The mind, and habits - Use it or lose it

And a lot of other things

Sometimes, I write an intermiment analysis, an amalgamation of papers that don’t fit an overall theme but are interesting, often, these are more centered around the benefits of doing something specific or just novel breakthroughs. Today is one of those days. This is a general overview, not a complete and complex breakdown of each topic.

We start with a “bad paper” and go towards a good answer shortly after =).

Multiple Sclerosis and Epstein-Barr

In recent years, it has been widely accepted that Epstein-Barr Virus, also known as Human Herpesvirus 4, plays a role and, under very specific circumstances, is the driver of developing MS (Multiple Sclerosis), an autoimmune disease in which the body attacks the brain, especially the spinal cord.

Here, the authors found one of the leading mechanisms in a large cohort (group of patients). EBV creates a reservoir in B cells (mostly memory, older cells), and once infected, it remains latent in the vast majority of people. Whenever your immune system or body gets taxed, the virus may go into the lytic phase, when it starts to replicate inside the cell, leading to lysis, meaning it replicates until the cell explodes and spreads around the region the cell finds itself.

One of the virus's key proteins, called EBNA1, is responsible for latency, survival during latency, and replication. It is highly expressed during active infection, and MS patients generally have higher levels than healthy people infected with EBV. EBNA1 is chronically expressed in B cells at low levels at all times, resulting in repeated exposure over years and decades. EBNA1 can also tightly (strongly) bind to human and viral nucleic acids, creating a more potent immune response.

EBNA1 has molecular mimicry with GlialCAM, a highly important protein in the brain. Thus, this is one mechanism by which your body attacks the brain and spinal cord, creating an autoimmune reaction that can lead to the development of MS. Higher antibody levels against EBNA1 and GlialCAM increase the risk for MS, this is further elevated by specific genes. The more pieces (peptides) of EBNA1 and GlialCAM the body develops, further increase the odds, given one mimics the other. Towards the good news.

High-Dose Vitamin D and dealing with the first symptoms of Multiple Sclerosis

One of the lowest-hanging fruits in immunology, molecular biology, and avoiding long-term disease is keeping your immune system working at optimum levels. Over the decades this lowers both the chances of dying and the chances of developing all forms of disease and cancer, and it keeps all the latent bugs at bay. This is even more significant towards Herpes Virus, where association between low levels of Vitamin D correlates pretty strongly with increased risk of Herpes infection.

The mechanisms by which Vitamin D can aid in lowering the risk of MS are many, and so are the reasons (as I proposed years ago) that high dosage could help manage its symptoms.

100.000 IU every 2 weeks for 24 months helped reduce CIS, which is a definition used to described MS when the diagnostic criteria is not met, and it also helped reduce relapse (when symptoms worsen). Given the low cost, low risk of using high dosage of Vitamin D, and the considerable benefits, testing even for 16 weeks shouldn’t be a problem. A funny one next.

Stimulants and lower mortality

As a stimulant user (the Brain Stack is basically a compounding stimulant centered around cognition), I saw this earlier today, and I was amused for a couple of hours. Stimulant usage when diagnosed with ADHD significantly lowers the all-cause mortality rate, with a more pronounced positive effect on unnatural causes. Perhaps I shall live forever (joking).

Of 148 578 individuals with ADHD (61 356 females [41.3%]), 84 204 (56.7%) initiated ADHD medication. The median age at diagnosis was 17.4 years (IQR, 11.6-29.1 years). The 2-year mortality risk was lower in the initiation treatment strategy group (39.1 per 10 000 individuals) than in the noninitiation treatment strategy group (48.1 per 10 000 individuals), with a risk difference of -8.9 per 10 000 individuals (95% CI, -17.3 to -0.6). ADHD medication initiation was associated with significantly lower rate of all-cause mortality (hazard ratio [HR], 0.79; 95% CI, 0.70 to 0.88) and unnatural-cause mortality (2-year mortality risk, 25.9 per 10 000 individuals vs 33.3 per 10 000 individuals; risk difference, -7.4 per 10 000 individuals; 95% CI, -14.2 to -0.5; HR, 0.75; 95% CI, 0.66 to 0.86), but not natural-cause mortality (2-year mortality risk, 13.1 per 10 000 individuals vs 14.7 per 10 000 individuals; risk difference, -1.6 per 10 000 individuals; 95% CI, -6.4 to 3.2; HR, 0.86; 95% CI, 0.71 to 1.05).

The Brain: Use it or Lose it

Skill changes after age 40: By background characteristics and skill usage.

