Melanocyte-stimulating hormone

In your hypothalamus, leptin resistance drives dysregulation of neuropeptides.

So all of a sudden, your MSH, your VIP, ADH, there we go.

And so the lab tests you do looking for ADH, and MSH is one of the master ones, that when that gets down, you mentioned it briefly before, how that helps with pain regulation in your reverse spinal tract, that when that's low, part of your innate system fighting off infections, so that sets people up for this thing called Marcon's.

Yeah.

So all of a sudden, this dysregulation of hypothalamus driven by leptin resistance comes forward to that.

It goes right up to your ethmoid plate.

And basically, if you can visualize the brain, this regulatory center, hypothalamus, like literally, it's like right on top of that ethmoid plate.

And all of a sudden now, these hemolysins go in and disrupt your POMC molecule, which turns into, affects cortisol, affects MSH.

And it's composed of seven amino acids in a sequence that is also found as part of the 13 amino acid sequence in alpha-melanocyte stimulating hormone.

which we normally abbreviate as alpha-MSH.

This hormone is produced by cells in the brain as well as in the skin, and it then circulates in the blood.

It acts as a chemical messenger, fitting into melanocortin receptors found on cells in the skin, the adrenal glands, and the brain.

In the brain, alpha-MSH can affect appetite, body weight, and energy expenditure.

In the adrenal glands, it can stimulate the production of various steroids, such as cortisol.

And in the skin, it can fire up cells called melanocytes that then release the pigment melanin responsible for tanning.

These have been keepers.

So the MSH deficiency and MMP9 increase and things we hear about and talk about were ones that I had stumbled upon mostly.

And I was about the only person doing this kind of work back in 1996.

But others joined, and we had situations where there was disagreement.

And it's almost that simple.

And if you don't have HLA, it's 99% of the time you will.

MSH deficiency comes in.

And with HLA not being 100%, but MSH accounting for the rest, we have now got two markers for who's sick, who's not.

So for intranasal KPV, we want to think of it in terms of neuroinflammation, post-injury brain resilience, or neuroimmune modulation, uh, rather than focusing on its, uh, common benefits seen with injectable KPV such as gut and, and, and skin applications.

So for the proposed intranasal benefits, we'll look at things like the neuroinflammation support, whereby KPV is the C-terminal tripeptide fragment of alpha MSH and has well-described anti-inflammatory activity.

In central nervous system-related models, alpha MSH KPV signaling has been associated with suppression of inflammatory pathways, including NF-kappa beta, interleukin-one beta, TNF alpha, interleukin-six, and inflammatory cell activation.

Then just like BPC-157, we'll look at TBI and head trauma resilience, whereby this is probably the most compelling central nervous system-specific research angle for KPV.

In a mouse-controlled cortical impact model, KPV administered after TBI produced an approximately twenty-four percent smaller secondary brain lesion, reduced microglial activation, and reduced neural, uh, neuronal apoptosis.

And this gives KPV a fairly specific neuroimmune regulation, uh, potential benefit.

Then we look at neuronal preservation, where KPV reduced markers of neuronal apoptosis after experimental brain trauma, suggesting potential protection of neurons during the inflammatory period following injury.

Then we have things like cytokine balance after neurological stress, where that broader alpha MSH KPV literature supports modulation of inflammatory cytokine signaling and immune cell migration, making KPV potentially interesting after neurological insults characterized by excessive inflammation.

but if you can get into a consistent schedule with it your body will feel better just being used to the same thing every day and what you can do to kind of boost the effects of that is to make sure that when you do wake up as soon as you possibly can get out into the morning light, even if it's just standing out on your patio or in front of your front door or on a balcony or wherever you're living and just absorbing a little bit of sun on your skin, preferably without sunglasses or glasses, just kind of let the natural light hit you.

That is one of the only researched ways to stimulate alpha MSH, or as we usually say MSH, which is of course notoriously low in SERS patients.

Notorious MSH.

It's our own rap song now.

We need to make t-shirts.

It's all good.

The next category we're going to talk about is hydration.

And the reason why hydration is so important for SARS patients is because low MSH causes dysregulation and ADH osmolality, which is basically like your body's balance of electrolytes and fluids.

They attach to the leptin receptors on your pituitary gland.

And you might've heard of leptin as being like the hung, or I guess the full signal hormone, but it actually has a lot of other things that it does, including creating this other thing called MSH or melanocyte stimulating hormone.

You hear Milano, you might think it only has to do with your skin.

But no, it has to do with basically every other hormone in your body.

And it's the cause of a lot of the, the symptom sets we see with service patients, including insomnia, because low MSH can lead to melatonin disruption.

It can also lead to other hormone disruption, like your cortisol, your sex hormones, et cetera.

So there's a lot of different ways that this low MSH can cause insomnia.

It's a very common symptom for SIRS patients.

So VCS was our first, HLA was our next.

In that group, there was a, a regulatory neuropeptide, melanocyte-stimulating hormone, which is essentially negative in all cases and normal in all controls.

And then with treatment, we saw the improvement in MSH, not as much as what we wanted, and that was the impetus to keep on.

Scott mentioned cytokines.

In nineteen eighty-six, nineteen eighty-five was the first publication of a paper on cytokines.