Why Drinking Diet Soda Makes You Crave Sugar

Recommendations on limiting sugar consumption vary around the world, with guidelines ranging from “[l]imit sweet desserts to one every other day” to “[k]eep sugar consumption to 4 or less occasions per day.” In the United States, the American Heart Association is leading the charge, “proposing dramatic reductions in the consumption of soft drinks and other sweetened products” and recommending fewer than about 5 percent of calories a day from added sugars, which may not even allow for a single can of soda.

Why is the American Heart Association so concerned about sugar? “Overconsumption of added sugars has long been associated with an increased risk of cardiovascular disease,” meaning heart disease and strokes. We used to think added sugars were just a marker for an unhealthy diet. At fast-food restaurants, for example, people may be more likely to order a cheeseburger with their super-sized soda than a salad. However, the new thinking is that the added sugars in processed foods and drinks may be independent risk factors in and of themselves. Indeed, worse than just empty calories, they may be actively disease-promoting calories, which I discuss in my video Does Diet Soda Increase Stroke Risk as Much as Regular Soda?.

At 1:14 in my video, you can see a chart of how much added sugar the American public is consuming. The data show that only about 1 percent meet the American Heart Association recommendation to keep added sugar intake down to 5 or 6 percent of daily caloric intake. Most people are up around 15 percent, which is where cardiovascular disease risk starts to take off. There is a doubling of risk at about 25 percent of calories and a quadrupling of risk for those getting one-third of their daily caloric intake from added sugar.

Two hundred years ago, we ate an estimated 7 pounds of sugar annually. Today, we may consume dozens of pounds of sugar a year. We’re hardwired to like sweet foods because we evolved surrounded by fruit, not Froot Loops, but this adaptation is “terribly misused and abused” today, “hijacked” by the food industry for our pleasure and their profits. “Why are we consuming so much sugar despite knowing too much can harm us?” Yes, it may have an addictive quality and there’s the hardwiring, but the processed food industry isn’t helping. Seventy five percent of packaged foods and beverages in the United States contain added sweeteners, mostly coming from sugar-sweetened beverages like soda, which are thought responsible for more than a 100,000 deaths worldwide and millions of years of healthy life lost. Given this, can we just switch to diet sodas? By choosing diet drinks, can’t we get that sweet taste we crave without any of the downsides? Unfortunately, studies indicate that “[r]outine consumption of diet soft drinks is linked to increases in the same risks that many seek to avoid by using artificial sweeteners—namely type 2 diabetes, metabolic syndrome heart disease, and stroke.” At 3:15 in my video, you can see data showing the increased risks of cardiovascular disease associated with regular soft drinks and also diet soda. They aren’t that dissimilar.

“In other words, the belief that artificially sweetened diet beverages reduce long-term health risks is not supported by scientific evidence, and instead, scientific data indicate that diet soft drink consumption may contribute to the very health risks people have been seeking to avoid.” But, why? It makes sense that drinking all that sugar in a regular soft drink might increase stroke risk, due to the extra inflammation and triglycerides, but why does a can of diet soda appear to increase stroke risk the same amount? It’s possible that the caramel coloring in brown sodas like colas plays a role, but another possibility is that “artificial sweeteners may increase the desire for sugar-sweetened, energy-dense beverages/foods.”

The problem with artificial sweeteners “is that a disconnect ultimately develops between the amount of sweetness the brain tastes and how much glucose [blood sugar] ends up coming to the brain.” The brain feels cheated and “figures you have to eat more and more and more sweetness in order to get any calories out of it.” So, “[a]s a consequence, at the end of the day, your brain says, ‘OK, at some point I need some glucose [blood sugar] here.’ And then you eat an entire cake, because nobody can hold out in the end.”

If people are given Sprite, Sprite Zero (a zero-calorie soda), or unsweetened, carbonated, lemon-lime water, but aren’t told which drink they’re getting or what the study is about, when they’re later offered a choice of M&M’s, spring water, or sugar-free gum, who do you think picks the M&M’s? Those who drank the artificially sweetened soda were nearly three times more likely to take the candy than those who consumed either the sugar-sweetened or unsweetened drinks. So, it wasn’t a matter of sweet versus non-sweet or calories versus no-calories. There’s something about non-caloric sweeteners that somehow tricks the brain.

The researchers did another study in which everyone was given Oreos and were then asked how satisfied the cookies made them feel. Once again, those who drank the artificially sweetened Sprite Zero reported feeling less satisfied than those who drank the regular Sprite or the sparkling water. “These results are consistent with recent [brain imaging] studies demonstrating that regular consumption of [artificial sweeteners] can alter the neural pathways responsible for the hedonic [or pleasure] response to food.”

