidelines for the Treatment of Blood Cholesterol to Reduce Cardiovascular Risk do not make a recommendation to add therapy to raise low HDL cholesterol in patients who are on maximal statin therapy.



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Vegetarian Diet – Will Going Vegan Reduce the Risk of Heart Disease?

I became a bit puzzled the other day when I read a blog article written by Kim A Williams MD, a cardiologist at Rush University in Chicago and the next president of the American College of Cardiology.

 

Doctor Williams describes how one of his patient’s history inspired him to change his dietary habits and adopt a cholesterol free, plant-based diet.

He finds it interesting that the American Heart Association prevention guidelines do not specifically recommend a vegan diet.

Dr. Williams writes: “…Wouldn’t it be a laudable goal of the American College of Cardiology to put ourselves out of business with a generation or two“…

Obviously, he’s implying that heart disease may be eliminated if we all go vegan.

To make my case clear I have to emphasize that my puzzlement has nothing to do with whether I believe Dr. Williams is right or wrong. In fact, he might very well be right. However, the question is whether his implications are supported by scientific evidence.

Should doctors base their treatment decisions on anecdotal evidence?

We often warn our patients to adopt the experience of other people and make it their own, both when it comes to interpreting symptoms and advising treatment strategies.

However, to be fair to Dr. Williams I will mention that he believes that studies on vegan diets are “either very large and observational or small and randomized“…

But, then he’s also implying that the scientific data isn’t strong enough to recommend heart patients or the general public to become vegetarians. So where is he going then?

 

Vegan Diet and Heart Disease

The health of vegetarians has been addressed in a number of studies. The health effects of foods that are preferred or avoided by vegetarians has also been studied. Most of these studies are of observational nature. Suffice to say that there is strong evidence that vegetarians have lower rates of coronary heart disease, lower LDL-cholesterol and lower rates of hypertension, diabetes and obesity.

A combined analysis of the five biggest cohorts published in 1999 showed a 24% lower mortality from coronary heart disease among vegetarians compared with non-vegetarians. Recently published data from the EPIC-Oxford Study showed that vegetarians had a 32% lower risk coronary heart disease than did non-vegetarians. Vegetarians had lower BMI, non-HDL cholesterol and blood pressure. 

Randomized studies of vegetarian diets are few and small. Ornish’s Lifestyle Heart Trial showed a regression of coronary artery plaques among patients who adopted a program consisting of a low-fat vegetarian diet, stopping smoking, stress management and moderate exercise, compared with a “usual care” control group. These results were achieved without the use of cholesterol-lowering drugs. Although the study was randomized, only 48 individuals participated.

Another old and often cited study by Lester M. Morrison published 1960 tested 100 patients with proved coronary atherosclerosis. Fifty patients were treated with a low-fat, low-cholesterol diet. The other 50 patients were not given any specific treatment and acted as controls. By the end of 12 years, 19 of the 50 patients treated with the diet survived. Of the 50 control patients, all had died by the 12th year of observation.

Caldwin Esselstyn’s studies have also shown positive effects of a low-fat strategy in patients with coronary atherosclerosis. But again very few patients were studied. In his book, Prevent and Reverse Heart Disease, Esselstyn writes: … “I believe that coronary artery disease is preventable, and that even after it is under way, its progress can be stopped, its insidious effects reversed. I believe, and my work over the past twenty years has demonstrated, that all this can be accomplished without expensive mechanical intervention and with minimal use of drugs. The key lies in nutrition—specifically, in abandoning the toxic American diet and maintaining cholesterol levels well below those historically recommended by health policy experts…”

Will we be seeing more heart surgeons having a good time on the golf course if the world goes vegan?

It’s the Cholesterol Stupid

Obviously, there is a lot of evidence suggesting that plant based diets positively affect atherosclerosis and coronary artery disease compared with a traditional Western dietary pattern. But many questions remain. Do we have to avoid all animal products? How about dairy foods, eggs and fish? What are the advantages and risks of soy consumption? What about compliance? Are vegetarian diets more difficult to stick with than other diets Well, clearly more research is needed before we can answer the question whether cardiologists will run out of business if the world goes vegan.

Now let’s get back to Kim A Williams blog article. Williams apparently believes that cholesterol is what defines a healthy diet. He writes: … “I thought I had a healthy diet — no red meat, no fried foods, little dairy, just chicken breast and fish. But a simple Web search informed me that my chicken-breast meals had more cholesterol content (84 mg/100 g) than pork (62 mg/100 g). So I changed that day to a cholesterol-free diet, using “meat substitutes” commonly available in stores and restaurants for protein. Within 6 weeks my LDL cholesterol level was down to 90″...

In a paper published 2010 in the American Journal of Cardiology, William C. Roberts famously wrote: … “The lower the LDL cholesterol, the better, and this principle has been established repeatedly despite voices of the anticholesterol, antistatin fallacy mongers! It’s the cholesterol, stupid!“…

Dr. Roberts has been editor-in-chief of the American Journal of Cardiology for 32 years. Although not within the scope of my article, I can’t but wonder how many of the “anticholesterol, antistatin fallacy mongers” have managed to get their papers accepted for publication in the journal.

Mixing medicine with anal retentiveness is bad. You may remember that according to Freudian psychoanalysis “the term anal retentive (also anally retentive), commonly abbreviated to anal, is used to describe a person who pays such attention to detail that the obsession becomes an annoyance to others, potentially to the detriment of the anal-retentive person”. 

So, let’s open our minds a little bit. Is it possible that the positive health effects of eating fruits and vegetables have to do with something else than cholesterol? I can assure you that by admitting that’s possible, you’re not saying that cholesterol doesn’t matter, and hopefully you’ll not be classified as an “anticholesterol fallacy monger.”

Last week The BMJ published a meta-analysis of sixteen cohort studies analysing the relation between fruit and vegetable consumption and risk of all cause, cardiovascular, and cancer mortality. Higher consumption of fruit and vegetables was significantly associated with a lower risk of all cause mortality. However, there was a threshold around five servings of fruit and vegetables a day, after which the risk of all cause mortality did not reduce further. Mortality from cardiovascular causes, but not cancer, was significantly related to less consumption of fruits and vegetables.

The authors discuss the possible mechanisms underlying their findings. Antioxidant compounds and polyphenols in fruit and vegetables—such as vitamin C, carotenoids, and flavonoids may play a role. These have been shown to prevent the oxidation of cholesterol and other lipids in the arteries and to increase the formation of prostacyclin with positive effects on arteries and blood clotting.

Reduction in blood pressure may play a role. Fruit and vegetables are good sources of magnesium and potassium, which have been inversely associated with mortality in previous studies. Fruit and vegetable increase plasma concentrations of antioxidants, such as alpha and beta carotene and other compounds such as vitamin C, carotenoids, and other phytochemicals may be important as well.

So, after all, it’s not only the cholesterol (stupid) …

 

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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.

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.

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.

A 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.”

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