New research suggests there’s a connection between nose-picking and dementia. While there’s many risk factors for dementia such as age, family history, poor diet, lack of sleep and not enough physical activity, nose-picking might be added to the list. The bad habit can result in bacteria traveling through the nasal cavity’s olfactory nerve and reaching the brain creating markers that are “a tell-tale sign of Alzheimer’s disease,” according to research by Australia’s Griffith University.
The study, which was published in Scientific Reports in February, has recently generated a lot of media attention after a press release from the university was sent out suggesting nose picking could increase the chance of dementia and Alzheimer’s. Professor James St. John, the study’s co-author and head of the Clem Jones Center for Neurobiology and Stem Cell Research, said in a press release, “We’re the first to show that Chlamydia pneumoniae can go directly up the nose and into the brain where it can set off pathologies that look like Alzheimer’s disease.”
Professor St. John added, “Picking your nose and plucking the hairs from your nose are not a good idea. We don’t want to damage the inside of our nose and picking and plucking can do that. If you damage the lining of the nose, you can increase how many bacteria can go up into your brain.” As of now, the research has only been conducted on mice and Dr. St. John states, “We need to do this study in humans and confirm whether the same pathway operates in the same way. It’s research that has been proposed by many people, but not yet completed. What we do know is that these same bacteria are present in humans, but we haven’t worked out how they get there.
Eat This, Not That! Health spoke with Dr. J. Wes Ulm, Harvard and MIT-trained MD, PhD with a background in bioinformatics, gene therapy, genetics, drug discovery, consulting and education who was not affiliated with the study, but explains the findings of the research and what to know about the data. Read on—and to ensure your health and the health of others, don’t miss these Sure Signs You’ve Already Had COVID.
Dr. Ulm tells us, “Although the Griffith University team’s research was conducted in mice — and the phenomenon has not yet been directly demonstrated in humans — nonetheless their findings represent a proof-of-principle demonstration that mechanical disruption of the mammalian nasal lining, within the nostrils, can provide a route for bacterial invasion and deposition of amyloid-beta (i.e. Aβ) protein, present within the amyloid plaques in the brain closely associated with Alzheimer’s disease.
There had already been a number of hypotheses and suggestions that such a phenomenon was possible. Clinicians and scientists have long been aware of the olfactory nerve, responsible for our sense of smell, as representing a kind of “back door” into the central nervous system (CNS) that bypasses most of the anatomical firewalls of the blood-brain barrier (BBB). The olfactory nerve is a cranial nerve, part of a group of specialized nerves involved in sensation, movement, and autonomic control (i.e. the involuntary regulation of things like heart rate, blood flow, and pupillary dilation, e.g. through the fight-or-flight response to an external threat).
But unlike the vast majority of cranial nerves — which originate in the brainstem, a lower-down portion of the CNS that acts as a bridge between the spinal cord and brain — the olfactory nerves (one on each side) originate much higher up, within a specialized brain structure called the olfactory bulbs. These then traverse a sponge-like structure called the cribriform plate, part of a skull bone called the ethmoid bone, from where they enter the nose.”
Dr. Ulm explains, “Both animal and human studies have indicated that so-called neurotropic viruses (viral types that can enter the brain, albeit mostly in rare cases) such as those involved in polio, rabies, and measles can utilize the olfactory nerve as a conduit, although the olfactory bulb has robust systems to effect an immune response to remove the microbial invaders as a rule. There is ongoing research on the neurotropic potential of SARS-CoV-2, the virus that causes COVID-19, and potential associations of brain fog and other neurological disturbances with the same processes that cause anosmia (loss of smell) in so many patients with acute COVID infections.
Likewise, Chlamydia pneumoniae — the bacterium mentioned in the study — has been identified as a potential agent in at least some cases of schizophrenia, which studies have identified as being closely linked with structural changes in the brain, visible for example in radiographic studies. Put all these puzzle pieces together, and there’s long been suspicion that Chlamydia pneumonia or other infectious agents might have a role in the deposition of amyloid plaques strongly associated with Alzheimer’s disease, with the Griffith University researchers among the first to provide experimental evidence of a physiological pathway that can lead to such observations.”
