Category: Diet

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Eggs, Heart Disease and Diabetes – Dreams of an Omelette

It was early Sunday morning. Mr. Mason watched his wife across the kitchen table. She appeared deeply engaged in the daily crossword puzzle. He swallowed his three diabetes pills with a large sip of orange juice.

There was a momentary sparkle of light, a glint of sunshine through the clouds. He would give it another try.

“I’m told that a highly prestigious nutrition journal published a paper recently showing that eating eggs is fine if you have diabetes. So, maybe I should have my omelette today.”

She raised her chin just enough to be able to stare at him over her reading glasses.

“William dear. We finished this discussion fifty years ago. The American Heart Association hasn’t changed its mind. You should thank me for not letting you eat all that pipe plugging cholesterol you seem to fantasize about all the time.”

A momentary silence. He wasn’t giving up. “But, that didn’t prevent me from getting diabetes though.”

“C’mon. You know as well as I do that if you’d eaten all those fats, your belly would be twice the size it is today, and it surely’s big enough. So don’t start that nonsense all over.

“Dreams of an Omelet.”

A book that never leaves my night drawer is The Lost Art of Healing by Bernard Lown, a respected Boston cardiologist, and Nobel Piece Price Recipient.

In his book, doctor Lown shortly describes his relationship with a certain Mr. H., “a schoolteacher in his mid-fifties, gentle thoughtful and undemanding.” Mr. H. suffered from a heart valve disorder and needed regular check-ups. This was many years ago when dietary cholesterol was much more dreaded than today.

Surprisingly, with many things to be concerned bout, he was culturally in tune by worrying about his cholesterol. Although he was free of risk factors for coronary heart disease, and his arteries were normal, he was on a rigorous low-animal-fat diet. “My wife is very strict with me; she makes sure that not a crumb of cholesterol passes my lips.”

When I saw him at Christmas, I asked what he would wish for most in the new year. Without hesitation, he responded, as though the thought had long been percolating, “I dream of an omelet”. He continued, “I have not had an omelet for ten years. My wife tells me it is poison for me because of my heart condition”.

I explained that his type of heart problem does not require rigorous avoidance of cholesterol. “As a matter of fact, I am now prescribing an omelet for you once a week, always on Sunday”. To make sure that his wife would believe the incredible, a cardiologist prescribing an omelet, I wrote a letter accompanying the prescription of a two-egg omelet once weekly. When he next visited, he was beaming. “I look forward to Sunday as never before.” His eyes lit up. “Doctor, it is the best gift I have had in a very long time.” 

                                                               The Los Art of Healing – Bernard Lown

However, William Mason’s cardiologist didn’t prescribe omelets.

Although eggs had been cleared by many specialists, research still suggested they might be harmful to diabetics.

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Eggs, Cholesterol and Heart Disease – Are We Done?

In 1989, a paper by Stamler and co-workers in The Lancet presenting data from a study of 1824 middle-aged men who were followed for 25 years, concluded that intake of dietary cholesterol increased the risk of death, particularly death from cardiovascular disease (1).

These data strengthened the belief that dietary cholesterol causes heart disease and should be avoided as much as possible. For the omelette, this was the final nail in the coffin.

In a 2000 revision of the American Heart Association (AHA) dietary guidelines (2) the message was pretty clear: “Although there is no precise basis for selecting a target level for dietary cholesterol intake for all individuals, the AHA recommends <300 mg/d on average.”

For the layperson, this wasn’t too hard to understand. If cholesterol causes heart disease, eating it doesn’t make sense. So eliminating eggs from our dishes didn’t need much convincing.

With more than 200 mg of cholesterol in each egg yolk, eggs were branded as unhealthy and were to be eaten sparingly.

In the 1940’s U.S. per capita, egg consumption averaged more than 400 eggs a year but dropped to an average of 236 in the 1990s. The primary culprit for this reduction in egg consumption is believed to have been the concern for the impact dietary cholesterol might have on blood cholesterol levels and the incidence of heart disease (3).

