Finally, proof that aspartame will destroy your kidneys?

Hot on the heels of claims about a study that supposedly correlated aspartame with lymphoma, but that turned out to be “weak”, a 2011 study linking diet sodas to “increased kidney decline” has been making the rounds of the anti-aspartame sites. I am not sure why it took until early 2013 for it to start popping up on the various blog sites.The way that the conspiracy sites tell it, the study was damning and demonstrated that aspartame will pretty much kill your kidneys.

Some headlines:

  • “Diet Soda, Aspartame Shown to Destroy Kidney Function”
  • “Aspartame alert: Diet soda destroys kidney function”
  • “Aspartame and Kidney Damage”

What does the study say?

But what does the study actually say and how does it fit into the larger body of evidence?

As of this writing, the full text of the study (“Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women” by Julie Lin, published in Clinical Journal of the American Society of Nephrology)  is available for free, so anybody can read it without a subscription.

The results:

Consumption of ≥2 servings per day of artificially sweetened (diet) soda was independently associated with eGFR decline ≥30% (OR 2.02, 95% CI 1.36 to 3.01) and ≥3 ml/min per 1.73 m2 per year (OR 2.20, 95% CI 1.36 to 3.55). No increased risk for eGFR decline was observed for <2 servings per day of diet soda. No associations were noted between diet soda and MA or sugar soda and MA or eGFR decline.

With the simplified conclusion of:

Consumption of ≥2 servings per day of artificially sweetened soda is associated with a 2-fold increased odds for kidney function decline in women.

Basically, the study looked at the results of two tests that are associated with a decline in kidney function. One of them, Estimated Glomerular Filtration Rate or eGFR, had apparently a larger decline for diet than for sugar sodas. The other measure, microalbuminuria or MA, did not have a statistically significant effect for either sugar or diet drinks.

Looking deeper into the study content itself, their Table 3 presents the OR values for eGFR decrease (using <1 day to represent OR=1.0) but they do not present a direct comparison between sugar-sweetened and diet drinks for each level of consumption. They show the 1 to 1.9/day (OR 0.9) and >=2/day (OR 2.02) for diet, but only show >=1/day (OR 1.56) for sugar-sweetened. The authors note:”…only 3% of the women in our study consumed ≥1 sugar soda per day”, versus 22% for >=1 for diet soda, which would obviously generate a much smaller sample set. But it seems like it should have been possible to calculate the >=1 per day for diet soda to at least get a better comparison (and perhaps just show it in the footnotes of the table). Forgetting about any sort of comparison (i.e. pretending that we have essentially two separate studies), the granularity makes sense because it was only after 2/day of diet that the potential problem manifests. But, if the two were nearly identical at >=1,it would imply an issue with soft drinks in general, not specific to diet drinks.

But in any case, there is still the 2-fold (100%) increase in risk from >=2 per day which should be looked at. Also note that from 1 to 1.9 per day actually has an OR < 1 (the authors note “No association between lower levels of artificially sweetened soda intake and eGFR decline was seen, implying a threshold effect rather than one that increases linearly”). I doubt that actually means diet beverages have a “protective” effect. But what must also be noted is the 56% increase for >=1 of sugar sweetened. The study is touted as showing diet beverages to “destroy” kidneys, but nobody talks about the increased risk from sugar-sweetened soft drinks. And if I am at all right and combining the diet data to produce a >=1 figure, it would very possibly come very close to the sugar number.

A little statistical support

As I am certainly no statistical expert, I actually consulted a friend who provides statistical support for research at one of the UC schools, and the relevant parts of his response were (emphasis mine):

It is odd that they would evaluate and report the non-equivalent intakes…my guess is that they are justifying this non-equivalency by trying to show “proof of concept” that artificially sweetened soda is, at higher intakes, associated with increased risk.

