Type I diabetics are put in a tough spot. From diagnosis on it's a bleak picture in terms of getting back to normal. And for us diabetics, where do we even start? The time and energy put into reacclimatizing to this new life is crucial to our survival and well-being, but also prevents us from looking into a cure with any real zeal or intent.
This isn't a simple fix. This isn't a "lose weight and things sort themselves out" or a "take care of variable x and you can achieve equilibrium". As diabetics, we need to remove the bad AND rebuild the good all on our own.
We're told it's our beta cells. Not only are they gone, but they don't grow back either. So curing it takes on a new degree of difficulty. Even if you did find out how it all happened in the first place, those beta cells are gone forever and we don't have a good way to get them back.
Until now...
People's knee jerk response to getting new beta cells is to have them transplanted or regrown from external stem cells. And why wouldn't it be? That's all modern medicine seems to fixate on.
But did you know there's recent research looking at some plant compounds that actually do regrow beta cells? This is a big deal.
A compound called harmine has been found to initiate beta cell differentiation in diabetic mice. It's a compound popularized in the herbal medicine realm. You can find harmine in the famous psychedelic brew ayahuasca.
It's a beta-carboline and a harmala alkaloid, which to common folk doesn't stand for much. But it's being used in mice and pig research for it's ability to regenerate beta cells. Harmine is unique in its ability to inhibit a specific pathway, called the DYRK1A pathway. I call it the "durka" pathway.
DYRK1A plays a critical role in cell differentiation and seems to be a part of several human health disorders. Things like Down's syndrome, leukemia, Alzheimer's, an assortment of cancers and now diabetes. It's main role is in cell proliferation, or cell growth. A dysfunctional DYRK1A spells either undeveloped cells or an overdevelopment of cells. For down syndrome, it plays a part in making too much of chromosome 21, for diabetics it could be halting the formation of beta cells.
Harmine has become pivotal in its ability to inhibit the DYRK1A pathway. For a diabetic, this allows for the proliferation of viable, insulin-producing cells. Weng et al. (2015) found that harmine is able to induce beta cell proliferation, increase islet mass and improve glycemic control in both humans and mice samples via inhibition of DYRK1A.
But not so fast. The same researchers lauding harmine as an excellent beta cell initiator have also noted that it isn't good at just growing beta cells. The pancreas has a number of other cell types, namely alpha cells, that also play a part in glycemic control. Alpha cells are the glucagon producing cells, opposite the insulin production of the beta cells. What researchers found was that harmine indiscriminately caused growth in both beta cells and alpha cells. This is problematic in that if the ratio of glucagon producing cells to insulin producing cells is off, would your blood sugar ever be truly regulated? Or would you be perpetually high because of the abundance of glucagon.
Ever wonder why your blood sugar inches higher and higher even during times of fasting? That's your alpha cells at work. Your basal rates? Or long lasting MDI? That's to account for the natural release of glucagon from these cells. The name of the game is to find a way to inhibit the alpha cells and selectively grow the beta cells.
In a beautiful stroke of diabetic luck, much of the money being dumped into Type II diabetes research is focusing on just that. That is, silencing alpha cells. I know you've seen the commercials: Ozempic, Rysvalta, Trulicity, Victoza. All these T2D medications are called glucagon-like peptides, or GLP-1s. They mimic glucagon and inhibit the release of additional glucagon into the blood stream, thus keep blood sugars lower.
Sure enough, Ackeifi et al (2021) found that combining GLP-1 and harmine significantly boosted beta cell proliferation rates by about 3x. This is a huge win in not only regrowing beta cells, but doing so at a faster pace and with fewer side effects.
So how do I get my hands on some harmine? Bowie, you said it was in ayahuasca before. Do I need to find an Amazonian shaman? Or trip balls in order to get my beta cells back?
Maybe? But no, not really.
Turns out harmine is also found in a perfectly legal and accessible seed of the Syrian Rue shrub. Syrian rue is fairly easy to locate and get your hands on. Syrian rue, or Peganum harmala, is a perennial, herbaceous plant that grows in temperate desert and mediterranean terrains. It's seeds naturally contain harmine and have been used in ayurvedic and shamanistic rituals for centuries. It's become invasive in the Western USA and is a part of local medicine in the Middle East and North Africa.
Its therapeutic use is not well documented, and especially not in any clinical sense. In my personal research, much of the information and dosing I found was related to those looking for the psychedelic experience people seek in ayahuasca. In Ackeifi et al (2021), the dosing they used to reach therapeutic dose was 10 µM combined with 5 nM of GLP-1. And while I understand what µM means from college chemistry class, I have no idea how that translates to syrian rue seeds.
So I've begun experimenting on myself. I've blended up 16 oz packages of Syrian Rue and stuffed into gelatin capsules. I've been dosing anywhere from 4 to 8 capsules a day. For GLP-1 agonists like Ozempic and Trulicity, I've found nature's equivalents in berberine, korean panax ginseng, and gentian tea.
I'm encouraged by the results. I think a cure is on its way.
We're almost there!
References:
https://www.science.org/doi/abs/10.1126/scitranslmed.aaw9996?intcmp=trendmd-stm
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