But the landscape has changed. Recent observational data suggest that egg consumption is not associated with risk of cardiovascular disease and mortality from heart disease in the general population. These conclusions are largely based on two systematic reviews and meta-analyses published 2013 (3,4).

However, both of these studies left doubts with regards to diabetes.

One of the studies suggested egg consumption may be associated with an increased risk of coronary heart disease among diabetic patients. The other study hinted that egg consumption may be associated with a raised incidence of type 2 diabetes among the general population, and increased cardiovascular risk among diabetic patients.

However, it was pointed out that people with high egg consumption were not following current dietary guidelines and thus more likely to have an unhealthy lifestyle in general.

So, in 2013 eggs were okay if you didn’t have diabetes. Not good enough for Mr. Mason and his omelette dream.

Eggs and Diabetes

Mr. Mason’s recent glint of hope has to do with a paper published in the current issue of the American Journal of Clinical Nutrition (5).

The authors of the paper hypothesize that “people with type 2 diabetes may benefit from egg consumption because eggs are a nutritious and convenient way of improving protein and micronutrient contents of the diet, which have importance for satiety and weight management.” 

The study performed in Sydney, Australia, randomized 140 participants to either a high-egg diet or a low egg diet. The former were instructed to eat 2 eggs/d at breakfast for 6 d/wk (12 eggs/wk), the latter were instructed to consume less than 2 eggs/wk.

After 12 weeks, there was no significant difference between the groups for blood levels of total cholesterol, LDL-cholesterol (the bad cholesterol), HDL-cholesterol (the good cholesterol), triglyceride or blood sugar control.

The high-egg group reported less hunger and greater satiety following breakfast.

The authors conclude that a high-egg diet can be included safely as a part of the dietary management of type 2 diabetes.

However, the study results are approached much more carefully by Peter M Clifton who writes an accompanying editorial in the same journal. After also citing a few other studies, Clifton concludes; “Given these data and the fact that coronary risk is not fully captured by fasting lipids, caution is needed in recommending daily egg consumption in people with type 2 diabetes.”

Interestingly, the issue of eggs and diabetes was recently addressed in another paper published on-line in the American Journal of Clinical Nutrition by Finnish investigators who studied the association between egg consumption and risk of type 2 diabetes in middle-aged and older men from eastern Finland (6).

This was a typical prospective cohort study that included 2,332 men aged 42–60 years participating in the population-based Kuopio Ischemic Heart Disease Risk Factor Study.

During an average follow-up of 19.3 years (after adjustment for potential confounders), those in the highest vs. the lowest egg intake quartile had a 38% lower risk of developing type 2 diabetes. Thus, higher egg intake was associated with a lower risk of type 2 diabetes in this cohort of middle-aged and older men.

Dear Mr. Mason …

Eggs have a high nutritional value. Although they are rich in cholesterol, the total amount of fat is not high (5.2 g). This fat is predominantly unsaturated (51% monounsaturated and 16% polyunsaturated).

The high protein content of eggs improves satiety. Eating eggs will probably reduce the risk of consuming energy dense, less nutritious alternatives.

Epidemiological studies suggest that high egg consumption is not associated with cardiovascular disease in the general population.

Recent evidence shows that high egg consumption does not affect blood cholesterol or other blood lipids in a negative way in patients with diabetes.

A recent Finnish study even suggests that high egg consumption may reduce the risk of type 2 diabetes among middle-aged and older men.

Still, US guidelines for diabetics recommend less than four eggs a week, unfortunately not allowing for many omelets (7). But, if you decide to visit or move to the UK, there are no limits with regards to egg consumption (8).

Anyway, I’m happy to go along with Dr. Bernard Lown and write you and Mrs. Mason a prescription for an omelette (or two).

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Benefits of Coffee – Caffeine Benefits Explained

It’s been almost forty years since Bob Dylan and Emmylou Harris sang about the guy who left his gypsy girl for a journey “to the valley below”. His final cup of coffee became a classic.

