Reduced dopamine D1 receptors and dopamine D2 receptors in the striatum have been reported in people with OCD, along with both increased and decreased reports of dopamine transporter (DAT) binding.
Preclinical, neuroimaging and neurochemical studies have provided evidence demonstrating that the dopaminergic system is involved in inducing or aggravating the symptoms that are indicative of OCD.
In OCD, people develop obsessions (intrusive thoughts or images that trigger significant emotional distress) and compulsions (behaviors someone engages in to decrease the upsetting obsessions). OCD may involve damped dopamine-receptor activity and also increased dopamine activity in some areas of the brain.
The neurobiological understanding of obsessive–compulsive disorder (OCD) includes dysregulated frontostriatal circuitry and altered monoamine transmission. Repetitive stereotyped behavior (e.g., grooming), a featured symptom in OCD, has been proposed to be associated with perturbed dopamine (DA) signaling.
Is OCD Caused by a Chemical Imbalance? Changes in the neurochemical serotonin, as well as in the neurochemicals dopamine and glutamate, are likely present in OCD. Indeed, medications like the antidepressants known as selective serotonin reuptake inhibitors (SSRIs) improve symptoms for many people.
Obsessive compulsive disorder, or OCD, is an anxiety disorder which, like many anxiety disorders, is marked by low levels of serotonin. Serotonin, a type of neurotransmitter, has a variety of functions that make a deficiency a serious and anxiety producing issue.
Vitamin D. Previous studies have demonstrated that vitamin D deficiency is associated with numerous neuropsychiatric diseases that include autism, major depressive disorder, schizophrenia and OCD.
Glutamatergic neurotransmission is the principal neurotransmitter implicated in the CSTC model of OCD. Hyperactivity in the CSTC loop implies a high level of glutamate in the cortical-striatal pathways as well as a dysregulation of GABAergic transmission, and could represent the pathophysiology of OCD.
Research suggests that OCD involves problems in communication between the front part of the brain and deeper structures of the brain. These brain structures use a neurotransmitter (basically, a chemical messenger) called serotonin.
You can test for low dopamine levels by taking a Dopamine Blood Test. This test measures the dopamine level in your body responsible for some brain functions such as movement, memory, behavior and cognition, pleasurable reward, attention, sleep, mood, and learning.
A consistent pattern emerged from the combined data: Compared with healthy volunteers, people with OCD had far more activity in the specific brain areas involved in recognizing that they were making an error, but less activity in the areas that could help them stop.
Total severity scores are usually assumed to indicate the following levels of OCD: subclinical (0–7), mild (8–15), moderate (16–23), severe (24–31) and extremely severe (32–40).
Neuroimaging studies have revealed differences in brain activity between people with OCD and those who are unaffected. In particular, there are differences in a circuit that links a part of the brain called the striatum, thalamus, and parts of the frontal cortex.
However, one thing that is clear is that comorbidities, stress, anxiety, and major life changes or circumstances can all play a significant role in how much worse OCD might become. As symptoms increase or intensify, people with OCD may also experience the following: Failure at work and/or school.
The study showed that the balance between glutamate (Glu) and γ-aminobutyric acid (GABA)—two major neurotransmitter chemicals—is disrupted in OCD patients in two frontal lobe regions of the brain, the anterior cingulate cortex (ACC), and the supplementary motor area (SMA).
Magnetic resonance imaging (MRI) scans conducted to compare the volumes of different brain regions in people with and without OCD have found smaller volumes of the orbitofrontal cortex and the anterior cingulate cortex in individuals with OCD.
Serotonin Reuptake Inhibitors (SSRIs) work well to help control OCD symptoms. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) are another type of antidepressant that can be helpful to people suffering from OCD symptoms. The following antidepressants are FDA approved to treat OCD: Anafranil (clomipramine)
Vitamin B12 and folate are thought to be effective in OCD treatment due to their associations with neurotransmitters. Depending on their antioxidant effect, zinc and selenium can be used in augmentation therapy for OCD. However, both trace elements and vitamin B12/folate can be affected by diet.
The study demonstrated that newly diagnosed OCD patients have lower vitamin D levels than healthy controls.
OCD has peaks of onset at two different life phases: pre-adolescence and early adulthood. Around the ages of 10 to 12 years, the first peak of OCD cases occur. This time frequently coincides with increasing school and performance pressures, in addition to biologic changes of brain and body that accompany puberty.
Estrogen plays a role in augmenting feelings of anxiety, so high levels of estrogen can increase or lead to the development of OCD symptoms. Conversely, progesterone tends to inhibit anxiety, so a deficiency in that might lead to similar effects on OCD symptomatology.
While brain structure may play a role in developing OCD, chemical imbalances in the brain have not been found to be a contributing cause of OCD.
Exposure Response Prevention Therapy (ERP) is extremely helpful in treating OCD. Therapy is difficult, but with the right resources, there is hope.
Symptoms fluctuate in severity from time to time, and this fluctuation may be related to the occurrence of stressful events. Because symptoms usually worsen with age, people may have difficulty remembering when OCD began, but can sometimes recall when they first noticed that the symptoms were disrupting their lives.