Study: Splenda, Sucralose Artificial Sweetener, Could Affect Body's Insulin Response
So don't go out and eat a whole bunch of sugar after eating splenda. Check.
If a non-nutritive sweetener *does* cause insulin to behave differently, the implications would go beyond just ingesting sugar following a period of eating Splenda. For example, if an elevated insulin response occurs while ingesting fats like heavy whipping cream with a non-nutritive sweetener then that could create a hormonal environment in which more of the ingested fat is transported into storage cells. I think that's a super interesting research question, so I hope the next step is to look at whether or not the storage environment changes if an elevated insulin response follows the ingestion of a non-nutritive sweetener. But that's a much more complicated and difficult and expensive thing to test for in humans because the process of testing when and where the body stores fat is a lot more invasive than just testing the subsequent reaction of insulin.
The study only had 17 participants. This sample size is too small to be statistically significant.
I think most people *believe* we know more about how the human body functions than current research has actually established. At this point, a lot of hormone research is done simply to establish *what* is happening inside the human body. It's not necessarily designed to tell an individual what's "good" or "bad" to do. Researchers are trying to establish what physiologically occurs under different conditions because they honestly don't know. So studies like this are necessary because they reveal functions and reactions that are currently undocumented, and that may somehow be connected to larger phenomena that we aren't yet aware of. First, we have to look at *what* happens and then track backwards to learn *why* it happens.
For example, two of the most significant regulators of human bodyfat were *discovered* during my lifetime: leptin function was identified in humans in the mid-1990s, and beta-3 adrenergic receptors were isolated in humans in the mid-1980s. Leptin choreographs a comprehensive series of hormonal and neurotransmitter operations that regulate the level of stored human bodyfat. Beta-3 adrenergic receptors orchestrate levels of fat release from storage AND the rate at which skeletal muscle consumes energy. Both of these research advances started by looking at *what* happens in obese bodies and then tracking back to understand *why* it happens.
Leptin research started with the identification of an "abnormal" gene pattern in obese mice, then the investigation tracked back to identify why the gene abnormality caused the accumulation of excess bodyfat. Beta-3 receptor research started with the observation that the metabolic rate of obese mice didn't down-regulate when the uptake of adrenal stimulants was blocked through all of the previously identified channels, so then the research tracked back to see why this happened. This research into leptin and beta-3 receptors started in animal models -- like the study in the original post, as noted in the abstract -- and the next step was to see if a similar reaction would be observed in humans. Humans are kind of *weird* mammals, so animal models don't always predict what actually happens inside our systems.
Little studies of 17 morbidly obese humans seems small and inconsequential but these tiny steps have to be taken, just to tell us "yes, this happens" or "no, this doesn't happen." Yes or no is the first step on the road to answering *why*.
lovely post, Trillex!
While I agree they used the glucose test to establish a baseline, it is questionable whether non-nutritive sweeteners impact insulin without glucose; unfortunately, this study says nothing about it. I think we can all attest to how differently a body operates in the absence of glucose.
Regardless, that and other studies I've read make it really clear: consuming non-nutritive sweeteners while also consuming nutritive sweeteners is a really bad idea.
I would love to see this study using a low-carb, high-fat control instead of a glucose control. In fact, I'll perform the n=1 experiment once my bgl meter shows up.
In this particular case, we need to know how and why insulin levels are *indirectly* affected, by factors other than serum concentrations of glucose. If non-nutritive sweeteners, which don't raise serum concentrations of glucose, are raising the serum concentrations of other hormones and, in that way, indirectly provoking an insulin response, then that's exciting information because it could reveal additional physiological operations that we may not yet be aware of.
For example, a lot of our information about the relationship between the hormone "leptin" and neurotransmitters in the human brain comes from testing dopamine "D1 agonists" and observing that D1 agonists produce some of the same metabolic effects that leptin produces, even while leptin levels are extremely low. Through that observation -- because the effects were observed in the effective *absence* of leptin -- researchers were able to trace some of the pathways through which leptin works in the human brain. So, if we can identify *indirect* pathways that stimulate an insulin response, those observations could provide valuable information about deeper levels of human metabolic pathways. For example, we know that sugar affects neurotransmitters in the human brain so, if research found that non-nutritive sweeteners also affect neurotransmitters in some way, then that would tell us things that we don't currently know about operations in the brain.
