Douglas.Curtis
Autistic Diplomat in Training
Thought that was already in here, good reference anyway. Thanks!
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Do you have Cannabinoid Hyperemesis Syndrome?
- Thread starter Thomas Paine
- Start date
That's a very interesting article.
It also proofs the general idea that consuming some pepper helps when a person used to much cannabis.
Good to hear there is finally found something that can relief the effects of CHS. And it even explains why hot showers/baths brings relief.
But this article also kinda disproofs your idea about azadirachtin.
Reading about the impact cannabinoids also has on the TRPV1 receptors (and not only CB1/2) and how capsaichin can 'reset' them.
I'm not saying that azadirachtin doesn't cause gastro-intestinals problems.
Can somebody confirm that consuming (or topical use) of Capsaichin (ie. spicy food, chilli pepper) brings relief from CHS?
Full length article:
https://acgcasereports.gi.org/succe...-hyperemesis-syndrome-with-topical-capsaicin/
It also proofs the general idea that consuming some pepper helps when a person used to much cannabis.
Good to hear there is finally found something that can relief the effects of CHS. And it even explains why hot showers/baths brings relief.
But this article also kinda disproofs your idea about azadirachtin.
Reading about the impact cannabinoids also has on the TRPV1 receptors (and not only CB1/2) and how capsaichin can 'reset' them.
I'm not saying that azadirachtin doesn't cause gastro-intestinals problems.
Can somebody confirm that consuming (or topical use) of Capsaichin (ie. spicy food, chilli pepper) brings relief from CHS?
Full length article:
https://acgcasereports.gi.org/succe...-hyperemesis-syndrome-with-topical-capsaicin/
Last edited:
Successful Treatment of Cannabinoid Hyperemesis Syndrome with Topical Capsaicin
Andrew M. Moon, MD, MPH1, Sarah A. Buckley, MD2, and Nicholas M. Mark, MD3
1Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, NC
2Hematology/Oncology Fellowship Program, University of Washington, Seattle, WA
3Division of Pulmonary and Critical Care, University of Washington, Seattle, WA
ACG Case Rep J 2018;5:e3. https://dx.doi.org/10.14309/crj.2018.3. Published online: January 3, 2018.
Abstract
Cannabinoid hyperemesis syndrome (CHS) is a clinical entity in which marijuana users develop nausea, vomiting, and abdominal pain that improves with hot water bathing or cannabis cessation. Previous models suggest that CHS arises solely from the derangement of cannabinoid receptor type 1 signaling. However, involvement of transient receptor potential vanilloid subtype 1 (TRPV1) receptor, which is activated by marijuana, capsaicin, and heat, could fill gaps in existing models, including the enigmatic role of hot water bathing. We propose that chronic cannabis use decreases TRPV1 signaling and alters gastric motility, and we report the case of a CHS patient whose symptoms improved after topical capsaicin.
Introduction
Cannabinoid hyperemesis syndrome (CHS) is a clinical entity characterized by chronic marijuana use, intractable vomiting, and relief of symptoms with hot-water bathing, exemplifying the enigmatic role of temperature in attenuating symptoms.1–3 A recent review proposed that transient receptor potential vanilloid subtype 1 (TRPV1) receptor, which is involved in gastric motility and is activated by cannabinoids, high temperatures, and capsaicin, is centrally involved in the pathogenesis of CHS (Figure 1).4
Case Report
A 47-year-old man with a decade-long history of marijuana use of up to several grams daily presented to the gastroenterology clinic with 8 years of abdominal pain, nausea, and vomiting relieved by up to 4 hours of hot-water bathing daily. Computed tomography (CT) of the abdomen and pelvis showed an unremarkable liver, no biliary duct dilatation, normal gallbladder, normal pancreatic body and head, normal spleen, and no bowel obstruction or inflammation. Abdominal ultrasound revealed a liver with normal size and echotexture, antegrade portal flow, non-dilated bile ducts, and a gallbladder without gallstones, wall thickening, or pericholecystic fluid. Upper endoscopy demonstrated a normal esophagus, normal gastric mucosa, and normal examined duodenum. Biopsies were negative for Helicobacter pylori. Colonoscopy showed normal colonic mucosa and terminal ileum. The patient had no improvement with dicyclomine, ranitidine, and twice-daily omeprazole. He was diagnosed with CHS and encouraged to discontinue marijuana.
