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.
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.
–– 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.