Diet Coke and other sodas have a bad rep: increased appetite, risk of diabetes, high blood pressure, etc. It’s time to clear their name.
In 2017, Science Daily cast an article into the internet ether that damaged the reps of Diet Coke and every other artificially sweetened beverage. It led off with the following thunderbolt:
“Artificial sweeteners may be associated with long-term weight gain and increased risk of obesity, diabetes, high blood pressure and heart disease, according to new study.”
Almost instantly, the jaw of nearly every body-conscious diet soda drinker who read that went slack. They all looked like the shocked-face emoji. What they read seemingly defied logic. It was as if they’d just learned that mom’s chicken soup made colds and flus worse.
True, the idea that artificially sweetened soft drinks are bad for you had, by 2017, already been permeating through the populace for at least a couple of years, but “bad for you” simply meant that they supposedly increased your appetite, causing you, weak-willed schlub that you are, to probably gain fat in the long run. Now came this new missive from hell, adding additional crimes to the rap sheet of artificially sweetened beverages.
Either way, a lot of people believed that stuff and rather than parse the studies or the specific allegations made against diet sodas, they stopped using them as a tool against unwanted pounds.
Further, their minds probably closed shut to any subsequent studies that might have exonerated artificially sweetened drinks, especially the latest one (Pearson, et al., 2021) that went so far as to suggest that when mixed with meals, Diet Coke – when compared to regular Coke – had positive effects on post-prandial (after eating) energy expenditure and insulin concentrations without any significant increase in appetite.
Let’s quickly kick to the curb some of those earlier studies before we get to the good stuff. The study reported on in Science Daily (Azad, et al. 2017) was, as pointed out by the fine people at Suppversity, based on observational links between diet drinks and obesity, diabetes, etc., and not causal ones.
I’ll give you an example, an absurd one at that, but it’s just to make a point: Let’s say I conduct a study and I observe that, for some unknown reason, people who eat New England style clam chowder are more likely to become tap dancers than people who eat Manhattan style clam chowder. Now, it should be clear to anyone whose I.Q. has a fightin’ chance at hitting 3 digits that it’s unlikely that a preference to eat New England style clam chowder would cause someone to become a tap dancer.
Regardless, scientists often make these kinds of observations and dutifully report on them in their research papers, but they don’t usually accept bookings on Good Morning America to discuss them. Most of them have too much integrity.
However, the lay press and social media don’t have the science training to make such distinctions – they run with it/them. And that’s what happened with that Azad study from 2017, even though none of the randomized controlled studies (RCTs) referenced in the Azad study pointed to a causal relationship between artificial sweeteners and increased fatness or worsening cardiometabolic risk factors.
To be more precise, none of the studies cited listed any experimental evidence that the link between artificially sweetened beverages and increased weight gain and heightened cardiovascular risk was a causal one. I mean, most of the people in the referenced studies were obese and the rest were just overweight. It takes no Brobdingnagian leap of faith to assume that many got fatter all on their lonesome, with or without diet sodas.
It’s also possible that drinking diet sodas convinces overweight souls that they’ve done good and deserve some sort of reward, resulting in additional fattiness.
Regardless, if you look carefully at the small number of RCT evidence available at the time, they showed that artificial sweeteners appeared to have some beneficial effects. The studies that found contradictory evidence, or that thought they did, including Azad’s, seem to have hung all their nay-saying ornaments on one thin branch: CPIR, or “cephalic phase insulin response.”
CPIR is a spike in insulin that’s mediated by neural mechanisms. In short, your brain registers a sweet taste and incorrectly identifies it coming from a carbohydrate source and then instructs the pancreas to release some insulin to counter it, even though the release isn’t needed. Hypoglycemia may occur, which elicits a hunger response and makes a body want to eat more.
The theory is that if it happens repeatedly, as might occur with habitual diet soda drinkers, fatness might ensue. But forget all that for now. Let’s look at the new study, one that’s based on apparently causal links and not observational ones.
One reason I like this new study is that it used Coke and Diet Coke, products that we’re all familiar with, rather than some fakakta concoction of “dihydrogen monoxide” [water] and N-(L-α-Aspartyl)-L-phenylalanine (Equal), and 1-methyl ester perfused with 3,5-Dimethyl-1,2-cyclopentanedione (caramel flavoring). Diet Coke and Coke are something we can relate to.
