cbd bladderDecember 15, 2021
Urothelial carcinoma, also known as transitional cell carcinoma (TCC), is by far the most common type of bladder cancer. As the name suggests, they start in the urothelial cells that line the inside of the bladder. Urothelial cells also line other parts of the urinary tract (incl., the renal pelvis, the ureters, and the urethra). People with bladder cancer sometimes have tumors in these places, too, so all the urinary tract needs to be checked for tumors.
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Invasive bladder cancers have grown into deeper layers of the bladder wall, meaning the cancer has grown into a deeper (muscle) layer of the bladder, or beyond. Some people have invasive bladder cancer when they are first diagnosed.
Bladder Cancer Types.
The wall of the bladder has many several layers, each of which comprises different cells. Bladder cancer is when the cells that make up the urinary bladder growing out of control. And as more cancer cells develop, they can form a tumor. Sometimes, it can also spread to other parts of the body.
They did this by using CBD (a known selective TRPV2 agonist) to investigate the association between TRPV2 and UC cell death as well as determine whether Ca2+ influx into UC cells through TRPV2 is involved in apoptotic cell death. Focussing on Ca2+ permeable TRP channels expressed abundantly in human bladder cancer cells, they examined, using Ca2+ imaging analysis and biochemical approaches, whether the regulation of channel activity could lead to an inhibitory effect on the viability of UC cells.
Radiation therapy , a form of that uses beams of powerful energy, such as X-rays and protons, to destroy the cancer cells. Radiation therapy for bladder cancer usually is delivered from a machine that moves around the body, directing the energy beams to precise points. It is sometimes combined with chemotherapy to treat bladder cancer in certain situations, such as when surgery isn’t an option or isn’t desired.
Chemotherapy in the bladder (intravesical chemotherapy), to treat cancers that are confined to the lining of the bladder but have a high risk of recurrence or progression to a higher stage.
Chemotherapy for the entire body (systemic chemotherapy), to increase the chance for a cure in a person having surgery to remove the bladder, or as a primary treatment when surgery isn’t an option.
Transient receptor potential (TRP) channels are calcium ion (Ca2+) permeable channels that are thought to contribute to calcium balance inside the cell. Evidence shows that these channels are implicated in the emergence and/or progression of certain epithelial cancers. Based on this, 2010 study published in Urology, investigated the role of vanilloid 2 (TRPV2) channel proteins in the development of human urothelial carcinoma (UC) cells.
CBD as a Complementary Treatment.
Non-invasive bladder cancers (also called early or superficial) are only in the inner layer of cells (the transitional epithelium) and have not yet grown into the deeper muscle layers.
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Most of the available evidence indicates that CBD may complement cancer treatment and that CBD may help people with cancer by helping reduce pain and inflammation. In addition, many people suffering from cancer also report having other side effects from chemotherapy treatment, including sleep problems, feelings of anxiety and depression. In one large case series study investigating the effects of CBD on anxiety and sleep, the results show CBD helps improve sleep and/or anxiety in clinical populations. Similarly, CBD can further support cancer patients by reducing stress, anxiety, depression while also helping to promote REM sleep that is thought to help improve overall mood.
Symptoms of Bladder Cancer.
The internet is full of stories from people who have effectively treated their bladder cancer with cannabis oil. However, when it comes to CBD and bladder cancer, the anecdotal evidence centres more around CBD being used as a complementary therapy (more on that below).
In a later study from 2017 published in Scientific Reports, researchers investigated cannabinoid receptor (CB) expression on normal and human bladder cancer (BC) cells using immunohistochemistry. Again, although the effect of CBD in particular was not investigated, they did draw conclusions about the effectiveness of cannabinoid such as CBD on BC cell growth and motility.
All the moist skin-like tissues lining body organs, including the bladder, have some gland cells that produce mucus. Adenocarcinoma is an uncommon malignancy in the urinary bladder that develops from these cells in the lining of the bladder.
