My passion is medicine – without drugs. I believe that the diseases so prevalent today, like diabetes, high blood pressure, high cholesterol and the complications thereof such as heart disease and strokes, are simply diseases of civilisation (bar those of purely genetic origin). We have created these plagues on our bodies simply by the way we live – they were unheard of in indigenous populations, not because of failure to diagnose but more likely because they did not plague those people.
But why? That is the question I am hoping to explore in this post. I credit the information to Gary Taubes and the research he carried out in writing ‘Good Calories, Bad Calories: Fat, Carbs, and the Controversial Science of Diet and Health’. Many of my blog posts to follow will be based upon this book – I have certainly challenged the education I have received at medical school through reading this book, and I hope to share with you some of this insight. Perhaps one day doctors may be following somewhat different guidelines…
So what is cholesterol and what of it is detrimental to optimal health? Cholesterol is only one of the fatty substances circulating through our blood; triglycerides is another. Both are carried by molecules called lipoproteins – the amount carried varies between lipoproteins. You may have heard of LDL and HDL, which get measured when you get a full lipogram at the doctor – these stand for low density lipoprotein and high density lipoprotein. The third is called VLDL or very low density lipoprotein. Cholesterol is mostly carried by LDL and triglycerides by VLDL.
So how is it that LDL came to be known as “bad” and HDL as “good”? A physician and chemist named Gofman in 1950 used a fancy instrument to measure the density of lipoproteins. Through his research he found that LDL was more numerous in patients with atherosclerosis (fatty plaques that can cause heart disease) than healthy subjects; however, he noted that the LDL did not reflect consistently how much cholesterol was actually in the blood. Thus, he proposed that lipoproteins are more important in heart disease than cholesterol itself. Unfortunately, in the meanwhile, a national council started funding research to replicate Gofman’s hypothesis – these groups already had difficulty with the technique and instrumentation that Gofman used, and thus when Gofman wanted to update the technique to prove that lipoproteins were the important factor, the groups did not want to accept any modifications. And so, in 1956, the research report published stated that cholesterol was a predictor of heart disease and that lipoproteins were too complex to be reliably measured and added little predictive power. Meanwhile, Gofman’s subsequent research with better techniques showed that LDL and VLDL were good predictors of heart disease, with the best predictor being the sum of these two classes. Nevertheless, due to funding and politics, the former majority opinion prevailed.
Gofman had showed that it was actually carbohydrates that elevated VLDL, and not fat. Saturated fats elevated LDL. Another researcher at the time, Ahrens, observed Gorman’s findings through blood samples: the milky white plasma from subjects on a high carbohydrate diet, versus the clear plasma from those on high fat diets or alternatively just low calorie diets (which explains the often low total cholesterol levels in Asian populations). Further research by a young physician named Albrink concluded that elevated triglyceride levels were far more common in heart disease patients than high cholesterol. However, again due to measuring difficulties and funding commitments, these hypotheses were not accepted by the greater medical community.
In 1967, the National Institute of Health funded large scale research to test the hypothesis. A decade later, the prospective data confirmed Gofman’s original hypothesis that “total cholesterol per se is not a risk factor for coronary heart disease at all”, that LDL is a marginal risk factor, and that triglycerides were a significant predictor of heart disease. The report also confirmed a new revelation: that HDL is inversely related to the risk of heart disease, and this lipoprotein had the largest impact of them all. The key was that things that raised HDL lowered triglycerides, most notably a low carbohydrate intake.
But somehow, these findings were not committed further to clinical trials and thus got dismissed by ignorant institutions that were already pouring money into research dedicated to the proposition that total cholesterol predicted heart disease. Furthermore, around the same time as the results were published, so were the Dietary Goals, which advocated a low-fat diet to reduce not only LDL, but now also VLDL as well as raise HDL – which is false. But what was the ideal recommendation really? Considering that carbohydrates were the devil for HDL and saturated fats the devil for LDL. In 1985, Grundy and Mattson provided the ideal compromise: monounsaturated fats, which both lower LDL and raise HDL (ironically, monounsaturated fats are the principal fat in red meat, eggs, and bacon).
The 80’s also revealed a new concept surrounding LDL: the size of the LDL varies depending on how much triglycerides and cholesterol it contains – the more it contains the larger and fluffier it is. Small, dense LDL is more likely to find its way through blood vessel walls, become oxidised, and cause plaques. A lipid metabolism specialist Krauss discovered through his research that the lower the fat and higher the carbohydrate, the smaller and denser the LDL; and that the higher the saturated fat, the larger and fluffier the LDL (rather than an increase in number). In addition, as VLDL is a precursor to LDL, any factor that increases VLDL (i.e. high carbohydrate diets) results in an increase in LDL in small, dense form.
In summary then, the most important factors to look out for with regards to the risk of heart disease are triglycerides and HDL. To achieve this, the evidence (not the guidelines) suggests a diet low in carbohydrates and high in monounsaturated fats. Saturated fats, previously demonised, have been shown to result in large fluffy LDL particles, the ones less likely to be atherogenic. So really, the guidelines we have all been taught (at medical school too!) is less based upon science than it is upon which research was funded more intensely… time to rethink? I think so.