Indeed, “[t]he only way really to prevent this problem—to break the addiction—is to go completely cold turkey and go off all sweeteners—artificial as well as fructose [table sugar and high fructose corn syrup]. Eventually, the brain resets itself and you don’t crave it as much.”

We’ve always assumed the “[c]onsumption of both sugar and artificial sweeteners may be changing our palates or taste preferences over time, increasing our desire for sweet foods. Unfortunately, the data on this [were] lacking”…until now. Twenty people agreed to cut out all added sugars and artificial sweeteners for two weeks. Afterwards, 95 percent “found that sweet foods and drinks tasted sweeter or too sweet” and “said moving forward they would use less or even no sugar.” What’s more, most stopped craving sugar within the first week—after only six days. This suggests a two-week sugar challenge, or even a one-week challenge, may “help to reset taste preferences and make consuming less or no sugar easier.” Perhaps we should be recommending it to our patients. “Eating fewer processed foods and choosing more real, whole, and plant-based foods make it easy to consume less sugar.”


Speaking of stroke, did you see my Chocolate and Stroke Risk video?

For more on added sugars, see:

You may also be interested in my videos on artificial and low-calorie sweeteners:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How the Egg Industry Tried to Bury the TMAO Risk

“Metabolomics is a term used to describe the measurement of multiple small-molecule metabolites in biological specimens, including bodily fluids,” with the goal of “[i]dentifying the molecular signatures.” For example, if we compared the metabolic profile of those with severe heart disease to those with clean arteries, we might be able to come up with a cheap, simple, and noninvasive way to screen people. If heart patients happened to have something in their blood that healthy people didn’t, we could test for that. What’s more, perhaps it would even help us understand the mechanisms of disease. “To refer to metabolomics as a new field is injustice to ancient doctors who used ants to diagnose the patients of diabetes” (because the ants could detect the sugar in the diabetics’ urine).

The first modern foray discovered hundreds of substances in a single breath, thanks to the development of computer technology that made it possible to handle large amounts of information—and that was in 1971, when a computer took up nearly an entire room. “[N]ew metabolomics technologies [have] allowed researchers to measure hundreds or even thousands of metabolites at a time,” which is good since more than 25,000 compounds may be entering our body through our diet alone.

Researchers can use computers to turn metabolic data into maps that allow them to try to piece together connections. You can see sample data and a map at 1:28 in my video Egg Industry Response to Choline and TMAO. Metabolomics is where the story of TMAO started. “Everyone knows that a ‘bad diet’ can lead to heart disease. But which dietary components are the most harmful?” Researchers at the Cleveland Clinic “screened blood from patients who had experienced a heart attack or stroke and compared the results with those from blood of people who had not.”

Using an array of different technology, the researchers identified a compound called TMAO, which stands for trimethylamine N-oxide. The more TMAO people had in their blood, the greater the odds they had heart disease and the worse their heart disease was.

Where does TMAO come from? At 2:19 in my video, you can see a graphic showing that our liver turns TMA into TMAO—but where does TMA come from? Certain bacteria in our gut turn the choline in our diet into TMA. Where is the highest concentration of choline found? Eggs, milk, and meats, including poultry and fish. So, when we eat these foods, our gut bacteria may make TMA, which is absorbed into our system and oxidized by our liver into TMAO, which may then increase our risk of heart attack, stroke, and death.

However, simply because people with heart disease tend to have higher TMAO levels at a snapshot in time doesn’t mean having high TMAO levels necessarily leads to bad outcomes. We’d really want to follow people over time, which is what researchers did next. Four thousand people were followed for three years, and, as you can see in the graph at 3:10 in my video, those with the highest TMAO levels went on to have significantly more heart attacks, strokes, or death.

Let’s back up for a moment. If high TMAO levels come from eating lots of meat, dairy, and eggs, then maybe the only reason people with high TMAO levels have lots of heart attacks is that they’re eating lots of meat, dairy, and eggs. Perhaps having high TMAO levels is just a marker of a diet high in “red meat, eggs, milk, and chicken”—a diet that’s killing people by raising cholesterol levels, for example, and has nothing to do with TMAO at all. Conversely, the reason a low TMAO level seems so protective may just be that it’s indicative of a more plant-based diet.

One reason we think TMAO is directly responsible is that TMAO levels predict the risk of heart attacks, strokes, or death “independently of traditional cardiovascular risk factors.” Put another way, regardless of whether or not you had high cholesterol or low cholesterol, or high blood pressure or low blood pressure, having high TMAO levels appeared to be bad news. This has since been replicated in other studies. Participants were found to have up to nine times the odds of heart disease at high TMAO blood levels even after “controll[ing] for meat, fish, and cholesterol (surrogate for egg) intake.”

