Happy December, ceiling fans 🙂 In September, I wrote a post reviewing Fat Chance, a book by Dr. Robert Lustig, that discusses the root causes of obesity and Metabolic Syndrome. The review caught the eye of Dr. Lustig’s business partner at the Institute for Responsible Nutrition, and we had a great exchange over the past couple of months. This was very exciting and a big deal for me! He asked me to write a guest post on their website, and coincidentally enough, it is about a topic that I’ve been meaning to explore for quite some time: Noncaloric sweeteners.
The blue, yellow, and pink rectangular packets are a visual staple on tables at American restaurants. Sweet’N Low, Equal, Splenda, and Stevia (with a new, green seat at the table) are alternatives to sugar that our country has adopted with open arms. I question, do they actually work in thwarting weight gain without sacrificing sweetness? Are they safe? Please check out my interesting and eye-opening post on their site here, or you can check it out below (They left out a few key graphs and figures). Either way, I appreciate your support, as always!
It is well known and undisputed that the increased consumption of sugar, in all its variations, has contributed to the ever-growing prevalence of obesity and metabolic syndrome over the past fifty-plus years. Once the exception, metabolic dysregulation and its related symptoms have now etched themselves as the rule in our global health picture. As a result, the industries involved in treating, rectifying, and capitalizing on this problem and its associated costs are estimated to be in the tens of billions of dollars.
Weight loss programs, pharmaceuticals, exercise techniques, surgical procedures, nutritional supplements, and diet products targeted to consumers and physicians permeate the media, literature, and our everyday vernacular. Rife among these countless products and initiatives designed as quick-fix remedies to lower blood sugar, boost weight loss, increase insulin sensitivity (and the like) are noncaloric artificial sweeteners (NAS).
NAS are commonly deemed as a safe and beneficial solution for weight loss, given their low caloric content, stunted insulin response, and reduced costs for use in commercial products. Yet, their surge in promotion, production, and consumption over the past twenty to thirty years has not done the average American’s waistline any favors. In fact, the opposite has occurred. So, what’s the rub??
Before I try to tackle this question, I would like to point out that there truly is not enough clinical research or epidemiological data out there to definitively conclude whether to label NAS as “good” or “bad” in comparison to sugar. Many of the studies that promote their safety and benefits for weight loss are industry-funded. Unbiased, evidence-based research is sparse. Further, the FDA’s approval of their portioned use in foods doesn’t really account for the surplus amounts of these substances most consumers actually ingest due to their ubiquity and our nation’s appetite.
All being said, my hope for this post is to illuminate two rather different mechanisms through which NAS can disrupt metabolic function and perhaps further negate the weight problems they were created to fix. The significant kind of weight gain that plagues many in our society is not just a matter of caloric indulgence; it is an overall reflection and byproduct of the inner workings of one’s body and health gone awry. Because of this, I would like to draw some attention away from the mouth, and focus instead on two different areas that NAS can considerably affect: the brain and the gut … and as a result, one’s clothing size.
Many of us, when we have just sampled a delicious dessert, have said, “Oh my goodness, this must be so bad for you.” Simply put, this is our body’s innate ability to determine the caloric contents of what we eat based on its sweet taste.
As a result of a sweet taste and our brain and body’s calibration of its caloric estimation, an assembly line of biochemical reactions occurs that determines how our body then regulates the caloric energy we have just received. Our metabolism revs up like an engine because it has fuel to burn. Our brain also tells us to stop eating (or drinking) because it received a negative feedback message that our body has enough energy to accomplish what it needs to.1,2
Now, if something were to disrupt this communication – like, keeping the sweet taste in tact but omitting the calories – don’t you think the body and brain would get a little confused? That nice give-and-take balance is thrown off; the sweet taste registers, but there are no calories, nutrients, or fuel to burn and utilize. It’s sort of like the boy who cried wolf. What a gyp! A predictive relationship, such as the sweet taste, caloric estimation, and metabolic adjustment is based upon a specific cue followed by a specific outcome. The relationship becomes progressively weaker when either the cue or the outcome occurs alone. In the case of NAS, the sweet taste occurs alone without the calories to produce a proper outcome.1,2
In a 2008 study1, Susan Swithers, the leading scientist on noncaloric sweeteners, successfully demonstrated this predictive relationship with sweet tastes and what ensues metabolically when it is disrupted by NAS. In a normal, healthy rat, they ingest a form of glucose, the sweet taste signals the imminent arrival of nutrients and calories into the gut where they will be broken down and used for energy. When the nutrients in the food are absorbed in the gut, their core body temperature rises, and the rats become more active to utilize and burn the energy provided by the calories. She found that, “impairing the ability of sweetness to predict the arrival of energy in the gut accurately reduced the efficient utilization of that energy,”1 thereby weakening the feedback loop to the brain in order produce satiation.