But you are right that the odds ratio for artificially sweetened drink does not appear to be statistically different than the odds ratio for sugar soda. You can tell by the confidence intervals (CI) they report. The 95% CI is 1.36 to 3.01 for artificially sweetened, meaning that we can be 95% certain that the true OR in the population is somewhere between 1.36 and 3.01 (this range is due to the fact that we are dealing with a sample – the range would be smaller if the sample was larger and/or variance in the outcome was smaller)… the OR for sugar soda, by contrast, is 1.56 (with CI = .84 to 2.91), which is a value that is captured within the CI for artificially sweetened soda and thus not statistically different from it… So what they are saying is that, on its own, drinking more than 2 artificially sweetened sodas a day is associated with increased risk…But they cannot say that this risk is statistically greater than the risk of drinking 1 sugar soda a day…What does the OR look like for 2 or more sugar sodas a day? Seems like that would be important to know….


So this seems to mostly confirm my hunch that perhaps there should be more highlighting the result that consumption of carbonated soft drinks (sugar-sweetened or no) is correlated with a decline in kidney function, in women at least. The authors themselves actually point out that the diet link was not hypothesised so the study was not actually designed to test for that effect. Further studies may nullify it (or strengthen it). This study is in no sense a smoking gun that diet drinks are going to destroy your kidneys.

I want to quickly note that there were two previous studies (both mentioned by the current Lin study). A 2004 study based on the National Health and Nutrition Examination Survey found no association between diet sodas and kidney damage but some association with sugary sodas. A separate 2009 study based on the Multi-Ethnic Study of Atherosclerosis (MESA) also found no association of sugar-sweetened sodas for people with pre-existing chronic kidney disease (CKD).

In all cases the authors mention that it could be other factors in the lifestyle or the beverage itself which relate to the kidney decline, because the studies were not designed to actually figure out what is causing the problem. One crucial thing is that aspartame is never identified as the crucial factor in any of the studies.


So it seems that the analysis here should be tempered — if you consume a lot of sodas (sugary or not), you might be at increased risk for kidney damage versus not consuming soda. But this is not how the anti-aspartame sites present the data, and that is the problem. If anything, this is a great case for moderation, both in consumption and analysis. As is frequently the case with these sort of studies, it seems to warrant further studies specifically intended to isolate the reason for the decline, such as an ingredient common to both sugar-sweetened and artificially-sweetened.

Lin, Julie, and Gary C. Curhan. “Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women.”Clinical Journal of the American Society of Nephrology 6, no. 1 (2011): 160-166.

Shoham, DA, et al. Sugary soda consumption and albuminuria: Results from the National Health and Nutrition Examination Survey, 1999-2004. PloS ONE 3(10): e3431. doi:101371/journal.pone.0003431.

Bomback, AS, et al. Sugar-sweetened beverage consumption and the progression of chronic kidney disease in the Multi-Ethnic Study of Atherosclerosis (MESA). American Journal of Clinical Nutrition, 2009, 90:1172-8.

UPDATE: Clarified the intro.

About Josh DeWald

I am a software engineer, husband and parent of two. I have been involved in the Skeptical movement for a few years now, especially since having children and so needing to fight pseudoscience related to parenting (vaccines, homeopathy, etc). I've been fortunate to attend TAM twice with my wife (who is also of a Skeptical bent). I also have a blog known as "What Does the Science Say?" (, where I have an odd habit of writing a lot about aspartame.
This entry was posted in Health, Science and tagged , , , . Bookmark the permalink.

11 Responses to Finally, proof that aspartame will destroy your kidneys?

  1. kiltederic says:

    Thank you for the write up Josh.

    I am currently a community college student and am taking a nutrition class (albeit a nutrition 101, so not delving very deep into some subjects) and we are finishing up sections on carbohydrates.

    While I am still following the overall conclusion that Aspartame is generally not bad for us, I personally think, what’s the point? Sugars are only 4 kcal’s, the same as proteins, and where fats (lipids) are 9 kcals.

    With such a low caloric amount, why not just consume sugar?

