02 Feb 2018 Sugar Does NOT Cause Inflammation (Part 1)
The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.
Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”
But sugar is about as far from a poison as you can get.
There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.
Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.
But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.
Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.
In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.
I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.
What is inflammation and why does it matter?
Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.
It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.
So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.
This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:
- We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
- We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats
Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.
But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.
So how does sugar fit into all of this?
Before we talk about that, let’s first clarify what sugar is.
What is Sugar?
White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.
This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.
When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.
On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.
I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”
While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.
The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.
Sugar and inflammation
As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.
The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.
Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.
Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.
Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).
But, when you feed the liver extra fructose, a couple remarkable things happen:
- It increases the amount of fructose it burns (2).
- It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.
I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!
But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.
This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.
But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.
And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.
Some concluding thoughts
Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”
It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.
We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)
This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.
This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.
Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.
That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”
In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.
- Wang, Zimian, et al. “Specific metabolic rates of major organs and tissues across adulthood: Evaluation by mechanistic model of resting energy expenditure.” The American journal of clinical nutrition, 92, no. 6, 2010, pp. 1369–77. doi:10.3945/ajcn.2010.29885.
- Delarue, J., et al. “The contribution of naturally labelled 13C fructose to glucose appearance in humans.” Diabetologia, 36, no. 4, 1993, pp. 338–45.
- Schwarz, J. M., et al. “Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection.” The Journal of clinical investigation, 96, no. 6, 1995, pp. 2735–43. doi:10.1172/JCI118342.
- Acheson, K. J., et al. “Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man.” The American journal of clinical nutrition, 48, no. 2, 1988, pp. 240–47.