As sugar consumption was found to be strongly associated with health risks such as obesity and diabetes, a simplistic solution seemed to be the use of non-caloric artificial sweeteners (NCAS) – we could have most things taste sweet with no harm. The problem has been that after 3-4 decades of consumption of NCAS, both diabetes and obesity have progressively increased.
Currently, 68% of the U.S. population is overweight or obese. The percentage of the population with type two diabetes has risen from 2% of the population prior to 1970 to over 7% currently. Another 28% have “prediabetes” which is a preview for the next 10-20 years.
An interesting exercise is to compare the curves looking at NCAS use and obesity over time. If the artificial sweeteners were introduced to be a solution, at some point in time we should have seen these two curves going in opposite directions when, in fact, they parallel each other. Sometimes theories get so entrenched that in spite of conflicting data they are not abandoned when proven false.
So, what went wrong with the artificial sweetener solving the obesity and diabetes hypothesis? The answer has multiple pieces. This requires a little being said about insulin. Insulin increases fat storage in a diet that supplies high amounts of energy. While sugars are a rich source of dietary energy so are fats.
Combining dietary fats with higher insulin leads to higher fat storage. It seems that NCAS increase insulin significantly. This is called cephalic phase insulin response. Cephalic meaning higher up nearer the head. The body has layers of preparedness. This cephalic insulin response comes not from blood glucose going up once sugar is absorbed but simply from the taste of sweet on the neurons on the tongue we call taste buds.
The taste of sweet, real or artificial, tells the brain to send a signal to the pancreas to release insulin as “early preparedness” for the increase in blood sugar whether it is coming or the brain just thinks it is. Perhaps the earliest biomarker of prediabetes is elevated blood insulin.
Other research has uncovered yet another layer of the NCAS relationship to obesity and diabetes. Back in 2014 Dr. Jothem Suez and his colleagues found that feeding artificial sweeteners to mice altered their gut microbiome which then caused increased glucose intolerance or a prediabetes state. In a just published study they have confirmed this relationship in humans. The relationship between the gut microbiome and altered glucose tolerance related to metabolites or breakdown products of the artificial sweeteners by the different gut microbes.
The artificial sweetener most associated with altered glucose tolerance was sucralose, but all were associated with some impaired effect. Even with a single artificial sweetener such as sucralose, the degree of the effect varied between individuals. This was related to variations in the microbiome between individuals. The microbiome is made up of 100 trillion organisms which is a cell mass 10 times greater than all of the cells in the human body. There is also great variation from person to person so differing effects on what metabolites are produced.
The next likely step will be to correlate how the composition of an individual’s microbiome may put them at risk, but this is an immense task given the size of the microbiome and its diversity across the approximately 1000 different species that compose it. From a practical standpoint it seems more prudent to simply not use artificial sweeteners. If we could learn how to tweak an individual’s microbiome to not produce the metabolites that alter glucose tolerance, that would not prevent the cephalic phase response that increases insulin.
The real solution seems to be “tame” the sweet addiction. I use that term as that is what it truly appears to be. Work by French researchers in 2007 found that rats addicted to cocaine would gradually choose the intense sweet taste of saccharine over that of cocaine if they could have access to either. These researchers quote “The supranormal stimulation of these receptors by sugar-rich diets, such as those now widely available in modern societies, would generate a supranormal reward signal in the brain, with the potential to override self-control mechanisms and thus to lead to addiction.”
Unfortunately, the food industry has learned this science and has increased the use of both caloric and non-caloric sweeteners to drive consumption. Both cocaine and sweet taste activates dopamine receptors in the accurate nucleus in the brain and over time this nucleus actually changes in architecture leading to addiction. Withdrawal of the addictive substance over time will allow this nucleus to recover reducing the desire for what caused the change.
For the vast majority of human existence on this planet we did fine without everything tasting sweet. We should get back to that pattern. Healthy may become the “new” norm.
Suez et al. ARTIFICIAL SWEETENERS INDUCE GLUCOSE INTOLERANCE BY ALTERING THE GUT MICROBIOTA. Nature, 2014;514:181–186.
Suez et al. PERSONALIZED MICROBIOME-DRIVEN EFFECTS OF NON-NUTRITIVE SWEETENERS ON HUMAN GLUCOSE TOLERANCE. Cell, 2022;185:1–22.
Lenoir et al. INTENSE SWEETNESS SURPASSES COCAINE REWARD. PLoS ONE , 2007;2(8): e698.
Olszewski et al. EXCESSIVE CONSUMPTION OF SUGAR: AN INSATIABLE DRIVE FOR REWARD. Current Nutrition Reports, 2019;8:120–128.