    • Josh DeWald says:

      Fair question. For me personally, it’s the whole “empty calorie” thing due to the sheer quantity of sugar. I am one of those people who drinks ~2 sodas a day. I looked at a can of Coke and it has 36g of carbohydrates (sugar) in it, for about 150 Calories. So with just two sodas you’ve got ~300 Calories in sugar alone vs “0” with the artificially sweetened (it’s probably closer to 5 or so perhaps). That’s a decent chunk of your intake if you’re shooting for something like a 2000 Calorie daily intake Most things with protein are only going to have a few grams (meat aside), and protein is certainly not going to be “empty” calories.

      That all said, I’m not sure if diet drinks are really correlated with weight less necessarily.

      Perhaps a nutritionist can chime in with a more academic response 😉

      EDITED: Corrected my faulty math.

  2. Freke1 says:

    Great info, thanks! Last time I tried a diet cola I had to pour it out, I got an odd feeling in my tummy. I used to drink 1.5 liter a day of that and loved it. Just my personal story, nothing can be concluded from that. It is nice that somebody follows aspartame.

  3. Eric Hall says:

    It is also of note that the study is a self-reporting study. Imagine if you got a questionnaire every other year and it asked you to recall things you eat and drink regularly and in the amounts. I drink a mix of regular and diet soda (2-3 per week total), but I wouldn’t know at what ratio. There are also days where I’ve had 2, and weeks where I’ve had zero. As your friend pointed out, I think the CI’s in this case reflect that uncertainty, and it is pretty hard to pin this effect on just that. It would be nearly impossible to eliminate all differences (pasta intake, apple intake, asparagus intake, etc) among the participants.

    Also of note – are all other ingredients in the soda at the same ratio? “Natural Flavors” – do they need to change the amount depending on the type of sweetener? I didn’t see if they mentioned that in the study.

    I agree with you – good to look at this result in additional study, but I don’t see much to worry about at this point.

  4. rmforallblog says:

    Josh DeWald, congratulations and thanks for an excellent, lucid, reasonable critique on this widely discussed study — I will copy it to my blog — epidemiological studies seem to me to be mostly a waste of time, especially for methanol-formaldehyde toxicity disorders in humans:

    1. ADH1 enzyme, that makes methanol into free floating formaldehyde right inside human cells, is itself free floating inside the cells of 19 specific tissues, especially the inner layers of blood vessels, the rods and cones of the retina, and in fibroblasts in skin and bone marrow — thus there are as many different disorders, varying with the amount and pace of methanol ingestion, and a host of genetic, dietary, infectious, and toxic co-factors.

    2. Folic acid in the blood offers some protection for some people, while many drugs and antibiotics impede folic acid function — notably aspirin.

    3. Ethanol, ordinary drinking alcohol, is a strong antidote for low levels in the blood, about an hourly oral dose of 3 ml 80 proof vodka , which in many people is provided by fermentation by bacteria in the GI tract (so the toxic “side effects” of antibiotics and many drugs may to some unknown degree be via disruption of this ethanol production, leading to formaldehyde toxicity within the cells of vulnerable tissues) — other ethanol sources include most fruits and many vegetables, which strongly reduces the harm from their high levels of methanol.

    Also, this explains the mystery that those who never drink have about twice the level of symptoms from many modern novel chronic diseases as those who drink about one shot (3 ounces volume) of 80 proof vodka daily, while larger daily doses leads to increased harm — called the U-shaped curve — which may be a major indicator that chronic methanol-formaldehyde toxicity is involved.

    Daily heavy drinkers end up with high blood methanol levels, as the ethanol stops the main process of methanol metabolism, so when in a lab experiment the intake was stopped suddenly after three weeks, the resulting high blood methanol levels, with a half-life of 3 hours, dropping 16 fold in 12 hours, generated dangerous alcohol withdrawal symptoms that only started when blood ethanol, with a half life of 20 minutes, dropped 36 fold to effectively zero, allowing the ADH1 enzyme to start making the methanol into formaldehyde within cells. 745 free full texts
    133. Majchrowicz E. Biochemical Pharmacology of Ethanol.
    New York: Plenum Press; 1973.
    134. Majchrowicz E, Mendelson J.
    Blood Methanol Concentrations During Experimentally Induced Ethanol Intoxication in Alcoholics.
    The Journal of Pharmacology and Experimental Therapeutics 1971;179:293-300.