Figure 1. Proposed pathophysiology of cannabinoid hyperemesis syndrome. TRPV1 is expressed in area postrema of the medulla, along gastric enteric and vagal nerves, and on cutaneous receptors in the dermis and epidermis. Prolonged exposure to cannabinoids inactivates TRPV1, potentially resulting in central nausea, altered gastric motility, and abdominal pain. Exposure to nociceptive heat, such as with compulsive hot-water bathing, may transiently augment cutaneous TRPV1 firing and restore gastric motility, temporarily mitigating symptoms. Use of another TRPV1 agonist, capsaicin, may also provide relief. Cessation of marijuana use gradually leads to normalization of TRPV1 function and fully ameliorates symptoms.
The patient continued marijuana use and presented several weeks later to the emergency department with severe, periumbilical, stabbing pain associated with nausea and vomiting. He had a temperature of 37.1°C, heart rate 86 beats/min, blood pressure 146/74 mm Hg, and oxygen saturation 98% on ambient air. Labs showed a white blood cell count 14,000 cells/µL, potassium 3.1 mEq/L, and normal hemoglobin, creatinine, blood urea nitrogen, aspartate aminotransferase, alanine aminotransferase, total bilirubin, albumin, lipase, and urinalysis. Abdominal CT scan was unchanged from the previous scan. He was treated with intravenous fluids, potassium, ondansetron, metoclopramide, prochlorperazine, fentanyl, viscous lidocaine, aluminum hydroxide/magnesium hydroxide/simethicone, and pantoprazole without improvement of symptoms. We applied capsaicin cream (0.075%) to a 15 × 25 cm area in the periumbilical region, with reapplications every 4 hours. The patient reported burning of the skin and improvement in the intensity of his stabbing abdominal pain and nausea a few hours after the first application of capsaicin. After the second dose, he noted complete resolution of his nausea. He received 2 more doses, which resulted in complete improvement of his abdominal pain. He was discharged the following day with a prescription for topical capsaicin. Over the following 3 months, the patient had no visits to our hospital system or any other providers included in Epic Care Everywhere within Washington State.
Discussion
The efficacy of capsaicin in CHS in our case lends credence to the role of TRPV1 in this syndrome. Previous models suggesting that cannabinoid receptor type 1 (CB1) is solely responsible for CHS are unsatisfying for several reasons. First, peripheral activation of CB1 slows gastric transit, but a case series of CHS patients described normal or increased transit time and no gastroparesis symptoms.5,6 Second, previous models suggested that hot-water bathing is an adaptive response to the hypothermic effects of cannabinoids. However, activation of CB1 should lead to hot-water bathing in all marijuana users, not just CHS patients who seem to engage in hot-water bathing as a learned behavior to treat symptoms. Finally, this model fails to explain why only some patients are susceptible to CHS, why there is latency from onset of marijuana use to symptoms, and why only chronic users are affected.
