Talk:Obsessive–compulsive disorder

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Inaccurate history of OCD is presented[edit]

The article neglects to mention that the first clinical description of OCD was by Abu Zayd al-Balkhi in the 9th century work Sustenance of the Body and Soul.

For details, see "Obsessional Disorders in al-Balkhi′s 9th century treatise: Sustenance of the Body and Soul" published in the Journal of Affective Disorders, Volume 180, 15 July 2015, Pages 185-189.

I am including the abstract below:

Morbid fears and phobias have been mentioned in religious, philosophical and medical manuscripts since ancient times. Despite early insights by the Greeks, phobias did not appear as a separate clinical phenomenon in Western medicine until the 17th century and has evolved substantially since. However, robust investigations attempting to decipher the clinical nature of phobias emerged in pre-modern times during the oft-overlooked Islamic Golden Era (9th–12th centuries); which overlapped with Europe’s medieval period. An innovative attempt was made by the 9th century Muslim scholar, Abu Zayd al-Balkhi, in his medical manuscript “Sustenance of the Body and Soul,” to define phobias as a separate diagnostic entity. Al-Balkhi was one of the earliest to cluster psychological and physical symptoms of phobias under one category, “al-Fazaá”, and outline a specific management plan. We analyze al-Balkhi’s description of phobias, according to the modern understanding of psychiatric classifications and symptomatology as described in the DSM-5.

Semi-protected edit request on 16 December 2018[edit]

Please chng hoarding related to hoarding-related Letateal (talk) 22:19, 16 December 2018 (UTC)

 DoneJonesey95 (talk) 01:57, 17 December 2018 (UTC)

Recent changes to the lead[edit]

IiKkEe, you need to discuss your changes because you are changing the context or meaning of some material. Keep in mind that this is a medical article, which is why WP:MEDRS has high standards. Why not just to stick to what the sources state? When reverting you here, I stated that checking things repeatedly is not necessarily performing certain routines repeatedly. For example, a person with OCD might feel the need to repeatedly check for an email reply. But this doesn't mean that doing so is a routine for them. After all, that is just one email reply. Once the other person replies, that matter is over. The person with OCD might not communicate via emails enough for repeatedly checking emails to become a routine. You went back to changing the lead. You made it so that the lead states "the need to perform certain routines repeatedly such as checking on the status of something (rituals)," which led Doc James to remove "checking on the status of something (rituals)." It's best to just leave the lead as it was and include "feel the need to check things repeatedly," just like we do in the infobox.

When you are reverted on something like this, don't just go back to tinkering with the lead, especially when an editor suggests that you discuss the matter on the talk page. Take it to the talk page and discuss. If you reply to me on this, I ask that you don't ping me. Flyer22 Reborn (talk) 14:05, 8 March 2019 (UTC)

It is important to be actively reading the sources when text is adjusted. Doc James (talk · contribs · email) 14:13, 8 March 2019 (UTC)

Semi-protected edit request on 31 May 2019[edit]

Please change "A myth propagated by Sigmund Freud regarding above-average intelligence in OCD was recently refuted"

to something more accurate eg,

"There is evidence and a consensus among psychiatrists that people with OCD have a higher average intelligence quotient than the general population. However, a recent study has questioned this."

Here is a large study that supports this opposing view: https://www.sciencedirect.com/science/article/pii/S0160289616303324 Dom.uk.1 (talk) 20:36, 31 May 2019 (UTC)

 Not done: please establish a consensus for this alteration before using the {{edit semi-protected}} template. MrClog (talk) 16:21, 6 June 2019 (UTC)

Semi-protected edit request on 3 December 2019[edit]

I would like to add additional information to the Neurobiological section of this page. I have integrated my research into the existing paragraph as below, with new information bolded.

