Myth “Some sugars are better for our bodies than others.”

Myth “Natural, raw or unrefined sugars are better.”

Myth “It is better to use honey, maple syrup, agave syrup, or coconut sugar.”

Myth “Corn syrup is worse for us than other sugars”

Myth “Natural sugar is better than processed sugar.”

Reality: None of those claims are really true. In reality our metabolism breaks down all sugars the same way.

Agave syrup, maple syrup, coconut sugar – none of these are sugar alternatives – they are just sources of sugar.

Sucrose, a common sugar, is a disaccharide. That means it is a two-part molecule, made of glucose and fructose.

And get this – sucrose is not absorbed by the human GI tract. Instead, our intestines secrete an enzyme, sucrase-isomaltase.

This breaks down any sucrose into glucose and fructose, and it is those smaller sugars which are absorbed. So our body doesn’t care which kind of sugar we eat; the result is the same.

Myth “Natural sugar is better than processed sugar.”

All sugars are processed.  The so-called “processed” white sugar that people are afraid of is just sugar from a natural source, sugar cane or beets.  Brown sugar? The same as white sugar, except that the molasses hasn’t been removed. Not healthier whatsoever.

“Raw honey” may be unprocessed, but it isn’t any healthier. It is just sugar mixed with water, pollen and a few other organic molecules. You’re not going to be helped by the microscopic amount of nutrients in raw honey unless you ate pounds of it a day.

Myth “High fructose corn syrup is worse for you than other sugar.”

Reality? Nope. It’s literally the same thing.

More details on this bit here – What is the difference between high fructose corn syrup (HFCS) and sugar?

Myth “Sugars higher on the glycemic index are worse for you.”

Nope. Such claims come from flawed studies, see below for details.

So, are we saying that sugar is good for you? No, we aren’t saying that either. Mainstream science already knows the answer, and people just refuse to hear it: For most people, having some sugar in our diet has always been fine. The problem comes from diets which have huge amounts of sugar, and not enough of other foods that actually are good for us.

While no one, single diet is best for everyone, science points to the same direction: Eat a balanced diet with whole grains, beans, legumes, vegetables and fruit. Have less meat, and certainly less processed meat. Eat far less fried foods. Watch your total calorie intake. Keep daily sugar and fat intake lower. There you go.

 

What’s wrong with those glucose versus sucrose studies?

In those studies, researchers did the following: They fed huge amounts of only one type of sugar molecule to one group of rats, and huge amounts of a different type of sugar molecule to another group of rats. Then they looked at how the health of the rats were affected over time.

Problem 1: These studies don’t resemble real world eating. Humans don’t spend entire days eating nothing but fructose or nothing but sucrose.  The way that our metabolism would handle that is different from how it would handle normal eating, in which sugar is only a small part of the diet. In real life, even in poor diets, sugar is still only a fraction of the total: there are also proteins, complex carbohydrates, fats, oils, vitamins, minerals, etc.

Problem 2: Some studies attempted to see how consuming different sugars affects one’s resulting blood sugar level. Sugar molecules which create a higher result are said to be higher on a glycemic index; sugar molecules which create a lower result are said to be lower on the glycemic index.  Yet these are unnatural diets in which rats ate only pure sugars. When we study the results of normal diets, with actual food, there’s almost no difference between sugars. A meal’s impact on resulting blood sugar levels depends on the amount of sugar and how fast it gets absorbed, not on the type of sugar molecule.

Problem 3: Rats do not metabolize sugars in the same ways that humans do. Hence, any inaccuracies due to the above problems become magnified, making the results non applicable to humans.

Result: The data from those studies are essentially useless.

Honors biology details
Glucose enters the glycolysis metabolic pathway at the top.

Here it is phosphorylated by Hexokinase.

Fructose enters glycolysis pathway two steps later, where it meets phosphofructokinase.

Thus, eating pure fructose allows the energy to be metabolized a bit faster than eating pure glucose.

But people don’t consume huge chunks of pure sugars. When eating anything resembling real life meals, the difference is very little.

Studies on High-fructose corn syrup (HFCS)

High-fructose corn syrup (HFCS) is also known as glucose-fructose, isoglucose and glucose-fructose syrup. There is no scientific evidence that HFCS itself causes obesity or metabolic syndrome, but rather overconsumption and excessive caloric intake of any sweetened food or beverage may contribute to these diseases.

Epidemiological research has shown that the increase in metabolic disorders, such as obesity and non-alcoholic fatty liver disease, is linked to increased consumption of sugars and calories in general.

A 2012 review found that fructose did not appear to cause weight gain when it replaced other carbohydrates in diets with similar calories.

A 2014 systematic review found little evidence for an association between HFCS consumption and liver diseases, enzyme levels or fat content.

The American Heart Association recommended that people limit added sugar (such as maltose, sucrose, high fructose corn syrup, molasses or cane sugar) in their diets.

