California Psychiatric Association Advocacy Day

This year, I had the distinct honor of being flown to Sacramento to participate in the California Psychiatric Association’s Advocacy Day. I went as a representative of Los Angeles psychiatrists and the Southern California Psychiatric Society (SCPS) with the goal to advocate for mental health.

In Sacramento, we were briefed on the bills that are currently being sponsored by the California Psychiatric Association (CPA). There are three main bills; two assembly bills (AB) sponsored by Assemblymember Susan Eggman and one senate bill (SB) sponsored by Senator Josh Newman.

According to the National Association of Counties, 64 percent of people in jail have a mental illness. Furthermore, 15 percent of male inmates and 31 percent of female inmates have what can be classified as a severe mental illness. AB 720 would allow for the involuntary medication of people in jail with a mental illness who are awaiting adjudication (i.e. sentencing). Of note, this law would only allow for involuntary treatment of people who are deemed to be dangerous to others, dangerous to themselves, or gravely disabled (as in not being able to care for their own food, clothing, or shelter usually due to a psychotic illness). This bill would not allow for involuntary medication of people with mild mental illness.

Already, law allows for inmates who have been sentenced to be medicated involuntarily; AB 720 would expand the scope of this law to include inmates who have yet to be sentenced. As a psychiatrist, it is clear to me that treating mental illness is of utmost importance. This bill has the potential to reduce harm to the inmate themselves, other inmates, and staff, and to reduce suffering by actively and effectively treating severe mental illness.

AB 1136 was the second bill on which we were briefed. This bill would mandate that the California Department of Public Health apply for federal funding under the 21st Century Cures Act for the creation of a web-based psychiatric bed registry. This registry would include inpatient psychiatric beds, crisis stabilization units, residential community mental health facilities, and residential substance use disorder treatment facilities. Currently, when patients come to an emergency department in an acute psychiatric crisis, social workers have to cold-call dozens of facilities to find out bed availability and if a particular patient would be appropriate. A bed registry that could be updated in real-time would greatly increase the efficiency of this process.

The third and final bill has to do with mental health parity. Mental health parity refers to the fight to end discrimination toward people with mental illness through ensuring equal access to treatment (i.e. the same types of benefits for mental illness as other medical illnesses). This takes the form of ensuring similar copays, similar numbers of doctor visits, and similar numbers of days in the hospital. SB 347 makes certain that regardless if the Affordable Care Act is repealed, the California Department of Insurance may continue to enforce mental health parity laws.

After being briefed on the three bills, I was paired with a senior psychiatrist (Dr. William Arroyo, president of CPA) and other resident-fellow members from the Los Angeles area. Together, we went to the State Capitol Building and met with Assemblyman Nazarian and Senator Bob Hertzberg’s Chief of Staff Diane Griffiths to discuss the importance of the three bills.

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Participating in CPA Advocacy day was an eye-opening experience on both the complicated nature of mental health policy in California and the relevance of the CPA and the SCPS in influencing that policy. I feel honored to be part of the wonderful team of psychiatrists who fight for mental health parity and increased access to care for all people.

If these topics interest you, I encourage you to reach out to your local California legislator to advocate for their support on these important topics.

 

Holiday Blues? Not so much. Trends in Psychopathology over the Holidays.

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The idea of “holiday blues” or “holiday stress” has been discussed extensively in popular culture and in the psychiatric literature. Interestingly, the majority of these articles presume its existence, yet do not cite data. Most of the literature comes from case studies or psychoanalytic teachings (as opposed to higher-quality research papers). As early as 1955, a psychiatrist described a “holiday syndrome” characterized by feelings of “helplessness, possessiveness, and increased irritability, nostalgic or bitter ruminations about the holiday experiences of youth, depressive affect, and a wish for magical resolution of problems.2 Not a small number of articles inundating my newsfeed are about how to “cope” with the added stress of holidays instead of how to enjoy a lovely season. Suggestions for how to manage this stressful time include living in the present (Oprah via HuffPo), making a budget and focusing on your breathing (US News), and just shaking it off (Today).

shake-off

You’d think that with all of this stress surrounding the holidays, psychopathology would increase. People would be visiting the psychiatric emergency room more frequently, people would be committing suicide, and there would be higher rates of depression, right? Wrong.