One more cup of coffee for the road
One more cup of coffee ‘fore I go
To the valley below

– Bob Dylan 1976

Coffee, second to water, is the most widely consumed beverage in the US (1). However, the US doesn’t reach the world’s top ten when it comes to coffee consumption per capita. Consumption is higher in Scandinavia and many other European countries (2).

About two-thirds of Americans drink coffee daily. Given its widespread popularity, small benefits or harms associated with coffee may have important implications for public health.

Caffeine is the best-known compound in coffee. However, coffee contains more than 1.000 substances, among them, are diterpene alcohols and chlorogenic acid.

Caffeine is known for its stimulating effects on the central nervous system; diterpene alcohols have been associated with elevation of cholesterol (3) and chlorogenic acid and flavonoids in coffee have antioxidant and anti-inflammatory effects.

Caffeine is the most widely used stimulant in the world and one of few that is socially accepted. In most cases, exposure to caffeine continues for many years, often throughout life. It is estimated that 80-90 percent of adults in the world consume coffee daily.

Habitual coffee consumption often leads to mild physical dependence. Withdrawal symptoms such as irritability, headache, fatigue, anxiety and depressed mood are common if consumption is stopped abruptly.

Most of the data on the health effects of coffee are derived from observational studies. Unfortunately, such studies can’t prove a causative relationship between habitual coffee consumption and different health issues. However, currently available evidence suggests that habitual coffee consumption may have important effects on health and wellbeing.

 

How Much Coffee is Safe?

The average US adult drinks about two cups of coffee per day which is equivalent to approximately 280 mg of caffeine. However, this depends on the caffeine content of the coffee that varies greatly.

Consuming high amounts of caffeine may cause palpitations, anxiety, tremors and sweating. Very high doses may even be lethal.

Men consume more coffee than women; smokers drink more than nonsmokers and coffee consumption is lower in the black than in the white population in the US (4).

For most adults, consumption of up to 400 mg of caffeine a day appears safe (5).

It is important to keep in mind that soft drinks and energy drinks are also a common source of caffeine.

Coffee and Cardiovascular Risk Factors

Habitual coffee consumption may affect risk factors for cardiovascular disease such as blood lipids and blood pressure. In theory, this may influence health, quality of life and risk of developing coronary heart disease or stroke.

Coffee and Cholesterol

Cafestol and kahweol are examples of diterpenes in coffee beans that may raise blood cholesterol and triglycerides (6).

The highest amounts of cafestol are found in unfiltered coffee drinks such as French press coffee or Turkish/Greek coffee. Kahweol is a similar molecule, typically found in Coffea Arabica.

Diterpenes are extracted from coffee by prolonged contact with hot water. When coffee is filtered, diterpenes are retained in the filter paper, and the coffee has much shorter contact with hot water. Consequently, boiled coffee has higher concentration of diterpenes than brewed/filtered coffee.

A meta-analysis of 14 randomized controlled trials showed a significant increase in total and LDL cholesterol following regular consumption of boiled coffee compared to filtered coffee (7).

Coffee and Blood Pressure

High blood pressure (hypertension) is a strong risk factor for coronary heart disease and stroke.

Coffee consumption may be associated with acute, short-term increase in blood pressure that may last for up to three hours. However, long-term blood pressure does not seem to be significantly affected by habitual coffee consumption (8).

A 2012 meta-analysis did not show any significant effect of coffee consumption on blood pressure or the risk of hypertension (9). However, the authors of the paper conclude that the quality of currently available evidence is low, and therefore “no recommendation can be made for or against coffee consumption as it relates to blood pressure and hypertension“.

In other words, scientific evidence has not shown an association between coffee consumption and the risk of developing hypertension. However, such a relationship can’t be ruled out.

Coffee, Insulin Resistance, and Diabetes

Habitual coffee consumption is associated with reduced risk of diabetes (10).

Drinking coffee, both caffeinated and decaffeinated was associated with lower risk of diabetes according to a recent analysis of a huge epidemiological database from the Nurse’s Health Study (11). A four to eight percent risk reduction in incident type-2 diabetes may be expected for every one cup increment in coffee consumption.