    4. Few indeed know that the smoke from a pack of cigarettes gives as much methanol as a liter of aspartame diet soda — so most of the long-term chronic symptoms of cigarette use may actually be evidence for methanol-formaldehyde toxicity: Alzheimer’s, multiple sclerosis, atherosclerosis, and birth defects spina bifida, autism, preterm birth, many cancers, etc.

    Methanol (wood alcohol) comes from wood smoke as well, while peat smoke gives three times higher doses — hence highest world incidence of multiple sclerosis is in Scotland, where smoked fish is a daily staple.

    5. So, modern methanol sources include:
    smoke from cigarettes wood peat,
    dark wines and liquors,
    fresh tomatoes,
    unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers,
    smoked, fermented, spoiled foods,
    jams jellies marmalades,
    mortuary medical chemical industrial facilities, especially wood and paper factories.

    6. New precision methods now make it possible to directly confirm toxic formaldehyde products in tissues from methanol:

    apoE4 protein scaffold allows growth of human neurons in lab,
    Kwang-Min Kim et al, Brown U — can test harm from formaldehyde made
    from methanol by ADH1 enzyme inside cells of inner walls of brain
    blood vessels, WC Monte paradigm: Rich Murray 2013.01.29

    Initial tests could use micro gram amounts of formaldehyde to show the
    typical processes of harm within neurons:

    confirms WC Monte paradigm: ingested methanol becomes toxic
    formaldehyde-induced hydroxymethyl DNA adducts in all tissues in rats,
    sensitive C13 test, Kun Lu, James A Swenberg, UNC Chapel Hill
    2011.12.08 Toxicol Sci: Rich Murray 2013.01.11

    Then, if neurons can be grown along with small brain blood vessels,
    with ADH1 enzyme free floating within the cells of the inner layers of
    the vessels, the effects of formation of formaldehyde in situ from
    micro grams of added methanol can be studied, confirming the WC Monte
    paradigm, described in detail at and backed
    by a free online archive of 745 full text medical research references.

    Rich Murray,
    MA Boston University Graduate School 1967 psychology,
    BS MIT 1964 history and physics,
    254-A Donax Avenue, Imperial Beach, CA 91932-1918
    505-819-7388 cell
    619-623-3468 home

  5. Stephen Propatier says:

    Josh Great post. Good job on the statistics, now a quick medical piece.
    “. Other self-reported clinical and lifestyle variables including weight, hypertension (HTN), smoking status, physical activity, cardiovascular disease (angina, myocardial infarction, coronary artery bypass surgery, percutaneous coronary revascularization, or stroke), and blood pressure (BP) medication use were reported on the biennial questionnaires. Questionnaire data collected closest to the year when kidney function was measured (the 1988 questionnaire for eGFR decline and the 2000 questionnaire for urinary ACR) were used (Figure 1). In addition, we obtained self-reported BP from the 1990 questionnaire.”
    this is a pointless variable collection for the purpose of this question. How about previous Kidney disease????
    “diabetes and BMI were the strongest confounders of the association between artificially sweetened sodas and MA.” There is your answer people.

    This is a short list of the major things that affect GFR; medication, dehydration, illness, surgery, alcohol consumption, variation in salt intake, variation in protein consumption. Total food and fluid intake for the day is critical. Even if you have a category of diabetics, what is there A1c are they insulin dependent? Self reported “diagnosis” data was used.
    Other methodological errors; I takes a 24 hour urine sample to properly determine any type of kidney malfunction, not one urinalysis. That group selected was older Caucasian women”nurses”, it was not a normal population distribution. As noted above by Eric, self reported study there was no statistical adjustment for under-reporting of sugar beverages, or any food. The original questionnaire was not developed to answer any questions about a kidney healthy lifestyle. on and on go the glaring methodological holes.
    From a medical standpoint this is a retrospective correlational study that did not properly control for variables and used a questionnaire meant to answer a different question in a select population. It is not representative of the general population in any way. If I was on this IRB committee it never would have gotten the go ahead, never mind published.
    It has no chance of determining anything useful about renal disease and any other variable.
    Does not even reach the level of guiding other research.
    As noted in study limitations other study shows no problem with kidney function in a larger population, they just didn’t tweak the variables the same way.
    Josh dead right again.

