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This article I read states that in adults over the age of 65 diet soda consumption triples waist circumference gain over people who did not consume diet sodas. Study: Diet Soda May Be Making You Fat:

According to a study published in the Journal of the American Geriatrics Society, people who daily drank diet soda for about 10 years gained almost triple the abdominal fat than those who did not drink diet soda.The waist circumferences of diet soda drinkers gained about 2.11 centimeters, while non-users gained 0.77 centimeters around the waist. Daily consumers gained a whopping 3.04 centimeters, while occasional users' waist increased 1.76 cm.

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    Careful. You are asking about a casual relationship but the article you cite does not claim to show causation, only correlation. – Nate Eldredge Mar 18 '15 at 19:14
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    And that waist gain isn't "whopping". In fact it sounds to me like the typical weight gain for people of that age group over that period of time. And maybe their consumption of diet drinks is caused by their increasing weight/size not the other way round. – matt_black Oct 31 at 1:31
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Diet soda intake is associated with long-term increases in waist circumference in a biethnic cohort of older adults is the journal article they're citing. The article you quoted is slightly incorrect in that the increase in waist circumference is what triples.

Adjusted for initial WC, demographic characteristics, physical activity, diabetes mellitus, and smoking, mean interval ΔWC of DS users (2.11 cm, 95% confidence interval (CI) = 1.45-2.76 cm) was almost triple that of nonusers (0.77 cm, 95% CI = 0.29-1.23 cm) (P < .001). Adjusted interval ΔWCs were 0.77 cm (95% CI = 0.29-1.23 cm) for nonusers, 1.76 cm (95% CI = 0.96-2.57 cm) for occasional users, and 3.04 cm (95% CI = 1.82-4.26 cm) for daily users (P = .002 for trend). This translates to ΔWCs of 0.80 inches for nonusers, 1.83 inches for occasional users, and 3.16 for daily users over the total SALSA follow-up. In subanalyses stratified for selected covariates, ΔWC point estimates were consistently higher in DS users.

Of course, correlation does not equal causation, so it may be that diet soda makes older people fat. It might be that fat old people drink more diet soda. It's also possible that there is some other factor or factors that both measures are influenced by. The article merely notes an association.

In a striking dose-response relationship, increasing DSI (Diet Soda Intake) was associated with escalating abdominal obesity, a potential pathway for cardiometabolic risk in this aging population.

  • that was my error, the article actually mentions specifically its the waist circumference that triples. – Himarm Mar 18 '15 at 18:52
  • {nods} Although it's still slightly incorrect in that waist circumference measures more than just belly fat. – Sean Duggan Mar 18 '15 at 18:53
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    but typically an increase in adults waist circumference comes almost entirely from either fat or muscle, and at the age in the study group 65 plus, its most likely purely fat over muscle as strenuous muscle building would be rare. And the conclusion itself is that its "increasing DSI(Diet soda Intake) was associated with escalating abdominal obesity" fat, not muscle, so in essence yes they are gaining 3x the abdominal fat. – Himarm Mar 18 '15 at 18:58
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    Clearly this study shows that diet soda makes fat people old. – Adam Phelps Mar 19 '15 at 4:38
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    So although they seem to correct for physical activity they don't seem to correct for non-soda diet. Maybe diet soda drinkers are the kind of people who enjoy a xxxl pizza with extra cream on the side? because, annecdotal evidence, my grandma ate like a bird and just drank tea. – Borgh Nov 8 at 9:10
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Diet soda refers to a calorie-free carbonated beverage sweetened by artificial sweeteners.

The current evidence does not provide a proof that diet soda causes weight gain, but the main points are:

  • Overweight individuals may drink diet soda to prevent further weight gain, but they still gain weight because they do not decrease calorie intake from foods, which gives an impression that diet soda causes weight gain.
  • Artificial sweeteners in diet soda may (or may not) increase appetite.

In some studies, regular use of diet soda for several years has been associated with weight gain:

Anyway, these studies alone do not provide any firm proof that drinking diet soda actually causes weight gain. There seem to be 2 main possible explanations:

1) Reverse causality

It is possible that overweight people drink diet soda with artificial sweeteners [ASs] to prevent additional weight gain (but they continue to gain weight), rather than drinking diet soda makes them fat. This is how the authors of this study Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long‐term Weight Gain (Obesity, 2012) explained it:

Individuals seeking to lose weight often switch to ASs in order to reduce their caloric intake. AS use might therefore simply be a marker for individuals already on weight‐gain trajectories, which continued despite their switching to ASs. This is the most obvious possible explanation of our findings. Increased fast food consumption among soda users might further confound apparent associations.

The same way, the authors of Sugar-sweetened and artificially sweetened beverage consumption and risk of type 2 diabetes in men (AJCN, 2011) explained the association between drinking diet soda and diabetes type 2:

However in...prospective cohort studies, consumption of artificially sweetened beverages was significantly associated with an increased risk of type 2 diabetes and the metabolic syndrome. One explanation for these findings is that artificially sweetened beverages stimulate appetite for sweet foods at subsequent meals. However, reverse causation and confounding are more plausible explanations.

