09 Feb Sugar Does NOT Cause Inflammation (Part 2)
In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.
In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.
But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).
There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)
Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.
Research Shows That Sugar Causes Inflammation
In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.
These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.
For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.
Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).
But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.
And it’s more than just that.
The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:
- We’re not rats
- We have self-regulating sugar consumption mechanisms
- Sugar’s inflammatory effects require more than just sugar
Let’s break these reasons down one by one.
1. We’re not rats
Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.
Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.
For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.
Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).
But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.
Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).
In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.
2. We have self-regulating sugar consumption mechanisms
One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).
However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.
The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.
And guess what increases the energy of our livers and hypothalamus the most…
That’s right, sugar!
In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.
3. Sugar’s inflammatory effects require more than just sugar
One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.
When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).
Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.
So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.
The Sweet Truth About Inflammation
Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.
As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).
But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!
What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.
- Zhang, Dong-Mei, et al. “High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions.” Nutrients, 9, no. 4, 2017, doi:10.3390/nu9040335.
- Żelewski, Mateusz, and Julian Świerczyński. “Comparative studies on lipogenic enzyme activities in the liver of human and some animal species.” Comparative Biochemistry and Physiology Part B: Comparative Biochemistry, 95, no. 3, 1990, pp. 469–72. doi:10.1016/0305-0491(90)90004-D.
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- Shrago, Earl, et al. “Comparative aspects of lipogenesis in mammalian tissues.” Metabolism, 20, no. 1, 1971, pp. 54–62. doi:10.1016/0026-0495(71)90059-X.
- Hellerstein, M. K., et al. “Regulation of hepatic de novo lipogenesis in humans.” Annual review of nutrition, 16, 1996, pp. 523–57. doi:10.1146/annurev.nu.16.070196.002515.
- Hellerstein, M. K. “De novo lipogenesis in humans: Metabolic and regulatory aspects.” European journal of clinical nutrition, 53 Suppl 1, 1999, S53-65.
- Rippe, J. M., and T. J. Angelopoulos. “Sugars and Health Controversies: What Does the Science Say?” Advances in Nutrition: An International Review Journal, 6, no. 4, 2015, 493S-503S. doi:10.3945/an.114.007195.
- Tappy, Luc, and Kim-Anne Lê. “Metabolic effects of fructose and the worldwide increase in obesity.” Physiological reviews, 90, no. 1, 2010, pp. 23–46. doi:10.1152/physrev.00019.2009.
- Chiavaroli, Laura, et al. “Does Fructose Consumption Elicit a Dose-response Effect on Fasting Triglycerides? A Systematic Review and Meta-regression of Controlled Feeding Trials.” Canadian Journal of Diabetes, 36, no. 5, 2012, S37. doi:10.1016/j.jcjd.2012.07.330.
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