    • Joe Perkins says:

      I love how it all focuses on “diet soda” with no delineation of WHAT KIND of sweetener was used. They’re not all Aspartame and not just “soda” alone. What about Diet Snapple, artificial sweeteners used in coffee and all other intake? Bet they didn’t “adjust” for those confounding elements.

  6. Anonymous says:

    fine critique by Josh DeWald of aspartame kidney harm survey, J Lin,
    GC Curhan 2011 — now labs directly prove formaldehyde harm inside
    cells from blood methanol via ADH1 enzyme — confirming methanol harm
    in alcoholics, lab study, E Majchrowicz 1971 — WC Monte paradigm:
    Rich Murray 2013.02.02

  7. rmforallblog says:

    ethanol is an antidote that prevents ADH1 enzyme from making methanol (11% of aspartame — liter diet soda or smoke from cigarette pack give 60 mg) into formaldehyde right inside cells in 19 specific human tissues, including pancreas — major cause of hangovers, probable diabetes 2 co-factor — WC Monte paradigm: Rich Murray 2013.02.08

    So, hangovers and other formaldehyde toxicity disorders start only when blood ethanol levels fall to 16 times less molar concentration than blood methanol, “the morning after the night before”, as blood ethanol half life is 1/3 hour, while blood methanol half life is 3 hours, reaching all parts of the body and the fetus every minute with the blood circulation.

    Human ADH1 enzyme is high within the cells of 19 specific tissues: inner walls of blood vessels, retina rods and cones, skin and bone marrow fibroblasts, and the islands of Langerhans in the pancreas.

    Also, the smoke from a pack of cigarettes gives as much methanol, 60 mg, as from a liter aspartame diet soda — so this may be the actual toxin that causes the correlation of cigarettes with Alzheimer’s and multiple sclerosis, atherosclerosis, diabetes 2, many chronic diseases, many cancers, and birth defects spina bifida, autism, preterm birth.

    ADH1 is “unusually highly concentrated” in the million tiny “islands of Langerhans” in the pancreas, where the beta cells make insulin — cigarette use pairs with diabetes 2 risk, with a doubling of risk for smoking over a pack daily.
    [ page 172, “While Science Sleeps”, 2012 January, Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004 includes free online archive of 745 full text medical research references: 5 pages
    637. Bühler R., Pestalozzi D., Hess M., Von Wartburg JP.
    Immunohistochemical localization of alcohol dehydrogenase in human kidney, endocrine organs and brain.
    Pharmacol Biochem Behav. 1983;
    18 Suppl 1:55-9 1983;18(Suppl 1):55-9. 12 pages
    648. Willi C., Bodenmann P., Ghali WA., Faris PD., Cornuz J.
    Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis.
    JAMA 2007;298(22):2654-64. 5 pages
    283. Wei M, Gibbons L, Mitchell T, Kampert J, Blair S.
    Alcohol intake and incidence of type 2 diabetes in men.
    Diabetes Care 2000;23(1):16-21. Ming Wei ]

    All these diseases, including diabetes 2, are twice as harmful for
    those who never drink ethanol, compared to those who have just one standard drink a day, due to the inhibition of formation of formaldehyde.

    Ethanol is also made by fermentation by bacteria in the colon.

