Fructose vs. High-Fructose: The Metabolic Difference Fruit and Concentrated Fructose
This post is mostly summarizing and citing from an interesting clinical research study I read published in February 2018 called The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids. The article can be obtained for free if you have an institutional or student login for most colleges and universities. If you are interested in the research of this topic, I highly recommend that you pick up the article as it is fascinating and more in depth than what I will be discussing here. For those of you who don’t delve past the abstract because you are afraid of getting a little too much science on your hands, that is fine too. I know scientific literature can be dry and daunting to read, so I will give you a little context and provide you with what, in my opinion, this study means big picture and how you can put this information into practice.
Glucose, fructose and fructose on crack (A.K.A. high-fructose)
Glucose is the primary fuel for the human body. Yes, being metabolically flexible (being able to use substrates like ketones for fuel) is a thing, but in normal physiology the body takes the food we eat and turns directly or indirectly into glucose. Glucose and fructose are chemically very similar. Glucose by itself is not sweet (like a potato, which has many grams of carbohydrate yet almost no fructose), but when you combine glucose with fructose you get what we traditionally call table sugar. Fructose is found in sweet carbohydrate foods like fruits, some grains, and to a lesser extent, some vegetables.
High-fructose has long been villainized, but many of us haven’t been able to give an articulate answer about whether and why concentrated levels of fructose differs from fructose naturally occurring in fruits. Apart from the desire to limit concentrated sweets, the argument has been incomplete at best. We have traditionally thought that fructose is metabolized by the liver (which it is to some extent) unlike glucose which enters the bloodstream where it metabolized at various body sites. The metabolism of excessive fructose at the liver can increase the chance of developing non-alcoholic fatty liver disease and it also directly results in the synthesis of triglycerides. Elevated triglycerides contributes to increased risk of heart disease, metabolic disease and degenerative brain diseases. Now, the problem with this model is that fruit and high-fructose corn syrup are theoretically metabolized identically in the body. So, whether you are eating a bowl of grapes or a Snickers bar you will be elevating your triglycerides and possibly causing irreversible damage to your liver.
Fructose Metabolism Revisited
This study used isotope tracers and metabolomics to examine the extent to which other organs assist in the metabolism of fructose. The research trial was done on mice, but the implications are important and aid in our understand of fructose metabolism in humans. These researchers found that in small doses, the small intestine was able to metabolize the blunt of ingested fructose, shielding the liver from fructose exposure. High doses of fructose overwhelm the shielding capacity of the small intestine which results in fructose toxicity in the liver. They also found that intestinal clearance of fructose is enhanced both by prior introduction of fructose, and by being in the fed state. The intestinal adaptions that yielded increase fructose metabolism from prior fructose exposure were reversible by removing the stimuli (fructose exposure).
What This Means
- Normal physiological doses of fructose can be almost entirely metabolized by the small intestine
- Large doses of fructose like that found in sugar sweetened foods or those sweetened with high-fructose overload the small intestine and must be metabolized in the liver
- Frequent over-consumption of fructose in supraphysiological doses is linked to toxicity in the liver and liver disease of which mechanism is not entirely known
- Consumption of normal physiological doses of fructose can improve intestinal clearance
What This Means in the Real World
- Fruit is metabolized differently than concentrated sweeteners and foods contain high-fructose, meaning that fruit can be consumed without posing the same inherent risks
- By eating fruit moderately and regularly you may be able to improve intestinal absorption and therefore decrease metabolic load delivered to the liver
- Eating fruit after or along with a meal may improve intestinal absorption
- Eating several pieces of fruit over the course of the day is much less likely to saturate the intestinal capacity to metabolize fructose than an exceedingly large portion of fruit at one sitting or concentrated sweeteners (whether sugar or fructose based)
- Sweetening foods with dates, honey, maple syrup or agave is not necessarily healthier if you are consuming them in excess. Note that agave is essentially all fructose and should be avoided as any high-fructose sweetener, even considering it is naturally occurring.
Moral of the story: Have your fruit and eat it too, just not too much.