2) Increased appetite due to artificial sweeteners in diet soda

There is a known hypothesis that artificial sweeteners may stimulate appetite, but the evidence is inconclusive.

Study reviews with NO ASSOCIATION between ASs and weight gain:

Study reviews that have found an ASSOCIATION between ASs and weight gain:

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    "So, we can assume that drinking diet soda does not contribute to any significant calorie intake and therefore does not cause weight gain." That is a simplistic theoretical model. It might be the case that diet sodas interfere with hormones in a way that promotes weight gain. It might be the case that they encourage a sweet tooth that promotes eating of sugar. It might be that people drinking them compensate by eating more. Of course, none of this could be true, but you need to reference this claim with empirical data.(I admit your second last conclusion addresses this in some ways.) – Oddthinking Oct 31 at 0:24
  • @Oddthinking while you make good logical points, there is a problem with the proofs you want to see. The most obvious base assumption would be that diet sodas don't contribute to weight gain as they don't contain calories. The onus of proof is to show this is wrong. Most studies don't show good evidence of this (see some analysis of other studies in answers to this related question. The weight of proof needs to show there is a fattening effect not that there isn't. – matt_black Oct 31 at 1:28
  • I reworded the answer. Reverse causality and increased appetite are 2 main hypotheses. – Jan Nov 7 at 18:18
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Yes.

As long as the diet soda is still a sweetened beverage containing artificial (ie non-caloric) sweetener, then they do help make people fat. Regardless of age. That is, as a tendency: eat more. And this is really old news.

Artificial sweeteners are for a long time now used to fattened pigs and cattle. The research there is now just how to optimise its use, no longer whether it does or not.

–– E. Roura, M. Fu: " Taste, nutrient sensing and feed intake in pigs (130 years of research: then, now and future)", Animal Feed Science and Technology, 2017. DOI

–– Laia Blavi Josa: "Exploring Dietary Strategies to Enhance Feed Intake and Growth of Piglets after Weaning by a Multidisciplinary Approach", Dissertation, University of Barcelona, 2016.

There is multitude of mechanisms working mostly in synergy.

These data support the hypothesis that long-term use of saccharin may blunt post-absorptive EE at rest in Wistar rats, which is related to weight gain. On the other hand, long-term sucrose intake can increase energy expenditure in rats. This effect combined can explain, at least partially, the weight gain increases associated to saccharin in relation to sucrose in these animals.
–– Pinto DE et al.: : "Long-term intake of saccharin decreases post-absortive energy expenditure at rest and is associated to greater weight gain relative to sucrose in wistar rats", Nutr Metab (Lond). 2017 Feb 20;14:18. doi: 10.1186/s12986-017-0165-7. eCollection 2017.

And the association for non-nutritive sweeteners with type 2 diabetes:

The average consumption of sweetened beverages in consumers was 328 and 568 mL/wk for SSBs and ASBs, respectively. Compared with nonconsumers, women in the highest quartiles of SSB and ASB consumers were at increased risk of T2D with HRs (95% CIs) of 1.34 (1.05, 1.71) and 2.21 (1.56, 3.14) for women who consumed >359 and >603 mL/wk of SSBs and ASBs, respectively. Strong positive trends in T2D risk were also observed across quartiles of consumption for both types of beverage (P = 0.0088 and P < 0.0001, respectively). In sensitivity analyses, associations were partly mediated by BMI, although there was still a strong significant independent effect. No association was observed for 100% fruit juice consumption.
CONCLUSIONS:
Both SSB consumption and ASB consumption were associated with increased T2D risk. We cannot rule out that factors other than ASB consumption that we did not control for are responsible for the association with diabetes, and randomized trials are required to prove a causal link between ASB consumption and T2D.

–– Fagherazzi G et al.: "Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidemiologique aupres des femmes de la Mutuelle Generale de l'Education Nationale-European Prospective Investigation into Cancer and Nutrition cohort", Am J Clin Nutr. 2013 Mar;97(3):517-23. doi: 10.3945/ajcn.112.050997. Epub 2013 Jan 30.

The body senses 'sweet' taste not only on the tongue but detects energy containing carbohydrates throughout the system. Artifical sweteners betray that system and not only via pre-emptive sensory insulin response the body tries to compensate this 'betrayal':

Ad libitum lunch intake was significantly higher for the NNS treatments compared with sucrose (P=0.010). The energy 'saved' from replacing sucrose with NNS was fully compensated for at subsequent meals … ––Tey SL et al.: "Effects of aspartame-, monk fruit-, stevia- and sucrose-sweetened beverages on postprandial glucose, insulin and energy intake", Int J Obes (Lond). 2017 Mar;41(3):450-457. doi: 10.1038/ijo.2016.225. Epub 2016 Dec 13.

