Many of you will remember the terrible catastrophe that befell the astronauts of Apollo I. On January 27, 1967, while still training for the first space expedition that would eventually lead to a manned mission to the Moon, all three crew members were killed in a fire that engulfed the cabin. There were several reasons why this runaway fire occurred, including faulty wiring and the fact that the cabin was locked from the outside. However, the single most significant cause was the use of pure oxygen in the cabin (normal air is 70% nitrogen and 25% oxygen), which literally caught fire after being triggered by a spark from an electrical short-circuit.
Perhaps the only benefit in the retelling of this sad story is that it illustrates the best way to interpret the role that fructose plays, and might play, in health and disease. In essence, it harkens back to the age-old observation of the famous medieval physician Paracelsus, that ‘the dose is what determines the poison.’
Some observational data shows that high fructose intake is associated with metabolic syndrome, obesity, and liver disease. Observational studies are ones where the researchers observe the effect of a risk factor, diagnostic test, or treatment without trying to change who is or isn’t exposed to it. These studies can be useful but are prone to bias. In other words, the researchers are at risk of finding what they are looking for. If you think I’m kidding, take a look at the notorious PLOS study, purported to ‘debunk’ the blood type diet link. We see this occur in most studies, wherein the highest fructose intake occurs not from high fruit intake but from high consumption of sugar-sweetened beverages and highly processed foods.
But what does the valid research say?
Your liver is indeed the primary organ that handles fructose, and almost all fructose you consume does pass through your liver. But it doesn’t really turn to fat; instead, about 50% is immediately burned as fuel; 30% converts to glucose and is metabolized, and another 25% is converted to lactate and shipped out of the liver. Less than 1% is converted into fat.
A review in the journal Diabetes Care  analyzed eighteen prior studies that had studied the effect of fructose consumption on blood sugar levels in people with diabetes, finding that overall fructose significantly improved blood sugar control. Even more promising, the researchers observed that the benefits were seen without adverse effects on body weight, blood pressure, uric acid, or cholesterol. This type of study is known as a meta-analysis- -a study that looks at the aggregate results of all prior studies and is considered a much more important finding than single observational-type studies.
Like almost anything in Nature, such as the level of oxygen in that ill-fated Apollo capsule, it is the dose that can create the problem. Most living things do rather nicely on oxygen –when it is in the proper amount and proportion, such as when we breathe atmospheric air. Increase the amount past a certain point and the characteristics change mightily.
A survey of the scientific literature indicates that this is the case with fructose. One study found that consuming 255 grams of fructose per day did lead to an increase in liver fat and reduced insulin sensitivity. It also showed the same result if you consumed 255 grams of straight glucose as well, suggesting it may not be just the fructose that is the issue.  A separate study found that people had to be in the 95th percentile of intake for fructose to create metabolic problems, while another found that individuals had to consume amounts greater than 100 grams of fructose per day over a lengthy period to see adverse effects on body fat or metabolic markers.  It turns out that the problems with fructose may simply be the problems with sugars in general, small amounts in healthy folks are acceptable, whilst large amounts in unhealthy folks are a problem.
This makes sense as fructose is nicknamed ‘fruit sugar’ for a reason. It is abundantly found in common plant foods we consume daily. If we eat enough apples, honey, grapes, pears, raisins, bananas, blueberries, and onions and we will get a significant dose of fructose in our diet. However, these foods are often healthy in the right person and come with many, many health-enhancing substances, such as antioxidants, polyphenols, vitamins, minerals, and fiber. Thus the illogic of wholesale demonizing fructose just becomes an exercise in ‘punching your nose to spite your face.’ For example, a single, medium-sized, raw apple contains approximately 11 grams of fructose, while one wedge of watermelon contains 18 grams of fructose and a one cup serving of pineapple contains 6.5 grams of fructose.
Based on the evidence, it appears that modest fructose intake does not pose a substantial health risk, or at least, any sort of risk over and above that of being in poor health and overconsuming any sugar in general. However, as fructose intake gets higher, as seen in those who eat a lot of highly processed foods with substantial amounts of high-fructose corn syrup, things change significantly. If your daily fructose intake is in a rational range and is derived from live foods there is no real reason to be concerned. If you smoke, drink alcohol to excess, carry a higher BMI, are less physically active, and your dietary fructose is coming from soda pop and highly processed foods, much of the fructose hysteria out there may well apply to you, and it may be time to consider adopting a healthier lifestyle. Also, certain folks can have genetic issues with fructose, such as polymorphisms in the ALDOB gene, which can lead to a condition known as such as hereditary fructose intolerance. In these individuals, fructose intake must be carefully monitored and controlled.
Finally, there is concern that dietary fructose may increase uric acid concentrations, which can be a problem in people with chronic kidney disease and is linked to gout. Yet in one meta-analysis the investigators concluded that ‘these analyses do not support a uric acid-increasing effect of isocaloric fructose intake in nondiabetic and diabetic participants. Hypercaloric (extreme doses (213-219 g/d)) of fructose intake may, however, increase uric acid concentrations.’ 
Again, as Paracelsus said, the dose makes the poison.
I certainly realize that the opinions expressed here put me at odds with many so-called experts on the subject who likely hold more extremist views on the subject. However, there are logical inconsistencies in the wholesale argument against fructose, in all doses and forms. Reminds me of what the author Philip K. Dick once wrote on the subject.
“Reality is that which, when you stop believing in it, doesn’t go away.”
- V. Lecoultre,L. Egli,G. Carrel,F. Theytaz,R. Kreis,P. Schneiter,A. Boss,K. Zwygart,K-A. Lê,M. Bortolotti,C. Boesch,L. Tappy. Effects of fructose and glucose overfeeding on hepatic insulin sensitivity and intrahepatic lipids in healthy humans. Obesity (Silver Spring) 2013 Apr;21(4):782-5
- Dolan LC ,Susan M. Potter SM, George A. Burdock GA. Evidence-Based Review on the Effect of Normal Dietary Consumption of Fructose on Development of Hyperlipidemia and Obesity in Healthy, Normal Weight Individuals. Crit Rev Food Sci Nutr. 2010 Jan;50(1):53-84
- Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. The American Journal of Clinical Nutrition, Volume 88, Issue 5, November 2008, Pages 1419–1437
- A.I. Cozma, J.L. Sievenpiper, R. J. de Souza, L. Chiavaroli, V. Ha, et al. Effect of Fructose on Glycemic Control in Diabetes: A systematic review and meta-analysis of controlled feeding trials. Diabetes Care\u200bVolume 35, Number 7, Pages 1611-1620
- D David Wang, John L Sievenpiper, Russell J de Souza, Laura Chiavaroli, Vanessa Ha, Adrian I Cozma, Arash Mirrahimi, Matthew E Yu, Amanda J Carleton, Marco Di Buono, Alexandra L Jenkins, Lawrence A Leiter, Thomas M S Wolever, Joseph Beyene, Cyril W C Kendall, David J A Jenkins . The effects of fructose intake on serum uric acid vary among controlled dietary trials. J Nutr. 2012 May;142(5):916-23. doi: 10.3945/jn.111.151951. Epub 2012 Mar 28.
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