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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 7 of 7. This is the beginning of the thread.
Posted by PeterMartin on March 13, 2022, at 23:46:44
I've taken Metformin off and on over the past few years so I was looking at the latest research. This is an interesting case study published last week:
"Reversal of insulin resistance is associated with repair of blood-brain barrier dysfunction and remission in a patient with treatment-resistant bipolar depression"
https://pubmed.ncbi.nlm.nih.gov/35247029/
Abstract
Our findings show that reversal of insulin-resistance using metformin (1000 mg with breakfast and supper for 14 weeks) led to remission in a patient with treatment-resistant bipolar depression (TRBD). Psychiatric symptom rating scales, laboratory tests and blood-brain barrier (BBB) imaging were all performed on one day before and one day after the 14-week trial of metformin. Remission of TRBD was associated with repair of BBB dysfunction. These results highlight BBB pathology as a mechanism contributing to TRBD, and a promising therapeutic and diagnostic target.
Posted by PeterMartin on March 14, 2022, at 0:11:49
In reply to New case study: Metformin Blood Brain Barrier/BP, posted by PeterMartin on March 13, 2022, at 23:46:44
Another recent one: https://pubmed.ncbi.nlm.nih.gov/35120288/
Treating Insulin Resistance With Metformin as a Strategy to Improve Clinical Outcomes in Treatment-Resistant Bipolar Depression (the TRIO-BD Study): A Randomized, Quadruple-Masked, Placebo-Controlled Clinical Trial
Abstract
Objective: Therapeutic options are limited for treatment-resistant bipolar depression (TRBD). Insulin resistance (IR) confers increased risk for TRBD. We investigated metformin, an insulin sensitizer, to reverse IR and improve clinical outcomes in TRBD.
Methods: Using a random-assignment (1:1), intent-to-treat, 2-site, quadruple-masked, parallel-group (metformin to 2,000 mg/d or placebo) clinical trial design, patients with DSM-5 bipolar disorder (BD) type I or II and IR received study medication for 26 weeks (February 2016 to October 2019). The primary outcome was the change in depression rating scores (Montgomery-Asberg Depression Rating Scale [MADRS]) at 14 weeks between those who no longer met IR criteria (converters) and those who still did (non-converters). Additional outcomes included scores on the Global Assessment of Functioning (GAF); the Clinical Global Impressions Scale, Bipolar Disorders version (CGI-BP); and the Hamilton Anxiety Rating Scale (HAM-A) and maintenance of improved outcomes up to 26 weeks.
Results: Forty-five BD patients were randomized to metformin (n = 20) or placebo (n = 25), and at 14 weeks or later, 11 subjects no longer met IR criteria (n = 10 with metformin, n = 1 with placebo; P = .0009). These converters experienced significant improvements in MADRS (P values ranged from .031 to .008) and GAF (P values ranged from .045 to .008) scores compared to non-converters beginning at week 6, sustained to week 26. HAM-A (P = .022 at week 14 and .019 at week 26) and CGI-BP change scores (P = .046 at 26 weeks) significantly favored converters over non-converters. Effect sizes were large for the MADRS and GAF (Cohen d > 1 at 14 and 26 weeks) and large for the HAM-A and CGI-BP at 26 weeks. Transient gastrointestinal side effects occurred under both treatment conditions.
Conclusions: Pending replication, this early study suggests that reversal of IR by metformin offers a path out of TRBD. Further characterization of metformin converters with TRBD will prove informative.
Posted by PeterMartin on March 14, 2022, at 0:26:10
In reply to Re: New case study: Metformin Blood Brain Barrier/BP, posted by PeterMartin on March 14, 2022, at 0:11:49
Annnnd one not so good one now in reference to potential risk increase for cognitive decline (AD). There have been studies showing it's preventative against AZD and other showing it may increase the risk. This paper seems pretty thorough....eh....
Posted by PeterMartin on March 14, 2022, at 0:33:25
In reply to Re: New case study: Metformin Blood Brain Barrier/BP, posted by PeterMartin on March 14, 2022, at 0:26:10
So that last one was in regards to diabetics. Here's another (2022) paper just published w/ mice that found in combo w/ Prozac Metformin has benefits in a parkinsons model:
https://pubmed.ncbi.nlm.nih.gov/34890997/
Metformin and fluoxetine improve depressive-like behavior in a murine model of Parkinsońs disease through the modulation of neuroinflammation, neurogenesis and neuroplasticityAbstract
Thereabout 30-40% of patients with Parkinson's Disease (PD) also have depression contributing to the loss of quality of life. Among the patients who treat depression, about 50% do not show significant improvement due to the limited efficacy of the treatment. So far, there are no effective disease-modifying treatments that can impede its progression. The current clinical approach is based on symptom management. Nonetheless, the reuse of drugs with excellent safety profiles represents an attractive alternative strategy for treating of different clinical aspects of PD. In this study, we evaluated the effects of metformin separately and associated with fluoxetine on depressive like-behavior and motor alterations in experimental Parkinson's disease. C57BL6 mice were induced with rotenone (2.5 mg/kg/day) for 20 days and treated with metformin (200 mg/kg/day) and fluoxetine (10 mg/kg/day) from the 5th day of induction. The animals were submitted to Sucrose Preference, Tail Suspension, and rotarod tests. Hippocampus, prefrontal cortex, and substantia nigra were dissected for molecular and morphological analysis. Metformin and fluoxetine prevented depressive-like behavior and improved motor impairment and increased TH nigral positive cells. Metformin and fluoxetine also reduced IBA-1 and GFAP positive cells in the hippocampus. Moreover, metformin reduced the phospho-NF-kB, IL-1β in the prefrontal cortex and iNOS levels in the hippocampus. Both metformin and fluoxetine increased neurogenesis by increasing KI67, but only the combined treatment increased neuronal survival by NeuN positive cells in the hippocampus. In addition, fluoxetine reduced cell death, decreasing caspase-3 and PARP-1 levels. Lastly, metformin potentiated the effect of fluoxetine on neuroplasticity by increasing BDNF positive cells. Metformin has antidepressant and antiparkinsonian potential due to anti-inflammatory neurogenic, and neuroplasticity-inducing effects when combined with fluoxetine.
Posted by Jay2112 on March 14, 2022, at 18:58:18
In reply to New case study: Metformin Blood Brain Barrier/BP, posted by PeterMartin on March 13, 2022, at 23:46:44
When I was in the hospital, they fed me very good, and I was on perfect insulin dose of one short acting, and one long acting. My blood sugar was almost ALWAYS near perfect, and I felt damn great! Now at home, probably because of poor diet, my sugar levels are all f'd up! Ugghhhh...
Jay
p.s. I am way too used of metformin. It does almost nothing for me. :(
Posted by Lamdage22 on March 15, 2022, at 2:07:54
In reply to Re: New case study: Metformin Blood Brain Barrier/BP » PeterMartin, posted by Jay2112 on March 14, 2022, at 18:58:18
I wonder the same thing. If it stil does anything for me. I am not diabetic, just trying to lessen sugar cravings. Could I just try for a few days if it is still beneficial?
Posted by Lamdage22 on March 15, 2022, at 2:14:24
In reply to Re: New case study: Metformin Blood Brain Barrier/BP, posted by Lamdage22 on March 15, 2022, at 2:07:54
Things went uphill since introducing Metformin. But there were changes to my life other than Metformin that could have made the difference.
This is the end of the thread.
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