What about the rest of the sequence, though? How can we be certain that our gut bacteria can take the choline we eat and turn it into trimethylamine in the first place? It’s easy. Just administer a simple dietary choline challenge by giving participants some eggs.

Within about an hour of eating two hard-boiled eggs, there is a bump of TMAO in the blood, as you can see at 4:51 in my video. What if the subjects are then given antibiotics to wipe out their gut flora? After the antibiotics, nothing happens after they eat more eggs. In fact, their TMAO levels are down at zero. This shows that our gut bacteria play a critical role. But, if we wait a month and give their guts some time to recover from the antibiotics, TMAO levels creep back up.

These findings did not thrill the egg industry. Imagine working for the American Egg Board and being tasked with designing a study to show there is no effect of eating nearly an egg a day. How could a study be rigged to show no difference? If we look at the effect of an egg meal (see 5:32 in my video), we see it gives a bump in TMAO levels. However, our kidneys are so good at getting rid of TMAO, by hours four, six, and eight, we’re back to baseline. So, the way to rig the study is just make sure the subjects hadn’t eaten those eggs in the last 12 hours. Then, you can show “no effect,” get your study published in the Journal of the Academy of Nutrition and Dietetics, and collect your paycheck.


Unfortunately, this appears to be part for the course for the egg industry. For more on their suspect activities, see:

For more on the TMAO story, see:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How to Get the Benefits of Aspirin Without the Risks

For people without a personal history of cardiovascular disease, aspirin’s risks may outweigh its benefits, but aspirin may have additional benefits. “We have long recognized the preventative role of daily aspirin for patients with atherosclerotic [heart] disease; however, it now appears that we can hatch 2 birds from 1 egg. Daily low-dose aspirin may help prevent certain forms of cancer, as well, as I discuss in my video Should We All Take Aspirin to Prevent Cancer? In an analysis of eight different studies involving more than 25,000 people, “the authors found a 20 percent decrease in risk of death from cancer among those randomized to daily aspirin…” The researchers wrote, “[T]he search for the most efficacious and safe treatments for malignant disease remains an enormous and burdensome challenge. If only we could just stop cancer in its tracks—prevent it before it strikes. Perhaps we can.” Indeed, perhaps we can with salicylic acid, the plant phytonutrient that’s marketed as aspirin.

How does aspirin affect cancer? The Nobel Prize for Medicine was awarded to the team who discovered how aspirin works. Enzymes named COX (cyclooxygenase) take the pro-inflammatory, omega-6, fatty-acid arachidonic acid our body makes or we get directly in our diet (primarily from eating chicken and eggs), and turns it into inflammatory mediators, such as thromboxane, which produces thrombosis (clots), and prostaglandins, which cause inflammation. Aspirin suppresses these COX enzymes. Less thromboxane means fewer clots, and less prostaglandin means less pain, swelling, and fever. However, prostaglandins can also dilate the lymphatic vessels inside tumors, allowing cancer cells to spread. So, one way cancer tries to kill us is by boosting COX activity.

We think one way aspirin can prevent cancer is by counteracting the tumor’s attempts to pry open the lymphatic bars on its cage and spread throughout the body. Indeed, reduction in mortality due to some cancers occurred within two to three years after aspirin was started. That seems too quick to be accounted for by an effect only on tumor formation . Cancer can take decades to develop, so the only way aspirin could work that fast is by suppressing the growth and spread of tumors that already exist. Aspirin appeared to cut the risk of metastases in half, particularly for adenocarcinomas, like colon cancer.

Given this, should we all take a daily baby aspirin? Previous risk-benefit analyses did not consider the effects of aspirin on cancer, instead just balancing cardiovascular benefits with bleeding risks, but these new cancer findings may change things.

If daily aspirin use were only associated with a reduction of colon cancer risk, then the benefits might not outweigh the harms for the general population, but we now have evidence that it works against other cancers, too. “[E]ven a 10% reduction in overall cancer incidence…could tip the balance” in favor of benefits over risks.

How does the cancer benefit compare? We know that using aspirin in healthy people just for cardiovascular protection is kind of a wash, but, by contrast, the cancer prevention rates might save twice as many lives, so the benefits may outweigh the risks. If we put it all together—heart attacks, strokes, cancer, and bleeding—aspirin comes out as protective overall, potentially extending our lifespan. There is a higher risk of major bleeding even on low-dose aspirin, but there are fewer heart attacks, clotting strokes, and cancers. So, overall, aspirin may be beneficial.