Requested text

From the observation of the efficacy of antidepressants in OCD, a serotonin hypothesis of OCD has been formulated. Serotonin, or 5HT, is a monoamine that is produced in the Raphe Nuclei. 5HT is known to be involved in a variety of bodily functions, including mood, digestion, memory, and sexual desire. 5-HT1 receptors act by inhibiting protein kinases and opening potassium channels to hyperpolarize the cell. 5-HT1 receptors are thought to promote feelings of happiness and calm when activated, while 5-HT2 receptors can lead to feeling overwhelmed. Studies of peripheral markers of serotonin, as well as challenges with proserotonergic compounds have yielded inconsistent results, including evidence pointing towards basal hyperactivity of serotonergic systems. The basal ganglia is responsible for planning and executing movements, receiving input from across the cortex and sending excitatory glutamate signals into the striatum. Serotonin receptor and transporter binding studies have yielded conflicting results, including higher and lower serotonin receptor 5-HT2A and serotonin transporter binding potentials that were normalized by treatment with SSRIs. Despite inconsistencies in the types of abnormalities found, evidence points towards dysfunction of serotonergic systems in OCD.

The orbitofrontal cortex, or OFC, is responsible for causing feelings of worry, preventing poor decisions, and changing behavior as appropriate to a new situation. Damage to the OFC leads to impulsivity and lack of inhibition. Orbitofrontal cortex overactivity is attenuated in people who have successfully responded to SSRI medication, a result believed to be caused by increased stimulation of serotonin receptors 5-HT2A and 5-HT2C. Ahmari et al. (2018) studied how activating inputs from the OFC into the striatum affect OCD-like behaviors. They injected wild-type mice with channelrhodopsin, a light-gated ion channel that stimulates a brain region when blue light is shined on it. Half of the mice had their OFC to striatum connection stimulated five times a day for 5-10 days, while the other half received no stimulation. Upon measuring spontaneous grooming when no blue light is being shined, they found that mice that received repeated activation exhibited obsessive-compulsive grooming while controls did not. These findings provide evidence that excessive OFC to striatum signaling causes OCD. This persistent overactivity may underlie the obsessions that are characteristic of the disease, which are intrusive, repeated thoughts that cause anxiety and worry. A complex relationship between dopamine and OCD has been observed. Dopamine is produced in the substantia nigra and ventral tegmental area, which are adjacent in the brainstem. Dopamine produced in the substantia nigra and sent to the striatum increases desire to move. Dopamine produced in the VTA can be sent to the frontal lobes, where it aids in attention and motivation, or to the nucleus accumbens, where it results in feelings of pleasure. Although antipsychotics, which act by antagonizing dopamine receptors may improve some cases of OCD, they frequently exacerbate others. Antipsychotics, in the low doses used to treat OCD, may actually increased the release of dopamine in the prefrontal cortex, through inhibiting autoreceptors. Further complicating things is the efficacy of amphetamines, decreased dopamine transporter activity observed in OCD, and low levels of D2 binding in the striatum. Furthermore, increased dopamine release in the nucleus accumbens after deep brain stimulation correlates with improvement in symptoms, pointing to reduced dopamine release in the striatum playing a role in generating symptoms.

Abnormalities in glutaminergic neurotransmission have implicated in OCD. Findings such as increased cerebrospinal glutamate, less consistent abnormalities observed in neuroimaging studies, and the efficacy of some glutaminergic drugs such as riluzole have implicated glutamate in OCD. Welch et al. (2007) utilized mice with the Sapap3 gene knocked out to study how synaptic inputs from the cortex into the striatum differ in OCD. Sapap3 is an excitatory protein that is highly expressed in the striatum, and caused mice to groom compulsively when removed. Researchers electrically stimulated inputs from the cortex into the basal ganglia, measuring the rate of grooming and size of the postsynaptic response in striatal cells. They found that there was weaker signaling in the Sapap3 knockout mice than in controls, suggesting that mice with obsessive-compulsive behaviors have less glutamate receptors in the cortex to striatum connection. OCD has also been found to have high rates of comorbidity with a variety of other disorders, including depression and Tourette Syndrome. Pauls et al. (1996) investigated the possibility of a common genetic mechanism between OCD and Tourette Syndrome. They compared probands with Tourette’s to their relatives and controls, measuring the rate of Tourette’s, rate of OCD, and rate of both diseases in all comparison groups. The researchers found that the relatives of the probands also showed increased rates of OCD and Tourette’s, suggesting that there exists a common genetic risk factor both both diseases that may manifest in different ways. OCD has been associated with reduced N-Acetylaspartic acid in the mPFC, which is thought to reflect neuron density or functionality, although the exact interpretation has not been established.

