Let’s take a closer look at several studies suggesting this type of harm from aspartame, including the one you cite using older people: Fowler, Williams et al., http://www.ncbi.nlm.nih.gov/pubmed/18535548. Another often cited critical study used diabetic/obese mice, Fowler, S.P., Halade, G.V., Fernandes, G. (2011). ‘Aspartame consumption is associated with elevated fasting glucose in diabetes-prone mice.’ Poster presentation. American Diabetes Association. San Diego Convention Center. June 27, 2011. San Diego, California. [If the study had been peer-reviewed, changes in the design and analysis may have been recommended and with implementation of the research, the findings could have been eliminated, see http://www.aboutaspartame.com/arc/article.asp?aid=204].
Frankly, my independent reviews of aspartame safety have discovered and can prove that all the papers criticizing aspartame represent scientific garbage often by activists with little understanding of the science involved. I have yet to find one that doesn’t suffer fatal experimental issues. My criticism differs from the comments by others about the first paper and the bracketed comment following the second. But in this case both these above papers are simply NOT credible works for yet other fundamental reasons. That explains why aspartame is judged safe by all the relevant world’s regulatory agencies. In this case the former is an epidemiological study; such studies actually mean little in general (unless are variables are controlled, which is very difficult) and even less when it comes to deciphering safety issues. The mouse research suffers from the same fundamental problem. What is worse than the papers lacking appropriate scientific controls, is that the authors are so clueless about the real science that they don’t even know what ARE the appropriate controls. Let me explain!
First, I need to provide the reader some background so that they can understand the errors of these works. Aspartame is metabolized completely before absorption to its two amino acid constituents and methanol. So it is not aspartame itself, but only these constituents, than can be responsible for any effects of aspartame. The amino acid constituents are more abundant in milk, meats, and other common foods than in aspartame. Thus all problems with aspartame reside not with these two amino acids, but with methanol and specifically not with even methanol nor its formaldehyde intermediate oxidation product, but with the final oxidation product formic acid (formate). Both formaldehyde and more importantly formate metabolism are nearly completely dependent on folate and folate status of the user. Not surprisingly treatment in methanol poisoning now days involves treatment (with vitamin) folic acid derivatives and inhibitors of alcohol dehydrogenase inhibitors that slow the very rapid rate of formation of that formate. So again the only issue here is formate and the serious acidosis it produces. Papers critical of aspartame invariably fail to take into account these critical folate issues, yet they have been known for methanol metabolism for 20 years (http://www.ncbi.nlm.nih.gov/pubmed/1997785).
Second, none of these papers even consider the folate status of their test subjects, human or mouse. And that consideration is vital for two reasons. First, a large percentage of the human population is deficient in folate and related vitamins like B12 and there are polymorphisms (enzyme differences) in the folate enzymes that make as many as 40% of the human population require substantially more folate. Older people are even more deficient. And second, the interested reader should be aware that folate deficiency is a substantial issue with regard to insulin resistance and insulin issues (http://www.ncbi.nlm.nih.gov/pubmed?term=folate%2Cinsulin; over 345 references). The mouse work is guilty for not one but two reasons, both of which are similar. First, it is entirely inappropriate to treat animals with aspartame alone and to think it means something. Aspartame metabolism generates methanol, which not only requires folate for metabolism, but the formate produced can also deplete folate selectively in the treated, but not the control group, since they did not receive any methanol. Such studies violate adequate control requirements. With this faulty control, folate status becomes the issue, not aspartame safety and the longer you run the experiments the more faulty results are produced—this was a critical problem in the Italian Soffritti et al studies reporting problems with aspartame, but which have been dismissed world-wide. But those Soffritti et al studies also used Sprague-Dawley rats that are known to become deficient in folate after just one year. Yet their experiment ran for a roughly three year lifetime of their rats. Hence, all the signs and symptoms they observed (mammary cancer, etc.) were really evidence of an induced-folate deficiency. Now, as to the mouse experiment, obese/diabetic mice have serious known issues with folate, http://www.ncbi.nlm.nih.gov/pubmed?term=folate%2Cdiabetes%20mice. So the third experimental paper suffers from the same fundamental problem as the epidemiology paper.
So why were these very-well-known factors not considered or even mentioned in these papers? There is always ignorance of the long-known issues. Thus, the reader must consider there may be another factor at play. There is an on-going effort to condemn aspartame mostly by scientifically illiterate, anti-aspartame zealots. But the acute desire for funding (and publicity) by some scientists makes many board any floating boat, whether their work is done correctly or not. So, the take home message is again that aspartame safety has been supported by all relevant scientific regulatory experts in the western world. It would seem that this issue discussed here represents but another effort to dredge some concern upon which to hang ones financial hat.
