Diabetes: the new panorama
There are some key facts crucial to an understanding of the current situation. WHO definitions of obesity reveal some of them. To date, obesity worldwide has more than doubled since 1980. In 2014, more than 1.9 billion (39% of the population) adults were overweight. Of these over 600 million (13%) were obese. 42 million children under the age of 5 were overweight or obese in 2013.
These numbers are of very great concern, sufficient to consider obesity an epidemic, which should be treated as an international emergency for many reasons. Firstly, most of the world’s population live in countries where excessive weight and obesity kill more people than malnutrition. Secondly, the cost of these illnesses will be “astronomical” according to Marion Nestle, PhD, MPH, and Chair of the Department of Nutrition and Food Studies at New York University. Unfortunately our current solutions to this huge health problem are not even close to helping cure or avoid complications in any of those patients. And one of the easiest ways of understanding why our strategies are so ineffective is to examine what causes obesity according to the WHO. They report that the “fundamental cause of obesity is an energy imbalance between calories consumed and calories expended. There has been a worldwide increase in intake of energy-dense foods that are high in fat, and an increase in physical inactivity due to the increasingly sedentary nature of many forms of work, changing modes of transportation and increasing urbanisation”. We would judge that it is now absolutely clear that obesity is due to an imbalance between food consumed and energy expended. Thanks to Robert H. Lustig (M.D. Professor of Pediatrics in the Division of Endocrinology at University of California, San Francisco, and Director of the Weight Assessment for Teen and Child Health (WATCH) Program at UCSF) it is clear that the concept of calories is wrong and cannot single-handedly explain obesity. It is also clear that the increased intake of energy-dense foods that are high in fat is not solely responsible for the obesity epidemic. We will examine here what seems to be the real culprit. R. Lustig explained it well when he said that “the problem in obesity is not excess weight, the problem with obesity is that the brain is not seeing the excess weight”.
Significantly, one person dies every 6 seconds from type 2 diabetes on the planet and we have seen an increase from 30 million diabetic people in the 1980’s to 415 million people today. Worldwide approximately 1 in 10 adults has type 2 diabetes mellitus. In the United States 29 million adults (1 in 11) have type 2 diabetes mellitus and another 86 million (over 1 in 3) have prediabetes. Put simply, approximately 40 % of US adults already have some degree of insulin resistance. Last November 14th was the World Diabetes Day which WHO wanted to use as an opportunity to promote efforts to prevent diabetes and ensure optimal disease management. But surprisingly sugar is still not a target in any of the plans to fight diabetes.
Fat or sugar?
Nutrition is one of the most significant fields where patient behaviours are central, as patients carry out their own purchase and consumption of food. As a result they need to take responsibility and so need to be able to understand all the ins and outs about food.
We have already explained elsewhere (1) why fat has long been considered the culprit for what is known as the metabolic disease and we will now explain why and how it has destroyed perfectly good food habits and ended up in what we may well consider as the worst food epidemic ever known.
For well-known reasons given elsewhere, fat has been removed from our food. The main subsequent problem was that low fat food is not palatable, so changes had to be made to make the low-fat food into something more appealing. For equally well-known reasons sugar was the cheapest and easiest substitute. It is a very cheap solution, palatable, and with the additional factor that it triggers a very strong reward response in the brain, resulting in an addiction leading to increased purchase. As R. Lustig said “Sugar is cheap, sugar tastes good, sugar sells, so companies will have little incentive to change.”
We would now like to set out why sugar is the culprit and not fat. The main reason is that your body fat also called endogenous fat is not made from exogenous fat but exogenous sugar. In other words the sugar you eat makes you fat.
Considering that today added sugars are consumed in excess by a majority of the population it is essential to explain here the effects of those sugars on our metabolism. As we stated in our previous paper (2) fructose is the only sugar we should focus on. From an evolutionary standpoint fructose was present in fruits to confer a survival advantage (in the event of famine or for the winter period). Our overconsumption of it is now killing us.
Metabolism of Sugars
We will now discuss the various stages of fructose metabolism to understand why overconsumption is the main reason for our general metabolic disturbance leading to obesity and diabetes, sometimes referred to as insulin resistance syndrome.
The first action of the metabolism pathway is absorption. As soon as you eat food containing fructose as an added sugar or the simple monosaccharide present in fruits, it is absorbed by a specific transporter in your jejunum (Glut5) and then taken up by your liver. It is important to note that this absorption process has a threshold and that this absorption is also facilitated if fructose is ingested with glucose (which is the case with most added sugars such as HFCS: High Fructose Corn Syrup).
Fructose is metabolised in the liver. It is also important to note that only a very small amount of fructose is transported in your blood for distribution to other organs. This is the reason why we do not measure the fructose concentration in your blood as we do for glucose (glycemia) for example. (Glycemia 5.5 mmol/l VS fructosemia 0.01 mmol/l) Other organs like the kidneys, muscles, adipose tissue and brain cells can express Glut5 and therefore can make use of fructose from the blood but as the concentration of fructose in the blood is so low, the metabolism in the periphery is very poor.
In the liver, fructose follows a very well known pathway avoiding the main control steps of glycolysis (breaking down of sugar mechanism). In the interests of simplicity you should understand that this mechanism is an enzymatic process by which we transform a sugar (glucose or fructose) into a metabolic product that will be used to produce energy.
