Less Heart Disease Despite More Diabetes; The Role of Diet

The diverging trends in heart disease and diabetes represent a public health paradox of immense importance.

Obesity and type 2 diabetes are well-known risk factors for coronary heart disease. However, whereas the prevalence of obesity and type 2 diabetes is increasing, the death rate from coronary heart disease is declining.

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This interesting paradox was recently addressed in two separate articles written by renowned experts in The Lancet Diabetes & Endocrinology (1,2)

Although the authors share some common ground, their views differ significantly in some important areas. It is of great interest to analyze their opinion on how the current paradox should affect dietary guidelines and our interpretation of the role of calories, cholesterol, saturated fats, and carbohydrates.


The Role of LDL Cholesterol and Total Energy Consumption

The first paper entitled “Diverging global trends in heart disease and diabetes: implications for dietary guidelines” is written by Jim Mann and coworkers from New Zealand.

The paper reflects a somewhat traditional view on the subject;

The decrease in coronary heart disease can be explained by several factors, including reductions in LDL cholesterol concentrations, blood pressure, and tobacco use and more recently, improvements in medical and surgical treatment.

The authors point out that reduced consumption of saturated, and more recently trans unsaturated, fatty acids with variable increases in unsaturated fatty acids have occurred in parallel with reductions in mortality from coronary heart disease.

Although everybody knows that correlation does not prove causation, they claim this dietary change has been a major contributor to the reduction in coronary heart disease, largely because of a reduction in LDL cholesterol.

Mann and colleagues believe there is accumulating epidemiological evidence suggesting that diets high in minimally processed carbohydrate and dietary fiber are associated with reduced risk of type 2 diabetes, coronary heart disease, and some cancers.

They also claim there is data supporting the potential of such dietary advice to improve the control of diabetes and to reduce cardiometabolic risks in general.

They also point out that early recommendations about dietary carbohydrates in the 1970-80s may have been misleading because they encouraged consumption of complex rather than simple carbohydrates.

They believe such distinction is unhelpful because complex carbohydrates may be very different from those associated with reduced risk, such as minimally processed fiber-rich cereals, whole grains, legumes, pulses, vegetables, and fruits.

Nonetheless, they acknowledge that for people who are insulin resistant, intake of total carbohydrate should be at the low end of the recommended range (45-60% total energy).

Although they agree that reduced carbohydrate diets may enable more short-term weight loss than do reduced fat diets, they believe that long-term weight loss relies on compliance with a prescribed diet rather than macronutrient distribution.

They conclude that existing evidence does not support a dietary pattern that involves radical restriction of carbohydrate and unlimited fat consumption, but they don’t cite studies that have compared this approach to their preferred dietary pattern.

However, they still believe that the food industry’s replacement of fat with sugar and rapidly digested starches is likely to have contributed to the increase in energy intake that is driving the epidemic of obesity and type 2 diabetes.

Furthermore, they point out that because increased bodyweight is a much weaker risk factor for coronary heart disease than for diabetes, it is readily counterbalanced by improvements in the major coronary risk factors. This, they believe, could lead to the uncoupling of trends in type 2 diabetes and coronary heart disease.

Although I think their assumption may be correct, I believe we have still not seen the full effect of the epidemic of obesity and diabetes on the prevalence of chronic lifestyle-related disease such as cardiovascular disease, cancer and dementia.

While they suggest that changes in emphasis are needed in nutritional recommendations, they believe that reduction of saturated fats and replacement of refined grains with fiber-rich whole grains should remain central to dietary advice,

Finally, they believe that a reduction in consumption of free sugars is important to reduce total energy consumption, and they emphasize that restricting consumption of manufactured energy-dense food and reducing portion size are important.

Saturated Fatty Acid Enthusiasts and Traditionalists

The other paper, written by Dariush Mozaffarian from Boston MA, USA, is entitled “Diverging global trends in heart disease and type 2 diabetes: the role of carbohydrates and saturated fats”.

Mozaffarian addresses the subject in a different manner by taking into account recent studies on the risk associated with saturated fat intake as well as evidence suggesting that focusing entirely on the role of energy intake could be misleading.

He claims that foods rich in refined starches and sugars are the primary culprits for obesity and type 2 diabetes. He writes:

To blame dietary fat or even all calories, is incorrect. Although any calorie is energetically equivalent for short-term weight loss, a food’s long-term obesogenicity is modified by its complex effects on satiety, glucose-insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure.

Mozaffarian explains two opposing schools of thought when it comes to defining the role of saturated fatty acids (SFAs).