Beverage type did not influence measures of satiety or the desire to eat foods with a specific taste. However, sweet snacks were more (p < 0.05) reinforcing relative to salty/savory snack foods after consuming a NSB than after a SSB. In conclusion, this is the first study to demonstrate that NSB can increase the motivation to gain access to sweet snacks relative to salty/savory snack foods later in the day.
–– Casperson SL et al.: "The relative reinforcing value of sweet versus savory snack foods after consumption of sugar- or non-nutritive sweetened beverages", Appetite. 2017 May 1;112:143-149. doi: 10.1016/j.appet.2017.01.028. Epub 2017 Jan 23.

With neuronal imaging the differences get colourful:

We did not observe an acute effect of NNS consumption on immediate food intake in humans who are not frequently drinking NNS beverages. Yet, we observed imminent changes in brain response patterns in brain areas that are key players in food intake regulation. The responsiveness of these brain areas to sweet taste has been shown to ‘fade’ as a function of longer-term NNS consumption [58,59]. Thus, it remains to be investigated whether such longer-term brain response alterations can also be observed to visual food cues, often mediating pre-ingestive food choices. Given such longer-term alterations, the brain response modulations observed under the NNS condition in our study might reflect an initial stage of adaptation to taste-calorie uncoupling, possibly indicating that longer-term alterations of food intake regulation (via responses to tempting visual cues) take place when NNS are repeatedly consumed over time. Our study thus provides first insights linking neuroimaging research in the gustatory modality and behavioral research on the impact of non-caloric sweetener consumption on food intake, by investigating the neural correlates of drives towards visually conveyed food cues.
–– Camille Crézé et al.: "The Impact of Caloric and Non-Caloric Sweeteners on Food Intake and Brain Responses to Food: A Randomized Crossover Controlled Trial in Healthy Humans" Nutrients. 2018 May; 10(5): 615. 2018 May 15. doi: 10.3390/nu10050615, PMCID: PMC5986495 PMID: 29762471

That this is a universal response with direct causality, also in humans, is shown here:

  • Chronic sucralose diet triggers increased food intake
  • Dietary sucralose creates a sweet/energy imbalance
  • Sweet/energy imbalance activates a conserved neuronal starvation response
  • Sucralose effect on feeding is conserved from flies to mammals

Non-nutritive sweeteners like sucralose are consumed by billions of people. While animal and human studies have demonstrated a link between synthetic sweetener consumption and metabolic dysregulation, the mechanisms responsible remain unknown. Here we use a diet supplemented with sucralose to investigate the long-term effects of sweet/energy imbalance. In flies, chronic sweet/energy imbalance promoted hyperactivity, insomnia, glucose intolerance, enhanced sweet taste perception, and a sustained increase in food and calories consumed, effects that are reversed upon sucralose removal. Mechanistically, this response was mapped to the ancient insulin, catecholamine, and NPF/NPY systems and the energy sensor AMPK, which together comprise a novel neuronal starvation response pathway. Interestingly, chronic sweet/energy imbalance promoted increased food intake in mammals as well, and this also occurs through an NPY-dependent mechanism. Together, our data show that chronic consumption of a sweet/energy imbalanced diet triggers a conserved neuronal fasting response and increases the motivation to eat.

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–– Qiao-Ping Wang et al.: "Sucralose Promotes Food Intake through NPY and a Neuronal Fasting Response", Cell Metabolism, Volume 24, Issue 1, p75–90, July 12, 2016. DOI

And these sweeteners also promote obesity via gut microbiota:

Over the last two decades, safety concerns about low/no-calorie sweeteners (LNCS) have been described in the archival scientific literature including elevated risk of metabolic syndrome, type 2 diabetes, excessive weight gain, cardiovascular disease, safety, and disruption of the gut microbiome. A recent review by Lobach, Roberts, and Roland in Food and Chemical Toxicology examined 17 research articles on modulation of gut bacteria by LNCS along with other selected publications. In the conclusions of their paper, they claim that LNCS 1) do not affect gut microbiota at use levels and 2) are safe at levels approved by regulatory agencies.

Both of these claims are incorrect. The scientific literature on LNCS clearly indicates that it is inappropriate to draw generalized conclusions regarding effects on gut microbiota and safety issues for compounds that vary widely chemical structure and pharmacokinetics.

Scientific studies on the sweetener sucralose, used here as a representative LNCS, indicate that this organochlorine compound unequivocally and irrefutably disrupts the gut microbiome at doses relevant to human use.

Results of dozens of additional research publications added and reviewed here also raise significant and extensive concerns about the safety of sucralose for the human food supply.
–– Schiffman SS, Nagle HT: "Revisited: Assessing the in vivo data on low/no-calorie sweeteners and the gut microbiota.", Food Chem Toxicol. 2019 Oct;132:110692. doi: 10.1016/j.fct.2019.110692. Epub 2019 Jul 24.

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