TRPV1 is a nonselective cation channel activated by noxious heat and capsaicin. This receptor is expressed throughout the gastrointestinal tract, including vagal sensory neurons, intrinsic enteric neurons in the myenteric plexus, and gastric epithelial cells.7,8 Within the central nervous system, there is a high density of TRPV1 in the area postrema, known as the chemoreceptor trigger zone. Activation of TRPV1 has potent anti-emetic effects, which may be mediated by depletion of substance P from neural circuits traveling to the nucleus tractus solitarius.9,10
Exogenous cannabinoids, including delta-9-tetrahydrocannabinoil, activate both CB1 and TRPV1.11 In vitro studies demonstrate that exogenous cannabinoids lead to dephosphorylation of TRPV1 and subsequent receptor desensitization.10 Therefore, chronic exposure to cannabinoids could downregulate or desensitize TRPV1 signaling, explaining how prolonged exposure to cannabinoids might lead to decreased TRPV1 signaling, altered gastric motility, and emesis. The learned behavior of compulsive hot-water bathing may be an attempt to normalize diminished TRPV1 activity by deliberate exposure to another TRPV1 agonist, nociceptive heat. Therefore, TRPV1 agonists such as topical capsaicin, which has a longer half-life than oral capsaicin, might augment TRPV1 activity and provide a less burdensome approach to treating CHS.12
One published case report and 2 case series have described successful treatment of 15 CHS patients with topical capsaicin.13–15 In all cases, patients with heavy marijuana use presented to the emergency department with nausea, vomiting, and abdominal pain improved by application of topical capsaicin preparation (0.075%). Some have questioned the lack of advanced diagnostics, such as endoscopic studies and CT imaging in these cases. In addition, these patients had a short period of observation in the emergency department with unclear clinical courses after discharge.16 These weaknesses do not apply to our case, given the extensive workup and prolonged inpatient observation.
Marijuana is the most frequently used illicit drug in the United States. Its recent legalization in many states has raised concerns of increased use and a resulting rise in CHS incidence.17,18 For these reasons, a better understanding of CHS pathogenesis and novel treatment strategies are increasingly important. Our case lends further credence to the role of TRPV1 in CHS, although only limited conclusions can be drawn from this single case with incomplete confirmed follow-up. We believe a prospective study, such as the planned randomized controlled trial examining capsaicin in cyclic vomiting syndrome, could adequately assess the efficacy of capsaicin for CHS.
Andrew M. Moon, MD, MPH1, Sarah A. Buckley, MD2, and Nicholas M. Mark, MD3
1Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, NC
2Hematology/Oncology Fellowship Program, University of Washington, Seattle, WA
3Division of Pulmonary and Critical Care, University of Washington, Seattle, WA
ACG Case Rep J 2018;5:e3. https://dx.doi.org/10.14309/crj.2018.3. Published online: January 3, 2018.
Abstract
Cannabinoid hyperemesis syndrome (CHS) is a clinical entity in which marijuana users develop nausea, vomiting, and abdominal pain that improves with hot water bathing or cannabis cessation. Previous models suggest that CHS arises solely from the derangement of cannabinoid receptor type 1 signaling. However, involvement of transient receptor potential vanilloid subtype 1 (TRPV1) receptor, which is activated by marijuana, capsaicin, and heat, could fill gaps in existing models, including the enigmatic role of hot water bathing. We propose that chronic cannabis use decreases TRPV1 signaling and alters gastric motility, and we report the case of a CHS patient whose symptoms improved after topical capsaicin.
Introduction
Cannabinoid hyperemesis syndrome (CHS) is a clinical entity characterized by chronic marijuana use, intractable vomiting, and relief of symptoms with hot-water bathing, exemplifying the enigmatic role of temperature in attenuating symptoms.1–3 A recent review proposed that transient receptor potential vanilloid subtype 1 (TRPV1) receptor, which is involved in gastric motility and is activated by cannabinoids, high temperatures, and capsaicin, is centrally involved in the pathogenesis of CHS (Figure 1).4
Case Report
A 47-year-old man with a decade-long history of marijuana use of up to several grams daily presented to the gastroenterology clinic with 8 years of abdominal pain, nausea, and vomiting relieved by up to 4 hours of hot-water bathing daily. Computed tomography (CT) of the abdomen and pelvis showed an unremarkable liver, no biliary duct dilatation, normal gallbladder, normal pancreatic body and head, normal spleen, and no bowel obstruction or inflammation. Abdominal ultrasound revealed a liver with normal size and echotexture, antegrade portal flow, non-dilated bile ducts, and a gallbladder without gallstones, wall thickening, or pericholecystic fluid. Upper endoscopy demonstrated a normal esophagus, normal gastric mucosa, and normal examined duodenum. Biopsies were negative for Helicobacter pylori. Colonoscopy showed normal colonic mucosa and terminal ileum. The patient had no improvement with dicyclomine, ranitidine, and twice-daily omeprazole. He was diagnosed with CHS and encouraged to discontinue marijuana.
