Soda consumption and the obesity rate have risen in tandem. And there is good reason to believe that they are causally related. For instance, one study found that for every additional 12-ounce soda that a child consumed each day, their likelihood of becoming obese was increased by 60% at follow-up.

Many nutritional studies have tried to better understand this relationship. Most of the focus has, of course, been on the sweetening agents found in these drinks (both caloric and non-caloric).

But what if we’ve been fixated on the wrong target all along? What if it is actually some other component, common to these drinks, that is the real culprit (or at least a meaningful contributor)?

For the first time ever, researchers from Birzeit University in Palestine have investigated the effects of carbon dioxide gas (like in a soda) on secretion of ghrelin. Ghrelin is a peptide hormone that is released from the stomach to stimulate hunger. Ghrelin levels increase with fasting and decrease after meals. Higher ghrelin, generally speaking, means greater appetite.

But ghrelin doesn’t just make you hungrier. It also increases nutrient storage and growth hormone release, essentially linking appetite and nutrient partitioning with growth and repair processes. Perhaps even more interesting, ghrelin also acts upon dopamine neurons in the brain (ventral tegmental area) to stimulate the intake of freely available food. In fact, ghrelin plays a key role in reward behaviors of various types, and is also important in mood regulation. 

So, could it be that the bubbles in soft drinks – and even in sparkling water – are boosting appetite, food intake, and fat storage, thus contributing to the obesity epidemic? Let’s take a closer look at this weird but interesting study.

 

Experiment I – Effects on Rats

16 young lab rats were randomly assigned into four different conditions:

• tap water
• degassed (flat) carbonated drink
• sugar-sweetened carbonated drink
• diet carbonated drink (sweetened with aspartame)

The rodents were given their assigned beverages for about a year. Their body mass and food intake were measured and recorded daily during the intervention, and blood levels of ghrelin were also assessed over the course of the study.

So what did the researchers find?

Rats consuming either the sugar-sweetened or diet drinks secreted significantly more ghrelin. Ghrelin levels in the rodents drinking soda were found to be 1.5- to 2.5-fold higher than their counterparts drinking the flat beverages or the tap water. They also ate more, and gained weight more rapidly.

But I know what most people are thinking: does this also happen in humans? That’s where the second part of this study comes in.

 

Experiment II – Effects on Humans

The team then recruited a group of 20 male volunteers at the university. First, they gave each of the men 330 mL of plain water, and got baseline ghrelin measurements. Then, on different days, the researchers randomly assigned each of the subjects to one of the following drinks:

• Regular (sugar-sweetened) carbonated beverage
• Diet carbonated beverage
• De-gassed (flat) carbonated beverage
• Carbonated water

Afterwards, they collected blood samples and analyzed for ghrelin.

Subjects who drank carbonated beverages (including carbonated water) experienced a 6-fold increase in ghrelin levels compared to water. Click To Tweet

So why does this happen?

In an effort to tease out underlying mechanisms, the researchers also harvested rodent stomachs and treated isolated portions with different beverages.

When exposed to carbonated liquids, ghrelin was secreted 3- to 4-fold more than control upon interaction with the stomach cells. The authors attribute the increased release of ghrelin to mechanosensation from pressurized carbon dioxide against the cell walls of the stomach.

 

So what does this mean?

Humans have been inexorably drawn to carbonated beverages for centuries, at least since the discovery of bubbling waters in natural springs, which were thought to promote good health. But why do we like them so much?

It’s actually not obvious why we do! The sensation that we all experience when we drink carbonated beverages is produced by a chemical excitation of nociceptors (sensory receptors for painful stimuli) in the oral cavity, when carbon dioxide is converted to carbonic acid. That’s why you feel a “bite” when you sip soda – the carbon dioxide triggers the same pain sensors that are triggered by wasabi.

Interestingly, other animals are reportedly not big fans of this, and indeed it has been suggested that our shared ability to detect CO2 may have evolved as a means to recognize and avoid foods that are fermenting. So what makes us different? Why do we like and even crave bubbly drinks?

Ghrelin could be a contributing factor. As mentioned, ghrelin is best known for its role in regulating appetite and stimulating food intake, but it has a wide array of peripheral actions, particularly in reward-seeking behavior. We now know that ghrelin does not only activate the homeostatic hypothalamus, but it also interacts with brain reward pathways to alter food preference and enhance food reward. Injecting animals with ghrelin, for instance, has been shown to increase dopamine release from the nucleus accumbens, a part of the brain that plays a vital role in processing rewarding stimuli. And in an fMRI study, when researchers injected ghrelin into human participants who had already eaten, they observed increased response in regions of the brain that are associated with reward and with encoding incentive value of food cues, but not with maintaining energy homeostasis.

Actually, the power of this pathway has perhaps been best illustrated with another bubbly beverage – beer. Giving people just 15 milliliters of their favorite beer – enough to taste but without a discernible rise in blood alcohol levels – triggers the release of dopamine in the brain. 

 

But before you stop drinking sparkling water…

So if we take this study at face value, it’s pretty alarming, especially if you like to drink sparkling water between meals. But there are a couple things about the study itself that give me pause.

For instance, Figure 1 (which presents the rate of weight gain), only presents the body mass of the rodents up to day 110, despite the fact that the study ostensibly continued for an entire year. Why stop there? What were the weights when they were euthanized? I can find no explanation for this in the paper.

Additionally, the explanation offered from the mechanistic study just doesn’t make a whole lot of sense to me, and I can find little support for it in the literature.

To be fair, there isn’t a ton of data available on the effects of carbon dioxide in beverages on appetite or on stomach function. But we have reason to believe that carbonated drinks may increase gastric volume, especially in relatively large amounts, and we have known for some time that mechanical distension of the stomach actually plays a role in inhibiting food intake. A lot of you probably find that to be the case as well – I have heard a number of anecdotal reports of physique competitors consuming loads of sparkling water to stave off hunger pangs.

One study, for instance, found that increasing the level of carbonation in a beverage led to increased satiety and lower caloric intake (though the effect didn’t last long). Other studies examining this phenomenon, however, have failed to find much of an impact of this distension on total food intake. This is probably in part because gastric distension from liquids tends to be very short-lived, and this is especially true for beverages that do not contain calories, which are rapidly cleared from the stomach.

Finally, I question if incubating stomach pieces with these beverages is a great representation of what happens when we drink soda, simply because much of the CO2 in carbonated drinks is lost before it even gets to the digestive tract.

So, this study is very interesting, but the purported underlying mechanism seems to be a little half-baked. Nevertheless, it’s worth investigating further. I would like to see this study replicated, and it would be really nice to see 1) a larger group of rodents (four rats per drink type is pretty low), and 2) a longer human follow-up that also assesses subsequent food intake.

In the meantime, I drink sparkling water pretty much every day, and I don’t plan to stop on account of this study alone. But I do think it makes sense to evaluate how carbonated beverages (or anything else you ingest for that matter) affects you and your relationship with food. If you personally find that drinking tasty carbonated drinks makes you hungry, or you’ve mysteriously gained weight since adding five cans of La Croix to your average day, then by all means cut out the sparkles and see if it makes a difference.

 

 

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