I’m currently gathering information in an attempt to build a model which gives some insight on the possibility of some unsettling trends in dementia and dementia like conditions in the near future and I’m left with some pretty unsettling questions.
Many people have read the book “Freakonomics” which proposed that abortion legality showed strong correlations to the reduction of violent crime rates in the US. The problem with this theory is that it does not track granularly by state permissiveness, nor is this data consistent with countries outside of the US. In the early 2000’s an intriguing correlation was offered with lead exposure, and indeed we can track the level of pre/post natal exposure to lead with violent crime in regions around the world, including the United States.
Just as interestingly, we can also tie lead exposure to granular levels of violent crime by examining the water systems of these regions. In nearly all regions with heavily contaminated water supply, we see significantly higher levels of violent crime compared to regional average. Unfortunately this type of water system neglect is tied to social and political mechanisms so there’s a pretty tangled web to walk through before asserting that environmental insults via the water supply are causal to violent crime, but… the data is there.
Most environmental insults occur cumulatively and many chemicals like lead and aluminum build up in pontine nuclei and many people’s bodies have no ability to remove them at all over the course of their life. And of course degradation of pontine nuclei like the locus coeruleus and pedunculopontine nucleus have direct links to all dementias, including “Alzheimer’s”, “Parkinsons”, and “Fronto-temporal” presentations.
While we’ve managed to reduce lead exposure and it clearly showed a significant impact in many health related social metrics, we reached a bit of a plateau in the mid 2010’s and many areas are starting to slide back again. My working assumption at this point is that we’ve introduced another pervasive insult that has slowly started taking the place of lead.
Have we reached a point of pervasiveness with aluminum use that we are generating enough micro-particulates to generate lead like effects not only in our water system, but in general atmospheric conditions? Could microparticulate plastic (which would be extremely difficult to detect in imaging) be reaching a critical mass and causing similar astrocyte dysfunction as the brains clearance systems simply have no way to remove these chemicals?
Going a bit further, could these types of pervasive convenience insults actually be the reason obesity rates around the world are expanding? As these non-clearable chemicals build up in a body in both the nervous and vascular systems, are they disrupting the metabolics just enough to trigger multi-system effects?
As it stands, the overwhelming amount of dementia conditions almost certainly go massively under-diagnosed. Among those that do get diagnosed, imaging to verify physiological insult is rare, and among those forensic autopsies to investigate these insults are even more rare. Is it possible the overwhelming hostility of the last decade in US politics has been driven not so much by ideology, but massively underestimated nervous system insult? Are we back on the upward trajectory of violent crime rates that we saw through the 60’s and 70’s as leaded gasoline became more and more pervasive until the absolute bomb we had in the 80’s/early 90’s?
Attempting to get accurate data when social, economic, and political forces are actively working against collecting that data as it would require modification to their behavior is proving to be quite challenging. Trying to avoid being controversial as possible, but is the stunning rise of populism over the past decade an artifact of cumulative neurological insult degrading dorsal stream mechanics?
Edit: Ancillary question – Are most “neuropsychiatric” conditions actually early or congenital dementia? Fine, fuck it, I like to run with scissors. Are “autism” and “ADHD” more accurately described as types of dementia?
I didn’t articulate this well I guess, but the jist here is that if “ADHD” and “Austism” represent congenital dementia types, and the epidemiology of these things are on rails, what does this look like for future dementia when natural degeneration starts kicking in? We’ve blamed the rise of epidemiology of these things on many things, from changes in diagnosis to legislative (no child left behind) influences. What if we actually are looking at a pervasive environmental insult that does not show up readily in imaging, and had a use/incidence rate that continues to peak but had slowing growth starting in the mid 2010’s?
What if when we are looking at dementia, we are conflating two completely separate problems, one is natural aging which imparts some level of degeneration naturally. About half of all humans degenerate “gracefully” and as such don’t show signs of the core issue in dementia, the cognitive issues. Back in the bad old days nearly all of these conditions were considered types of childhood dementia/dementia praecox until psychiatry started creating arbitrary diagnostic categorizations which have perceptually separated these conditions from the core symptoms which are consistent in a 10 year old or a 100 year old.
