Last week my wife showed me a study that found as little as a drink per day increases a woman's risk of breast cancer. We hugged, kissed, and lamented a misguided life.
This week she found a new study that says drinkers live longer than non-drinkers. We hugged, kissed, and threw back a couple of Dewar's.
I suspect our reaction is similar to most when discussing the risks of drinking, overeating or a myriad of other life choices. Yet, if these studies had anything to do with chemicals in our environment, all logic and common sense would be suspended.
I recently read a blog that implied environmental chemicals conclusively caused autism. When you see headlines like this, be it autism, puberty, or ADHD, the authors almost always base their conclusions using three sleight of hand ploys:
- "Big E" vs. "Little e" - They rely on research that uses "Environment" to mean the world around us (Big E), but use "environment" to mean manufactured chemical entities that permeate our lives (Little e). Big E includes viruses, bacteria, diet, and medicines: the set of things we either have some control over (i.e., life choices) or are incapable of controlling (i.e., the vagaries of life). Little e is all about something that is being done to us for which we have no control (i.e., big brother against the masses).
- Group vs. List - They avoid applying any qualitative assignment to the myriad of other known risk factors. This allows the authors to treat all the risk factors as a group and focus on the pollutant du jour. If they had presented a list in order of possible affects, then the reader might be able to evaluate a reasonable approach.
- Ignore the Tone of the Original Research - Peer-reviewed research usually concludes with the authors cautiously making statements about the possible ramifications of the findings. Yet, authors that want headlines in the press use exclamatory statements that do not capture the tone of the original underlying research.
Here are a few "Big E" alternatives that offer better plausible blame than mere chemicals in our environment:
Vaccines and Demographics - I suggest anyone who wants to blame the explosion in autism rates solely on environmental chemicals should read a couple of other epidemiological papers that suggest, rather convincingly, that the culprit may be vaccinations: An Investigation of the Association Between MMR Vaccination and Autism in Denmark states:
Trends in prevalence data in Denmark suggest a temporal association between the introduction of MMR vaccine and the rise in autism. Because thimerosal was not used in any pediatric vaccine in Denmark since 1992 and the greatest increase in autism prevalence followed that year, it is likely that one or more of the viral components or their combination in the MMR vaccine contributed to the reported increase;
Commentary: MMR and Autism in Perspective: the Denmark Story states:
The Institute of Medicine, in seeking to bring an end to research into MMR and autism, appears to have learned little from prior experience. The CDC, for its part, is likely to be accused of adding conspiracy to confusion through its latest Physician Survey Study on vaccines and adverse reactions. In the only question relating to concerns over specific individual vaccines and autism, no box has been provided for MMR.
A recent paper touted by CDC only dispels the notion that Thimerosal is the culprit. This paper does NOT address the vaccine program. In addition a recent study identifies both maternal and paternal age as risks for autism. Milk - If you are ready to jump on BPA as an environmental estrogen causing all forms of dire consequences, then please look at the literature on estrogen and progesterone in cow's milk. One article states:
This is a study in humans NOT mice. Seriously, consider the diet of American children and the level obesity that creates excess leptin which is associated with early production of estrogen. Milk, cheese and calories are ultimately more potent sources of estrogen than BPA.
After the intake of cow milk, serum estrone (E1) and progesterone concentrations significantly increased, and serum luteinizing hormone, follicle-stimulating hormone and testosterone significantly decreased in men. Urine concentrations of E1, estradiol, estriol and pregnanediol significantly increased in all adults and children. (emphasis added)
None of the above says: "Don't look at environmental chemicals." My point is simply that the rhetoric is out of control given the substantial literature of alternative realistic explanations that are bolstered by actual human data. It would be a travesty of science to ignore these data. They should be pursued with at least the same (if not more) zeal that people seem to address environmental chemicals.