One of the things that makes humans so different from other mammals is the role that our brain plays in orchestrating our metabolic balance. We *know* that we are a lot more complicated in this regard than other mammals. But we don't really know *why*. In humans, the metabolic balance *appears* to be governed by more than just simple hormonal balancing and rebalancing. For example, injecting additional leptin into rats that have a leptin imbalance causes the rats to rapidly shed their excess bodyfat and to change their eating behavior. Injecting additional leptin into humans does *not* have the same effect. Leptin therapy doesn't work on humans (partly) because the human brain has levels of integration between hormonal and neural and biochemical reactions that we don't yet have a way of fully understanding. We're still missing too many pieces of the puzzle.
New to forum...Wont eat Artificial Sweeteners of any kind!!
I'm new to this forum and have only been eating low carb for a month or so. In that time I have spent many hours looking at blogs and websites for recipes. The thing that struck me most was how much artificial sweetener was featured!!!
I am in Australia and we just dont have the same reliance on AS as you guys in the US seem to. In fact, most people I know wont go near it due to its carcinogenic properties.
Besides which, I just cant handle the horrible aftertaste (which I also find with stevia).
Genuine question, not a criticism.....Do people in the US really use that much AS?????
Artificial Sweeteners and Cancer
Artificial sweeteners are regulated by the U.S. Food and Drug Administration.
There is no clear evidence that the artificial sweeteners available commercially in the United States are associated with cancer risk in humans.
Studies have been conducted on the safety of several artificial sweeteners, including saccharin, aspartame, acesulfame potassium, sucralose, neotame, and cyclamate.
What are artificial sweeteners and how are they regulated in the United States?
Artificial sweeteners, also called sugar substitutes, are substances that are used instead of sucrose (table sugar) to sweeten foods and beverages. Because artificial sweeteners are many times sweeter than table sugar, smaller amounts are needed to create the same level of sweetness.
Artificial sweeteners are regulated by the U.S. Food and Drug Administration (FDA). The FDA, like the National Cancer Institute (NCI), is an agency of the Department of Health and Human Services. The FDA regulates food, drugs, medical devices, cosmetics, biologics, and radiation-emitting products. The Food Additives Amendment to the Food, Drug, and Cosmetic Act, which was passed by Congress in 1958, requires the FDA to approve food additives, including artificial sweeteners, before they can be made available for sale in the United States. However, this legislation does not apply to products that are “generally recognized as safe.” Such products do not require FDA approval before being marketed.
Is there an association between artificial sweeteners and cancer?
Questions about artificial sweeteners and cancer arose when early studies showed that cyclamate in combination with saccharin caused bladder cancer in laboratory animals. However, results from subsequent carcinogenicity studies (studies that examine whether a substance can cause cancer) of these sweeteners have not provided clear evidence of an association with cancer in humans. Similarly, studies of other FDA-approved sweeteners have not demonstrated clear evidence of an association with cancer in humans.
What have studies shown about a possible association between specific artificial sweeteners and cancer?
Studies in laboratory rats during the early 1970s linked saccharin with the development of bladder cancer. For this reason, Congress mandated that further studies of saccharin be performed and required that all food containing saccharin bear the following warning label: “Use of this product may be hazardous to your health. This product contains saccharin, which has been determined to cause cancer in laboratory animals.”
Subsequent studies in rats showed an increased incidence of urinary bladder cancer at high doses of saccharin, especially in male rats. However, mechanistic studies (studies that examine how a substance works in the body) have shown that these results apply only to rats. Human epidemiology studies (studies of patterns, causes, and control of diseases in groups of people) have shown no consistent evidence that saccharin is associated with bladder cancer incidence.
Because the bladder tumors seen in rats are due to a mechanism not relevant to humans and because there is no clear evidence that saccharin causes cancer in humans, saccharin was delisted in 2000 from the U.S. National Toxicology Program’s Report on Carcinogens, where it had been listed since 1981 as a substance reasonably anticipated to be a human carcinogen (a substance known to cause cancer). More information about the delisting of saccharin is available at http://ntp.niehs.nih.gov/ntp/roc/ele...ppend/appb.pdf on the Internet. The delisting led to legislation, which was signed into law on December 21, 2000, repealing the warning label requirement for products containing saccharin.