Scientific and anecdotal evidence both suggest that CBD can support bladder cancer patients, especially by helping to reduce chemotherapy-induced neuropathic pain, inflammation, nausea and vomiting. If you or a loved one are suffering from bladder cancer and want to try CBD, talk to your medical practitioner first. He or she can help put together a plan that includes CBD along with other treatment options to help you deal with your symptoms safely and effectively.
Targeted therapy to treat advanced cancer when other treatments haven’t helped.
The localization of CB 2 receptor with nerves argues for a role of CB 2 in bladder afferent signals which can be best demonstrated by cystometric studies. These in vivo effects of CP55940 (CB 1 /CB 2 receptor agonist) on urodynamic parameters. MI and TP may be considered parameters that indirectly represent sensory functions during cystometry. Lack of a direct effect of CB 1 /CB 2 agonist CP55,940 and the nonselective agonist anandamide on carbachol induced contractions indicated the absence of direct CB mediated functions of isolated detrusor smooth muscle.
Pharmacology of ECBs is complex due to their ability to act on multiple receptors.
Local action of CB agonist in the bladder may involve action at receptors on peripheral nerves or an indirect modulation of immune cell responses decreasing peripheral nerve excitability [ Figure 5 ]. Similar pharmacological studies in gut have shown that activation of CB 1 receptor inhibits intestinal motility by reducing the acetylcholine release from enteric nerves. Possibility of a similar action of CB 1 agonists in bladder, to explain higher MI, cannot be ruled out. Locally administered cannabinoids can also inhibit NF-kB activation to suppress hyperalgesia. These findings support the notion that cannabinoid system participates in buffering the pain signals emerging from the peripheral sites.
Cannabinoid receptors in human and primate bladder.
As described in earlier sections here, experimental factors such as drug concentration, timing of drug delivery and location of drug administration can influence the therapeutic and adverse response of cannabinoids. The acute adverse effects reported with the consumption of cannabis by smoking or by oral route includes increased food intake, tachycardia, orthostatic hypotension, pulmonary irritation, impaired motor coordination, cognitive impairment, anxiety, paranoia, and psychosis. In addition, the bioavailability of CBs from the oral route is uncertain as illustrated by unpredictable pharmacokinetics of (Δ 9 – THC) after oral administration. This has generated a lot of interest in alternative routes for delivering cannabinoids. It was recently shown that topical application of 30 µg of Δ 9 -THC reduced allergic inflammation in mouse ear model of allergic dermatitis. The activation of cutaneous CBs lead to attenuation of nociceptor excitation, pain and itch perception, and decreased the release of neuropeptides, particularly CGRP, from terminal afferents.
To further confound the pharmacology of anandamide in bladder, the responses to anandamide as reported by Gratzke et al., (2009) were attenuated but not abolished after desensitization by capsaicin. Further, anandamide response were partially attenuated by an prostaglandin receptor EP1 antagonist and almost abolished by indomethacin, a cyclooxygenase inhibitor. Neither the CB 1 antagonist AM251 nor the CB 2 antagonist AM630 had any effect on the response to anandamide, to suggest possible role of EP1 receptor.
The distribution of these CB 1 /CB 2 receptors at key sites involved in nociceptive processing is instrumental in the analgesic effects of phytocannabinoids (plant source) or synthetic cannabinoids developed in last 30 years. Synthetic cannabinoids are chemicals having action similar to cannabis on their cognate receptors. Studies have shown that synthetic and semi-synthetic cannabinoids that lack psychotropic effects are effective against severe pain states refractory to even opioids. The activation of nociceptive sensory neurons leads to nociception. However, CB 1 /CB 2 agonists are capable of altering nociceptor activity without producing nociceptive behavior.[13,43] CB 1 /CB 2 agonists have been able to suppress the nociceptive transmission and inhibit pain-related behavior in animal models of acute and persistent nociception by their activity at spinal, supraspinal and peripheral sites.
