- The gut microbiome consists mostly of bacteria and that is largely the portion of the microbiome we are focusing on (fungi and viruses exist but their function is largely unknown)
- Communication pathways exist between the microbiota-gut-and brain.
- Multiple mechanisms exist that allow gut microbiota to signal to the brain and control physiological processes.
- These include release of gut peptides from enteroendocrine cells which activate receptors of the immune system and vagus terminals in the gut.
- Studies indicate that these bacteria can manufacture and secrete essential neurochemicals including serotonin, dopamine, NE, GABA, and acetylcholine
- Depression and anxiety have been linked to a less well diversified gut microbiome.
- What can help diversify the gut microbiome? Diet, processed food, sugar, saturated fats, and red meat. Medication can also alter the gut microbiome, a good example is oral antibiotics used to treat an acute infection, sleep, exercise. Sounds a lot like a healthy lifestyle will get you the microbiome you need for optimal mental health.
- However, if you want a treatment there have been several studies that looked at fecal transplant to treat psychiatric disorders. Fecal transplants are much easier these days and now there is a capsule version that you take orally. There is not enough data to recommend this as a practical treatment and if the patient goes back to eating a poor diet, sleeping poorly, not exercising then the gut microbiome will revert after the transplant.
- What are the practical things you can do? Stop eating processed food, sugar, and red meat. Increase your fiber intake and select a diet like the Mediterranean diet or a plant based whole food diet that will provide those prebiotics. You could supplement with a probiotic but most of what you need can be had from a good diet alone and I think it’s far better to change the diet then to try using supplements to treat a poor diet. Fermented products like kimchi, kombucha and sauerkraut are good sources of live bacteria.
- If you choose to take a probiotic make sure it’s a quality, 3rd party tested product.
- Increase aerobic activity, I think if you goal is overall general health and you have limitted time, I think aerobic activity is a better bang for your buck.
- The way I believe you get and keep a healthy gut microbiome is through lifestyle modification. Improving your diet, exercise, and sleep is a good place to start. If you want to supplement with food products like kimchi or kombucha, go for it. I do not believe there is enough evidence to support a probiotic supplement for psychiatric disorders at this point, but if you want to spend $30 or more per month on a product if it’s a quality one that’s fine. Remember you cannot supplement away a bad diet.
In this video I focus the discussion on the exercise/physical activity portion of lifestyle medicine for psychiatry. Exercise is an underrated and underutilized tool for fighting depression. It can have a profound impact on mood, and helps people learn to be more resilient.
Key Findings Include:
- For resistance training, higher intensity and shorter duration provides improvement in mood symptoms
- For aerobic exercise, durations of 45-60 minutes appear to provide the most improvement in mood symptoms. Longer and shorter durations showed less benefit.
- Keep it simple and just get started. There are a million different programs, and you can easily find yourself worrying to much about getting all the information and not enough time worrying about exercising.
- The simplest way to start is with a daily walking routine. Spend six months consistently walking for 45-60 minutes. That’s it, no special equipment or significant out of pocket expenses required.
- A walking routine will set the foundation for adding additional forms of exercise including resistance training
My clinical experience indicates that most psychiatric disorders would benefit from the use of lifestyle medicine. As a member of the American College of Lifestyle Medicine, I’ve used lifestyle interventions to treat many of my patients. It’s an underutilized and undervalued part of health care in general and these are my thoughts about why that is the case.
MOA: mu opioid receptor antagonist which prevents exogenous opioids from binding blocking the pleasurable effects of opioid use. Reduces alcohol consumption through modulation of the opioid system, blocking the reinforcing effects of alcohol.
FDA Indications: alcohol use disorder (oral or injectable), Prevention of relapse to opioid dependence (injection)
Oral Dose: 50 mg/day
Injection Dose: 380 mg/month
Caution: patient must be opioid free for 7-10 days prior to starting, conformed with a negative urine
For alcohol use disorder start with 50 mg/day or 380 mg/month for IM formulation (injection may be preferred because it eliminates the daily decision to take the medication)
Side effects: nausea, vomiting, decreased appetite, dizziness, injection site reaction, life-threatening side effect is hepatocellular injury in overdose
Who is it good for?: Those ready to abstain completely from alcohol and for binge drinkers. Good evidence for reducing heavy drinking days. There is some risk of apathy or loss of pleasure with chronic use. The combination of naltrexone and bupropion has been used as a treatment for obesity.
