"A dangerous chemical, natural or unnatural, enters the blood through the skin, gut or lungs and travels to the liver, the primary organ of detoxification."
The liver attempts to "detoxify" the chemical creating metabolites — sometimes the metabolites are less toxic and sometimes they're not — in order to excrete the chemical and any remnants of it out of the body.
So for us to believe that fructose is a poison, it needs to follow, in some respects, the pathway I just described — and I'll get to that soon.
But first, let's clarify something...
Natural vs. Unnatural Fructose
Natural fructose is a sugar found in fruits. It's chemically distinct from glucose and does not require insulin to enter into cells. Once inside cells, it can be used, like glucose, in cell energy pathways.
Unnatural fructose is stripped of naturally occurring fibers resulting in a crystalline form of fructose that can be used in the manufacturing of processed sweeteners and syrups. The processed, fiber-stripped fructose is found in many everyday packaged foods, cereals, breads, and drinks.
The Difference Comes Down to Quantity
I am writing about fructose — whether it is natural or unnatural. The effect on the body, as you will see, is the same. With one important exception though: quantity.
Unnatural fructose absorbs into your blood unabated by the missing natural fibers. For example, all 15 grams of fructose from a glass of orange juice or two slices of white bread absorb into your bloodstream. In contrast, the fibers found in fruits will minimize the absorption of natural fructose limiting the net influx of fructose into your circulatory system.
Bottom line: Serving for serving, higher amounts of unnatural, fiber-stripped fructose absorb into your body than natural fructose. Processed sugars and syrups containing unnatural fructose are more dangerous to your body than natural fructose, based solely on quantity.
The Pathological Effects of Fructose
Fructose is metabolized primarily by the liver, just like most poisons. The liver cell begins by taking a phosphate group from ATP, adenosine triphosphate, and adds it to fructose. The result is fructose-1-phosphate and ADP, adenosine diphosphate.
First, let's follow what happens to ADP. Excessive fructose consumption requires such a tremendous amount of ATP that it decreases the availability of phosphate groups, known as "sequestering of phosphates." This means that the ADP formed initially doesn't have phosphate groups readily available to convert back to ATP.1
Without phosphate groups, ADP catabolizes into AMP, adenosine monophosphate, and eventually into IMP or inosine-5-monophosphate. IMP is the initiating compound for uric acid production. In high concentrations, uric acid crystallizes causing the painful joint disorder known as gout.1
Additionally, it inhibits nitric oxide (NO) production which can raise blood pressure.2 So as a result of fructose inside the liver and the production of uric acid, we see two possible negative outcomes: gout and hypertension.
Remember, this isn't going to happen by drinking one soda with high fructose corn syrup. It takes excessive (daily) consumption of soda - which actually characterizes most Americans! - or other sources of fructose to accumulate uric acid.
The Fate of Fructose-Phosphate
What happens to fructose-1-phosphate? Some of it is metabolized into pyruvate, a compound used to initiate cell energy production.
However, in excessive amounts, it converts into xylulose-5-phosphate which then activates pathways that produce fat, called lipogenesis.3 This can increase the number and size of fat cells, along with raising blood triglycerides levels - a marker of metabolic disease and a known risk factor of heart disease.
And the Verdict Is...?
Well, let's review the facts:
- Fructose (natural or unnatural) enters the liver because that's the primary organ that can metabolize it.
- The liver cell converts fructose into metabolites (uric acid and xylulose-5-phosphate) that are known to have negative health effects in high concentrations: gout, hypertension, body fat, and high blood triglycerides.
- Champe, P. (2008). Biochemistry, 2nd edition. New York, New York: Lippincott Williams & Wilkins (Pages 128, 350).
- Nitric Oxide. 2013 Aug;1(32):36-42. doi: 10.1016/j.niox.2013.04.003. Epub 2013 Apr 23
- Endocr J. 2008 Aug;55(4):617-24. Epub 2008 May 19.