I see another side of the coin: the data brought by Billioti de Gage et al. seem to corroborate a narrative that aluminum intake can increase the risk for Alzheimer's disease. This relationship - aluminum and Alzheimer's disease - has been documented in the literature for over a decade. The basic science suggests aluminum interacts with proteins involved in amyloidogenesis. This is relevant to this study because Klonopin, a prescription drug, contains aluminum lake. So does, Xanax, Valium, and a host of other benzodiazepines. It is plausible that daily intake of aluminum-containing products over a long span of time can be a risk factor for Alzheimer's disease. Indeed, aluminum toxicity can lead to encephalopathies (See "dialysis dementia") that mimic symptoms of Alzheimer's disease such as confusion, memory loss, disorientation, and loss of coordination.
While it is true that aluminum is poorly absorbed and efficiently cleared from the body, this is not true for patients suffering from renal insufficiency. Further, aluminum has an extraordinarily long terminal half-life (>100 days) which could lead to the accumulation of the metal in tissues after multiple dosing regiments, thus precipitating aluminum toxicity, which has been shown to potentiate Alzheimer's disease. It would be interesting to see this study coupled with the analysis of aluminum plasma levels of the participants; that is, do the patients who consume benzodiazepines containing aluminum have an altered plasma profile? In this study, for example, were there any benzodiazepines without aluminum lake? Are there any differences in AD outcomes between those who took benzodiazepines with aluminum lake and those who didn't?
Competing interests: No competing interests