Dave Atherton of Freedom2Choose (which claims to seek “to protect the informed choices of consenting adults on the issues of smoking”) has written a piece that touches on the issue of smoking and SIDS. I found it quite interesting. But probably not for reasons that would please the author.
The article in The Commentator introduces SIDS to the argument here:
The accusations are that second hand smoke (SHS) leads to “cot death (sudden infant death syndrome, or SIDS), asthma, lower respiratory infections, glue ear, bacterial meningitis as well as coughs and wheezes.”
This is no more than the triumph of faith over science, in this case creating a platform of prejudice, intolerance and bigotry against smokers. The Department of health (DH), the BMA and other anti-smoker groups are fabricating evidence, called publication or wish biases. The perversion of science knows no limits.
Atherton “deals with” the BMA by pointing to a single correction they have issued. Well, that’s their credibility gone forever. Imagine having to correct something you’ve written. It doesn’t bear thinking about. I bet Dave’s never done it. He goes on:
As for cot deaths or SIDS: in the UK, from 1970 to 1988, SIDS deaths rose by 500 percent while smoking rates and, by definition, exposure to SHS, reduced from 45 percent to 30 percent of the population.
If that doesn’t sound alarm bells, in 2010, Harvard Medical School, funded by the National Institute of Health, found the true cause, and I quote: “The researchers found that serotonin levels were 26 percent lower in tissue from infants who died of SIDS than in tissue from the group of infants who had otherwise died unexpectedly. Measurements of tryptophan hydroxylase, an enzyme needed to make serotonin, also were 22 percent lower.”
The most famously famous thing I can think of in relation to SIDS involves something that we did during that time period (and for some time before that, mind) that was thought to be a good idea but was later estimated to have killed as many as 50,000 infants in Europe, Australia, and the US. Coincidentally, 1988 is the same year mentioned here as being the end of the promotion of this behaviour: PDF.
For those ‘pro-choice’ advocates who want to know what that thing is, here’s a quote from that PDF:
Sleeping on the front was recommended in books between 1943 and 1988 based on extrapolation from untested theory.
Surprisingly for an expert on SIDS and Teh Science, Dave Atherton seems to be unaware of this obscure bit of history that is almost never mentioned and certainly does not appear prominently on the Wikipedia page for SIDS.
Now, onto the second paragraph in that quote. What are the researchers quoted as saying in the article he links to? That they’ve found “the true cause” of SIDS? Er. Not quite. While keen to quote their findings regarding serotonin levels and tryptophan hydroxylase levels, Atherton seems less keen on quoting other bits of the report he links to. Especially the bits that contradict his “the true cause” schtick or make clear what risk factors the researchers found in cases of SIDS.
The researchers theorize that this newly discovered serotonin abnormality may reduce infants’ capacity to respond to breathing challenges, such as low oxygen levels or high levels of carbon dioxide.
In earlier work comparing SIDS cases with other infant deaths, Kinney and her coauthors showed that the brains of infants who died of SIDS had higher concentrations of cells that use serotonin in the medulla oblongata, a region of the brain stem. For the current study, the researchers set out to see if this meant the SIDS infants’ brains in fact had altered levels of the brain chemical.
This abnormality appears to fit into the triple-risk model of SIDS, which holds that SIDS occurs only when three elements come together: an infant with an underlying vulnerability, a critical period of development, and an external stressor. The researchers speculate in this case that the low serotonin level would cause the underlying vulnerability. The first year of life is the critical period of development for stabilizing vital functions such as breathing. The final element of the model, sleeping face down, might provide the external stressor.
“Our research suggests that sleep unmasks the brain defect,” Dr. Kinney said. “When the infant is breathing in the face-down position, he or she may not get enough oxygen. An infant with a normal brainstem would turn his or her head and wake up in response. But a baby with an intrinsic abnormality is unable to respond to the stressor.”
“It’s no one single factor but a culmination of abnormalities that result in the death,” Dr. Kinney said. In fact, in 88 percent of the SIDS cases they examined, the researchers found two or more risk factors, such as the infant’s sleep position, an illness, or exposure to cigarette smoke.
Did Dave Atherton not read the article he linked to, or did he simply hope that his readers would not?
Wiki’s citations for the inclusion of smoking as a prenatal and postnatal risk factor for SIDS include this: http://www.surgeongeneral.gov/news/speeches/06272006a.html “Infants who die from SIDS tend to have higher concentration of nicotine in their lungs and higher levels of cotinine (a biological marker for secondhand smoke exposure) than infants who die from other causes. We have also found that infants who are exposed to secondhand smoke after birth are also at increased risk of dying of SIDS. ” and this: http://www.ncbi.nlm.nih.gov/pubmed/20642831 “We observed a wide spectrum of ependymal pathological changes in sudden death victims, such as desquamation, clusters of ependymal cells in the subventricular zone, radial glial cells, and the unusual presence of neurons within and over the ependymal lining. These alterations were significantly related to maternal smoking in pregnancy.”
You may also find this interesting: http://www.ncbi.nlm.nih.gov/pubmed/16898673.
Over 60 studies have examined the relation between maternal smoking during pregnancy and risk of SIDS. With regard to prone-sleep-position intervention programs, the pooled relative risk associated with maternal smoking was RR = 2.86 (95% CI = 2.77, 2.95) before and RR = 3.93 (95% CI = 3.78, 4.08) after. Epidemiologically, to distinguish the effect of active maternal smoking during pregnancy from involuntary tobacco smoking by the infants of smoking mothers is difficult. Clear evidence for environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking when the mother is a non-smoker. Seven such studies have been carried out. The pooled unadjusted RR was 1.49 (95% CI = 1.25, 1.77).