Fructose can make you fat and even affect mental capabilities. Here's what you can take to protect yourself.
Let's Get This Out of the Way
Worrying about high-fructose corn syrup (HFCS) and not worrying about regular fructose is like worrying about Dracula and not worrying about his younger brother, Alan, who's just a tad shorter than Dracula and has a bad haircut. Either bloodsucker will drain you of blood and condemn you to an eternity of never ending night.
Regular sucrose – Dracula's presumably less formidable younger brother – is a 50/50 blend of fructose and glucose. HFCS – Dracula himself – is a 55/45 blend of fructose and glucose. That means that if you drank 100 grams of a HFCS Coke made in America, you'd be ingesting a measly 5 extra grams of fructose than if you drank 100 grams of the cane sugar (sucrose) version made in Mexico. Big deal.
That being said, it's not entirely certain that either fructose or HFCS are guilty of all the crimes they're accused of. There's sufficient evidence, or lack thereof, out there to make us at least question how and to what degree fructose makes us fat.
But despite the inconsistencies in the data, it's starting to look like fructose is guilty of affecting genes in the brain, and that's pretty damning. Luckily there's a naturally occurring supplement that can act like a crucifix to fructose's vampiric heart and reverse its harmful effects on genes.
A Thousand Messed Up Genes
Scientists at UCLA found that fructose affects more than 700 genes in the rat hypothalamus (the structure that control's metabolism) and 200 in the rat hippocampus (where learning and memory are regulated).
The vast majority of these genes are comparable to those found in humans and subjecting the ones in the hypothalamus to fructose can cause inflammation and a dysfunctional metabolism, leading to elevated glucose, triglycerides, insulin sensitivity, and fatness. Likewise, introducing fructose to genes in the hippocampus can lead to Parkinson's, depression, bipolar disorder, and other brain diseases.
Not to worry, though. The same researchers found that the omega-3 fatty acid DHA (docasahexaenoic acid) can turn these genes off after fructose has turned them on.
What They Did
- The researchers trained rats to navigate a maze.
- They then divided the rats into three groups. One group drank fructose-sweetened water (the amount was roughly equivalent to a human drinking a liter of Yoo Hoo Chocolate Beverage, Mountain Dew, or whatever your fructose-y preference). Another group was given the same fructose-water plus a DHA-rich diet. The third group was given plain water.
- After 6 weeks, the rats were re-introduced to the maze.
The rats that were given only fructose water navigated the maze only half as fast as the water-only group. The fructose water plus DHA group performed equally as well as the water-only group, suggesting that the DHA eliminated or reversed fructose's harmful effects.
Blood tests also revealed that the high-fructose rats had much higher blood glucose, triglyceride, and insulin levels than the other two groups. Apparently, fructose was removing or adding another biochemical group to cytosine, one of the four DNA nucleotides. This results in the gene either being turned on or turned off, but DHA flips the switch the other way.
How To Use This Info
Unless you're a farmer or a Whole Food's employee who gets a discount on healthy food, it's hard to entirely avoid fructose. The chemical is insidious in Western society, so it makes sense to use a little insurance in the form of a DHA supplement.
Omega-3 fatty acid supplements almost always contain both DHA and EPA (eicosapentaenoic acid) and that's great, but the vast majority of said supplements are heavily disproportioned towards EPA. Look for one that contains more DHA than EPA, like Flameout®, and use it daily to protect against fructose's detrimental effects on metabolism and brain function.
- Qingying Meng, Zhe Ying, Emily Noble, et al. "Systems Nutrigenomics Reveals Brain Gene Networks Linking Metabolic and Brain Disorders," EBioMedicine, Volume 7, May 2016, Pages 157–166.