Ray on lidocaine for bowel complaints
I've had a very stubborn bowel condition, don't know if he'd recommend this for everyone. I smoked weed many years and felt that it had changed my gut. At first i thought it was SIBO but I didn't consider the epigenetic componment.

Me:" I have burning eyes, burning throat and sinus cavity, etc. Definitely related to gut."

Ray:"Years ago I swallowed a sip of 2% lidocaine gel, and within a few minutes felt something changing in my intestine, and from then on, without any more lidocaine, some of my bowel symptoms were gone."

Me: "Excellent! I just happen to have some on hand. Epigenetic?"

Ray: "I think that must be it, for the improvement to be so stable."

Br J Anaesth. 2014 Jul;113 Suppl 1:i32-8. 
Lidocaine and ropivacaine, but not bupivacaine, demethylate deoxyribonucleic acid
in breast cancer cells in vitro.
Lirk P(1), Hollmann MW(2), Fleischer M(3), Weber NC(2), Fiegl H(4).
(1)Department of Anaesthesiology, Academic Medical Center, University of
Amsterdam, Meibergdreef 9, Amsterdam 1105AZ, The Netherlands p.lirk@amc.uva.nl
heidelinde.fiegl@i-med.ac.at. (2)Department of Anaesthesiology, Academic Medical 
Center, University of Amsterdam, Meibergdreef 9, Amsterdam 1105AZ, The
Netherlands. (3)Department of Gynaecology and Obstetrics, Innsbruck Medical
University, Anichstr. 35, Innsbruck 6020, Austria. (4)Department of Gynaecology
and Obstetrics, Innsbruck Medical University, Anichstr. 35, Innsbruck 6020,
Austria p.lirk@amc.uva.nl heidelinde.fiegl@i-med.ac.at.
   BACKGROUND: Lidocaine demethylates deoxyribonucleic acid (DNA) in breast cancer
cells. This modification of epigenetic information may be of therapeutic
relevance in the perioperative period, because a decrease in methylation can
reactivate tumour suppressor genes and inhibit tumour growth. The objectives of
this study were to determine the effect of two amide local anaesthetics,
ropivacaine and bupivacaine, on methylation in two breast cancer cell lines and
to detect whether the combination of lidocaine with the chemotherapy agent
5-aza-2'-deoxycytidine (DAC) would result in additive demethylating effects.
METHODS: Breast cancer cell lines BT-20 [oestrogen receptor (ER)-negative] and
MCF-7 (ER-positive) were incubated with lidocaine, bupivacaine, and ropivacaine
to assess demethylating properties. Then, we tested varying concentrations of
lidocaine and DAC to assess whether their demethylating effects were additive.
Cell numbers and global methylation status were analysed.
RESULTS: Lidocaine decreased methylation in BT-20 and MCF-7 cells, ropivacaine
decreased methylation in BT-20 cells, and bupivacaine had no demethylating
effect. When combined, lidocaine and DAC had additive demethylating effects.
CONCLUSIONS: At clinically relevant doses, lidocaine and ropivacaine exert
demethylating effects on specific breast cancer cell lines, but bupivacaine does 
not. The demethylating effects of lidocaine and DAC are indeed additive.
 © The Author [2014]. Published by Oxford University Press on behalf of the
British Journal of Anaesthesia. All rights reserved. For Permissions, please
email: journals.permissions@oup.com.
Br J Anaesth. 2012 Aug;109(2):200-7. 
Lidocaine time- and dose-dependently demethylates deoxyribonucleic acid in breast
cancer cell lines in vitro.
Lirk P(1), Berger R, Hollmann MW, Fiegl H.
(1)Department of Anaesthesiology, Academic Medical Center, University of
Amsterdam, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands. p.lirk@amc.uva.nl
Erratum in
    Br J Anaesth. 2013 Jan;110(1):165.
  BACKGROUND: Anaesthetic management of cancer surgery may influence tumour
recurrence. The modulation of gene expression by methylation of deoxyribonucleic 
acid (DNA) (epigenetics) is increasingly recognized as a major hallmark of
cancer. Next to direct effects of local anaesthetics upon tumour cells, the
ester-type local anaesthetic, procaine, has been shown to affect methylation
status in several tumour cell lines, promoting the reactivation of tumour
suppressor genes. We sought to determine whether the prototype amide-type local
anaesthetic, lidocaine, influences the survival and epigenetic status of
oestrogen receptor (ER)-positive and -negative breast cancer cell lines in vitro.
METHODS: Breast cancer cell lines BT-20 (ER-negative) and MCF-7 (ER-positive)
were incubated with lidocaine and procaine as the reference substance. We
performed cell count and determined apoptosis using TUNEL stain. Further, we
assessed global methylation status, and methylation of three known tumour
suppressor genes (RASSF1A, MYOD1, and GSTP1) using the MethyLight assay and
real-time quantitative polymerase chain reaction, respectively.
RESULTS: Baseline methylation was 100-fold higher in BT-20 cells. Here, we
observed a dose-dependent decrease in DNA methylation in response to lidocaine
(1, 0.01, and 0.01 mM) after 72 h (P<0.001, <0.001, and 0.004, respectively). The
corresponding changes were smaller in MCF-7 cells. Global methylation status was 
profoundly influenced, but the methylation and mRNA expression status of three
tumour suppressor genes was unchanged.
CONCLUSIONS: Our findings suggest that demethylating tumour-suppressive effects
of anaesthetic interventions may only be detectable in specific types of cancer
due to differential methylation profiles. In conclusion, at clinically relevant
concentrations, lidocaine demethylates DNA of breast cancer cell lines in vitro.