Concerning glucose this enzymatic chain reaction is tightly controlled and certain enzymes are regulated mostly by the energy status of the liver (if we need energy the enzymes are free to work as much as required as they have a substrate breaking down glucose into a metabolic product and then ATP [adenosine triphosphate] )
With fructose the control steps are absent, which means that if there is a substrate (fructose) then we will have a chain reaction and production of the metabolic product. The reason why the control process is non-existent is clear, during evolution we needed to make extra fat out of the ingested fructose in order to have reserves of energy to be able to survive in periods when food was scarce (winter/ famine).
Metabolic products of this chain reactions are dihydroxyacetone phosphate and glyceraldehyde 3-phosphate (DHAP, GA-3P). After the glycolysis is simple, it can either continue into the citric acid cycle in the mitochondria, the anaerobic lactic acid formation, “de novo lipogenesis” pathway or undergo gluconeogenesis to form glucose.
To simplify, we can either make energy for immediate usage as ATP molecules or synthesise lipids in order to store it and use it later depending on the energy state of the body. For instance any organism in a low energy state ( sedentary humans) will prefer de novo lipogenesis because there mitochondria are not working, and they don’t need so much ATP molecules.
Now that we understand the theory let’s see what happens in practice when we consume sugar in our diet.
After fasting if we haven’t eaten for a long time, 50% of the fructose will be transformed into glucose, a process needed to control glycemia and to distribute glucose to the other organs in order to deliver a substrate for energy formation.
In the present set up of over and continuous consumption of sugar – which is the case most of the time since we eat too often during the day and most of our food contains added sugars – fructose now goes into the de novo lipogenesis pathway in order to make fat. As explained earlier this pathway is not regulated so the more fructose you consume the more fat is produced via non regulated de novo lipogenesis. The greater potential of fructose to stimulate de novo lipogenesis is the main reason why it has been portrayed as particularly harmful.
The fat accumulated in the liver causes hepatic disturbances and global insulin resistance leading to decreased hepatic function and diabetes. It has been shown that a hypercaloric state rather than macronutrient composition is significant for the accumulation of lipids in the liver meaning that too much sugar as added sugars or carbohydrates induces accumulation of fat in the liver leading to NAFLD (nonalcoholic fatty liver disease an alarming twin epidemy with central obesity or T2D.).
After this long metabolic explanation it is time to propose solutions in order to help you fight against obesity and diabetes.
One of the first pieces of advice is straightforward: you should cut down your intake of added sugars in order to reduce the amount of sugar you are eating.
As we explained previously (2), most of the sugar in your food is usually added and hidden. As you probably remember we listed almost 40 different names for added sugar, which makes it more complicated for you to read and understand exactly which ingredients are sugars. One of the simplest ways to avoid sugar is to not buy processed food and make the effort to eat mainly whole fresh foods. One of the most recurrent FAQ is whether you can eat fruit because of the presence of fructose. Remember that the concentration of fructose in a peach is nothing compared to the quantity of added fructose in processed food. So it is absolutely ok to eat fruits.
Secondly you should introduce fat into your diet; raw fats are healthy and won’t make you fat!
This is the most important point in our discussion, and we will try to explain why fat does not make you fat and does not increase your cardiovascular risk.
First it is really hard to over-eat fat because fat is very satiating. The best way for you to understand it is to try to eat raw fat like butter without any bread (you will have a normal, rapid, instinctive stop reflex). Eating fat in a low carbohydrate diet makes it easier to access fat for energy (2). To sum up, you will eat less and make your fat storage more accessible for fat burning so you might even lose weight.
The second important point is to understand that the fat you are eating (called exogenous fat) is not the exact same fat you will find in your arteries. It first has to be digested and absorbed then made soluble in the form of chylomicrons and eventually transported in the blood to the different organs. From there several factors are to be taken into consideration to evaluate the cardiovascular risk. If your inflammatory status is elevated (a consequence of over consumption of carbohydrates and sugar, stress, cigarette smoking and obesity) the odds are high for you ending up with oxidized LDL that will have to be removed from the artery and therefore enters the wall of your artery forming atherosclerotic plaques. Eating fat will not increase your LDL particles; instead it will increase your total cholesterol and HDL.
In conclusion, you should remember that you have the opportunity to decide whether you will eat it or not despite hacking of your brain. Deciding not to buy is deciding not to eat. If you quit your soda habit, the sugar in your morning coffee, your bread addiction and start eating more unprocessed fats (butter, olive oil, animal fats), your health will improve rapidly.
by Alexandre Jean Pelouze MD, Surgery resident, Geneva University Hospital, Geneva Switzerland, and Guy-André Pelouze MD, Thoracic and cardiovascular surgeon, St John’s hospital, Perpignan, France.
References:
1. Fats: an inaccurate hypothesis
Guy-André Pelouze, Global oils and fats, Vol 13 issue 2 (Apr-Jun) 2016, 8-11
3. Journal of Nutrition and Metabolism, Volume 2015 (2015), http://dx.doi.org/10.1155/2015/823081
Fructose Metabolism and Relation to Atherosclerosis, Type 2 Diabetes, and Obesity, Astrid Kolderup and Birger Svihus