He writes: “SFA enthusiasts deem all previous nutritional evidence to be erroneous, recommending meat-and-butter rich so-called paleo diets as a route to good health.”

On the other hand, SFA traditionalists, Mozaffarian writes, “uphold the conventional paradigm that because SFAs raise LDL cholesterol, a causal risk factor for coronary heart disease, SFAs must be an important cause of coronary heart disease.”

Mozaffarian thinks both schools are wrong. He writes: “Unsurprisingly, each viewpoint is extreme, simplistic and inconsistent with the full body of contemporary evidence”.

He highlights the fact that SFAs are a heterogeneous group. Some, like palmitic acid, may have adverse metabolic effects whereas other may have metabolic benefits (3). Furthermore, SFA’s in blood and tissues are often synthesized from dietary carbohydrates.

He also points out that SFAs are obtained from foods that have ingredients that may modify its health effects. Therefore, “judging the long-term health effects of foods or diet based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations.”

He concludes: “To summarize, these lines of evidence – no influence on apolipoprotein b, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources – provide powerful and consistent evidence for absence of appreciable harms of SFA’s.

Although Mozaffarian believes a reduction in consumption of starchy and sugary foods is important to reduce obesity and type 2 diabetes, he seems to write off the possibility that a radical restriction in carbohydrate consumption may be helpful.

Declining in Mortality from Coronary Heart Disease – The Role of Saturated Fats?

Although the incidence and mortality from coronary artery disease have declined, it is important to understand that the burden of the disease remains high. This is partly due to the aging of the population and the fact that people with heart disease have a better prognosis than before.

Evidence suggests that the decline in mortality from coronary heart disease seen in most western countries is due to reduction in important risk factors such as smoking, high blood pressure and blood cholesterol as well as improved medical treatments.

SFA traditionalists like Mann and colleagues usually point out that lowering of blood cholesterol has played a major role in reducing the prevalence and mortality from coronary heart disease. Furthermore, they assume that the lowering of blood cholesterol has been achieved by reducing the amount of SFA’s and trans fat in our diet.

However, Dariush Mozaffarian points out that “changes in dietary fats simply cannot explain most of the reductions in blood cholesterol in most western countries.” He cites evidence showing that “whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France (4).

Furthermore, Mozaffarian points out that ” a common mistake made by SFA traditionalists is to consider only slices of data – for example , effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trend; and expedient nutrient contrasts.”
Less Heart Disease Despite More Diabetes; The Role of Diet

The Low Carb Denialists

The first thing that comes to mind when reading Mann’s and Mozaffarian’s viewpoints is their striking disagreement on the role of saturated fats and the importance of LDL cholesterol. Their different interpretation of the medical literature in this particular area is bewildering.

Otherwise, they seem to agree on the basic elements of a diet that is likely to positively affect both heart disease and diabetes, favoring fruits, non-starchy vegetables, nuts, yogurt, fish, vegetable oils and whole grains.

Although they believe that free sugars and processed carbohydrates should be minimized they still claim that a diet with a relatively high amount of carbohydrates is the one best suited to address the epidemic of obesity and diabetes.

Unfortunately, their approach to the possible usefulness of carbohydrate restriction is arrogant and condescending.

In a large study published last week on the trends in diabetes among US adults the prevalence of prediabetes was 37% to 38% in the overall population, and consequently 49% to 52% of the population was estimated to have either diabetes or prediabetes (5). Without intervention, prediabetes is likely to become type 2 diabetes in 10 years or less (6).

Most of the increase in diabetes is due to an increase in obesity.

The seriousness of diabetes requires that we evaluate all of the evidence that is available (7). However, both Mann and Mozaffarian completely disregard data supporting the usefulness of intensive carbohydrate restriction in people with established insulin resistance or metabolic syndrome (8, 9, 1011). Low-carbohydrate diets tend to lead to more weight loss, less insulin resistance, lower levels of triglyceride-rich lipoproteins, and higher levels of HDL-cholesterol.

The Bottom-Line

During the last few decades, health authorities, together with the food industry have managed to create an obesogenic environment that will have disastrous consequences for public health.

Although the incidence and mortality from coronary heart disease have declined significantly, the burden of disease remains high.

But, while the experts disagree on the culprits, solutions may be hard to find.

Firstly, we must understand the complexity of the situation and abstain from extreme and simplistic viewpoints.

Although we certainly bought the cholesterol hypothesis easily from the beginning, we have to abandon the belief that it can explain everything.

We have to stop putting all the blame on dietary fats, calories and lack of exercise.

The seriousness of the diabetes epidemic does not allow us to refute contradictory evidence for the sake of preconceived notions.



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