This is what we know from research: though your mood may worsen, overall utilization of psychiatric services goes down. There are fewer visits to the Psychiatric Emergency Room in the days and week before Christmas. The psychiatric wards are emptier, suicide rates go down, and people engage in less self-injurious behavior (i.e., cutting and face-picking).1

Theories abound as to this apparent discrepancy. Perhaps the hope inherent in the Christmas season leads to the belief that problems will be fixed.2 Perhaps increased contact with family members bolsters social support, which is protective against psychopathology.2 Or, perhaps there needs to be a greater distinction: demoralization, disappointment, and merely revisiting intrapsychic conflicts do not a disorder make.3

Maybe the idea of Christmas blues is merely that, “blues,” and most people cope appropriately.

My first impulse when researching holiday stress was to assume that people struggle and that there would be increased utilization of psychiatric services. I was pleasantly surprised to find that the majority of people tolerate the holiday season and many even fare better during the month of December than other months of the year. Older adults, those who are single or widowed, people who struggle with alcoholism, and those who have had traumatic past holiday experiences may be at increased risk of having a difficult time during the holidays. Furthermore, those who have a prior or current diagnosis of depression or other mental illness may experience shame when surrounded by [presumably happy] family members.4 If you’re a member of one of these groups, I encourage you to seek out appropriate supports in the form of family, friends, or a trusted therapist or psychiatrist. [You can also take a look at this infographic from Happify, which did actually have some great suggestions for coping with holiday stress.]

The take home? While the holidays might be tough for some, in general mental health pathology and utilization decrease. Though people may feel intermitently blue, let’s allow the hope of the season to seep into our psyche, and let’s enjoy the season as we continue to show each other love and compassion.

References:
1. The Christmas Effect
2. Holiday Blues as a Stress Reaction
3. What is it About the Holidays?
4. A Season of Hope

Sleep Basics: OTC Antihistamines

Many over-the-counter (OTC) medications used for insomnia have primary effects on the H1 receptor. At this receptor, these medications serve as an antagonist; hence the name antihistamine. The H1 receptor is primarily implicated in allergic reactions, so blockade of this receptor decreases the allergic response. Histamine receptors in the central nervous system also have a role in wakefulness; blocking them causes sedation. Studies report that nearly 25 percent of patients with sleep disturbances use OTC sleep aids such as antihistamines, and 5 percent use them at least several nights a week.

Routine use of OTC antihistamines such as diphenhydramine (Benadryl) and doxylamine (Unisom SleepTabs and Nyquil) for insomnia is controversial. I know that on inpatient psychiatric hospitals, these medications are frequently used for sleep because 1) they are relatively safe and 2) they are not addictive. However, the evidence supporting the use of these medications for long-term treatment of insomnia is lacking.  Additionally, many OTC antihistamines (especially Benadryl and doxylamine) have effects at cholinergic receptors leading to uncomfortable side effects such as dry mouth, blurred vision, constipation, urinary retention, and more importantly cognitive impairment and possibly delirium 1.

Recent literature has explored the long term implications of use of anticholinergics (one of the more common being OTC antihistamines). A large prospective cohort study demonstrated that greater cumulative use of anticholinergic medicine in people >65 is associated with an increased risk of dementia 2. To quote from the study:

Higher cumulative anticholinergic medication use is associated with an increased risk for dementia. Efforts to increase awareness among health professionals and older adults about this potential medication-related risk are important to minimize anticholinergic use over time 2.

 

In cases where use of a medication is controversial; its important to be an informed consumer. Benadryl or Doxylamine? What dose is effective? Is Tylenol PM different than Benadryl? Is Nyquil? Is it okay to take these medications if you’re >65?

With regard to insomnia, diphenhydramine has been studied more thoroughly and is noted with short-term use to lead to improvements on self-reported sleep efficiency and the Insomnia Severity Index, and a decrease in participant-reported number of awakenings 3. Unfortunately, most studies fail to observe significant changes on the polysomnogram for sleep-onset, sleep efficiency, and total sleep time 3. Thus, although you may feel like you’re sleeping better, the data doesn’t show this. Furthermore, long-term use of OTC antihistamines may be futile. In fact, studies demonstrate that diphenhydramine may lose its sleep-promoting effects after just 3 days. Furthermore, when dosed at 50mg versus 25mg (i.e. 2 Benadryl vs 1) participants had significant psychomotor impairment and a decreased level of wakefulness the next morning 3.