In earlier studies, the presence of CB 1 receptors has been indirectly demonstrated in the rodent bladder using specific  Results from an isolated bladder strip study suggested that these receptors are located in the prejunctional neuron. Further, systemic administration of CB agonist and antagonists in spinal cord injured rats with detrusor overactivity demonstrated the role of a tonically active ECB system in pathological voiding.
It can be a challenge to determine the in vivo mechanism of CB agonists administered systemically or intravesicallygiven the ability of CB ligands to activate other receptors, namely TRPV1, at varying concentrations. This can also explain the difficulty faced by researchers engaged in investigating the role of CB 1 and CB 2 receptors using pharmacological antagonists and agonists. For example, SR-141716, a CB 1 receptor antagonist, can also show agonist property because of its other effects. Therefore, the use of a genetic approach has gained favor among scientists to complement the pharmacological analysis of the cannabinoid system, and mice with targeted deletions in the cannabinoid receptor genes have been generated to study role of of the endocannabinoid system in addiction research. The pharmacological specificity of CB 1 /CB 2 agents administered systemically or intravesically can be easily determined by comparing results in knockout mice with wild type littermates. The development of transgenic CB 1 -/- and CB 2 -/- receptor knockout mice using homologous recombination has opened up the opportunity to study the role of the CB 1 and CB 2 receptor system in lower urinary tract. The concerns of global deficit of CB 1 and CB 2 receptors, in the survival of these mice, can be ameliorated using time-dependent and bladder specific deletion of CB 1 and CB 2 receptors.
Proposed mechanism of locally administered cannabinoid agonist in irritated bladder. Bladder irritated by acetic acid, in the animal model, activates TRPV1 on urothelium and adjoining nerves to release CGRP. Irritation evoked release of CGRP is blocked by mixed CB 1 /CB 2 agonist ajulemic acid entrapped into liposome that activates CB 1 and CB 2 receptors on bladder surface and nerves.
The new drugs based on pharmacology of cannabinoids can be classified into two categories: Direct and indirect agonists. Direct agonists selectively activate either CB 1 or CB 2 receptor. CB 2 receptor agonists are not associated with the adverse side-effects of CB 1 -selective agonists and therefore may provide an alternative analgesic target. Indirect agonists work on the principle that metabolic degradation is the rate-limiting step in the therapeutic effects of ECB and the efficacy can be magnified by blocking the ECB metabolism either through cellular reuptake or enzymatic hydrolysis. Such compounds can theoretically act selectively on tissues with ongoing synthesis and degradation of ECB, thus producing fewer unwanted effects than direct agonists. By acting through up-regulation of ECB, another advantage of indirect agonists is that they may produce beneficial actions through actions on other receptors as well such as CB 1 , CB 2 or TRPV1 receptors.
Take home message and important points.
Cystometric effect of mixed CB 1 /CB 2 receptor agonist, ajulemic acid on bladder irritation induced by infusion of acetic acid (0.125%). Rats were pretreated with either saline or ajulemic acid entrapped in liposomes. Baseline cystometry (CMG) was done under saline infusion prior to bladder irritation induced by acetic acid. Activation of local cannabinoid receptors in the bladder blunted the decrease in micturition interval MI induced by acetic acid. Decrease in MI is evident from reduced time interval between the peaks of cystometrogram of saline treated rat relative to rat treated with ajulemic acid. The urodynamic parameter, MI, indirectly represents sensory functions and reduced MI is an integrated response of irritated bladder.
The receptor CB 1 is the most abundant of all receptor types in the brain and other CNS regions involved with pain transmission and modulation, specifically in the spinal dorsal horn and periaqueductal gray.[4,5] CB 1 receptors are also located peripherally in both neuron and non-neuronal tissue, while CB 2 receptors are mainly found in immune cells and brain glial cells.[4,6] These receptors have been found to have many physiological and patho-physiological functions, including mood alteration, control of feeding and appetite, motor and co-ordination activities, analgesia, immune modulation and gut motility.