John E. Garst, Ph.D. (Medicinal Chemistry, Pharmacology, Toxicology, and Nutrition)
Comment Reply
Let’s take a closer look at several studies suggesting this type of harm from aspartame, including the one you cite using older people: Fowler, Williams et al., http://www.ncbi.nlm.nih.gov/pubmed/18535548. Another often cited critical study used diabetic/obese mice, Fowler, S.P., Halade, G.V., Fernandes, G. (2011). ‘Aspartame consumption is associated with elevated fasting glucose in diabetes-prone mice.’ Poster presentation. American Diabetes Association. San Diego Convention Center. June 27, 2011. San Diego, California. [If the study had been peer-reviewed, changes in the design and analysis may have been recommended and with implementation of the research, the findings could have been eliminated, see http://www.aboutaspartame.com/arc/article.asp?aid=204].
Frankly, my independent reviews of aspartame safety have discovered and can prove that all the papers criticizing aspartame represent scientific garbage often by activists with little understanding of the science involved. I have yet to find one that doesn’t suffer fatal experimental issues. My criticism differs from the comments by others about the first paper and the bracketed comment following the second. But in this case both these above papers are simply NOT credible works for yet other fundamental reasons. That explains why aspartame is judged safe by all the relevant world’s regulatory agencies. In this case the former is an epidemiological study; such studies actually mean little in general (unless are variables are controlled, which is very difficult) and even less when it comes to deciphering safety issues. The mouse research suffers from the same fundamental problem. What is worse than the papers lacking appropriate scientific controls, is that the authors are so clueless about the real science that they don’t even know what ARE the appropriate controls. Let me explain!
First, I need to provide the reader some background so that they can understand the errors of these works. Aspartame is metabolized completely before absorption to its two amino acid constituents and methanol. So it is not aspartame itself, but only these constituents, than can be responsible for any effects of aspartame. The amino acid constituents are more abundant in milk, meats, and other common foods than in aspartame. Thus all problems with aspartame reside not with these two amino acids, but with methanol and specifically not with even methanol nor its formaldehyde intermediate oxidation product, but with the final oxidation product formic acid (formate). Both formaldehyde and more importantly formate metabolism are nearly completely dependent on folate and folate status of the user. Not surprisingly treatment in methanol poisoning now days involves treatment (with vitamin) folic acid derivatives and inhibitors of alcohol dehydrogenase inhibitors that slow the very rapid rate of formation of that formate. So again the only issue here is formate and the serious acidosis it produces. Papers critical of aspartame invariably fail to take into account these critical folate issues, yet they have been known for methanol metabolism for 20 years (http://www.ncbi.nlm.nih.gov/pubmed/1997785).
Second, none of these papers even consider the folate status of their test subjects, human or mouse. And that consideration is vital for two reasons. First, a large percentage of the human population is deficient in folate and related vitamins like B12 and there are polymorphisms (enzyme differences) in the folate enzymes that make as many as 40% of the human population require substantially more folate. Older people are even more deficient. And second, the interested reader should be aware that folate deficiency is a substantial issue with regard to insulin resistance and insulin issues (http://www.ncbi.nlm.nih.gov/pubmed?term=folate%2Cinsulin; over 345 references). The mouse work is guilty for not one but two reasons, both of which are similar. First, it is entirely inappropriate to treat animals with aspartame alone and to think it means something. Aspartame metabolism generates methanol, which not only requires folate for metabolism, but the formate produced can also deplete folate selectively in the treated, but not the control group, since they did not receive any methanol. Such studies violate adequate control requirements. With this faulty control, folate status becomes the issue, not aspartame safety and the longer you run the experiments the more faulty results are produced—this was a critical problem in the Italian Soffritti et al studies reporting problems with aspartame, but which have been dismissed world-wide. But those Soffritti et al studies also used Sprague-Dawley rats that are known to become deficient in folate after just one year. Yet their experiment ran for a roughly three year lifetime of their rats. Hence, all the signs and symptoms they observed (mammary cancer, etc.) were really evidence of an induced-folate deficiency. Now, as to the mouse experiment, obese/diabetic mice have serious known issues with folate, http://www.ncbi.nlm.nih.gov/pubmed?term=folate%2Cdiabetes%20mice. So the third experimental paper suffers from the same fundamental problem as the epidemiology paper.
So why were these very-well-known factors not considered or even mentioned in these papers? There is always ignorance of the long-known issues. Thus, the reader must consider there may be another factor at play. There is an on-going effort to condemn aspartame mostly by scientifically illiterate, anti-aspartame zealots. But the acute desire for funding (and publicity) by some scientists makes many board any floating boat, whether their work is done correctly or not. So, the take home message is again that aspartame safety has been supported by all relevant scientific regulatory experts in the western world. It would seem that this issue discussed here represents but another effort to dredge some concern upon which to hang ones financial hat.
John E. Garst, Ph.D. (Medicinal Chemistry, Pharmacology, Toxicology, and Nutrition)
September 11, 2011 - 2:11pmThis Comment
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