VEGF, AKT and You

Hello all,
I’ve been interested in VEGF, (Vascular Endothelial Growth Factor) to varying degrees for PE purposes for a long time now, and recently I’ve been looking into other naturally occurring proteins in the body which may play sympathetic roles in angiogenesis (the creation of new blood vessels). Today, while trying to find some new angle on the soft glans/spongiosum injury I’ve been dealing with for a number of years I found a study referring to a family of proteins called AKT, (protein kinase B), which suggests the inkling of a novel treatment for blood vessel damage.…40610205400.htm
More on that in a minute…

Largely, I’d like to see this thread stay on topic in exploring either lifestyle, chemical, behavioral or other acute strategies for prompting physiological angiogenesis responses, either locally or systemically. It’d also be very welcome to hear those with medical or biological backgrounds giving some insight into VEGF and its variants, AKT, EPO , BPC-157, or edothelial growth proteins or the systems which these interact with in a way that might suggest actionable tools for PE or PE injury recovery (which frankly ought to be thought of as half of PE itself).

Just for those who may need to crash-course, my broad understanding of VEGF is that it is a family of signal proteins that affect a number of changes in the endothelial cells of the vascular system (endothelial cells being those which line the inside of your blood vessels). But it’s most relevant function to our interests is that it seems to play a central role in prompting angiogenesis.
One important caveat is that elevated VEGF levels can play a role in hastening cancerous growth for at-risk populations. This is not necessarily worrisome exactly as for most healthy people the downregulation of VEGF expression is strongly linked to vascular disease, and populations with higher VEGF levels tend to be healthier for longer. It is also worth noting that many many naturally occuring proteins that are necessary for a healthy functioning body do play roles in feeding or hastening cancerous growth, and that while blocking VEGF receptors can play a role in cancer treatment, systemically VEGF is overall playing a very positive role in our vascular system, and higher levels generally accompany people in very strong health, with good habits.

AKT is another protein our bodies naturally produce which, as I understand, inhibits endothelial apoptosis (apoptosis = killing off older or senescent cells). Apoptosis generally is something our bodies greatly benefit from, but interestingly, when inhibition of endothelial apoptosis occurs, we seem to see elevated angiogenesis. So there appears to be an inverse relationship between endothelial apoptosis and active angiogenesis. Interesting but very dense study on this subject linked here:…p=rep1&type=pdf

Anyway, connecting the dots with all of this is not such a simple task but there is some very provocative data around that does some of the trick of doing this for us. Namely, that temporary ischemia appears to cause acute elevations in VEGF levels. This may not yet click for those few of you still reading along, but ischemia refers to cutting off or acutely restricting blood supply to some part of the body. Where in the PE world do we see very temporary ischemia being harnessed? I have linked to [ before, in discussions about CLAMPING.

So, anecdotally, some share of the growth that we see from clamping may conceivably be the result of these remote ischemic states spurring temporary elevations of VEGF, which we can interpret as correlative support for the perhaps strong link between VEGF and growth or repair of penile endothelial tissues.


Some of the anecdotally suggested behavioral/lifestyle methods of elevating VEGF systemically that I’ve come across that I’d say warrant further exploration or discussion:
- exercise
- cold exposure
- high altitude exposure

Some potential chemical VEGF modulators or similarly functioning proteins:
- BPC-157: a lot of recent excitement about this substance recently, and its link with VEGF may explain why.
- Erythropoietin (EPO): I know very little about this substance, but a cursory search suggests that
which I would say prompts serious consideration. EPO
- Statins: I only came across this referenced in a reddit thread (…o_increase_vegf ) by someone referring to an unpublished study conducted in the laboratory they worked in. Full disclosure, yes a lot of the strategies I’ve listed here I first read about on this reddit thread.
- Lithium: Although this may be restricted to neural/brain VEGF

Anyway, I’m not sure there’s anyone else interested in this angle, but this conversation would be very exciting for me, especially if there are others who wither have some expertise in the relevant physiology or are interested in doing some amateur research to find some footholds where we might find a way to leverage some preexisting and understood endothelial growth processes in our favor for either tissue growth or repair.