Figure 1. Proposed pathophysiology of cannabinoid hyperemesis syndrome. TRPV1 is expressed in area postrema of the medulla, along gastric enteric and vagal nerves, and on cutaneous receptors in the dermis and epidermis. Prolonged exposure to cannabinoids inactivates TRPV1, potentially resulting in central nausea, altered gastric motility, and abdominal pain. Exposure to nociceptive heat, such as with compulsive hot-water bathing, may transiently augment cutaneous TRPV1 firing and restore gastric motility, temporarily mitigating symptoms. Use of another TRPV1 agonist, capsaicin, may also provide relief. Cessation of marijuana use gradually leads to normalization of TRPV1 function and fully ameliorates symptoms.
The patient continued marijuana use and presented several weeks later to the emergency department with severe, periumbilical, stabbing pain associated with nausea and vomiting. He had a temperature of 37.1°C, heart rate 86 beats/min, blood pressure 146/74 mm Hg, and oxygen saturation 98% on ambient air. Labs showed a white blood cell count 14,000 cells/µL, potassium 3.1 mEq/L, and normal hemoglobin, creatinine, blood urea nitrogen, aspartate aminotransferase, alanine aminotransferase, total bilirubin, albumin, lipase, and urinalysis. Abdominal CT scan was unchanged from the previous scan. He was treated with intravenous fluids, potassium, ondansetron, metoclopramide, prochlorperazine, fentanyl, viscous lidocaine, aluminum hydroxide/magnesium hydroxide/simethicone, and pantoprazole without improvement of symptoms. We applied capsaicin cream (0.075%) to a 15 × 25 cm area in the periumbilical region, with reapplications every 4 hours. The patient reported burning of the skin and improvement in the intensity of his stabbing abdominal pain and nausea a few hours after the first application of capsaicin. After the second dose, he noted complete resolution of his nausea. He received 2 more doses, which resulted in complete improvement of his abdominal pain. He was discharged the following day with a prescription for topical capsaicin. Over the following 3 months, the patient had no visits to our hospital system or any other providers included in Epic Care Everywhere within Washington State.
Discussion
The efficacy of capsaicin in CHS in our case lends credence to the role of TRPV1 in this syndrome. Previous models suggesting that cannabinoid receptor type 1 (CB1) is solely responsible for CHS are unsatisfying for several reasons. First, peripheral activation of CB1 slows gastric transit, but a case series of CHS patients described normal or increased transit time and no gastroparesis symptoms.5,6 Second, previous models suggested that hot-water bathing is an adaptive response to the hypothermic effects of cannabinoids. However, activation of CB1 should lead to hot-water bathing in all marijuana users, not just CHS patients who seem to engage in hot-water bathing as a learned behavior to treat symptoms. Finally, this model fails to explain why only some patients are susceptible to CHS, why there is latency from onset of marijuana use to symptoms, and why only chronic users are affected.