Anyhow, Pearson, et al., recruited eight healthy, recreationally active college males. I won’t get into all the minutiae associated with the study, but over the course of several weeks, each participant completed three randomly assigned trials.
Each subject was required to eat a pre-trial meal consisting of 50% carbs, 30% fat, and 20% protein. Four hours later, they were fed a semi-nightmarish test meal of chocolate Ensure (57 grams), heavy whipping cream (47 mL), and a ZonePerfect Nutrition bar, individualized so each participant hit his prescribed macros.
The “meal” was washed down with 20 ounces of Coca-Cola, Diet Coke, or water. One week separated each trial and participants were restricted from consuming alcohol and caffeine or do anything else that might muck up the results.
Naturally, the researchers practiced due diligence by measuring their height, weight, and body comp, along with taking pre- and post-meal blood pressure and blood samples.
Here are the biggest takeaways from their study:
Fat and Carbohydrate Oxidation: Coca-Cola suppressed fat oxidation and increased carbohydrate oxidation. (“Oxidation” is a sciencey word meaning, essentially, “burned for energy.”) No real surprise there. However, post-meal carbohydrate oxidation was also increased in the Diet Coke trial, albeit briefly.
Post-Meal Calorie Burning: Both Coca Cola and Diet Coke elevated post-meal energy expenditure. You’d expect that from regular Coke because of all the sugar, but not so with the Diet Coke. Granted, both drinks contain caffeine, but the scientists didn’t think it was enough to explain all the results. As to how Diet Coke accomplished this increase in post-meal energy expenditure, they weren’t really sure.
Blood Glucose: While regular Coke strongly affected blood glucose (raising it), they didn’t see any such effect from Diet Coke or, of course, water.
Insulin: Regular Coke bent the insulin curve skyward, but contrary to what many other nutritionists have believed, Diet Coke didn’t. This is where the aforementioned CPIR surfaces again. Sixty percent of the participants experienced this brain-activated release of insulin after Diet Coke, but the scientists didn’t think it was physiologically relevant: “Chronic consumption of NS (Coca Cola, or similarly sweetened beverages) can lead to reduced insulin sensitivity and ultimately the development of Type II diabetes. We conclude that the consumption of artificially sweetened beverages does not elicit the same metabolic risk as NS beverages.”
Triglycerides: Things got a little screwy with triglyceride, or blood fat, measurements. Coke, to no one’s surprise, elevated triglyceride levels, but so did Diet Coke, which isn’t consistent with some other studies. This is one category in which additional studies are definitely needed.
Appetite: While sweeteners, particularly aspartame, have been implicated in appetite stimulation as far back as 1986, the findings of the current study didn’t support it. In fact, they found no differences in post-meal hunger or satiety between the three conditions (Coke, Diet Coke, water).
Blood Pressure: This category was a wash. While Diet Coke seemed to temporarily raise systolic blood pressure among the subjects (possibly as a side effect of ingesting one or both of the amino acids that comprise aspartame, the artificial sweetener used in Diet Coke), a much bigger study of 200 college students conducted in 2017 found that aspartame lowered systolic blood pressure.
Diet Coke (and presumably similarly sweetened drinks) doesn’t affect post-meal fat oxidation. In other words, you’ll continue to burn fat as efficiently, or inefficiently, as you did before. Neither did Diet Coke negatively affect insulin levels or, as a lot of people believe, increase your appetite and lead to more fatness.
The biggest benefit, though, was that Diet Coke increased resting energy expenditure.
Together, this study, and several others, reinstates the usefulness of diet drinks as a fat fighting tool. At the very least, drinking a diet beverage instead of one sweetened with sugar or fructose is going to save you from ingesting empty calories. Oh yeah, to those that think artificial sweeteners somehow change your microbiome to the worse, there’s no evidence to support that.
You might still want to avoid these drinks because of the artificial chemicals they contain or the not-proven, but not entirely ridiculous notion that they might somehow cause certain types of cancer, but those are entirely different arguments.
- Azad MB et al. Nonnutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies. CMAJ. 2017 Jul 17;189(28):E929-E939. PubMed.
- Pearson RC et al. Comparison of aspartame- and sugar-sweetened soft drinks on postprandial metabolism. Nutr Health. 2021 Nov 29;2601060211057415. PubMed.