• Members of the previous forum can retrieve their temporary password here, (login and check your PM).

DMT in clinical death

Migrated topic.
E

efrecska

Rising Star
We have started a crowd funding project on DMT in clinical death (in other words: against oxidative stress). Please, help us sharing this link with those who might be interested or supportive:
www.indiegogo.com

DMT for Extending Life When You Need It the Most

Please, fund us to develop our study on extending the phase of clinical death to save lives. | Check out 'DMT for Extending Life When You Need It the Most' on Indiegogo.
www.indiegogo.com www.indiegogo.com

Brief Summary of the project:
We are a group of basic and clinical researchers who follow the line of investigation started by Stephen Szara’s groundbreaking clinical studies with dimethyltryptamine (DMT). We are among the first ones who broke away of the mainstream scientific view of DMT as a psychopathological agent and proposed a somatophysiological role for this endogenous tryptamine, which is naturally occurring in the body. Our main tenet is that DMT is involved in the healing and regeneration of cells, it helps the body to survive extreme stress like clinical death. Our group has already provided experimental support of this concept in the field of immunology.
We need your support to expand our work into hypoxia (low oxygen) studies, which are in the stage of in vitro ("test tube") phase.

Thankfully,

Ede Frecska
 
Bump. Lets give this some attention.

The results of this research will probably lay new ways for future development. I hope that you get the funding that is needed for a project like this.


Kind regards,

The Traveler
 
Thanks for your interest!
The role of DMT in clinical death is an intriguing idea, however, there is more to it. Oxidative stress is possibly the key concept in the physiological function of DMT.
Oxidative stress is an emerging platform in explanation of a wide array of degenerative illnesses. If DMT is proven to mitigate its effect then we will learn how ayahuasca works as medicine at the molecular level, which is the basic layer in her multifaceted therapeutic effects.
 
Look on the CF main page what a strong statement we have received from Dennis McKenna:
"This is possibly the most important DMT research to happen since Rick Strassman forced open the gates 20 years ago!"
 
For the balance, I have to report that last night I got critical comments from an outstanding researcher of the field. Here they are with my responses:
1. "Farfetched protocol." Indeed, the goal (we spelled out DREAM) is very ambitious, but we stated clearly that the project is one step on the road toward the "attractor" (use in clinical death). If we only say DMT is against oxidative stress that can be enough for the scientific community. The public may need more: "And what is it good for then?"
2. "It has low probability of success." For what? Against oxidative stress? We have pilot data from microglia cells supporting that, though in micromolar concentration (I will address below this really important question), but microglia has no uptake mechanisms. Against clinical death? Perhaps less probable, but isn't worth a try?
3. "DMT’s affinity for the sigma-1 receptor is very low." This is typical, thinking in a neurotransmitter affinity range. Neurotransmission is a strictly regulated process (by feedback mechanisms). The process we discuss is a ballistic, flooding phenomenon. One cannot flood in the nanomolar range because without feedback it can easily overshoot. Anyhow, not the same mechanism like neurotransmission.
3. "The notion of endogenous DMT having physiological relevance is quite unlikely." For 40 years this has been the mainstream agenda. Then why is the three uptake processes and the one week storage for a physiologically insignificant drug? Vital molecules glucose, amino acids pass the blood-brain barrier by active process. And DMT. Perhaps not alone in its group, other tryptamine analogues my pass actively as well. Well, if bufotenin turns out to be the winner that would be fine with me! I can face a mistake like this: a terrible-horrible-no good-very bad hallucinogen drug has physiological effects. BUT it is not DMT, it is bufotenin. What a bummer! Our study still has relevance, next after showing DMT's anti-oxidative effects in neuronal cells, we may turn toward bufotenin.
4. “Sigma receptor function in dying is unclear.” But not in stroke, myocardial infarct, and other type of local ischemia. If local yes, why not general?
5. "Levels of free tryptamine (the substrate of DMT) in the body are low" That is a really good point! We have to think about it. At least in the study we use DMT exogenously (yet it is not consistent with our argumentation using converging data).
6. "It is like the romantic idea of pineal DMT." Barker et al. identified pineal DMT recently (2013): Rick Strassman was proven right.
 
"Barker et al. identified pineal DMT recently (2013): Rick Strassman was proven right."


...So it's true then?..very interesting stuff! Are we talking about presence of DMT in the pineal, or actual biosynthesis via the pineal?
 
Barker stated: "We report here, for the first time, the presence of N,N-dimethyltryptamine in pineal gland
microdialysate obtained from the rat." The pineal gland has the enzyme - known from the 70's - therefore very probably DMT is synthetized there.
 
This is quite a fascinating line of thinking.

Is there a reason 5-MEO-DMT isn't also considered along with DMT and bufotenine? Does DMT appear to be a more likely candidate than these other tryptamines?
 
efrecska said:
Barker stated: "We report here, for the first time, the presence of N,N-dimethyltryptamine in pineal gland
microdialysate obtained from the rat." The pineal gland has the enzyme - known from the 70's - therefore very probably DMT is synthetized there.
Click to expand...
For reference, the study is posted here, as well as attached.

Excellent work efrecska. GL on the campaign!
 

Attachments

  • PinealDMT.pdf
    896.7 KB · Views: 0
dreamer042 said:
This is quite a fascinating line of thinking.

Is there a reason 5-MEO-DMT isn't also considered along with DMT and bufotenine? Does DMT appear to be a more likely candidate than these other tryptamines?
Click to expand...

Indeed, a line of thinking. Thus far we have composed a fairly well built story from the little data we have out there. This has lead to the immunological finding. I hope soon we will have more hard data at hand on the oxidative stress effects.

The sigma receptor effect of bufotenin is less known. Who knows? It may turn out to be the winner. As far as the anti-inflammatory effects DOI is brutally strong (in the picomolar range). It is not endo though.
 
So let me see if I've got this right. The general idea goes like this:

Endogenous DMT acts as an agonist at the sigma-1 receptor, which, when activated, reduces cellular activity, prolonging the life of the neuron and extending the window before terminal death sets in.

I'm a little unclear about why exactly you've chosen to make DMT the centerpiece of this research (which is pretty cool, all told). There are other endogenous sigma 1 ligands (DHEA + derivatives, which also have low affinity). I don't have numbers, but I imagine that DMT is not the only endogenous tryptamine to have sigma 1 activity either.

From a clinical perspective, using DMT as a therapeutic agent also seems like an odd choice - there are tons of synthetic drugs out there with sigma 1 activity (it seems like most serotonergic drugs, like antidepressants also act there). Research into a scheduled psychedelic seems like it's making life unnecessarily difficult for you [mod edit: removed statement for privacy].

All told the choice to look at DMT seems kind of random.

Blessings
~ND
 
"...the choice to look at DMT seems kind of random."
Since DMT is considered to be an endogenous ligand of the sigma-1 receptor, therefore it's choice is not random. One may say (like us): primary.
It makes more sense to start from the natural ligand than from a synthetic one. An important physiological function is usually mediated by multiple channels and by choosing an "unnatural" compound one may miss out other pathways of the process.
In case of positive findings without doubt the pharmaceutical industry will step in with a synthetic derivative (there is little money in a natural drug). Will that chemical utilize the three transport mechanisms into the brain? Or like the SSRI fluvoxamine while exerting potent sigma-1 agonism is working against the "natural" ligand by blocking its uptake into neurons.
 
Back
Top Bottom