TRPV1 is a nonselective cation channel activated by noxious heat and capsaicin. This receptor is expressed throughout the gastrointestinal tract, including vagal sensory neurons, intrinsic enteric neurons in the myenteric plexus, and gastric epithelial cells.7,8 Within the central nervous system, there is a high density of TRPV1 in the area postrema, known as the chemoreceptor trigger zone. Activation of TRPV1 has potent anti-emetic effects, which may be mediated by depletion of substance P from neural circuits traveling to the nucleus tractus solitarius.9,10
Exogenous cannabinoids, including delta-9-tetrahydrocannabinoil, activate both CB1 and TRPV1.11 In vitro studies demonstrate that exogenous cannabinoids lead to dephosphorylation of TRPV1 and subsequent receptor desensitization.10 Therefore, chronic exposure to cannabinoids could downregulate or desensitize TRPV1 signaling, explaining how prolonged exposure to cannabinoids might lead to decreased TRPV1 signaling, altered gastric motility, and emesis. The learned behavior of compulsive hot-water bathing may be an attempt to normalize diminished TRPV1 activity by deliberate exposure to another TRPV1 agonist, nociceptive heat. Therefore, TRPV1 agonists such as topical capsaicin, which has a longer half-life than oral capsaicin, might augment TRPV1 activity and provide a less burdensome approach to treating CHS.12
One published case report and 2 case series have described successful treatment of 15 CHS patients with topical capsaicin.13–15 In all cases, patients with heavy marijuana use presented to the emergency department with nausea, vomiting, and abdominal pain improved by application of topical capsaicin preparation (0.075%). Some have questioned the lack of advanced diagnostics, such as endoscopic studies and CT imaging in these cases. In addition, these patients had a short period of observation in the emergency department with unclear clinical courses after discharge.16 These weaknesses do not apply to our case, given the extensive workup and prolonged inpatient observation.
Marijuana is the most frequently used illicit drug in the United States. Its recent legalization in many states has raised concerns of increased use and a resulting rise in CHS incidence.17,18 For these reasons, a better understanding of CHS pathogenesis and novel treatment strategies are increasingly important. Our case lends further credence to the role of TRPV1 in CHS, although only limited conclusions can be drawn from this single case with incomplete confirmed follow-up. We believe a prospective study, such as the planned randomized controlled trial examining capsaicin in cyclic vomiting syndrome, could adequately assess the efficacy of capsaicin for CHS.
Douglas.Curtis
Autistic Diplomat in Training
Since the 'kinda' is all speculation... I too am looking forward to concrete study results. The double blind I was going to set up involved a couple people I now believe to be psychotic, literally. Gonna have to st something else up.
Douglas.Curtis
Autistic Diplomat in Training
dr spaceman
New member
I recently moved back to Colorado and only have access to dispensary cannabis while I setup the grow. We all know how ubiquitous neem products have become in commercial cannabis... I've lost some weight (10 lbs) since moving from a strong lack of appetite, some stomach pain. I went to the gastroenterologist, given a 3 week antibiotic treatment for H. pylori, but they didn't do any tests. Ended that today, pain subsided after taking the antibiotic.
Last summer I grew cannabis using Neem seed meal as a soil amend and oil as a foliar only in veg. First time using Neem oil on plants, I've used meal in soil mixes before though. Grow was limited and for personal use, organic soil based on coots. Smoked it from aug-oct until I ran out. Experienced pretty bad gastro pain, irregularity, but not the current level of appetite loss.
So here I am, searching for some answers. I probably shouldn't have put neem oil on my face for acne several years ago... lol... or last summer.
Looks like I'll have to abstain for a bit until I can find and grow neem free cannabis. Unfortunate, I just mixed 30 gallons of organic soil with neem seed meal in it. RIP
Last summer I grew cannabis using Neem seed meal as a soil amend and oil as a foliar only in veg. First time using Neem oil on plants, I've used meal in soil mixes before though. Grow was limited and for personal use, organic soil based on coots. Smoked it from aug-oct until I ran out. Experienced pretty bad gastro pain, irregularity, but not the current level of appetite loss.
So here I am, searching for some answers. I probably shouldn't have put neem oil on my face for acne several years ago... lol... or last summer.
Looks like I'll have to abstain for a bit until I can find and grow neem free cannabis. Unfortunate, I just mixed 30 gallons of organic soil with neem seed meal in it. RIP
dr spaceman
New member
Also, any idea on the rate of azadirachtin uptake through roots? I tried to find the persistence of azadirachtin in soil but couldn't. The NSM is being actively degraded in an organic soil, would azadirachtin not also be degraded by microbes?
Going neem free on my setup for the sake of validation. Too many people with their anecdotes to ignore the pattern.
