I was lucky. My mentors were great. I went to all the big cardiology conferences. I read the best books and I learned from the great masters.
Early on, I was taught the fairly well established relationship between blood cholesterol and coronary heart disease.
The message to our patients was very clear; lowering blood cholesterol is the main target. It can be achieved by reducing fat intake, avoiding dietary cholesterol and replacing saturated fat with polyunsaturated fatty acids and complex carbohydrates.
But I wonder why we didn’t ask more questions. Why didn’t we request more data? Cardiologists are very research-oriented and usually claim scientific proof for everything.
Was our belief in the diet-heart hypothesis so strong that we didn’t need studies to confirm that our dietary advice would be of benefit?
The Warning Signs
Of course, there were those who warned that we might be on the wrong trail.
In 1977, Dr. George V. Mann wrote in The New England Journal of Medicine: “A GENERATION of research on the diet-heart question has ended in disarray (1)”. Mann later wrote a book called Coronary Heart Disease: The Dietary Sense and Nonsense – An Evaluation by Scientists. His book understandably evoked mixed emotions (2).
Mann’s book contained the views of members of the Veritas Society, who in November 1991 met to voice their objections to the diet-heart hypothesis, which they believed was “based upon fragile and selected data.” The society called “for a return to scientific and informational honesty.”
Mann wrote in the preface to his book that “the regulatory agencies have been derelict in their duties, allowing fraudulent health claims to continue in food and drug advertising.”
In 2001, journalist Gary Taubes highlighted the soft science behind the dietary fat hypothesis in a famous article published in Science (3).
US journalist Nina Teicholz took these arguments a step further in her book The Big Fat Surprise that was published 2014.
Uffe Ravnskog, a Danish doctor, has fought relentlessly for decades to convince the medical society that we were wrong about dietary fats and their proposed role in heart disease.
Of course, many physicians still believe that a low-fat diet is the best food choice, and the most effective one to reduce the risk of cardiovascular disease.
In fact, vegetarians appear to have low risk of cardiovascular disease. But nobody has proved it’s because they eat less fat and cholesterol. Vegetarians eat less sugar as well. Antioxidant compounds and polyphenols in fruit and vegetables—such as vitamin C, carotenoids, and flavonoids may be beneficial. Fruit and vegetables are good sources of magnesium and potassium, which have been inversely associated with mortality in previous studies.
In 1988 a small paper reported findings from a group of seven patients with food allergy and elevated serum cholesterol levels who were forced to follow a diet in which most of the calories came from beef fat (4). Their diets contained no sucrose, milk, or grains. During the study, their cholesterol and triglyceride levels decreased significantly, and levels of HDL cholesterol increased.
The investigators wrote:
These findings raise an interesting question: are elevated serum cholesterol levels caused in part not by eating animal fat (an extremely “old food”), but by some factor in grains, sucrose, or milk (“new foods”) that interferes with cholesterol metabolism?
Sadly, our delusive focus on dietary cholesterol and saturated fat dismisses a huge amount of scientific data suggesting that the effects of diet on cardiovascular health are mediated through many biologic pathways other than cholesterol, including oxidative stress, low-grade inflammation, insulin sensitivity, endothelial dysfunction and blood clotting mechanisms.
By claiming the diet-heart hypothesis is the sole key to our understanding of the role of diet in heart disease, medical professionals like myself have kept the lid on proper understanding of the role of the relationship between dietary factors and cardiovascular disease.
In his book, Pure, White and Deadly, published in 1972, UK doctor John Yudkin wrote:
One of my main reasons for taking up research in this field was that I became more and more uneasy about the prevalent simplistic view of how people get coronary disease – the idea that it is just a matter of cholesterol levels in the blood. This idea is now so firmly held by so very many people that they end up believing that anything that increases cholesterol in the blood is likely to cause coronary disease, anything that reduces cholesterol helps to prevent the disease or even cure it, and anything that does not invariably increase the cholesterol in the blood must have nothing whatever to do with the cause of heart disease. – I know I’m biased, but this picture – in my view a rather naive one, has hindered a proper understanding of its prevention.