Several mechanisms have been proposed to explain the protective effects of coffee on the risk of developing diabetes. Coffee is rich in chlorogenic acid, an antioxidant that may improve glucose metabolism and insulin sensitivity (12).

Another study found that consumption of 5 cups of coffee per day increased adiponectin levels and decreased insulin resistance (13).

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Coffee and Cardiovascular Disease

Caffeine has diverse effects on the cardiovascular system. It has been associated with increased heart rate, palpitations and elevated blood pressure, in particular among non-habitual coffee drinkers.

Coffee and Coronary Heart Disease

Studies performed in the 1970s suggested that habitual coffee consumption was associated increased risk of heart attack (myocardial infarction) (14,15). Today it is believed that confounding factors such as smoking, alcohol use, and physical activity may have flawed those early studies.

Since then, many observational studies have addressed the association between habitual coffee consumption and coronary heart disease. Most of these studies have shown neutral effects.

A 2009 meta-analysis of prospective cohort studies showed that moderate coffee consumption was associated with lower risk of coronary heart disease (16).

A recent Korean study showed  that middle-aged individuals who drank 4-5 cups of coffee a day had less calcification in their coronary arteries compared to those who drank less coffee (17). Coronary artery calcium score is  a known risk factor for developing clinical coronary heart disease.

Coffee and Arrhythmia (Irregular Heartbeat)

There is widespread belief that habitual coffee consumption is associated with heart palpitations and irregular heartbeat. However, data linking coffee consumption to arrhythmia is inconsistent.

Atrial fibrillation is a common arrhythmia and has sometimes been associated with habitual coffee consumption. However, a 2013 meta-analysis suggests that caffeine exposure is not associated with increased risk of atrial fibrillation (18).

Recent studies suggest that coffee does not cause arrhythmia. In fact, one large study suggests that  people who drank four cups of coffee per day were less likely to be hospitalized for arrhythmias (19). Therefore it is unlikely that moderate caffeine intake increases the risk of clinically significant arrhythmia.

Coffee and Stroke

A recent meta-analysis of prospective studies that have examined coffee consumption and risk of cardiovascular events in a general population found that moderate intake is associated with a decreased risk of stroke (20).

In the Swedish Mammography Cohort, coffee consumption was associated with lower risk of stroke among 34,670 women without a history of cardiovascular disease or cancer (21). The authors of the paper concluded that low or no coffee consumption is associated with an increased risk of stroke in women.

Data from the large Nurses’ Health Study showed an association between coffee consumption and decreased risk of stroke in a large cohort of women (22). The authors of the paper concluded that coffee consumption may modestly reduce the risk of stroke.

Coffee and Cancer

Caffeine has not been shown to cause any type of cancer (23).

The relationship between caffeine consumption and breast cancer is uncertain. Some studies have found coffee consumption to be associated with lower risk of breast cancer while others have not (24).

Some studies suggest that coffee consumption is associated with increased risk of lung cancer (25). However, this association became only marginally significant when the analysis was stratified by smoking status. Smokers, in general drink more coffee than non-smokers. Therefore, these results have to be interpreted with caution.

Observational studies have suggested that coffee consumption is associated with a decreased risk of some cancers of the gastrointestinal tract, particularly cancer of the mouth and throat (oropharyngeal cancer)(26) and cancer of the liver.

The relationship between coffee consumption and bowel cancer (colorectal cancer) is unclear (27). Although some studies suggested an association between coffee consumption and decreased risk of colorectal cancer, other studies have not supported this finding.

Habitual coffee consumption is associated with reduced risk of prostate cancer according to a number os studies (28). It has been suggested that this effect is related to other components of coffee than caffeine as a similar level of protection was found for those drinking caffeinated and decaffeinated coffee (29).

Other Health Benefits of Coffee

Studies have shown habitual coffee consumption to be associated with decreased rate of depression in women. This effect seems to be largely related to the caffeine content because similar association was not found for decaffeinated coffee (30)

Coffee is associated with reduced risks of Alzheimer’s disease (31) and Parkinson’s disease (32).

