You will have to make your own mind up but from my research this will be a good starting point for you.
From the day that high fructose corn syrup (HFCS) became a standard in the American diet (and in many other western countries) it has been hypothesized to be the culprit in everything from obesity to diabetes to heart disease.
The problem is that the available science doesn’t back any of these claims up.As it turns out, HFCS is almost identical to sucrose (table sugar) and no reputable study to date has demonstrated a difference between the two in terms of health consequences.
When solid evidence destroyed the claim that HFCS was to blame for a nation’s health problems, proponents of the claim simply shifted their focus slightly. These people have been unwilling to admit that increases in diabetes and obesity are simply a result of an imbalance in calorie intake and outtake.
Rather than accept the claims made by tomes of scientific research that obesity is best combated through increased exercise and decreased calorie intake, they look for some other factor that will remove personal responsibility from the equation.
The newest claim is that it is the type of calories consumed that matters and not the total quantity. This is really just a generalization of the argument that its HFCS that is to blame.
What is the culprit this time?
Fructose they say.
Fructose is found in both sucrose and HFCS, so it was a natural target for new claims about obesity and diabetes. In fact, fructose makes up about 50% of each of those compounds. The other 50% is glucose, a slightly different and less sweet sugar.
Proponents of the “fructose is bad” theory couldn’t go after glucose because too much is known about it.
Of course, fructose is the sugar found in fruits and some vegetables, which we are told to consume more of because they are healthy.
There is clearly a contradiction here, so the questions are:
1. Who is wrong in this dispute?
2. What claims are accurate?
In this research article, the claims surrounding fructose are explored and the weight of the science behind them is evaluated. The goal I have is to reach a conclusion for you out there about one question:
Is it ‘total calories’ or ‘type of calorie’ that matters most in regards to obesity and diabetes?
Claim 1 – 2004: Fructose in HFCS is causing a rise in Obesity.
The problem here is that fructose content in HFCS is the same as fructose content in sucrose. Substituting one for the other should have no effect. As it turns out, studies do not back this claim.
Rather, it is the quantity of sugar ingested and not whether it is HFCS or sucrose that matters. Ingesting more calories means a person will gain more weight (not rocket science is it?).
It doesn’t matter if those calories are in the form of sucrose or HFCS. Of course, this finding doesn’t rule out that fructose is the culprit. After all, it is found in both sweeteners.
Claim 2 – 2005: Fructose Decreases Leptin Levels, Leading to Overeating.
Some thought they had found the smoking gun when it was determined that fructose does not lead to a rise in leptin levels the way that glucose does. In fact, it causes leptin to decrease. This is substantial because leptin regulates hunger. High levels of leptin suppress appetite so it follows that low levels would lead to overeating.
Unfortunately for believers in the “fructose is evil” theory, this research has never been substantiated. Numerous studies have been performed and have yielded very conflicting results.
In some studies, fructose does have an impact.
In other studies, it is no different from any other sugar (like glucose for instance). The current consensus is that fructose does not lead to undue leptin suppression and therefore is not responsible for overeating and hence weight gain.
What is more, the role of leptin in controlling hunger is not well understood. In some people, it has a tremendous effect. In other people, leptin seems to have almost no effect at all. As it turns out, leptin injections have been found to work only on people who are genetically deficient in leptin.
For the rest of us, changes in leptin levels have much less impact. The only real correlation that has been found is that the more fat you have, the more leptin you make. It has much less to do with eating than was previously thought. Research is ongoing.
Claim 3 – 2008: Fructose Elevates Levels of Uric Acid, which leads to Diabetes
There is no link between urate (uric acid), and diabetes. There is also no relationship between urate (uric acid) and dietary fructose intake. In other words, there is no evidence at all to back this claim.
Claim 4 – Unknown: Fructose causes Non-Alcoholic Fatty Liver Disease, which leads to Triglyceride Synthesis and Obesity.
It is true that fructose causes a slight increase in serum triglyceride (fat) levels, especially when compared to glucose. However, the increase in triglycerides is small, especially when compared to elevations that result from eating fats and other carbohydrate rich foods.
There is still a lot of research going on in this area because the pathway isn’t well understood.
Recent studies have shown that only a very small percentage of fructose is used to make triglyceride, suggesting that this pathway is of little consequence in fat production.
Claim 5 – 2010: Differences in the Biochemical Metabolism of various sugars result in less regulation of Fructose compared to Glucose and hence ill health effects.
This claim has several problems.
First, fructose, even in fruit, is almost never found alone. It is almost always ingested along with other sugars.
This undermines results from tests in which only fructose or only glucose are administered because they don’t represent reality. HFCS and sucrose contain both fructose and glucose, so they are represented well by these studies.
The second problem is that glucose and fructose appear to be inter-converted in the liver. Tracer studies, in which radioactive sugars are ingested, have shown that the bits and pieces of these sugars are often interchanged.
In other words, the process is far more complex than we realize and the simplistic argument that “fructose is bad” is untenable.
Claim 6 – Unknown: Fructose is only Metabolized in the Liver where too much of it can overwhelm available Enzymes such that it must be Converted to Fat.
It is true that fructose is mostly metabolized in the liver (small amounts are used elsewhere, such as in sperm), but it is not true that it is necessarily converted to fat if it overwhelms the enzymes that convert it to glucose.
It turns out, according to tracer studies, that much of the excess fructose is converted to lactose and excreted from the liver. Most all cells can use lactose, so it isn’t necessary to convert fructose to fat just to get it out of the liver.
Take Away Message
The take away message is that weight loss is difficult and so is science. There is no magic bullet when it comes to controlling weight and the basic mantra that calories in must not exceed calories out still holds true.
It is also true that some foods are not as easily absorbed (fibre) as others (sugar) and therefore yield fewer calories per volume. Eating a poorly absorbed food can satiate an appetite while not providing as many calories as easily absorbed foods do.
Of course, eating large quantities of these foods will still lead to weight gain.
The bottom line is pretty simple – your weight is best controlled by eating a healthy diet, watching calorie intake, and exercising (in other words calories in = calories out). As I said earlier, all this stuff is not rocket science but merely taking some care and responsibility with what you eat and drink.
Relying on gimmicks or shifting blame to “bad foods” is not healthy and is not backed by science.
Like to know more? Then this article from The American Journal of Clinical Nutrition tells us: “How safe is fructose for persons with or without diabetes?”
Cheers – John – your Active Ageing Coach and Activist.
P.S. Help a friend to better health……..like and share. Thanks.