In Swithers’ study, two separate groups of rats were fed yogurt; one was sweetened with glucose, the other with saccharin (Sweet’N Low). It was found that those who were fed the saccharin had increased overall caloric intake (despite saccharin being noncaloric), greater weight gain, increased body fat, and lowered temperature change (reflecting a lowered metabolic rate) when other caloric foods were introduced.
As we know, a normal diet doesn’t consist solely of NAS or zero calories; one is bound to encounter calories and glucose at some point. This study revealed that, with the presence of NAS in the diet, the aforementioned predictive relationship is no longer tightly regulated, and when one eats or drinks anything with calories going forward, the body doesn’t quite know what to do with itself. In response, it cannot find its satiety point, stores fat, and does not burn energy as efficiently.
As you can see, it’s not to say that sugar is by any means an innocent bystander. This study, however, effectively shows that NAS are certainly not a magic bullet for weight loss either. In fact, they fare worse on almost all accounts.1
While Swithers’ research indicates that NAS do not have much influence on glucose homeostasis, a 2014 study3 by Suez et al. discovered a secondary route through which these noncaloric sweeteners do affect our glucose metabolism – via our microbiome.
Most of the noncaloric sweeteners fail to elicit an insulin response because, well, they go right through us. They slide through our GI system without being absorbed into the gut. Through their transit, though brief, they interact with our glorious microbiome and the intestinal bacteria colonies residing there, which we are learning play integral roles in regulating multiple physiological processes.3 This groundbreaking study went on to research how NAS may directly impact the microbiome, and as a result, the many processes to which it is intimately connected, including glucose metabolism.
In a set of experiments, Suez et al. monitored the glucose tolerance of mice ingesting water sweetened with aspartame (Equal, NutraSweet), saccharin, and sucralose (Splenda). At week 11 of this experiment, the NAS-mice had developed marked glucose intolerance compared to those ingesting sucrose, glucose, and plain water.
To determine whether their glucose intolerance was specifically induced by changes to their microbiome, antibiotics were administered to address their cultured dysbiosis. Lo and behold, once their dysbiosis was eradicated by the antibiotics, their glucose tolerance returned to healthy curves, despite the mice maintaining their NAS-laden diets. Further, the researchers took a fecal transplant from the dysbiotic guts of these mice and placed them into healthy germ-free mice. Six days after the transfer, glucose intolerance ensued in the recipients, illustrating a clear relationship between NAS use, resultant dysbiosis, and causative metabolic dysregulation.3 To note, saccharin-consuming mice displayed considerable dysbiosis, engendering the most significant changes in microbial overgrowth.
The researchers then went on to confirm the same effects in humans. Following seven healthy volunteers who do not consume NAS, the researchers asked the participants to ingest the upper limits of the FDA-approved daily allowance of saccharin for one week. Through monitoring glucose measurements, researchers found that the participants developed poorer glycemic responses compared to controls. Most importantly, there were significant changes to their microbiome composition after NAS ingestion.
To determine whether the dysbiotic changes to their microbiome caused their metabolic changes, fecal transplants from Day 1 and Day 7 of the trial of the NAS-participants and controls were placed into healthy germ-free mice. Day 7 transplants induced significant glucose intolerance in the mice compared to Day 1. However, both Day 1 and Day 7 transplants from controls had no effect on the mice’s glucose tolerance.
This study showcased that, in both mice and humans, increased incidence of glucose intolerance was mediated by modulation of the composition and function of their gut microbiota.3 As we know, one’s glucose tolerance plays a significant and direct role in their risk for developing obesity and metabolic syndrome.
As Suez nicely put it, NAS are “enhancing the exact epidemic they themselves intended to fight.”3
As I mentioned before, but it doesn’t hurt to reiterate, this is not a post recommending sugar consumption over NAS. Minimal to no amounts of both should be consumed in efforts to lose weight and restore metabolic and hormonal communication. However, I hope these studies revealed that a calorie certainly is not just a calorie, and this notion of weight management is antiquated at best. There are multiple players in the game and multiple avenues by which one can treat and improve such derangements. NAS add insult to injury by impairing multiple systems simultaneously.
A balanced diet, rich with wholesome, unprocessed, nutrient-dense foods will eliminate the need for sugars and the artificial sweeteners that were created to replace them. Once you’ve made the switch, you will find out that life without both of them is, well, a whole lot sweeter.
If you would like a heads-up for when I write a future follow-up post to this one, detailing the most relevant research on all of the sweeteners out there (including Stevia, Lo Han Guo, and sugar alcohols) and their effects on our body, please fill out the subscription link on this page.
Thanks for reading!
- Swithers, S.E.; Davidson, T.L. A Role for Sweet Taste: Predictive Relations in Energy Regulation by Rats. Behavioral Neuroscience 2008, 122, 161-173.
- Swithers, S.E. Artificial Sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends in Endocrinology and Metabolism 2013, 24, 431-441.
- Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 2014, 514, 181-188.