According to Dr. Ulm, “There’s been an intriguing series of medical discoveries, over recent years and decades, that are increasingly linking at least some patient cohorts afflicted by chronic diseases — including many autoimmune disorders — with subtle and often unappreciated microbial infections or activity, upending our understanding of their pathophysiology and pathogenesis (the sequence of events in the body that give rise to the condition). Perhaps the most classic example is that of peptic ulcers, once associated simply with stress or the consumption of spicy or fatty foods, but now known to be firmly linked with GI tract colonization by the Helicobacter pylori bacterium in a vast swath of cases. The practical significance of this finding has been incalculable, since it means that a large cohort of peptic ulcer patients can be cured or at least solidly managed with sequential courses of two antibiotics (e.g. clarithromycin and amoxicillin) and a proton pump inhibitor (such as lansoprazole, omeprazole, or esomeprazole), in a so-called triple therapy regimen. Similarly, the primary culprit responsible for cervical cancer is now known to be infection (often silent) by HPV, the human papillomavirus. More recently, a firm nexus has been found between multiple sclerosis and, in many cases, a prior infection by the Epstein-Barr virus (EBV), the cause of infectious mononucleosis or, as it’s more commonly been known by generations of school kids who’ve felt its wrath, mono.
There is likewise mounting evidence that Type 1 diabetes, an autoimmune disease entailing widespread loss of pancreatic beta-islet cells (the insulin-producing islets of Langerhans), may ensue in many cases from a cross-reaction from an immune response against certain enteroviruses, in particular the coxsackievirus, which can cause persistent infections especially in children. And of course, of particular significance over the past two years, SARS-CoV-2 — the infectious agent behind COVID-19 — has been increasingly (and quite unnervingly) connected to a broad array of post-viral syndromes and findings of lingering tissue and organ damage, with or without a formal diagnosis of long COVID. In other words, clinicians and researchers are becoming ever more aware of subtle and once-underappreciated links between infectious disease and chronic conditions, with Alzheimer’s and other forms of dementia likewise garnering interest in the prospects for such an etiology (i.e. a coherent, mechanistic explanation of their causes). Furthermore, and as discussed above, researchers have long been interested in the potential for the nasal passages, and the route of the olfactory nerve in particular, to serve as a gateway for pathogenic microbes to enter the central nervous system. And since nose-picking can disrupt the structural integrity of the mucous membranes in the nose, it goes without saying that researchers would hypothesize (and many indeed have hypothesized) that resulting mechanical damage could serve as a route for infectious pathogens to contribute, at least in part, to the pathogenesis of dementias or other disease processes affecting neural tissue.”
Dr. Ulm tells us, “There remain many unanswered questions and further investigations needed on this topic, and more broadly speaking, the pathogenesis of Alzheimer’s Disease and similar disorders (such as Lewy Body dementia, or LBD) continues to be somewhat murky and unexplained. As a result, researchers can’t firmly attribute much to any proposed cause, let alone one with a still somewhat tenuous linkage like the Chlamydia pneumoniae bacteria tracking the olfactory nerve into the CNS as a result of recurrent nose-picking.
It’s been challenging to tease out the physiological chains of events that lead to disease onset, alongside the ongoing riddles about causes vs. correlations (e.g. the exact role of the alpha-synuclein protein, found in the Lewy body deposits of LBD, as a trigger for the disease vs. a mere association). The pathophysiology of such dementias is likely to be multifactorial, however, in which case these bacteria may well be a contributor in at least some cases if, indeed, amyloid plaques are firmly established as a true causative factor.”
Dr. Ulm says, “On the one hand, as with other intriguing but still somewhat preliminary research findings, we can’t yet fully extrapolate the results in mice to humans. There are distinctive anatomical and structural features in the nasal passages and the conduits that link the murine olfactory nerves (in mice) to the central nervous system in these animals, along with potentially some differences in subtle physiological hallmarks (such as the olfactory bulbs, for which there is mounting evidence of a robust immune protective function humans) that may pose some challenges in applying the mouse results to people. In addition, there’s an ongoing chicken-and-egg debate about whether amyloid plaques in the brain (which are extracellular deposits) are truly a source of causation at all for Alzheimer’s Disease, or whether they are simply correlated (i.e. if the plaques arise merely in association with the condition as opposed to actually causing it).
On the other hand, many such findings in animal models have been at least partially applicable to human physiology and pathophysiology (the processes that give rise to disease), and so they should undoubtedly be regarded seriously and further explored. Moreover, this study is hardly the only one to suggest potential health hazards from any activity that mechanically disrupts the somewhat friable mucous membranes of the nostrils. There’s a solid body of evidence to support the notion that well-maintained, intact, uninjured nasal passages contribute non-trivially to overall health even outside the upper respiratory tract. Put another way: We already have a host of hygienic, social, and cosmetic reasons to discourage nose-picking, and now, there’s a good chance we have yet another health-related basis to come to the same conclusion!”