According to some studies coffee may increase the risk of bone loss. This may partly be offset by daily milk consumption (33).

Numerous observational studies have shown a relationship between coffee consumption and decreased all-cause mortality, suggesting that drinking coffee may prolong life (34,35,36).

Two prospective cohorts studies published 2015 showed that habitual intake of coffee was with lower risk of total mortality and less mortality from heart disease, cerebrovascular disease, respiratory disease, diabetes and influenza (37,38).

Health Benefits of Coffee – The Take Home Message

The association between habitual coffee consumption and health is mainly based on observational studies. Although such studies can’t prove a causative relationship, currently available evidence does not suggest that moderate coffee consumption is associated with health risks or increased risk of cardiovascular disease or cancer.

There is an association between habitual coffee consumption and decreased risk of diabetes, coronary heart disease, stroke and some cancers. However, the possibility that coffee consumption is a surrogate marker for other lifestyle factors can’t be ruled out.

Current evidence suggests that habitual coffee consumption can be a part of a healthy lifestyle, and there is no reason to advise individuals with established cardiovascular disease to abstain from moderate coffee consumption.

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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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Cholesterol and Heart Disease – A Quick Look Beyond

The word cholesterol is inherent to heart disease. Just like Paris is the capital of France and the Moon orbits the Earth, so cholesterol is associated with heart disease.

And common knowledge extends further. Most people know that cholesterol is measured in blood and that there’s is supposed to be both good and bad cholesterol. Bad cholesterol may clog arteries, so by all means make sure it’s low.

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

A standard lipid panel provides numbers for total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C) (1) and high-density lipoprotein cholesterol (HDL-C)(2).

LDL-C is often termed “the bad cholesterol” because high levels are associated with increased risk of heart disease.

On the other hand, HDL-C is usually nicknamed “the good cholesterol” because high blood levels are associated with less risk of heart disease and low levels are associated with increased risk.

Recently many experts and non-experts have cast doubt on the role of cholesterol as a causative factor for cardiovascular disease (CVD). The internet is flooded with articles and books have been published with titles such as the “Cholesterol Conspiracy” and “The Great Cholesterol Myth”. Some have suggested that the fat hypothesis is the biggest lie in medicine.

The opposite view is usually found among medical professionals. Cholesterol is regarded as a key player when it comes to cardiovascular disease;dietary recommendations aim at lowering LDL-C and cholesterol lowering drugs are often prescribed.

In a paper (3) published 2010 in the American Journal of Cardiology, William C. Roberts, editor-in-chief of the American Journal of Cardiology for the last 33 years 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!“

I believe healthy scepticism is the lifeblood of modern science. It is not about choosing teams and ignoring evidence that contradict our believes. Dogmatic assertions may get in the way of scientific progress.

So, let’s have a quick look at recent scientific results that may strengthen our understanding of the role of lipid measurements in assessing the risk of cardiovascular disease.

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Lipid Combinations

It is well known that high levels of LDL-C, low levels of HDL-C and high levels of triglycerides (TG) are each by itself a major risk factor for developing CVD (4,5,6).

But what about lipid combinations. What if both LDL-C and HDL-C are high? Will high HDL-C wipe out the risk associated with high LDL-C? And what about TG? How do they affect the mixture?

Interestingly these questions have not been addressed until lately. A paper published in the American Heart Journal in December 2014 (7) reports results from the Framingham Heart Study Offspring Cohort where the association between different lipid combinations and the long-term risk of cardiovascular disease was studied.

The study addressed 3,501 healthy middle-aged individuals without any history of cardiovascular disease who were followed for a median of 20 years.

The authors defined levels of high LDL-C as >130 mg/dL (3.4 mmol/L), high TG as > 150 mg/dL (1.7 mmol/L), and low HDL-C as < 40 mg/dL (1.0 mmol/L).