The metabotropic CB 1 receptor exhibit 48% amino acid sequence identity with CB 2 receptors and both of them are negatively coupled to adenylyl cyclase to inhibit cyclic AMP that indirectly inhibit L-type Ca 2 + channel. CB 1 receptors couple via pertussis toxin -sensitive Gi/o proteins to inhibit N − , and P/Qtype Ca 2 + channels and K + channels. The inhibitory effects of cannabinoids on Ca 2 + channels in nerve terminals are similar to other endogenous anti-nociceptive agents such as opioids. GP1a (N-(Piperidin-1-yl)-1-(2,4-dichlorophenyl)-1,4- dihydro-6-methylindeno[1,2-c]pyrazole-3-carboxamide) is a highly selective CB 2 agonist with Ki values of 0.037 and 363 nM for CB 2 and CB 1 , respectively. The Δ 9 -THC mimics the action of endocannabinoids and acts non-selectively on both CB 2 and CB 1 receptors.
The diverse effects of CB 1 and CB 2 receptor system in lower urinary tract may be novel targets for therapies designed to treat diseases afflicting lower urinary tract. The growth-inhibiting action of cannabinoids acting on these receptors expressed on transformed cells might be useful for the management of malignancy in bladder. Recently published pre-clinical studies have demonstrated that cannabinoids appear to act principally as prejunctional modulators of neurotransmission to affect the micturition process indirectly by affecting the nociceptive responses pathways. It is likely that CB 1 and CB 2 receptors located in periphery such as in bladder participate in the intrinsic control of initiation of afferent stimulus. Emerging studies show that ECBs are mediators of spinal activity-dependent pain sensitization to create a future role for pharmacological antagonists CB 1 and CB 2 receptors in control of neuropathic pain.
The presumed expression of CB receptors on capsaicin- sensitive sensory nerves, being coupled to inhibition of neurotransmitter release, was demonstrated in an isolated rat bladder model. Application of the mixed CB 1 /CB 2 receptor agonist, ajulemic acid (AJA) inhibited the evoked release of CGRP from afferent nerve terminals in isolated rat bladder. Sensory afferent axons in the bladder are the only structures in the bladder that contain high levels of CGRP released upon nerve depolarization or chemical stimulation by capsaicin [ Figure 3 ]. Pharmacological specificity of the inhibitory effect of AJA on sensory neuronal activity originating from the bladder through CB 1 and CB 2 receptors was demonstrated using selective receptor antagonists.
Local administration of cannabinoids inside bladder.
It is definitely more logical to develop local CB delivery with predictable bioavailability that rules out central side effects. Route of inhalation is also a distinct possibility for the therapeutic delivery of cannabinoids, as shown by the recent approval of an oromucosal (sublingual) spray standardized for the Δ 9 -THC and CBD (1:1 ratio) in Canada, as adjunctive treatment for neuropathic pain of multiple sclerosis patients. (53) The rationale for the combination of CBD and Δ 9 -THC is that CBD can antagonize some undesirable effects of THC including intoxication, sedation and tachycardia, while contributing analgesic, anti-emetic properties. This is because Δ 9 -THC can activate cannabinoid CB 1 and CB 2 receptors but CBD possesses no, or very weak affinity for these receptors. The spray is administered with a device equipped with an electronic tool to facilitate accurate dosing.
Expression of CB 1 and CB 2 receptor in lower urinary tract is relevant to effects of cannabinoids on voiding dysfunction.
In an open-label pilot study on advanced MS patients, daily inhalation from the oromucosal spray (Sativex ® ) for 16 weeks improved the refractory lower urinary tract symptoms of these patients. The spray also reduced neuropathic pain, spasticity, muscle spasms and sleep disturbances. Most common adverse events reported were dizziness, sleepiness, fatigue, feeling of intoxication and a bad taste.