Going neem free on my setup for the sake of validation. Too many people with their anecdotes to ignore the pattern.
Douglas.Curtis
Autistic Diplomat in Training
I've root fed azamax at 3ml/gal and had issues 80+ days later at harvest. No idea how long it lasts either. Sorry to hear the issues, glad to hear you're ok and in Colorado.
same way
none of my flower has caused issues ever but i stopped using neem entirely (aza included)
i believe neem to be a profit margin increaser for grow suppliers.... it alll comes from india so the shit must be dirt cheap
peeps package it up all nicely and over-charge it to weed growers
i don't need that shit
dr spaceman
New member
Thanks Douglas. Perhaps something to test in a future grow.
Avinash, that's probably more true than not. Someone's making a lot of money selling all that neem. Biological products from India carry a questionable reputation for sure.
So we have CHS anecdotes that claim neem, and CHS research that claims it is caused by cannabinoids. Aza poisoning a separate issue?
Avinash, that's probably more true than not. Someone's making a lot of money selling all that neem. Biological products from India carry a questionable reputation for sure.
So we have CHS anecdotes that claim neem, and CHS research that claims it is caused by cannabinoids. Aza poisoning a separate issue?
possibly separate issues that express themselves similarly
Nedstark815
New member
Any updates from anyone whos found a way to smoke regardless of chs and without feeling like crap 24/7?
Douglas.Curtis
Autistic Diplomat in Training
I removed H.Pylori and aza from my system, I can use all the clean cannabis I want now.
Nedstark815
New member
How were you able to get rid of h pylori and how do you know if it's aza free? Grow yourself?
Douglas.Curtis
Autistic Diplomat in Training
The H.Pylori was a simple test to determine I had it. The treatment was 2 antibiotics and a proton pump inhibitor (like a whole system antacid). The treatment took over a month and I had drastic improvement in weeks.
Yes, I grow myself because it's damn difficult finding clean cannabis. Aza products and neem are still the "go-to" organic treatment for most growers and dispensaries.
Douglas Curtis = TheCleanGame
Douglas Curtis = TheCleanGame
hey Doug still pushing your nonsense i see...
Just to be clear Doug is actually an old banned member 'TheCleanGame'
https://steemit.com/newauthor/@thecl...ers-free-intro
https://www.icmag.com/ic/showthread.php?threadid=351334
https://www.icmag.com/ic/showpost.ph...80&postcount=6
why is thecleangame doing this? maybe a case ASW (Attention Seeking Whore)...
You sir are a fraud...how about you cut the bullshit and move on...
Douglas Curtis = TheCleanGame
hey Doug still pushing your nonsense i see...
Just to be clear Doug is actually an old banned member 'TheCleanGame'
https://steemit.com/newauthor/@thecl...ers-free-intro
https://www.icmag.com/ic/showthread.php?threadid=351334
https://www.icmag.com/ic/showpost.ph...80&postcount=6
why is thecleangame doing this? maybe a case ASW (Attention Seeking Whore)...
You sir are a fraud...how about you cut the bullshit and move on...
Douglas.Curtis
Autistic Diplomat in Training
You seem to be stuck on only associating CHS with cyclical vomiting. Sad to see you so narrow minded. In time I will be proven correct and you will not. I have done the research and you have not. I am confident and you are a seriously angry person.
Someone suggested a liver cleanse to help with bad attitude, perhaps you should look into it. I'm truly trying to help here, and I hope you figure it out one day.
Back to ignore for you, I'm done with you in this thread.
You seem to be stuck on only associating CHS with cyclical vomiting. Sad to see you so narrow minded. In time I will be proven correct and you will not. I have done the research and you have not. I am confident and you are a seriously angry person.
Someone suggested a liver cleanse to help with bad attitude, perhaps you should look into it. I'm truly trying to help here, and I hope you figure it out one day.
Back to ignore for you, I'm done with you in this thread.
and whats the 'cure' for your bullshit??
ignore me...yeah sure, like the way you respond to my posts..