    Other methanol sources include wood and peat smoke, fresh tomatoes, unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers, some dark wines and liquors, smoked fermented spoiled foods, jams jellies marmalades.

    diet soda (mostly aspartame, 11% methanol — becomes formaldehyde inside cells, WC Monte paradigm) pairs with increased diabetes 2 in 66,118 women 1993-2007, Francoise Clavel-Chapelon, Guy Fagherazzi AJCN: Rich Murray 2013.02.08

    Study: Diet Soda Increases the Risk of Diabetes. Why Do We Still Drink This Stuff?
    By Lylah M. Alphonse, Senior Editor, Yahoo! Shine | Healthy Living – 8 hours ago

    Why do we keep drinking diet soda? (Photo: Getty Images)

    Yet another study confirms what people have been saying for ages:
    Stop drinking diet soda.
    Like, right now.
    Drinking just one 12-ounce can of an artificially sweetened fizzy
    drink per week can increase your risk of Type 2 diabetes by 33
    percent, French researchers found.
    And given that most people don’t stop at a single weekly serving, your real risk for diabetes could actually be much higher.

    Diet Soda May Increase Risk of Depression

    The study, which was announced Thursday and will be published in the American Journal of Clinical Nutrition, was conducted by France’s National Institute of Health and Medical Research and covered 66,118 middle-aged women whose dietary habits and health were tracked from 1993 to 2007.

    Diet Soda May Be Making You Fat

    The results were unexpected.
    Though it’s well-known that people who consume a lot of sugar are more likely to develop diabetes, the researchers found that participants who drank “light” or “diet” soft drinks had a higher risk of developing Type 2 diabetes than those who drank regular, sugar-filled sodas.
    Those who drank 100 percent natural squeezed fruit juices instead had no additional risk.
    Women who choose artificially flavored soft drinks usually drink twice as many of them as women who choose regular soda or juice — 2.8 glasses per week compared to 1.6 glasses.
    “Yet when an equal quantity is consumed, the risk of contracting diabetes is higher for ‘light’ or ‘diet’ drinks than for ‘non-light’ or ‘non-diet’ drinks,” the researchers, epidemiologists Francoise Clavel-Chapelon and Guy Fagherazzi, said in a statement.

    Women who drank up to 500 milliliters (about 17 ounces) of
    artificially sweetened beverages per week were 33 percent more likely to develop the disease, [ about 2.4 ounces daily ] and women who drank about 600 milliliters (about 20 ounces) per week had a 66 percent increase in risk. [ about 2.7 ounces daily, a quarter of a 12-oz can — aspartame [ E951 ] also is in packets, many foods and medicines, and most chewing gums. ]

    Am J Clin Nutr. 2013 Jan 30. [Epub ahead of print]

    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.
    Fagherazzi G,
    Vilier A,
    Saes Sartorelli D,
    Lajous M,
    Balkau B,
    Clavel-Chapelon F.
    Institut National de la Santé et de la Recherche Médicale U1018,
    Center for Research in Epidemiology and Population Health,
    Villejuif, France.


    It has been extensively shown, mainly in US populations, that
    sugar-sweetened beverages (SSBs) are associated with increased risk of type 2 diabetes (T2D), but less is known about the effects of artificially sweetened beverages (ASBs).

    We evaluated the association between self-reported SSB, ASB, and 100% fruit juice consumption and T2D risk over 14 y of follow-up in the French prospective Etude Epidémiologique auprès des femmes de la Mutuelle Générale de l’Education Nationale — European Prospective Investigation into Cancer and Nutrition cohort.

    A total of 66,118 women were followed from 1993, and 1369 incident cases of T2D were diagnosed during the follow-up.
    Cox regression models were used to estimate HRs and 95% CIs for T2D risk.

    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. [ Body Mass Index ]

    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.
    PMID: 23364017

    Rich Murray,
    MA Boston University Graduate School 1967 psychology,
    BS MIT 1964 history and physics,
    254-A Donax Avenue, Imperial Beach, CA 91932-1918
    505-819-7388 cell
    619-623-3468 home

  8. harold davis says:

    I have gfr rate of 27 and drink approx.2 cans of diet root beer /day.the root beer has no caffeine and no sugar but has aspartame.should I quit drinking the soda?

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