How the low fat obsession enabled the obesity epidemic

02/11/2018 How the low-fat obsession enabled the obesity epidemic
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- Article of the week -
How the low-fat obsession
enabled the obesity
epidemic
By Guy-André Pelouze & Alexandre Pelouze - 22.01.2018
Diabetes: the new panorama
There are some key facts crucial to an understanding of the current situation.
WHO de nitions 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
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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, suf cient 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”.
Signi cantly, 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
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prediabetes. Put simply, approximately 40 % of US adults already have some
degree of insulin resistance. Last November 14 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 ght diabetes.
Fat or sugar?
Nutrition is one of the most signi cant elds 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.
th
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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 rst 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 speci c 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
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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.
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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
signi cant 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 ght against obesity and diabetes.
One of the rst 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!
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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 re ex). 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 nd in your arteries. It rst
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 in ammatory 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:
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1. Fats: an inaccurate hypothesis
Guy-André Pelouze, Global oils and fats, Vol 13 issue 2 (Apr-Jun) 2016, 8-11
2. https://www.contexte.com/article/article/added-sugar-rather-than-fat-
endangers-public-health_42969.html
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
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cardiovascular risk diabetes diet Fat obesity sugar
GUY-ANDRÉ PELOUZE & ALEXANDRE PELOUZE
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How the low fat obsession enabled the obesity epidemic