The first days of the new year brought us a reminder that the hypothesi shared by the majority of scientists about a complex system where controlled experiments are hard to do may often be wrong.
For around three decades, the majority of neuroscientists had believed that one of the major plagues of aging, Alzheirmer’s disease, was primarily caused by the accumulation of misfolded amyloid beta protein. However, finally, now a study has been conducted that was capable of at least strongly indicating whether the amyloid hypothesis is true. And the results are not encouraging for it, despite its seemingly overwhelming plausibility. As Science Alert reports:
According to the amyloid cascade hypothesis, knotted fragments of a common protein found in cell membranes are responsible for the degeneration behind Alzheimer’s symptoms of memory loss and confusion.
Since its proposal back in the eighties, the explanation has gathered support in the form of studies showing how aggregates of beta-amyloid have a debilitating effect on health of neurons.
[…]This latest research involved 747 participants from the initiative — 305 classed as cognitively normal, with the remainder diagnosed with some form of cognitive impairment.
One form of testing found 289 had a mild form of decline, but a more specific set of objective psychological assessments determined 153 had subtle cognitive difficulties — indicating they had very early stages of the disease.
A close look at positron emission tomography (PET) scans taken over four years revealed individuals who were objectively assessed for very early, subtle signs of impairment did, in fact, accumulate amyloid at a faster rate than clinically normal participants.
Plaques were also found to accumulate faster over time, as expected in those who might receive an Alzheimer’s diagnosis.
But comparisons with clinically normal brains found no statistical difference in plaque concentrations during the condition’s earliest stages, indicating the protein clumps weren’t necessarily responsible for kicking off the condition.
And interestingly, while the study found those with mild cognitive impairment had comparatively high levels of amyloid in their brains in early scans, these levels didn’t increase with time.
What interests us here is that the situation with CO2 and climate change may be remarkably similar to amyloid and Alzheimer’s. Not in the sense that CO2 may not be a driver of warming at all, it certainly is. But its effects are quite possibly wildly exaggerated.
Just like in the amyloid case, the culprit is certainly strongly present at the crime scene but there are clear signs that something may be quite wrong about just pointing the finger at it, and calling for action. The concentrations of CO2 started rapidly increasing only after WW2 but there had already been quite some warming before that and then almost none until 1978. The major escalations in warming since 1978 mostly coincided with El Nino episodes, although there no theory with a plausible explanation why that should be the case. Finally, the ensemble of climate models all taking the “CO2 is the only culprit” for granted have so far mostly failed to track the global temperatures, especially since 2005, often being on the verge of falling out of the 95% confidence interval.
And the psychological mechanism leading most climate scientists to the strong belief in the CO2’s decisiveness may be similar, too. The issue is considered as hyper-urgent one to solve, and CO2 is the most obvious chief culprit candidate. It is right there for all to see, it is the only factor that is clearly correlated with the warming since the Industrial Revolution, etc. The temptation to implicate it and move on is enormous. The planet cannot wait, just like tens of millions of Alzheimer’s sufferers.
Add to this the huge politicization which was absent in the amyloid case, and anyone should become really cautious about CO2 alarmism. One needs just to recall how the politicized campaign against dietary fat has worked out.