Curr Cancer Drug Targets. 2013 May;13(4):379-99.
DNA methyltransferase-1 inhibitors as epigenetic therapy for cancer.
Singh V(1), Sharma P, Capalash N.
(1)Department of Biotechnology, Panjab University, Chandigarh, India.
  DNA methylation is an epigenetic modification involved in gene expression
regulation. In cancer, the DNA methylation pattern becomes aberrant, causing an
array of tumor suppressor genes to undergo promoter hypermethylation and become
transcriptionally silent. Reexpression of methylation silenced tumor suppressor
genes by inhibiting the DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B) has
emerged as an effective strategy against cancer. The expression of DNA
methyltransferase 1 (DNMT1) being high in S-phase of cell cycle makes it a
specific target for methylation inhibition in rapidly dividing cells as in
cancer. This review discusses nucleoside analogues (azacytidine, decitabine,
zebularine, SGI-110, CP-4200), non-nucleoside ihibitors both synthetic
(hydralazine, RG108, procaine, procainamide, IM25, disulfiram) and natural
compounds (curcumin, genistein, EGCG, resveratrol, equol, parthenolide) which act
through different mechanisms to inhibit DNMTs. The issues of bioavailability,
toxicity, side effects, hypomethylation resistance and combinatorial therapies
have also been highlighted.

Mediators Inflamm. 2016;2016:9607946. 
Epigenetic Modulation as a Therapeutic Prospect for Treatment of Autoimmune
Rheumatic Diseases.
Ciechomska M(1), O'Reilly S(2).
(1)National Institute of Geriatrics Rheumatology and Rehabilitation, Department
of Pathophysiology and Immunology, Warsaw, Poland. (2)Faculty of Health and Life 
Sciences, Northumbria University, Newcastle upon Tyne, UK.
  Systemic inflammatory rheumatic diseases are considered as autoimmune diseases,
meaning that the balance between recognition of pathogens and avoidance of
self-attack is impaired and the immune system attacks and destroys its own
healthy tissue. Treatment with conventional Disease Modifying Antirheumatic Drugs
(DMARDs) and/or Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) is often associated
with various adverse reactions due to unspecific and toxic properties of those
drugs. Although biologic drugs have largely improved the outcome in many
patients, such drugs still pose significant problems and fail to provide a
solution to all patients. Therefore, development of more effective treatments and
improvements in early diagnosis of rheumatic diseases are badly needed in order
to increase patient's functioning and quality of life. The reversible nature of
epigenetic mechanisms offers a new class of drugs that modulate the immune system
and inflammation. In fact, epigenetic drugs are already in use in some types of
cancer or cardiovascular diseases. Therefore, epigenetic-based therapeutics that 
control autoimmunity and chronic inflammatory process have broad implications for
the pathogenesis, diagnosis, and management of rheumatic diseases. This review
summarises the latest information about potential therapeutic application of
epigenetic modification in targeting immune abnormalities and inflammation of
rheumatic diseases.
[color=#222222][size=medium]"I have no religion, no political affiliation: I believe in me, above everything else." -Chasing Good & Evil[/size][/color]
Interesting! I wonder if this could work to reverse conditions such as varicose veins.
So Chasing, have you tried your lidocaine? I wonder if it could cause anxiety by increasing stress neurotransmitters.

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