The studies on doxylamine are few and far between. Similar to diphenhydramine, studies show improvement with self-reported sleep but not with the polysomnogram 3. The main drawback to doxylamine? It has a longer half-life than Benadryl, and thus is likely to cause more morning impairment than a comparable dose of Benadryl.

Diphenhydramine Doxylamine
Brand Name Benadryl, ZZQuil, Tylenol PM, All Unisom products except SleepTabs Nyquil, Unisom Sleep Tabs
Half-Life 3-9 hours (usually reported as 8) 10 hours
Dosing 25-50mg 12.5-25mg

My recommendation? If you’re having insomnia and you want a quick fix, go with 25mg of diphenhydramine each night for a short period of time (I’d recommend no more than 1 week). If you’re over 65, be extremely judicious with your use of OTC antihistamines. Likely due to their anticholinergic effects, long-term use is associated with an increased risk of dementia. Short-term use is probably okay, but if you continue to have sleepdisturbances after 1 week of use, ask your doctor for a better, more evidence based, long term solution.

  1. New Developments in Insomnia
  2. Anticholinergics and Dementia
  3. H1 Blockers for Insomnia

Go Outside, It’s Good for You

Everyone knows that spending time outside is “good for you,” but how many of us know exactly how much time we need to spend outside, or what type of outside areas (beaches, forests, or parks) would achieve the most health benefits?

As urban areas attempt to incorporate more green space (think the High Line in New York City), public health experts are attempting to nail down the characteristics of these areas that have the most population-wide benefit.  A recent study published in Nature examined the relationship between the duration of exposure to green space and public health outcomes such as mental health, physical health, and social health.

The study found that with 30 minutes per week spent in a green area people had reduced rates of depression. This was dose-dependent up to 1 hour and 15 minutes (meaning that increased durations were associated with decreased depression). The mental health benefits were present regardless of the intensity of the green space (i.e. low versus high vegetation complexity). This article estimated there would be a 7% reduction in depression prevalence for the population if every person achieved this minimum time.

The point here is short and sweet; get outside and spend some time in a green space (however you define it). It’s good for you!

Eagle's Nest

Photo taken during a time spent outside hiking in Topanga Canyon to Eagle Rock. Link to trail here, highly recommended!


As an aside, I found the idea that vegetation complexity could influence the magnitude of mental health benefits pretty fascinating. Apparently, vegetation complexity may mediate this through increased feelings of restoration (i.e. higher levels of plant, butterfly, and bird species richness have been shown to enhance a person’s feeling of restoration 1) and by possible parasympathetic nervous system activation (which lowers your blood pressure and heart rate) which may decrease your experience of stress 2. Other fun facts, “more people tend to visit public green spaces with moderate levels of vegetation cover (rather than high or low), and vegetation is also likely to influence the perception of safety of an area.” That’s enough nerdiness for today, until next time!

Psychiatric Applications of Psilocybin

fungi-steve-axford-11
Photo Credit Fungi Steve

Psilocybin is a member of the tryptamine class of hallucinogens. It is the active compound found in dozens of mushroom species and is responsible for the typical features associated with “shroom” or “magic mushroom” ingestion. Classic effects of psilocybin ingestion are similar to LSD, and include:

week6-psilocybin

 

  1. Oceanic boundlessness: the experience of unity while also being boundless
  2. Visionary restructuralization: auditory and visual distortions and hallucinations

These effects, while each fascinating in their own right, are not the topic of today’s post. Rather today, we’re going to focus on psilocybin’s antidepressant effects.

Psilocybin acts directly on serotonin 5HT-2A receptors. Interestingly, blocking, or antagonizing these receptors leads to improvements in parkinson’s disease-induced psychosis (discussed in a separate blog post here). Psilocybin, acting as an agonist at this same site, appears to have potent antidepressant effects.

Research on psilocybin has shown promise in the treatment of end of life anxiety, obsessive compulsive disorder, and smoking and alcohol dependence. A study from 2008 showed that 14 months after a single dose of psilocybin, greater than half of the participants continued to report an increased sense of wellbeing. Now, in a recent article published in the Lancet, psilocybin has demonstrated preliminary efficacy in the treatment of unipolar (i.e. not bipolar) depression.