Juliakim2 (talk) 01:42, 3 December 2019 (UTC)

Not done. Please provide reliable sources that support this information. –Deacon Vorbis (carbon • videos) 01:59, 3 December 2019 (UTC)

Remove unreliable information in Research section with dubious citation[edit]

Please remove claims of the usefulness of vitamin and mineral supplements for OCD patients in the Research section. The only cited source (Lakhan SE, Vieira KF (2008)) fails to verify these claims, makes additional claims of a particular brand of supplement being effective for OCD, and supports this by citing studies which mention neither OCD nor the supplement.


The claim "Nutrition deficiencies may also contribute to OCD and other mental disorders." cites no sources and should be removed unless a reliable source can be found to verify it.

The claim "Vitamin and mineral supplements may aid in such disorders and provide nutrients necessary for proper mental functioning.[126]" should be removed because it cites Lakhan SE, Vieira KF (2008) which fails to verify this claim. It repeatedly makes general claims of "deficiencies" contributing to "mental disorders" but supports this with multiple citations focused solely on Omega3/Folate intake in Depression and a single study on L-Tryptophan and Mania - no citations are directly relevant to OCD. It also contains fear mongering about the side effects of drugs used to treat "these disorders" but only supports this with citations related to lithium toxicity in Bipolar Disorder, an extreme example which does not apply to other disorders.

In Table 1, the only "Proposed Cause" of OCD listed is "St. John's wort deficiency" - St. John's wort is an exogenous substance not normally present in the human diet; deficiency is therefore impossible.


In the section focused on OCD in Lakhan SE, Vieira KF (2008) first paragraph, the following claim is made:

"...the amino acid tryptophan is a precursor to serotonin, and tryptophan supplements (which are better than 5-Hydroxytryptophan) will increase serotonin levels and treat OCD [68]."

The citation [68] is: Yaryura-Tobias JA, Bhagavan HN. L-tryptophan in obsessive-compulsive disorders - 1977

This is a 42-year-old preliminary study with n=7. It does not contain the term 5-Hydroxytryptophan. Patients did not receive tryptophan alone but a combination of tryptophan, nicotinic acid, and pyridoxine HCL. The study also noted increased aggression in 2 cases (28%) as a result of this regimen which is not mentioned in the citing article.


The second paragraph in the OCD section of Lakhan SE, Vieira KF (2008) is significantly more dubious and reads like an advertisement:

"A commercially available supplement called Amoryn has recently proven to help patients suffering from depression, anxiety, and OCD [69,70]."

The citations supporting this claim are:

[69]: Acute treatment of moderate to severe depression with hypericum extract WS 5570 (St John’s wort): randomised controlled doubleblind non-inferiority trial versus paroxetine
[70]: A Double-blind, Randomized Trial of St John’s Wort, Fluoxetine, and Placebo in Major Depressive Disorder

Neither of these studies pertain to OCD but rather to MDD. A text search for the terms OCD, Obsessive, Compulsive, Intrusive, and Ritual yielded 0 results in both papers. In addition, neither paper contains the term "Amoryn" even though their citations ostensibly confirm that Amoryn specifically has been proven effective by these studies. The first study excluded patients with acute anxiety disorders from the study population, yet Lakhan SE, Vieira KF cite this to support the claim that it is "proven to help patients suffering from ... anxiety". The second citation does not even contain the term anxiety.


The second paragraph of the OCD section in Lakhan SE, Vieira KF goes on to claim that this supplement is superior to SSRIs for OCD:

"Two double-blind, placebo-controlled studies were recently performed that compared the affects of a 900 mg daily dose of St. John's wort extract to 20 mg daily doses of Paroxetine (Paxil) or Fluoxetine ... In comparison to patients taking Paxil, those who took the St. John's wort supplement showed a 57% decrease in OCD symptoms and were 47% less likely to exhibit side effects [69]. In comparison to patients taking Fluoxetine, consumption of the St. John's wort extract reduced 48% of OCD patient's symptoms [70]. These results clearly depict how the use nutritional supplements can be effective treatments for mental disorders."

Again, neither of these citations even mention OCD, and one study specifically excluded patients with acute anxiety disorder, making any generalization to OCD highly suspect.

Jamedeus (talk) 03:26, 6 December 2019 (UTC)

 Done After having read this request and the cited sources, I agree these statements failed to be verified by the cited source. I have removed them as requested. Eggishorn (talk) (contrib) 18:02, 8 December 2019 (UTC)