The participants were grouped into eight distinct groups according to “normal”, or “low” or “high range” values of LDL-C, HDL-C, and TG.

The group with normal LDL-C, normal HDL-C and normal TG had a 5.9% risk  of cardiovascular events (age- and sex-adjusted 10 year CVD incidence) compared to 18.4% in the group with high LDL-C, low HDL-C and high TG.

Evidently, lipid combinations can tell us quite a lot about the risk of developing CVD.

What Is Most Important, LDL-C, HDL-C or TG?

Interestingly, low HDL-C alone or in combination with a high LDL-C and/or high TG was the category associated with the greatest risk of CVD.

When compared with HDL-C, LDL-C alone was associated with only a marginally increased risk of CVD. For example, the hazard ratio for the group with low HDL-C but normal LDL-C and normal TG was 1.93 while the group with high LDL-C but normal HDL-C and normal TG had a hazard ratio of 1.28.

In contrast to HDL-C or LDL-C alone, no increase in CVD risk was associated with high TG alone.

In my opinion, the most interesting finding of this study is that a lipid combination with low HDL-C is associated with a much higher risk than a lipid combination with high LDL-C. If HDL-C is low, it makes a little difference whether LDL-C is high or not.

On the other hand, it can be argued that lowering LDL-C with statins seems to reduce CVD risk while raising HDL-C has not been found to be helpful.

How can this discrepancy be explained?

HDL-C and Insulin Resistance

The authors of the above paper cite two recent studies that suggest that HDL-C is a surrogate marker (8,9). This may imply that low HDL-C is not problematic in itself but is associated with some other factor that can increase risk. But, where is the missing link?

It is known that low HDL-C and high TG commonly occur together. In fact, the TG/HDL-ratio (10) is strongly associated with the incidence (11) and the extent (12) of coronary artery disease.

Low HDL-C and high TG are very often related to obesity and metabolic syndrome. These situations are characterised by the phenomenon we call insulin resistance.

Insulin resistance is a condition in which cells fail to respond to the normal actions of insulin. Most people with this condition have high levels of insulin in their blood. Insulin resistance appears to play an important role in CVD and is associated with increased mortality (13).

Interestingly, previously published data from the Framingham Heart Study have shown that the risk associated with low HDL-C or high TG is increased only in the presence of insulin resistance (14) .

Another study showed the benefit of fibrate therapy was much less dependent on levels of HDL-C or TG than on the presence or absence of insulin resistance (15).

Accordingly, there is evidence that in the absence of insulin resistance, low HDL-C is much less relevant as a marker of risk than when insulin resistance is present. Therefore, insulin resistance may be the missing link between low HDL-C and the risk of CVD.

So, possibly, to reduce the risk of low HDL-C, we should aim at reducing insulin resistance instead of targeting low HDL-C in itself.

Should These Findings Affect Modern Dietary Advice?

For fifty years, dietary advice has aimed at lowering LDL-C. Therefore, a low-fat diet rich in fruits, vegetables, nuts, legumes, whole grains, low-fat dairy products, fish, and lean cuts of meat is recommended to lower the risk of CVD.

But what if low HDL-C is a stronger marker of risk than LDL-C as suggested by the above study. Should we approach individuals with low HDL-C with the same dietary approach? Is a “Prudent” low-fat diet best for individuals with insulin resistance?

Today there is abundant evidence available suggesting that carbohydrate restriction is more effective than a low-fat approach to treating insulin resistance (16).

Therefore, modern dietary recommendations have to take into account recent scientific evidence suggesting that a low fat approach may not always be the best advice to cut the risk of CVD.

Don’t misunderstand me though. I’m not suggesting we should skip fresh foods such as fruits, vegetable, fish and nuts.

However, evidence suggests we have to abandon the fat phobia, the fear of saturated fat, and the view that preferring carbs rather than fat is always the best option to reduce the risk of CVD.

But, should we abandon LDL-C and the low-fat approach? Absolutely not. There are situations when lowering LDL-C is of prime importance.

But, it is time we broaden our perspective.

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