刊行物
｜ ENGLISH ｜
Hemant Poudyal
Research over the past couple of decades has given scientific credence to an old English proverb “the way to a man's heart is through his stomach”. However, in our time, the “stomach way” usually leads to obesity, diabetes and a diseased heart in both men and women! The modern human diet is characterised by high amounts of refined sugars and fat and low amounts of vegetables and fruits (infamously called the cafeteria diet) which is thought to increase the risk of many chronic diseases including heart disease.
There are several hypothesis on how the cafeteria diet damages the heart. The most popular since the 1970s has been that nutritionally-poor, energy-dense diets primarily cause dyslipidaemia (increased cholesterol and triglycerides), obesity, and diabetes that ultimately leads to heart damage. As a young(er) researcher at the start of my Master’s degree research project almost a decade ago, this hypothesis raise many questions for me including:
1. Which components of the cafeteria diet (sugar, fat, or lack of fruits/vegetables) causes obesity and diabetes?
2. Can nutrients also directly damage the heart?
3. Does obesity and diabetes cause comparable damage to the heart?
My research during my Master’s degree and PhD naturally focused on the first question. I looked at the effects of different types of dietary fat in animal models and showed that not all fats induce heart damage but the ones that do almost always also promote obesity and diabetes. Further, adding fruits and vegetable to the cafeteria diet also prevented obesity, diabetes, and heart damage.
In my Hakubi project, I sought to explore the role of sugars in heart disease. Specifically, I looked at the effects of glucose and fructose, the two most common sugars in our diets, the latter being predominant in the cafeteria diet. These studies suggests that a fructose-rich diet does not promote obesity or diabetes, at least in the short-term, but still damages the heart, suggesting a direct action. In contrast, a glucose-rich diet promoted body fat storage but did not induce diabetes or heart damage. This result clarifies my first two questions, and I have now identified some of the specific dietary sugars and fats that cause obesity and diabetes. I have also found evidence that some of these nutrients may have a direct effect on the heart.
At the start of my Hakubi project, I had also started exploring my third question, which is quite controversial. I started monitoring heart structure and function in rats that are either obese or diabetic due to genetic predisposition but are consuming a balanced rodent diet. Preliminary results suggest that diabetes but not obesity caused extensive heart damage! This result supports recent paradoxical findings that obesity may even be protective for the heart and obese individuals have better survival in certain population groups such as the elderly (the obesity paradox).
There fore the generalisation that nutritionally-poor, energy-dense diets cause obesity and diabetes that ultimately leads to heart damage may not be accurate. We are now beginning to understand that specific nutrients within nutrient super-families of fats and sugars are unique and some may directly affect the heart independent of diabetes and obesity. Perhaps, it is time to consider dietary recommendation frameworks based on specific nutrients instead of the current nutrient super-family based framework. Also diabetes, irrespective of the diet, can cause heart damage. However, I am now developing two new questions that I aim to address in the next few years:
1. What is the mechanism for the direct effects of fructose?
2. Does obesity really increase the risk of heart diseases in humans?
Goto-Kakizaki (left) and Zucker Fatty (right)
rats-Models of diabetes and obesity-induced heart damage.
（へまんと ぽうどやる）
