Is Sugar Fattening?
The debate we all recognize and the first instalment of our “12 days of Christmas Nutrition” series, sees us explore the pitiful argument that sugar is inherently fattening.
Since the 1970s, the war on sugar has gained significant traction and with each preceding decade the polarization of sugar has amplified.
Sugar has been implicated in having a role in the epidemic of cardiometabolic diseases and has been rivalled against fat as one of the primary causes of cardiovascular disease. Additionally, sugar is widely purported to be “fattening” and the true cause of weight gain, but is this really the truth?
As a result of these narrow viewpoints, we are sadly at a point where sugar and sugar demonization is becoming normalized. This further feeds into the ever worsening issue of disordered eating. Something needs to change.
So the question on the tip of the tongue is, is sugar fattening?
First off and as with every article written, context must be provided. Let’s begin with a little background information on sugar!
Sugar (the devil’s dust as some call it), otherwise known as a saccharide, is part of the carbohydrate family. Carbohydrate is an energy containing macronutrient that is built on carbon, hydrogen and oxygen. Each gram of substrate contains 4 kcal/Calories.
Carbohydrates are classified according to the amount of saccharides that are present in each.
Monosaccharides are individual saccharides, of which there are three (glucose, fructose and galactose), and each have a very similar chemical structure. Disaccharides are combinations of two monosaccharides, again of which there are three (sucrose, lactose and maltose). Together, these mono and disaccharides are known as the “simple sugars”.
Simple sugars are found in fruits, fruit juices, honey, maple syrup, sports drinks, sugar sweetened beverages, table sugar, sweets/candy, baked goods, jams, chocolates etc. The tasty stuff.
Oligosaccharides are combinations of 3 to 9 saccharides (found in most fruits and vegetables) while combinations of 10+ saccharides are known as polysaccharides, poly meaning many. Polysaccharides are commonly referred to as complex carbohydrates. Complex carbohydrates (starches & fibers) are found in fruits, vegetables, breads, rice, pasta, oats dried beans and peas, cereals and whole grains/brown versions. These are the more boring foods but these typically contain more abundant promoting nutrients like fiber, vitamins, minerals and phytochemicals.
When it comes to the argument about sugars, it is the simple sugars that are center of the argument.
But not all simple sugars, mainly “free sugars” (simple sugars) which are added to a food product and especially fructose containing foods.
To be quite honest, the basis of the argument against fructose can seem very plausible and easily believed (hence why the viewpoint exists). The argument that sugar itself is fattening holds no basis. When the evidence is examined and a basic understanding of the principle of energy balance is held this all becomes clearer.
First off, let’s assess the assumption that fructose is fattening. Fructose, unlike glucose, bypasses the rate-limiting step in glycolysis and is indicated to act as an unregulated metabolic de novo substrate for fatty acid synthesis in the liver. Fructose can only be metabolized by the liver. Glucose on the other hand can be metabolized by both the liver and muscle. Secondly, there is the carbohydrate-insulin hypothesis which explores the notion that carbohydrate intake drives weight gain as a result of the increase in insulin secretion which drives a partitioning of energy to favor fat storage.
While both sound-like promising arguments, in substitution trials, markers of non-alcoholic fatty liver disease showed no adverse effects with varying levels of fructose intakes, ranging from 22.5g per day to 300g per day in isocaloric conditions (Chiu et al., 2014). Isocaloric conditions refer to where equal calories are consumed in each condition but with varying amounts of sugar.
Additionally, in similar trials, there were no adverse effects on body weight (Sievenpiper et al., 2012) using isocaloric conditions with varying sugar intakes.
Meta-analysis of randomized controlled studies have shown to refute both claims (Te Morenga et al., 2013; Khan et al., 2016).
If sugar intake is not the primary cause of weight gain, then what is?
The evidence repeatedly points towards the fact that excess energy consumption and the resulting positive energy balance is the cause of weight gain, not unique metabolic effects of sugar.
If sugar is not the direct cause, can it be an indirect cause of weight gain? This is certainly plausible, but again nuanced, as diet alone is not the only confounding variable when it comes to weight gain. Nonetheless, let’s discuss these valuable points.
The first hypothesis points towards the inability of fructose to stimulate insulin or leptin while it also does not suppress ghrelin (the hunger hormone). The impact of this is an impaired satiety. But this can’t possibly explain weight gain as weight gain is a result of energy intake greater than expenditure. What it does point towards though is the fact that satiety is negatively impacted upon which can influence the amount of energy consumed and the frequency of eating. This has the ability to drive total energy intake to a calorie surplus, leading to weight gain.
Another theory that states fructose intake can lead to weight gain is that it stimulates the regions in the brain associated with the regulation of food intake and rewards differently when compared to glucose. Again this is similar to the former point, it is only an indirect link to weight gain. It is a state of viewing food as a reward and thus increasing exergy intake as a result of the heightened desire to eat.
The final theory relates to food hedonics and that overconsumption of sugar is due to its addictiveness. This idea that sugar is addictive is wildly inaccurate. If sugar was addictive people would be snorting lines of sugar for at every opportunity and people would be walking around with withdrawal symptoms, begging for a fix. This is not the case.
Sugar is rapidly digested and absorbed when compared to complex carbohydrate sources. Sugar is highly palatable (tasty as f*ck) and this combination makes it extremely easy to overeat. Sugar is not a satiating food and it does not satisfy hunger to the same extent as complex carbohydrates or other satiating foods like protein sources such as chicken. Again, all this means is that energy intakes can easily be increased and weight gain is possible when diet quality is lower.
So there you have it. Sugar itself cannot be blamed for weight gain.
It needs to be explicitly clear that individual foods or lifestyle choices do not exist in isolation. Analyzing one food in isolation is not adequate for determining whether or not they are the cause of weight gain, the same goes for behaviors. It can show a relationship but not a cause. Weight gain is a result of a disruption of energy balance (EB = Ei – Eo) whereby energy intakes exceed energy expenditures creating a net positive energy balance.
Lifestyle patterns and dietary patterns are major determinants of intakes and expenditures, and individual foods should not be demonized or blamed for such a complex topic. This black and white thinking is sure fire way to disordered eating behaviors.
Chiu S, Sievenpiper JL, de Souza RJ, Cozma AI, Mirrahimi A, Carleton AJ, Ha V, Di Buono M, Jenkins AL, Leiter LA, Wolever TMS, Don-Wauchope AC, Beyene J, Kendall CWC, Jenkins DJA (2014) Effect of fructose on markers of non- alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials. Eur J Clin Nutr 68(4):416–423.
Khan, T. and Sievenpiper, J., 2016. Controversies about sugars: results from systematic reviews and meta-analyses on obesity, cardiometabolic disease and diabetes. European Journal of Nutrition, 55(S2), pp.25-43.
Te Morenga, L., Mallard, S. and Mann, J., 2012. Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ, 346(jan15 3), pp.e7492-e7492.
Sievenpiper JL, Chiavaroli L, de Souza RJ, Mirrahimi A, Cozma AI, Ha V, Wang DD, Yu ME, Carleton AJ, Beyene J, Di Buono M, Jenkins AL, Leiter LA, Wolever TMS, Kendall CWC, Jen- kins DJA (2012) ‘Catalytic’ doses of fructose may benefit gly- caemic control without harming cardiometabolic risk factors: a small meta-analysis of randomised controlled feeding trials. Br J Nutr 108(3):418–423.