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Technical_Sir_9588 t1_jc0m60m wrote

The interesting thing is that I learned about this from a similar study probably about 6-7 years ago. Capsaicin damages the mitochondria in sensitized nerve cells (which are currently dysfunctional due to sending information to the brain that is incorrect). After the capsaicin application, the nerve cells first retract to some degree from the tissue they're inervating (such as the skin). Eventually those nerve cells regrow but apparently without dysfunctional signaling. I work in health care and I'm always looking for options to help my patients, especially those with chronic pain. I've never found a practitioner that utilized the capsaicin approach. If any, I would expect physiatrists to be the most open-minded to utilize this as a treatment option.

Edit.

This may be the study: https://openaccesspub.org/article/549/ijp-17-1581.pdf

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snappedscissors t1_jc1w1q2 wrote

You should check out the recent research on the receptors TRPV1 and TRPA1, among others. They are best known as external environment sensors, as receptors for heat and capsaicin. In the last decade or so work has shown them to be present in the central nervous system as well. Which begs the question: what is the effect of activating these receptors in neurons and nerve cells? Because the brain isn't getting much direct exposure to hot sauce right?

I read one paper recently looking at capsaicin as an agonist against TRPV1 in mouse neurons in a model for Alzheimer's disease. They showed rescue of a number of metabolic defects seen in neuronal cells during this disease, including increased mitochondrial metabolism. This might indicate a refresh of mitochondria, or a general increase in energy production.

A bunch of research groups are working on receptors like these now, trying to see where they are being activated and by what. They may have applications like this paper, or more!

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Technical_Sir_9588 t1_jc1xrfi wrote

What I understand from some other research is that when these peripheral nerves become sensitized they spontaneous sends afferent signaling to the spinal cord - > brain without any external stimuli. This sustained signaling drives central sensitization. The idea is that central nervous system plasticity allows the reversal from central sensitization to the norm if these external stimuli reinforcing the [pain/damage/harm] are removed, especially since no actual sustained damage to the tissues is present.

I also educate my patients on the benefits of prolonged fasting, with the potential "repair" of peripheral nerves, spinal cord, etc. via autophagy. There is definitely research out there using mouse subjects and I wish more research funds would go towards this end but fasting isn't sexy more is its profitable.

The combo of fasting and capsaicin seem to provide the best outcomes.

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BlueSkyToday t1_jc899wj wrote

I imagine that what you're saying is that just the multi-branched portion of the axion that's near the surface of the skin is what atrophies and then regenerates. Kind of like if I were to sever an axion and then regenerate from the stub.

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