This is a somewhat complicated paper analyzing data from Germany, analyzing adults over an extended period, which enables the evaluation of skills across the adult lifespan. The findings here go contrary to cross-sectional data (comparing data of different groups at the same time) that suggested early decline, longitudinal data (data over a longer period) showed that average literacy and numeracy skills exhibit significant increase at first, peaking at mid-40’s, and following these peaks, a modest decline was observed in literacy, while numeracy demonstrates a more significant decline in later ages.

Further examination of the data revealed a remarkable trend. Individuals with above-average median skill usage at work and home, measured by reported frequency of reading and mathematical activities, don’t exhibit age-related decline. In fact, they show continued skill improvement into their fifties. The opposite is also true, below-media usage experience a much earlier decline, starting in their mid-thirties.

Consistent with the “use it or lose it” concept, white-collar and tertiary-educated workers (people who went to a university) usually exhibit higher skill usage and maintain or even enhance their skills as they age if they use above the average. This means that active engagement with cognitive tasks, be they your work or daily life, can both mitigate and even reverse age-related decline.

As a big proponent of both never stopping learning and always being curious, but especially handwriting, using pen and paper, this is particularly interesting and positive. And as we talk about the brain, cognition…

Mind over matter and mitochondria

I am a big believer in the concept of mind over matter, meaning how your mind and your beliefs can shape not only your body but also the reality around you. Your mind can “make it or break it” from any perspective you choose to analyze. Recovery, resilience, overcoming odds, achieving goals, from health to overall success, the mind can impact the outcome.

Your psychological state alone can influence how your body breaks down certain proteins, with special importance to Tryptophan, where it plays a highly impactful role by diverging from normal metabolism into the Kynurenine Pathway, which becomes neurotoxic and creates a psychologically negative feedback loop. Given the importance and complexity of mitochondria (they are not merely the powerhouse of the cells, they are more akin to being the GPUs, processors, and Language Models of the cell and the body), what is the impact of the mind over mitochondria ?

The multifaceted roles of mitochondria

Psychosocial experiences predict health trajectories, but the underlying mechanism remains unclear. We report that positive psychosocial experiences are linked to greater abundance of the mitochondrial energy transformation machinery, whereas negative experiences are linked to lower abundance. Overall, psychosocial experiences accounted for 18 to 25% of the variance in protein abundance for complex I, the largest and most upstream mitochondrial oxidative phosphorylation (OxPhos) enzyme. At single-cell resolution, positive psychosocial experiences were particularly related to glial cell mitochondrial phenotypes. As a result, opposite associations between glial cells and neurons were naturally masked in bulk transcriptomic analyses. Our results suggest that mitochondrial recalibrations in specific brain cell types may represent a potential psychobiological pathway linking psychosocial experiences to human brain health.

Psychocosial experience is usually defined as “the subjective experiences, perspectives, feelings, and views of the influences on mood status, cognitive behavioral responses, and social factors of a person”. In this paper, the authors used data from living patients and analyses of the proteins from postmortem brains.

How you perceive everything around you directly affects how your mitochondria function, and how your mitochondria function will inevitably affect how you perceive the world around you. Stress, toxins, and other variables will affect this, but a more positive outlook on life will inevitably benefit your overall health, especially in the long term. In this line of thought, of mind affecting your long-term health, especially neurological health.

Long-term mindfulness meditation increases occurrence of sensory and attention brain states

Interest has been growing in the use of mindfulness meditation (MM) as a therapeutic practice, as accumulating evidence highlights its potential to effectively address a range of mental conditions. While many fMRI studies focused on neural activation and functional connectivity during meditation, the impact of long-term MM practice on spontaneous brain activity, and on the expression of resting state networks over time, remains unclear. Here, intrinsic functional network dynamics were compared between experienced meditators and meditation-naïve participants during rest. Our analysis revealed that meditators tend to spend more time in two brain states that involve synchrony among cortical regions associated with sensory perception. Conversely, a brain state involving frontal areas associated with higher cognitive functions was detected less frequently in experienced meditators. These findings suggest that, by shifting attention toward enhanced sensory and embodied processing, MM effectively modulates the expression of functional network states at rest. These results support the suggested lasting effect of long-term MM on the modulation of resting-state networks, reinforcing its therapeutic potential for disorders characterized by imbalanced network dynamics.

Overall, the results of the current study support the potential of MM to impact brain function by altering the dynamics of functional connections between the different brain regions, even outside of meditation (i.e., as a long-term trait effect), suggesting that MM may increase the stability of neural states that support embodied momentary bottom-up cognition, shifting away from top-down reflective self-related processing.

So I leave you with a message tonight. Thank you for your support =) !