One of the key problems this line addresses is the heterogeneity we see in psychiatric conditions (which should be impossible at this point). A mechanic must exist which allows nearly any type of brain construction to exhibit this type of behavioral pathology, and that commonality seems very likely to be particulates which manipulate astrocytic actin dynamics and modify cognition at it’s core level.
Another note, I’ve given a lot of shit over the whole “spectrum” construct that psychiatry has embraced for many of it’s conditions, mostly because it indicates poorly defined conditions. It appears I was wrong here, literally all of them are a spectrum. Not because the “traits” blend together, but because common environmental insults can effect most brains the same way, and in the case of “ADHD”, certain types of construction are susceptible to certain types of environmental insults than others. So this is a mea culpa on my part, albeit for completely different reasons.
One of the most interesting artifacts of “autism” is the apparent “youthful” appearance of many phenotypes, what we could be observing are the reduced actin dynamics resulting in less strand breaks over the same period of time.
The construct here is ultimately that these conditions are not “genetic” per se, but certain genetic constructions respond in similar ways to these pervasive environmental insults. By tracking the epidemiology of conditions like “ADHD” and “Alzheimer’s”, observing the rate that environmental insults have compounded in the past, we may be able to get a better estimate of future epidemiology rates of dementias.
This really does speak a bit to pscyhology/psychiatric origins and the “ordered/disordered” construct. The bleed over has resuled in us looking for “ordered/disordered” genes, which probably don’t exist at all leading to the heterogeneity. Because these conditions are only diagnosed through social mechanisms, they are particularly vulnerable to social confounds.
Further reading:
Plastic Deformation and Fragmentation of Strained Actin Filaments – Actin dynamics are the process astrocytes use to physically record “memory” into their morphology. This suggests microparticulates may be literally stripping and distorting memory at a cellular level. (To clarify “plastic” here doesn’t mean the chemical plastic, it refers to cell plasticity. Not even sure how to make that more clear given the context, lol)
Dendritic spine loss caused by AlCl3 is associated with inhibition of the Rac 1/cofilin signaling pathway – The spines are literally “memory”.
Role of Cofilin in Alzheimer’s Disease – Full tie to dementia.
Formation of Cytoplasmic Actin-Cofilin Rods is Triggered by Metabolic Stress and Changes in Cellular pH – Back to the beginning, how AlCl may change metabolics.
Aluminum can activate grapevine defense through actin remodeling – I know, it’s a plant but the actin mechanics are well preserved. Here, they manage to strip pathogen binding sites using Al, tying us back into immune related pathologies like MS inflamation.
Deletion of the Autism-Associated Protein SHANK3 Abolishes Structural Synaptic Plasticity after Brain Trauma – Cofilin deletions in “autism”.
Neuroligin-3 and neuroligin-4X form nanoscopic clusters and regulate growth cone organization and size – Altered actin dynamics in “autism”.
Novel Contribution of Secreted Amyloid-β Precursor Protein to White Matter Brain Enlargement in Autism Spectrum Disorder – “Autism”, “Alzheimer’s” and the particulates in between.
The prevalence and incidence of early-onset dementia among adults with autism spectrum disorder Symptomatic, Genetic, and Mechanistic Overlaps between Autism and Alzheimer’s Disease
Disrupted Timing of MET Signaling Derails the Developmental Maturation of Cortical Circuits and Leads to Altered Behavior in Mice – Similarly broken actin dynamics between dementia and “autism”, difference being development vs. degeneration cycle.
Imaging of aluminium and amyloid β in neurodegenerative disease
Aluminium co-localises with Biondi ring tangles in Parkinson’s disease and epilepsy
Aluminum and Tau in Neurofibrillary Tangles in Familial Alzheimer’s Disease