Sugar and Heart Disease
Lately, we’ve seen epidemiological data suggesting that increased intake of sugar-sweetened beverages increases the risk for metabolic syndrome, type 2 diabetes, coronary heart disease, and stroke (5).
Human intervention studies have showed accumulation of fat in the liver, muscle, and the visceral fat depot induced by sugar sweetened beverages. Most of the studies support the fact that fructose is the main driver of these metabolic aberrations presumably by inducing lipid synthesis and fat release from the liver (6).
A large survey based on NHANES data and published in JAMA 2014 showed a significant relationship between added sugar consumption and risk for mortality from cardiovascular disease (7). The main findings were that individuals who reported more of their total calorie intake as added sugar did have a significantly increased risk of dying from cardiovascular disease.
Interestingly, Ancel Keys, the father of the dietary-heart hypothesis found an association between sucrose consumption and the risk of coronary heart disease but didn’t think it was an issue. As highlighted in Robert H. Lustig’s book Fat Chance, he believed high sucrose consumption was only a surrogate that correlated with high intake of saturated fat.
The fact that the incidence rate of coronary heart disease was significantly correlated with the average percentage of calories from sucrose in the diets is explained by the intercorrelation of sucrose with saturated fat.
A very recent paper published in the American Journal of Clinical Nutrition by US investigators addresses the link between sugar intake and cardiovascular risk factors (8). The study tested the effects of consuming beverages sweetened with different doses of high fructose corn syrup on blood lipids and uric acid in 187 adult participants.
The study found that blood levels of LDL-cholesterol, non-HDL cholesterol, and apolipoprotein B, postprandial triglycerides apoCIII and uric acid increased in a dose-dependent manner within two weeks following consumption of different doses of high-fructose corn syrup.
The authors believe their findings provide a plausible mechanistic link to the increased risk of death from cardiovascular disease associated with increased intake of added sugar.
In Pure White and Deadly, John Yudkin describes findings from several laboratories clearly showing that sugar in the diet increases plasma levels of cholesterol and triglycerides. Sugar consumption was also associated with a rise in insulin levels and increased stickiness of platelets that may increase the risk of blood clotting.
A very interesting finding from Yudkin’s studies was that a quarter or a third of their study subjects showed a special sensitivity to sugar while the remainder did not. These individuals showed more rise in insulin levels and they put on more weight than the others.
Yudkin suggested that it might be useful to screen for individuals who were “sucrose sensitive” because they might by at increased risk of coronary heart disease.
Another mechanism whereby sugar consumption may increase the risk of cardiovascular disease is through its effects on blood pressure.
It is well known that high blood pressure increases the risk for cardiovascular disease. Yudkin describes a study performed by Richard Ahrens from the US, who carried out an experiment with young men who were given diets containing varying amounts of sugar. Their blood pressure rose proportionally to the quantity of sugar in the diet.
Decades later, a meta-analysis of randomized controlled trials showed that high intake of sugar is associated with elevated blood pressure (9).
In a 2014 review paper in Open Heart BMJ Journals, the authors highlight that recommendations to reduce consumption of processed foods in order to reduce hypertension are highly appropriate and advisable. However, they propose that the benefits of such recommendations might have less to do with sodium and more to do with highly-refined carbohydrates (10).
The Bottom Line
High intake of sugar and refined carbohydrates is associated with increased risk of diabetes, metabolic syndrome, non-alcoholic fatty liver disease, lipid disorders and high blood pressure.
Recent findings showing an association between sugar consumption, fructose in particular, and the risk of cardiovascular disease suggest that we have to broaden our perspective in order to understand the relationship between dietary choices and cardiovascular disease.
For years, our overemphasis on the role of dietary fats and blood cholesterol has blurred our understanding of a multifactorial and much more complicated association between diet and heart disease.
Understandably, the medical community and public health authorities may have a hard time admitting their ingenuousness. Furthermore, considering all the commercial interests involved it may be guileless to think that honesty and belief in the scientific method will prevail.
However, let us remember Winston Churchill’s words
To improve is to change; to be perfect is to change often