Aspartame, distributed under several trade names (e.g., NutraSweet® and Equal®), was approved in 1981 by the FDA after numerous tests showed that it did not cause cancer or other adverse effects in laboratory animals. Questions regarding the safety of aspartame were renewed by a 1996 report suggesting that an increase in the number of people with brain tumors between 1975 and 1992 might be associated with the introduction and use of this sweetener in the United States. However, an analysis of then-current NCI statistics showed that the overall incidence of brain and central nervous system cancers began to rise in 1973, 8 years prior to the approval of aspartame, and continued to rise until 1985. Moreover, increases in overall brain cancer incidence occurred primarily in people age 70 and older, a group that was not exposed to the highest doses of aspartame since its introduction. These data do not establish a clear link between the consumption of aspartame and the development of brain tumors.
In 2005, a laboratory study found more lymphomas and leukemias in rats fed very high doses of aspartame (equivalent to drinking 8 to 2,083 cans of diet soda daily) (1). However, there were some inconsistencies in the findings. For example, the number of cancer cases did not rise with increasing amounts of aspartame as would be expected. An FDA statement on this study can be found at FDA Statement on European Aspartame Study on the Internet.
Subsequently, NCI examined human data from the NIH-AARP Diet and Health Study of over half a million retirees. Increasing consumption of aspartame-containing beverages was not associated with the development of lymphoma, leukemia, or brain cancer (2).
Acesulfame potassium, Sucralose, and Neotame
In addition to saccharin and aspartame, three other artificial sweeteners are currently permitted for use in food in the United States:
Acesulfame potassium (also known as ACK, Sweet One®, and Sunett®) was approved by the FDA in 1988 for use in specific food and beverage categories, and was later approved as a general purpose sweetener (except in meat and poultry) in 2002.
Sucralose (also known as Splenda®) was approved by the FDA as a tabletop sweetener in 1998, followed by approval as a general purpose sweetener in 1999.
Neotame, which is similar to aspartame, was approved by the FDA as a general purpose sweetener (except in meat and poultry) in 2002.
Before approving these sweeteners, the FDA reviewed more than 100 safety studies that were conducted on each sweetener, including studies to assess cancer risk. The results of these studies showed no evidence that these sweeteners cause cancer or pose any other threat to human health.
Because the findings in rats suggested that cyclamate might increase the risk of bladder cancer in humans, the FDA banned the use of cyclamate in 1969. After reexamination of cyclamate’s carcinogenicity and the evaluation of additional data, scientists concluded that cyclamate was not a carcinogen or a co-carcinogen (a substance that enhances the effect of a cancer-causing substance). A food additive petition was filed with the FDA for the reapproval of cyclamate, but this petition is currently being held in abeyance (not actively being considered). The FDA’s concerns about cyclamate are not cancer related.
Where can people find additional information about artificial sweeteners?
For more information about artificial sweeteners, contact the FDA at:
10903 New Hampshire Avenue
Silver Spring, MD 20993
U S Food and Drug Administration Home Page
Soffritti M, Belpoggi F, Esposti DD, Lambertini L. Aspartame induces lymphomas and leukaemias in rats. European Journal of Oncology 2005; 10(2):107–116.
Lim U, Subar AF, Mouw T, et al. Consumption of aspartame-containing beverages and incidence of hematopoietic and brain malignancies. Cancer Epidemiology, Biomarkers and Prevention 2006; 15(9):1654–1659.
Thanks for that :)
I think I will still stay away from them. Quite apart from anything else, I cant stand the taste!!!!
Interesting study. It was only 17 individuals, but we have a bunch of anecdotal evidence on this board here. Theory says that after a while the emotional and the hunger response to LC cheesecake should be the same as a 6 oz steak.
However we get posts of getting the munchies after sf treats and diet soda even more so. The point to take away to my mind from this study is that we do have an insulin response when eating "sweet" and that this can mean the munchies, something a lot of us empirically know. Another question would be why would you put aspartame in animal food if not to increase their appetite? I am sure the farmer is highly delighted about the pig being overweight.
Swine Nutrition : The good taste of pigs (part I): let it be sweet - pig333, pig to pork community
Beyond that it is interesting to see what happens with the protein/carbs ingested at the same time, but we are just not there yet in the research.
PS : There is now talk of the FDA allowing aspartame in milk without an appropriate label. Shudder!
Aspartame In Milk: Big Dairy Wants To Sneak In Sweeteners Without Labels, But There
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