Irritable Bowel Syndrome (IBS)

IBS and the link between the brain and gut

Irritable bowel syndrome (IBS) is a common gastroenteric condition that presents as bloating, abdominal cramps and diarrhoea. It is long been suspected that there is a link between IBS and neuropsychiatric dysfunction, as the condition is often comorbid with psychiatric conditions such as anxiety, depression and PTSD; acute symptoms often arise in times of mental distress. However, as endocannabinoids are expressed in the enteric nervous system (ENS), as well as the areas of the brain affected by such psychiatric disorders, their effect may be independent.

Serotonin also plays a part in IBS, influencing gut motility (the peristaltic actions of the colon, which become “spastic” or uncontrolled during bouts of IBS), sensitivity and secretion of fluid. Interestingly, IBS-D (characterised by diarrhoea) sufferers have been shown to have increased blood serotonin levels, while sufferers of IBS-C (characterised by constipation) experience reduced levels of serotonin.

Cannabinoid receptors in the enteric nervous system

It has been demonstrated that activation of the cannabinoid receptors in the ENS decreases hypersensitivity of the gut, as well as reducing gut motility  and inflammation. Many sufferers of IBS use cannabis to alleviate their symptoms, although some report that symptoms worsened subsequent to commencing use; some even postulate cannabis as a trigger for IBS in certain individuals.

The overlap between instances of these conditions has led to the hypothesis that they are all expressions of the same underlying somatic disorder. Many sufferers of IBS also report symptoms of migraine, and up to 70% of fibromyalgia sufferers also present IBS symptoms. Many have all three, but it is not strictly necessary for all three to be present for an underlying condition to be the cause, as many spectrum disorders manifest markedly different symptoms from patient to patient, and other related conditions may be involved.

Is an underlying condition responsible?

The idea that a dysfunctional endocannabinoid system is responsible for this postulated somatic disorder first arose within the last few years. In 2004, the condition CECD was first proposed; researchers suggested that the high degree of comorbidity, along with the common feature of unusual cannabinoid receptor activity, pointed to an underlying disorder of the endocannabinoid system. Many known conditions can be attributed to dysfunction of a specific neurotransmitter system: Alzheimer’s is caused by deficiency of the acetylcholine neurotransmitter, and Parkinson’s by age-related dopamine deficiency. It is therefore logical to assume that deficiency of the cannabinoid neurotransmitters would also cause a specific disorder, or set of related disorders.

The relationship with the serotonin signalling system cannot be ignored when researching the possibility of CECD’s existence. Behavioural studies suggest that the effects of endocannabinoid signalling are mediated by regulation of the serotonin system: THC has been shown to inhibit serotonin release from the platelets in migraine sufferers, as well as increasing synthesis of serotonin in the brain; 2-AG and cannabidiol have demonstrated similar effects. However, the independent effects of cannabinoids on the cannabinoid receptors are thought to be the underlying cause of CECD, despite this possibly fundamental relationship with serotonin signalling.

If the existence of CECD is proven, targeted therapies can be investigated, which would pinpoint the precise nature of the deficiency and determine the appropriate ration and dosage of supplemental exogenous cannabinoids. At present, treatment of these conditions is usually through ingestion of crude cannabis extract, or through smoking, which may involve wildly different cannabinoid ratios between cannabis strains. Due to the dose-dependent effect of many cannabinoids, relief of symptoms may not be adequate with some varieties.

https://sensiseeds.com/en/blog/what-is-clinical-endocannabinoid-deficiency/
Clinical Endocannabinoid Deficiency?