Earlier this week, we learned from the wonderful world of junk science that eating egg yolks is as dangerous as smoking. Now we learn that eating canned vegetables will harden your arteries! These stories are hard to believe for good reasons, but they sure do make catchy headlines for news sites and green bloggers.
Consider just a few. “BPA Now, Heart Disease Later: The scary new connection between bisphenol A and heart disease,” reads a headline on Prevention Magazine’s website. “BPA may boost artery disease risk” reads another headline on FoxNews.com. But the award for the most amusing “hype-line” on the topic goes to Treehugger: “Link Between BPA and Heart Disease Seen in Urine, New Study Reports.” That’s a new spin on fortune telling!
Trace residues of BPA enters the body when we consume food packaged in containers made using the chemical. For example, aluminum/steel cans are lined with BPA-based resins to control development of dangerous pathogens and extend shelf-life. BPA does not accumulate in the body, but instead passes out in urine.
This study measures the levels of BPA found in urine to assess whether high levels are associated with coronary artery disease. The authors divided 591 patients into three groups based on each individual’s degree of coronary artery disease: severe, intermediate, or normal. The researchers found: “BPA exposure was higher in those with severe coronary artery stenoses compared to those with no vessel disease.”
In addition to the fact that the association was weak and associations do not show cause and effect, there are a number of reasons to seriously question the “findings” of this study. Consider just three:
The study’s method for measuring BPA exposure is a scam.
The study authors admit: “One limitation of this study is that the BPA measures are from single spot urine samples, which could be considered as limited measures of long term exposure.” BPA levels fluctuate substantially on an hourly basis. As a result, a person placed in the “highly exposed” group one day could end up in the “low-exposure” group the next or maybe even in just a matter of hours. Accordingly, these measurements tell us nothing about long-term exposure and cannot be used to classify one group as high exposure and another as low. Studies that use this method are meaningless and not useful for drawing any conclusions.
BPA does not readily enter the blood stream.
BPA is unlikely to affect heart patients because very little, if any, ends up in our blood stream nor does it accumulate anywhere else in the body. The human body metabolizes BPA very quickly; passing through the body as a waste product before it can have any effect. In fact, very little is found in the bloodstream as shown in an EPA-funded study that measured BPA levels in blood an urine. The study’s volunteers consumed a diet containing relatively high level of BPA — levels up to 4 times higher than the highest exposed people in the U.S. population. Out of 320 blood samples, 83 percent had no measurable BPA despite their high exposures. Of the small percent that contained some BPA in the blood, the traces were extremely low. The authors concluded: “reported BPA concentrations in human blood …are highly unlikely in the general population exposed orally to amounts as much as ~4 times greater than the 95th upper percentile of aggregate exposure in the general U.S population.”
There are no plausible explanation for the heart disease study’s conclusions.
The study can’t even postulate a plausible reason, or mechanism, to explain why BPA would impact coronary heart disease. Instead, it notes: “Much remains unknown about the mechanisms involved in the association between BPA and CAD (coronary artery disease) in humans.”
These are not small problems. They render the study meaningless. And this study is not unique. We hear daily about “dangers” from BPA lurking everywhere from dental fillings to supermarket receipts to our food containers. But the research behind those claims, like this latest one, is flimsy. See this paper for more information on BPA safety.