High fructose corn syrup article

Is Sugar Really Toxic? Sifting through the Evidence

Scientific American Staff and Ferris Jabr, Scientific American, July 15, 2013

https://blogs.scientificamerican.com/brainwaves/is-sugar-really-toxic-sifting-through-the-evidence/

By consuming so much sugar we are not just demonstrating weak willpower and indulging our sweet tooth – we are in fact poisoning ourselves according to a group of doctors, nutritionists and biologists, one of the most prominent members of which is Robert Lustig of the University of California, San Francisco…

A few journalists, such as Gary Taubes and Mark Bittman, have reached similar conclusions. Sugar, they argue, poses far greater dangers than cavities and love handles; it is a toxin that harms our organs and disrupts the body’s usual hormonal cycles.

Excessive consumption of sugar, they say, is one of the primary causes of the obesity epidemic and metabolic disorders like diabetes, as well as a culprit of cardiovascular disease. More than one-third of American adults and approximately 12.5 million children and adolescents in the U.S. are obese. In 1980, 5.6 million Americans were diagnosed with diabetes; in 2011 more than 20 million Americans had the illness.

…. Because fructose metabolism seems to kick off a chain reaction of potentially harmful chemical changes inside the body, Lustig, Taubes and others have singled out fructose as the rotten apple of the sugar family. When they talk about sugar as a toxin, they mean fructose specifically.

In the last few years, however, prominent biochemists and nutrition experts have challenged the idea that fructose is a threat to our health and have argued that replacing fructose with glucose or other sugars would solve nothing.

First, as fructose expert John White points out, fructose consumption has been declining for more than a decade, but rates of obesity continued to rise during the same period. Of course, coinciding trends alone do not definitively demonstrate anything.

A more compelling criticism is that concern about fructose is based primarily on studies in which rodents and people consumed huge amounts of the molecule – up to 300 grams of fructose each day, which is nearly equivalent to the total sugar in eight cans of Coke – or a diet in which the vast majority of sugars were pure fructose. The reality is that most people consume far less fructose than used in such studies and rarely eat fructose without glucose.

…. Not only do many worrying fructose studies use unrealistic doses of the sugar unaccompanied by glucose, it also turns out that the rodents researchers have studied metabolize fructose in a very different way than people do—far more different than originally anticipated.

… Even if Lustig is wrong to call fructose poisonous and saddle it with all the blame for obesity and diabetes, his most fundamental directive is sound: eat less sugar. Why? Because super sugary, energy-dense foods with little nutritional value are one of the main ways we consume more calories than we need, albeit not the only way.

Glycemic index and obesity

Janette C Brand-Miller, Susanna HA Holt, Dorota B Pawlak, Joanna McMillan

Glycemic index and obesity, The American Journal of Clinical Nutrition

Volume 76, Issue 1, July 2002, Pages 281S–285S

https://doi.org/10.1093/ajcn/76.1.281S

Although weight loss can be achieved by any means of energy restriction, current dietary guidelines have not prevented weight regain or population-level increases in obesity and overweight. Many high-carbohydrate, low-fat diets may be counterproductive to weight control because they markedly increase postprandial hyperglycemia and hyperinsulinemia.

Many high-carbohydrate foods common to Western diets produce a high glycemic response [high-glycemic-index (GI) foods], promoting postprandial carbohydrate oxidation at the expense of fat oxidation, thus altering fuel partitioning in a way that may be conducive to body fat gain.

In contrast, diets based on low-fat foods that produce a low glycemic response (low-GI foods) may enhance weight control because they promote satiety, minimize postprandial insulin secretion, and maintain insulin sensitivity.

This hypothesis is supported by several intervention studies in humans in which energy-restricted diets based on low-GI foods produced greater weight loss than did equivalent diets based on high-GI foods.

Long-term studies in animal models have also shown that diets based on high-GI starches promote weight gain, visceral adiposity, and higher concentrations of lipogenic enzymes than do isoenergetic, macronutrient controlled, low-GI-starch diets.

In a study of healthy pregnant women, a high-GI diet was associated with greater weight at term than was a nutrient-balanced, low-GI diet.

In a study of diet and complications of type 1 diabetes, the GI of the overall diet was an independent predictor of waist circumference in men.

These findings provide the scientific rationale to justify randomized, controlled, multicenter intervention studies comparing the effects of conventional and low-GI diets on weight control.

Straight talk about high-fructose corn syrup: what it is and what it ain’t,

Straight talk about high-fructose corn syrup: what it is and what it ain’t,

John S. White, The American Journal of Clinical Nutrition

Volume 88, Issue 6, December 2008, Pages 1716S–1721S, https://doi.org/10.3945/ajcn.2008.25825B

High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice concentrates.

HFCS was widely embraced by food formulators, and its use grew between the mid-1970s and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness comparable with that of sucrose, improved stability and functionality, and ease of use.

Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike.

In particular, I evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same.

Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is supported neither in the United States nor worldwide.

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