Currently preparing a study on the relationship between Substance Abuse relapses and personality disorders , I want theories about the relapses and cognition for people relapsing,
I suggest focusing on the borderline personality disorder. From my experience, I found that alcohol, in particular, is commonly used in patients with this disorder, and it is associated with suicide and severe depression in patients with borderline personality. These patients use drugs in general because they have a fear of abandonment. Good luck in your project
Imaging studies in addiction show a decrease in D2 dopamine receptors and dopamine release in the striatum. The magnitude of this decrease is seen across addictions, independent of the substance abused. Increasing data suggests that low D2 dopamine receptor binding and low dopamine release occurs prior to drug exposure.
ADHD, Autism and PTSD which are frequently diagnosed in Borderline Personality Disorder, show the same decrease in dopamine transmission and childhood ADHD is considered a risk factor for later development of BPD.
Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis
I think the answer you're looking for is neuroinflammation.
There is neuroinflammation in Borderline Personality Disorder as well as several conditions often diagnosed in Borderlines (ADHD, Autism and PTSD) and multiple studies have shown a correlation between levels of cytokines and inflammatory endotoxins from leaky gut and alcohol/drug abuse, suggesting that activation of innate immune signaling increases alcohol craving/consumption and contributes to alcohol dependence and relapse. Recent studies provided further evidence that neuroimmune activation and inflammation contribute to alcohol dependence when targeted disruption of TLR4 in the central amygdala reduced alcohol consumption (but one single injection of LPS from leaky gut increases it).
"Repeated cycles of alcohol and stress cause a progressive, persistent induction of HMGB1, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, coupled with increasing ventral striatal responses that promote reward seeking behavior. "
Dopaminergic cell death is TLR4-dependent and Borderlines have reduced dopamine because of genetics.
Article The role of neuroimmune signaling in alcoholism
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1. Low dose Naltrexone- When used in doses of 1 to 5 mg it acts as a glial modulator with a neuroprotective effect via inhibition of microglial activation. It binds to Toll-like receptor 4 and acts as an antagonist, therefore inhibiting the downstream cellular signaling pathways that ultimately lead to inflammatory response. Its other mode of action involves transient opioid receptor blockade which increases enkephalin.
In one study, low dose Naltrexone reduced use of psych meds and opioids by 40%.
2. Cromolin- During stress Corticotropin Releasing Hormone and neurotensin stimulate mast cells and microglia resulting in focal brain inflammation and neurotoxicity. Cromolin stabilizes mast cells.
3. Probiotics like Lactobacillus Rhamnosus which is a NFkB inhibitor and can heal leaky gut. In studies using autistics, L Rhamnosus decreased behaviors shared by Borderlines.
Obviously, this is all theory since neuroinflammation seems to be an unexplored factor in Borderline Personality Disorder.
Article The Role of NFkB in Drug Addiction: Beyond Inflammation
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