Th2

And so it's inflaming against stuff it doesn't even know what it is.

And you get all this nonspecific inflammation called TH2 response.

Specific is I try to kill that virus.

Nonspecific is, oh my God, what's that? It's not me.

Right.

And so then you're taking things to calm the system.

And so these mast cell stabilizers, queristin, luteolin, vitamin C to break down the histamines, diendylelmethane, which is for, people think of it for estrogen metabolism, actually pulls back that TH2.

TH17 is this other runaway inflammatory response, brings you T regulatory dominance.

Also, this triggers a histamine response.

So our immune cells, our Th17 immune cells, our Th2 immune cells are being triggered they are releasing inflammatory cytokines mass cells are secreting histamine when we have yeast and dysbiosis and this is a means to try to take care of the infection but unfortunately the infection is so aggressive and our immune response is so weakened that our body is not successful in clearing infection.

So it's continuing on and our body's making this continuous, excuse me, low-grade inflammation every single day that is inflaming our cells, our tissues.

So the gut is really a big starting point.

or it might work momentarily and then you relapse like you flare so you want to do it right do it right food is medicine focus on healing the gut you also need to work on the liver so this is where like when protocols come in you do liver drainage with homeopathics you're opening up those organs of elimination to allow all the toxins and acidity acidity and everything flush and drain out through urine and stool via liver and kidneys so it is no longer triggering an immune response And you also then need to be doing, you know, other things too.

So immune modulation is a big one.

When you have psoriasis, you're usually Th2 and Th17 dominant.

You want to quiet that part of the immune system that's making those inflammatory cytokines and upregulate the anti-inflammatory part of your immune system, which is your Th1 immune response.

And the other one is developing, developing tolerance and a downpl- and kind of balancing out the TH1, right? So you need to have a balance, but be more or- oriented toward the TH1.

But when you're more oriented towards TH2 and less to TH1, is that's associated with what they call autoimmune conditions.

So that means that there's an imbalance on this side.

Okay? That's what it is.

You've got an immune dysregulation.

Something's going on.

You're oriented towards the TH2 side of, of the lim- of the, uh, immune system's, uh, possible responses.

So we need to do really good cleansing with you.

So immune system age is kind of a, kind of a paradox, um, where you have immunosa insufficiency and then inflammatory aging, which is overreaction.

So again, it's the two sides where you have the TH1 is too low, TH2 is too high.

Welcome to the Peptides and Longevity Podcast.

Each week, we'll dive into groundbreaking science, innovative therapies, and the future of health and longevity.

And, but the one we're gonna really concentrate on is kind of the upper tier, and everything flows from that, is the immune dysfunction, and especially natural killer cell dysfunction, stem cell dysfunction.

What we find is with age or chronic illness, inflammation, stress, and w-with age, you get involution of the thymus that's in your breastbone, and that kinda controls basically two sides of your immunity.

Now, immunity is very complex, but a good way to look at it from a clinician's point, and again, it's also used in, you know, standard textbooks, is look at the TH1 and the TH2 ratio.

Now, on the TH1 side, you could add Tregs, and on the TH2 side, add TH17.

Now, In conventional T-cells, mTOR signaling will inhibit FOXP3 induction, partly by inducing the hypoxia-inducible factor 1-alpha expression.

And in an HIF1-alpha-dependent glycolytic pathway organized around mTOR signaling, that will promote Th1, Th2, and Th17 cells, and indeed even an effector CD8 positive T cell differentiation.

But mTORC1 signaling does negatively regulate memory CD8 positive T cell differentiation.

So you see how lipid metabolism is working through the immune response.

So there's a lot of taking what we've discussed these last now 14 lectures, trying to give you an understanding of what I'm trying to get at when we just look at dyslipidemia.

We could take this, all this information, all this new knowledge you're developing, couldn't we? And we could take it into the laboratory and we could start thinking about, before we start generating experiments, What are the hypotheses that we can deduce from all this lipid regulation, for example, of immune cell populations? And how will that render some mediated control over dyslipidemia? Well, we've been discussing all that rendered control already.

We've been explaining how different lipid populations control relative activity of Th1, Th2, Th17, and now Treg cells today.

We brought in retinoic acid, vitamin D3, and we've already been talking about cholesterol directly via membrane association and oxysterols also directly functioning through T-cell receptor-mediated responses.