Most TRPV1 receptor-expressing cells are also known to co-express the CB 1 receptors as well.  The close proximity of CB 1 and TRPV1 may facilitate the dual, concentration- dependent effect of anandamide observed in different studies. Dual dose dependent effect of cannabinoids have also been previously noted in relation to immune system where low doses of cannabinoids may enhance cell proliferation and high doses of cannabinoids may induce growth arrest or apoptosis. The ability of same ligands to activate both metabotropic CB 1 /CB 2 receptors and ionotropic TRPV1 receptors suggest possible interactions between the two signaling systems. Stimulation of CB 1 and desensitization of TRPV1 could be a strategy to protect against inflammation in bladder.
Route of administration have a drastic influence on therapeutic index of of cannabinoids.
Anandamide has also been noted to aggravate cyclo phosphamide induced cystitis in rodents through its activation of TRPV1 ion channels and thereby causing detrusor overactivity and hyperalgesia. In contrast, anandamide have been also shown to mediate attenuation of detrusor overactivity induced by nerve growth factor instillation in bladder. The attenuation of detrusor overactivity by anandamide unmasked the role of CB 2 receptors expressed in bladder in controlling the pain initiated locally in bladder.  Concentration and time of exposure may be critical in determining which of these opposite effects of anandamide ultimately prevails.
So, if you’re going to try CBD to help with bladder leaks, you may want some back up protection just in case. Lily Bird pads and underwear are designed just for that.
There’s a lot of acronyms out there, but one that has been popping up everywhere is CBD. It’s becoming so popular that you can find it at most pharmacy store chains and even at your local grocery. Yet, despite seeing it everywhere, you probably still don’t know exactly what it is. You’ve likely heard claims that it reduces pain, fights anxiety, and alleviates insomnia. So, if it can do all of that, then we can’t help but wonder if it could help your bladder too. Sit tight and get comfortable as we explore what CBD is and if it can put a stop to bladder leaks (aka incontinence).
When CBD comes into the picture and interacts with CB1 receptors, it could possibly improve urinary incontinence conditions by enhancing the detrusor muscles. The detrusor muscles are what expand and contract to hold or eliminate pee. Studies have also shown that cannabis might have a role in reducing the brain/bladder signals that tell you to go when you don’t have to. But scientists need to do a lot more research.
For this part, I’m going to need you to bare with me. I know science class didn’t cover this back in high school, but this background will help make sense of things later. Our bodies actually have two receptors for cannabinoids, which are CB1 receptors and CB2 receptors. CB1 receptors are more present in the brain and have an impact on movement, emotions, mood, and more. CB2 receptors, on the other hand, are found in the immune system, and affect inflammation and pain. While THC binds with these receptors, CBD actually suppresses receptors, specifically CB1 receptors. CBD may activate and produce physiological changes by binding with these receptors, such as decreasing pain or improving mood.
You can take CBD in many ways, but most of the studies involving its impact on the bladder involve subjects taking it orally (i.e. pill form). You can also take it in the following ways:
But, How Does This Help My Bladder?
With information like this you’re probably wondering how you can get your hands on it as soon as possible. However, hold your horses, cowgirl. While CBD sounds great, it is not yet FDA approved. It’s legal under federal law (if it doesn’t contain more than 0.3% of THC), but it’s still subject to regulation if it’s sold with a claim for therapeutic benefit. So, in other words, you can buy and use CBD, but be careful where you’re getting it from because it’s not exactly policed by public health entities.
First things first, cannabidiol, also known as CBD, is not marijuana . It is a compound that is found in both marijuana and hemp plants, but it will not affect you like smoking marijuana would. The reason why marijuana is mind-altering is due to the main ingredient, THC (tetrahydrocannabinol) that is found in the plant. While CBD does contain about .3% of THC, it’s not enough to have an intoxicating experience.
What’s interesting is that the pathways related to bladder function have lots of CB1 receptors. This pathway includes the bladder, central nervous system, and the parts of the brain that communicate with the bladder.
In addition, scientists need to do more research to explore the potential side effects and risks of using CBD. So far, the only real side effect of taking CBD is tiredness, but it’s best to speak with your doctor first to see if it may interact with any medications you’re taking. In the meantime, we’ll stay on the lookout for more updates on CBD and its impact on bladder leaks.
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