Today, researchers from Yale announced new findings that demonstrate the mechanism by which the fructose sugars found in both refined table sugar and high fructose corn syrup cause a reduction in insulin sensitivity, a key stage in the development of both obesity and diabetes.
Researchers led by Yoshio Nagai had postulated that the PGC-1b gene, normally responsible for triggering fat production in the liver, also played a significant role in insulin resistance – an umbrella term for when the body slowly numbs itself to insulin. Remember that metabolic syndrome, the condition determined largely by insulin resistance, includes bad cholesterol and excess triglycerides as some of its markers.
You may not know all these conditions by name or how they affect one another but the take home idea is that researchers all knew these bad disorders (cholesterol, triglyceride and insulin problems) were related, but not quite how. Watch this great run down of the HFCS debate and its health effects to better understand the background of this issue:
Nagai, et al went about testing their hypothesis by taking genetically modified mice, who specifically had their PGC-1b genes ‘knocked out’, and observing what happened to them as they ate fructose. The results showed that mice without PGC-1b significantly reversed their insulin resistance, thereby showing that the metabolism of fructose created the bad cholesterol, excess triglycerides and insulin resistance.
Precedents Point to Harm
At first it may seem odd that the liver would process fructose at all but, in an interesting biological turn, fructose does not get metabolized like other sugars. Fructose loads (common when you chug a soda) end up putting a heavier stress on the liver because its the only organ that can do anything about it – that gave researchers their first clues as to why fructose sweeteners like HFCS might have a special role in obesity and diabetes.
Technically speaking, the researchers’ findings link only fructose to the gene but both refined table sugar and HFCS are roughly half fructose, so this surely applies to both of them. But beyond these findings, a host of significant milestones demonstrate that researchers have been on the right trial for awhile now. Observe these hints and see if you can follow the logic of the research:
- Hint #1 (A start…) – The only organ in the human body that can actually break fructose down is the liver, so all fructose gets routed through there.
- Hint #2 (Big Hint!) – Excess fructose activates fatty liver enzymes, which create a rise in triglycerides and cholesterol levels . In fact, fructose was found to increase the more dangerous VLDL cholesterol carriers while mostly ignoring LDL and HDL cholesterol carriers .
- Hint #3 (Almost there) – The VLDLs in circulation find their way into your muscles where they disrupt blood sugar absorption , while the triglycerides back in the liver crowd out and eventually block the liver cells responsible for insulin production .
And with todays findings, we are finally seeing the proof piece fall into place; inhibiting the liver fat/cholesterol producing gene renders fructose less harmful, proving fructose’s role in insulin resistance.
Many Lines of Thinking, All Myopic
Immediately following the announcement of these study findings, the Corn Refiners Association tried to get out in front of the situation by making a blanket statement, discounting the study’s methods.
“Recent studies using pure fructose that purport to show that the body processes high fructose corn syrup differently than other sugars due to fructose content are a classic example of this problem because pure fructose cannot be extrapolated to high fructose corn syrup. The abnormally high levels of pure fructose used in these studies are not found in the human diet.”
The Corn Lobby has a point here. Typically added sugars in the Western diet take the form of HFCS and sucrose (table sugar), both of which are chemically very similar in the ratio of glucose/fructose they contain – about 50/50. However, humans were never intended to eat added sugars in the volume we do now and they are likely the source of obesity and diabetes epidemics. Both need to be reduced, so HFCS gets a minor pass here. Very minor (but also consider that the Sugar Lobby gets a free pass on the whole issue by simply not having ‘fructose’ in their name).
Still, we would like to remind you these are the same people running this ad campaign right now:
The other piece of their quote is suspicious though [emphasis ours]:
“Fructose consumption at normal human dietary levels and as part of a balanced diet has not been shown to yield such results. Moreover, human fructose intake is nearly always accompanied by the simultaneous and equivalent intake of glucose – a critical and distinguishing factor from pure fructose used in these studies.”
Human fructose intake is NOT always accompanied by an equivalent amount of glucose. Up until about 100 years ago, most sweeteners in the diet simply came from fruit – and those sweeteners were mostly fructose tightly bonded to fiber in the fruits, in much smaller amounts. Think of the sweetness of an apple versus a lollipop and you get the idea. The science community added an interesting aside in the same article that further tears down the corn refiner argument, if you read between the lines:
“The findings …support the emerging role of gene/environment interaction in modulating the metabolic phenotype and disease pathogenesis. Thus, perturbations of the same regulatory motif may produce vastly different metabolic responses, depending on the specific combinations of dietary nutrients.”
In English, they are saying the findings change based on what you are eating fructose in (an apple or a soft drink?) – which is especially interesting in light of the Corn Lobby’s incorrect statement earlier. The lower amounts of sugars in some of your favorite fruits – namely apples, pears and watermelon – contain a ratio of twice as much fructose to glucose (feel free to run the numbers in the USDA’s database of food).
This is yet another example of why whole, real foods are always better choice. Despite having high ratios of fructose to glucose, we know apples are not causing the obesity epidemic. Fiber is likely helping lower the glycemic index of apples, something that has been stripped away in the processing of HFCS and refined sugar. Flavonoids are also having an effect but the exact mechanisms are unknown. Further research will uncover how these complex nutrient interactions fully impact diet – and we will cover them – but rest assured, natural foods and not refined sugars, are the answer to these nutritional crises.
An Evolution, Not A Revolution
The bottom line with this new wrinkle in the HFCS debate is that these new findings show the casual mechanisms that turn a soda into a health problem. That is a major step in the research but remember that this is not a new line of science as the monied players might subtly suggest with their ‘balanced diet‘ talk.
A long cannon of research has led up to this point. HFCS and refined sugar consumption was first brought to the attention of researchers when they noticed that the rise in its use throughout the 70s, 80s and 90s in America closely mirrored the obesity and diabetes epidemics. They compared that to the science of fructose metabolism, further implicating it in cholesterol and triglyceride complications. All that happened today is that the science has finally connected the dots of causation.
What You Can Do
We know the solution to this mess – reduce your excess sugar intake. Here are some easy ways:
- Try tea and coffee without sweeteners
- Substitute soft drinks with club soda and squeezed citrus juice
- Use natural unrefined syrups (agave, maple) in place of refined HFCS
- Have some organic berries in place of candy
- Eat dark chocolate instead of milk chocolate