“How bad is Diet Coke for me?”
When someone asks me this, the first thing that comes to mind is aspartame (APM).
It’s the artificial sweetener in the beloved drink of so many. But does it increase one’s risk for cancer?
Let’s dive in.
APM was originally approved by the FDA commissioner in 1981, despite the FDA board of inquiry and several FDA scientists advising against the approval of the product due to brain cancer concerns. (1)
Between 1974 and 2018, several rodent studies were done to determine the effects of aspartame. In the end, different conclusions were made regarding cancer risk (2). Although we can gain some insight in rodent studies, in my professional opinion, conclusions based on rodent studies aren’t conclusive enough for us humans.
That’s not to say all human studies are entirely conclusive either:
An 18-week study on patients with diabetes found no serious adverse effects APM intake. (2)
A 5-year study of high levels of APM intake found no association with increased risk of hematopoietic (blood) cancer. (3)
A 10-year study found no association with an increased risk of lymphoma. (4)
Harvard conducted a long-term study following medical professionals for 18 years. It became the longest, most comprehensive study between the association of aspartame consumption and cancer risk in humans.
What did they find?
Researchers found a positive association between the consumption of diet soda and total aspartame intake with an increased risk in non-Hodgkin's lymphoma and multiple myeloma in men. Plus, an increased risk of leukemia in men and women. (5)
Meaning, the higher the consumption of aspartame, the higher the risk for these types of cancer.
Further studies also found an increased risk of pancreatic cancer in men who consume diet soft drinks containing APM. Interestingly enough, beverages sweetened with natural sugar were not associated with increased risk. (6)
Among other types of sugars researched (lactose, fructose, and sucrose), only lactose (milk sugar) was also associated with increased pancreatic cancer risk. (6)
Why the increased risk?
Aspartame is made from a methyl ester of dipeptide of phenylalanine and aspartic acid.
Whoa! That takes me back to biochemistry and organic chemistry class!
I’ll explain in English.
This component in APM is broken down into methanol in our bodies and then into formaldehyde -- a known human carcinogen.
APM itself is not a human carcinogen, but what it breaks down into is.
So, what does all of this information tell us?
Short-term human studies don’t tell us the whole picture. Even though the short-term studies found no cancer risk, it isn’t enough--in my opinion. The 18-year study was the first to find risk. Think about this, since APM’s introduction to foods and drinks was in 1971, many individuals have regularly consumed this product for a large chunk of their lifetime.
It is likely true that small doses of APM or Diet Coke here and there may not lead to increased risk, but regular consumption is certainly not recommended.
What if you love your Diet Coke? Consider reducing the amount you consume regularly. Switch to carbonated waters flavored with natural flavors, unsweetened teas, or water flavored with fresh fruit.
Although we know consumption of processed sugars isn’t considered “healthy” for us, I still live by the philosophy of, “Eat real sugar, just less.”
(3)Lim U, Subar AF, Mouw T, Hartge P, Morton LM, Stolzenberg-Solomon R, Campbell D, Hollenbeck AR, Schatzkin A. Consumption of aspartame-containing beverages and incidence of hematopoietic and brain malignancies. Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1654-9.
(4) McCullough ML, Teras LR, Shah R, Diver WR, Gaudet MM, Gapstur SM. Artificially and sugar-sweetened carbonated beverage consumption is not associated with risk of lymphoid neoplasms in older men and women. J Nutr. 2014 Dec;144(12):2041-9.
(5) Schernhammer ES, Bertrand KA, Birmann BM, Sampson L, Willett WC, Feskanich D. Consumption of artificial sweetener- and sugar-containing soda and risk of lymphoma and leukemia in men and women. Am J Clin Nutr. 2012 Dec;96(6):1419-28.