How to use Pramipexole
- Selective D3 agonist thought to be related to hedonic drive.
- FDA approved for Parkinson’s disease and restless leg syndrome
- 5 randomized controlled trials indicating effectiveness in depression as monotherapy or adjunctive therapy and in bipolar disorder as adjunctive therapy with a mood stabilizer
- Side effects; nausea, hypotension, and fatigue, titrate slowly and give the dose at night
- Start with 0.125-0.25 mg QHS and rise by 0.25 mg every 5-7 days towards a target dose of 0.75-2 mg QHS
- Watch for hedonistic homeostatic dysregulation (HDD) including pathological gambling and shopping
I get a lot of questions that go something like this, I’ve been on X, Y, Z medications and nothing seems to help. It seems that what most are asking about is what is the algorithm for treating depression and when does it become treatment resistant. This video will provide a look at what treatment resistant depression is and provides a 5-stage strategy to medication selection.
I received a question asking me to discuss acamprosate as a medication and specifically to address any evidence to support its use to reduce urges to self-harm. I did the research, and this is what I found.
As a psychiatry trainee you will never forget that the two medications that reduce suicide are lithium and clozapine. In the case of clozapine, it has been shown in RCTs to reduce suicidal thoughts but not necessarily completed suicides. Lithium on the other hand has RCT data that indicates it reduces suicidal thoughts as well as completed suicide.
Lithium has anti-suicidal effects even at low doses. Lithium’s anti-suicidal effects are beneficial for both unipolar and bipolar depression. Unlike standard antidepressants that can increase the risk of suicide specifically in younger patients under the age 24, lithium has a prophylactic effect to prevent suicide.
While lithium overdoses can be fatal, this outcome is less likely given the anti-suicidal properties of this medication. We should not avoid prescribing it for this reason.
I get a lot of comments that go something like this “All psychiatrists do is prescribe medications.” Naturally, people are shocked when I talk about nutritional psychiatry, lifestyle modification, or the value of psychotherapy. I cover a lot of medication information on social media because there is significant confusion, misinformation, and a general benefit for patients to know more about the medications they routinely use.
While medication management is a substantial portion of the work most psychiatrists do it’s not the only things we do.
Most psychiatrists are well trained in at least one type of psychotherapy. The most common ones include cognitive behavioral therapy, interpersonal therapy, and motivational interviewing. Some are trained extensively in psychoanalysis which usually requires a 5-year commitment and engagement in psychoanalysis as a patient.
Many psychiatrists offer procedure-based interventions such as electroconvulsive therapy (ECT), and trans cranial magnetic stimulation (TMS). We may also consult on cases of vagus nerve stimulation or deep brain stimulation used to treat severe depression.
As a psychiatrist you are trained to handle some of the common neurological disorders (e.g. migraine). One third of our board examination is focused on neurological disease. In rural parts of the United States sometimes there is no one else to treat these disorders and the responsibility falls to psychiatry.
Most psychiatrists can treat things like hypertension or hypothyroidism. Many make the choice not to if the patient has a primary care physician. Like the treatment of neurological disorders sometimes there is no choice, and a psychiatrist will need to treat the medical condition.
Not everyone is lucky enough to have designated social workers so they can focus exclusively on the treatment of patients. We all know how important social determinates of mental health are, and sometimes altering these circumstances is the responsibility of the psychiatrist.
The result of research to develop a nonaddictive cough suppressant produced dextromethorphan. It was FDA approved in 1954 but the pharmacology of this cough suppressant is complex. It functions as an uncompetitive NMDA-glutamate blocker (thin ketamine), sigma-1 stimulator, and serotonin reuptake inhibitor. It should start to become clear why there is renewed interest in this medication.
Bupropion functions as a selective norepinephrine/dopmaine reuptake inhibitor. It’s currently used to treat depression, seasonal affective disorder, and nicotine dependence. Recent research suggests it acts as a potent inhibitor of cytochrome P450 2D6 (CYP2D6). Understanding the cytochrome P450 system is not a primary concern here but this enzyme metabolizes dextromethorphan.
The combination of these two drugs dextromethorphan 45 mg and bupropion 105 mg two times per day is AXS-05. The proposed mechanism is prolongation of dextromethorphan activity by CYP2D6 inhibition with the added benefit of norepinephrine/dopamine reuptake inhibition.
A phase-3 RCT of AXS-05 in patients with MDD outperformed placebo and improved depression scores over 6 weeks.