It’s important to note that the age categories in that study only went up to 74 years, though. Why? Because the “risk of bleeding on aspirin increases steeply with age,” so the balance may be tipped the other way at 75 years and older. But, in younger folks, these data certainly have the research community buzzing. “The emerging evidence on aspirin’s cancer protection highlights an exciting time for cancer prevention…”

“In light of low-dose aspirin’s ability to reduce mortality from both vascular events and cancer to a very notable degree, it is tempting to recommend this measure…for most healthy adults…However, oral aspirin, even in low doses, has a propensity to damage the gastroduodenal mucosa [linings of our stomachs] and increase risk for gastrointestinal bleeding; this fact may constrain health authorities from recommending aspirin use for subjects deemed to be at low cardiovascular risk”—that is, for the general population. “Recent meta-analyses estimate that a year of low-dose aspirin therapy will induce major gastrointestinal bleeding (requiring hospitalization) in one subject out of 833…”

If only there were a way to get the benefits without the risks.

Those who remember my video Aspirin Levels in Plant Foods already know there is. The aspirin phytonutrient salicylic acid isn’t just found in willow trees, but throughout the plant kingdom, from blackberries and white onions to green apples, green beans, and beyond. This explains why the active ingredient in aspirin is found normally in the bloodstream even in people not taking aspirin. The levels of aspirin in people who eat fruits and vegetables are significantly higher than the levels of those who don’t. If we drink just one fruit smoothie, our levels rise within only 90 minutes. But, one smoothie isn’t going to do it, of course. We need to have regular fruit and vegetable consumption every day. Are these kinds of aspirin levels sufficient to suppress the expression of the inflammatory enzyme implicated in cancer growth and spread, though? Using umbilical cord and foreskin cells—where else would researchers get human tissue?—they found that even those low levels caused by smoothie consumption significantly suppressed the expression of this inflammatory enzyme on a genetic level.

Since this aspirin phytonutrient is made by plants, we might expect plant-eaters to have higher levels. Indeed, not only did researchers find higher blood levels in vegetarians, but there was an overlap between people taking aspirin pills. Some vegetarians had the same level in their blood as people actually taking aspirin. Vegetarians may pee out as much of the active metabolite of aspirin as those who take aspirin do, simply because vegetarians eat so many fruits and vegetables. “Because the anti-inflammatory action of aspirin is probably the result of SA [salicylic acid, the active ingredient in aspirin], and the concentrations of SA seen in vegetarians have been shown to inhibit [that inflammatory enzyme] COX-2 in vitro, it is plausible that dietary salicylates may contribute to the beneficial effects of a vegetarian diet, although it seems unlikely that most [omnivores] will achieve sufficient dietary intake of salicylates to have a therapeutic effect.”

Aspirin can chew away at our gut. With all that salicylic acid flowing through their systems, plant-eaters must have higher ulcer rates, right? No. Both vegetarian women and men appear to have a significantly lower risk of ulcers. So, for the general population, by eating plants instead of taking aspirin, we may not only get the benefits without the risks, we can get the benefits with even more benefits. How is this possible? In plants, the salicylic acid can come naturally pre-packaged with gut-protective nutrients.

For example, nitric oxide from dietary nitrates exerts stomach-protective effects by boosting blood flow and protective mucus production in the lining of the stomach—“effects which demonstrably oppose the pro-ulcerative impact of aspirin and other NSAIDs.”

The researcher notes that while “[d]ark green leafy vegetables…are among the richest dietary sources of nitrate…it may be unrealistic to expect people to eat ample servings of these every day,” so we should just give people pills with their pills, but I say we should just eat our greens. People who’ve had a heart attack should follow their physician’s advice, which probably includes taking aspirin every day, but what about everyone else? I think everyone should take aspirin—but in the form of produce, not a pill.


To see the pros versus cons for people trying to prevent or treat heart attacks and stroke, see my video Should We All Take Aspirin to Prevent Heart Disease?.

Does the COX enzyme sound familiar? I talked about it in my Anti-Inflammatory Life Is a Bowl of Cherries video.

Where does one get “dietary nitrates”? See Vegetables Rate by Nitrate and Veg-Table Dietary Nitrate Scoring Method. I also discuss nitrates in Slowing Our Metabolism with Nitrate-Rich Vegetables and Oxygenating Blood with Nitrate-Rich Vegetables.

Do some plant foods have more aspirin than others? Definitely. In fact, some foods have the same amount as a “baby” aspirin. Check out Plants with Aspirin Aspirations.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations: