LSD and Type 1 Diabetes

[Shivonivore]

Greetings all! I've been doing lots of reading about around here since stumbling across the site and I have to say that this community blows my mind with amount of friendliness and constructiveness! With that said, I've been tossing about a good first topic to break the ice, so to speak, and having recently looked into the subject of this topic (while having diabetes myself) thought this would be a fun/good one.

Has anyone else looked into the what effects that LSD may possibly play on Diabetes. Including and not limited to; effects on blood glucose (BG), absorption rate of insulin, or other effects than the "norm" when having high/low BG readings.

*note: by no means was this experiment done in any precise or controlled way, but more as a "wonder what if..." way. I have intentions of looking further into this.*

I don't have the data on me at the moment (will have to dig through some files) but will update when I find them.
- Insulin seemed to be absorbed easier/at a more effective rate than usual which resulted in overall lower BG readings throughout the experience.
- There was no noticeable effects outside what is usually expected with regards to high or low BG readings.
- There was limited to no exercise involved which can affect BG readings.
- Reports of many various temperature fluctuations which may have been cause to many low BG feelings/readings. In personal experience when exposed to very warm temperatures for extended times (such as sitting in a hot tub or sauna) BG readings tend to drop significantly.

With the seemingly endless increase in insulin prices I am constantly looking for alternatives to either limit the amount of insulin needed or to find a way to forgo the use of it altogether (wishful thinking, I know). So with the little bit I have learned from this more than other times documented experiment I am beginning to be convinced that LSD has possibly, in some way, an effect on the body's ability to better regulate insulin. This in turn would allow an individual to theoretically use a lower dose of insulin and achieve the same results as if they were to take a full dose of insulin.

I realize this isn't exactly the best constructed experiment or display of results, but hopefully with practice I will get better at it! I appreciate any and all input and I look forward to many future discussions, cheers!

-Shiv

 

[Shivonivore]

The data as promised:

*notes: BG == Blood Glucose. u == unit/cc. N == Novalog. Average acceptable BG range is 80-140. 1u of Novalog is taken for every 15g of carbohydrates. 1u of Novalog is used to bring down the BG by about 48 points. All BG readings are measured in mg/dL.*

~*~START LOG~*~
Date: 2017 Apr 01
Dose: 1 tab (exact measurement is unknown)
Time: 00:05 | BG: 267 | 4u N | 20g carbs | start dose
Time: 01:08 | BG: 168 | Effects begin about 30-45 minutes after dose. Body temp fluctuations are prevalent. Arms seem to have more weight to them, akin to the feeling of deadweight. Focus is still sharp.
Time: 01:36 | BG: 166 | Increase in intensity. Excessively more fidgety. Colours are exciting and largely vibrant. Music feels "flowy". Everything appears to be slightly wavy, as if looking at a distant horizon on a very hot day. BG felt low; weakness of the body and light shakes as is common with low BG was observed.
Time: 02:15 | BG: 141 | 1u N | 20g carbs | Effects continue to amplify.
Time: 03:20 | BG: 106 | 2u N | 50g carbs | *3u should have been taken instead of 2u; however due to the unwanting of dealing with a hypoglycemic episode only 2u was taken.* The meal was looked upon for a good few minutes questioning it, "What is this? What do is to be done with it? What is the purpose of it? Why?"
Time: 03:43 | Observation: time sensitivity seems incredibly skewed.
Time: 04:20 | BG: 108 | It would appear the decision with regards to the earlier meal was correct. Had 1u N more been taken, BG could have dropped to below 60.
Time: 05:54 | BG: 59 | 41g carbs | Observation: snacks are very important. Notes claim that there was increased activity which could be the reason for the lower BG reading.
Time: 09:00 | BG: 58 | 20g carbs
Time: 10:15 | BG: 108 | A few handful of grapes were consumed; unknown carb count.
Time: 14:00 | BG: 57 | 26g carbs | Effects have completely dissipated.
Time: 21:00 | BG: 191
~*~END LOG~*~

Now, I know this data seems to be quite useless without a control set to go with it. Due to an incredible laziness/uncare, there is not much data (a downside to diabetes is the tediousness of the constant upkeep it requires which can cause many to become complacent in their care) however, there is an attempt at getting a CGM (continuous glucose monitor) that will provide constant BG measurements without the need of pricking one's finger, thus making the collection of BG readings incredibly easier.

Anyways, as mentioned before this is something that continues to fascinate so I will be looking at getting more data as time goes on. Hopefully this can prove to be insightful or helpful to others; cheers.

-Shiv

 

[Stelliuma]

Hi Shiv,
Not a medical expert. I'm a secretary aka God herself. But I have a lot of endocrine issues that run in my family, diabetes being one of them...which is also linked to various mental disorders.

I have not looked deeply into your connection, but I have been looking into the function/malfunction (gene mutations) of the VDR (vitamin D receptor). The down syndrome gene RCAN1 ("inhibits calcineurin-dependent transcriptional responses by binding to the catalytic domain of calcineurin, could play a role during central nervous system development) is now linked to diabetes.

After going down the rabbit hole (because I knew nothing of science/medical research), I found that RCAN1 maybe affected by VDR function.

The regulator of calcineurin (RCAN1) an important factor involved in atherosclerosis and cardiovascular diseases development

Atherosclerosis, one of the main causes of cardiovascular diseases, is a complex process that involves manifold factors. Besides the vascular lipids accumulation, inflammatory factors could be considered as a proatherogenic factor – RCAN1. RCAN1 ...

www.ncbi.nlm.nih.gov

"Enabling vitamin D action in VDR (vitamin D receptor) gene-deleted mice may lead to an increased RCAN1 gene expression and these mice models may display cardiac hypertrophy"

"Collectively, these studies demonstrate that the vitamin D-VDR signaling system possesses direct, anti-hypertrophic activity in the heart. This appears to involve, at least in part, suppression of the pro-hypertrophic calcineurin/NFAT/MCIP 1 pathway."

Cardiomyocyte-Specific Deletion of the Vitamin D Receptor Gene Results in Cardiac Hypertrophy

A variety of studies carried out using either human subjects or laboratory animals suggest that vitamin D and its analogues possess important beneficial activity in the cardiovascular system. Using Cre-Lox technology we have selectively deleted the vitamin ...

www.ncbi.nlm.nih.gov

So I just looked up LSD's interaction with this gene:

"a number of genes encoding for chromatin modifiers and remodelers, such as HDMs of the Jumonji C (JmjC)-domain containing proteins and lysine-specific demethylase (LSD) families are primary targets of VDR and its ligands"

Vitamin D and the epigenome - PubMed

Epigenetic mechanisms play a crucial role in regulating gene expression. The main mechanisms involve methylation of DNA and covalent modifications of histones by methylation, acetylation, phosphorylation, or ubiquitination. The complex interplay of different epigenetic mechanisms is mediated by...

www.ncbi.nlm.nih.gov

Based on the results of my genetic mutations (PCOS, insulin resistant, but not diagnosed with diabetes), I'd say if you are diabetic, there is a chance that a genetic test will show that you are both VDR Taq (Vitamin D Receptor) ++, COMT V158m ++ & COMT H62H ++.

COMT refers to Catecholamine, which is a type of monoamine, which "are derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan, and the thyroid hormones by the action of aromatic amino acid." The types of catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine"

Having the COMT ++ tag in your results will prove that there is an issue with your regulation of these hormones. There are also studies that suggest that VDR function has a powerful affect on COMT expression/regulation. Which is what I really want more information on.

Researching these types of catecholamines you will obviously see the connection with the adrenal gland/endocrine system. So here you have insulin regulation, interaction with exocrine glands. I believe it's because the pancreas is both a endocrine gland, and a exorine gland, that where you have have PCOS, arthritis, and diabetes in your family/self, you also may have skin issues, or a family history of kidney issues. I personally can't drink without spending the whole day throwing up. You'll see a posts from people asking why do I get so sick from drinking? "You're allergic to alcohol" is your answer. Dosen't seem fair for a 18 yr old college kid to be put through the torture!

All of this leads back to Pineal Gland malfunction of course! These are all pineal gland disorders.

If you've submitted DNA results to any ancestry site, you can grab your raw data file & interpret them here: https://www.knowyourgenetics.com/.

I used 23&Me for free when it started years ago. Not sure how people feel about giving away their DNA because there is profit in gene mutation study obviously. But wouldn't you rather pay for things that help?

The knowyourgenetics site belongs to Dr. Amy Yasko. The program is built around the methylation cycle, and once you upload your raw data file, what you will get are recommendations for HER very expensive vitamins based on your results. Her program is completely built around treating your genetic mutations and has been interesting to research. But I have not started her program and I don't want to be given instructions I want to find my way there. & I haven't had time to dig into her research but she isn't alone in her studies around the methylation cycle.

So you're clearly on to something.

 

[downwardsfromzero]

lysine-specific demethylase (LSD)

Given that this is a forum concerned with psychedelic drugs, it's probably useful to distinguish this use of the acronym from the more widely understood and usual usage referring to lysergic acid diethylamide - which, incidentally, is a good reason for including the '25' in LSD-25.

So, is the OP still referring to the lysergic acid derivative? There have been studies on the effects of LSD-25 on carbohydrate metabolism at least, and a search engine turned up this: Insulin potentiates LSD?!
which does actually cite a reference: Butterworth A.T., 1962, Some aspects of an office practice utilizing LSD 25, Psychiatric Quarterly, vol. 336: 734-53, p. 737

Or of course, both could apply.