Twelve patients (6 women and 6 men) with treatment resistant depression were dosed with two oral doses of psilocybin (10mg and 25mg) 7 days apart. Typical recreational doses of psilocybin range from 10-50mg (i.e. 1-2 grams of dried mushrooms, or 20-30 grams of fresh mushrooms). The participants were dosed in pre-decorated (i.e. low lighting) rooms with music playing through high quality speakers. Patients had psychiatrists sit on either side of them and perform psychological support in the form of check-ins, making sure that the patient experienced a mostly uninterrupted “inner journey.”

Incredibly, at one week and at three months depressive symptoms were markedly reduced. Although clearly not a placebo controlled trial, this study demonstrates significant promise for the future of psilocybin as a treatment for depression and may offer hope for those with treatment resistant depression.

Supplements for Depression

As a psychiatrist in LA, I’m always looking for novel techniques and other ways to help my patients. I recently became aware of a meta-analysis published in the American Journal of Psychiatry that showed great promise for Vitamin D, Omega 3 (fish oil), Methylfolate, and S-adenosylmethionine (SAMe) as adjunctive treatments for depression in patient’s already receiving antidepressants.

Many people take multivitamins and cite reasons like “health” but have no idea what the effects could be. These four supplements could actually help improve your depression. In the meta-analysis the only cited adverse effect was minimal digestive upset.

So, let’s talk about each one individually.

First off, vitamin D. We should probably all be taking vitamin D because 1) we know it serves an important role immune function 2) it is required for proper mineralization of bones 3) it may help prevent falls in the elderly and 4)there are very few (if any) side effects. Now, there is new evidence that vitamin D may help treat depression in depressed patients.  To quote the study, the results were positive and significant. A reasonable starting dose? 1000-2000 IU/day. I personally take 2000IU daily.

Second, Omega 3, or fish oil. Omega 3 is another one we should probably all be taking because it positively impacts cardiovascular risk factors through a myriad of methods including acting as an antiarrhythmic, lowering the heart rate, lowering blood pressure, preventing clot formation, and decreasing the level of triglycerides in your blood. This meta-analysis reveals that there is new evidence for a fish oil as adjunctive treatment for depression. A reasonable starting dose would have a combination of EPA&DHA approximating 1gm. This is the brand and formulation I buy.

Last but not least, methylfolate and SAMe. The evidence for taking these without depression is less robust. Both are participants in essential chemical reactions that happen in your body constantly and a deficiency in folate (related to methylfolate) causes anemia. Both showed positive effects when used as augmentation for antidepressant treatment.

The take home? Vitamin D and Fish Oil are rockstars with few to no side effects. This new meta-analysis only further serves to reinforce that these should both be prominent in your diet, either through naturally-occurring sources or as a high-quality supplement.

Article after the jump: Link

Inflammation, Depression, and … Statins?

There are multiple theories regarding the pathophysiology of depression. The most common (and the one you’ve probably heard about) is the monoamine hypothesis. This theory posits that depression is an imbalance (or depletion) of certain key neurotransmitters in the brain. The imbalance of these key neurotransmitters, namely dopamine, serotonin, and norepinephrine, is believed to cause depression. As such, most common antidepressants fit into classes that limit the uptake and/or breakdown of serotonin (SSRIs), serotonin and norepinephrine (SNRIs and TCAs), or serotonin, norepinephrine, and dopamine (MAOIs).

Today, we’re interested in a different hypothesis involving inflammatory proteins called cytokines. Cytokines are increased within our body when we are having an immune response and with inflammation in general. In patients with depression, certain cytokines have been found to be elevated before treatment (associated with a pro-inflammatory state) and decreased after treatment 1. This implies that cytokines and other inflammatory molecules may cause a pro-inflammatory state that causes our brain to be “inflamed,” thus causing depression. If there were a way to decrease inflammation in our body, perhaps depressive symptoms would improve as well.

On to statins. Statins (think Lipitor, Crestor) are commonly prescribed to treat high cholesterol. Incidentally, they are also believed to have anti-inflammatory properties. This is believed to be the reason why statins decrease the risk for stroke and heart attack independent of their cholesterol lowering effect.

A recent study in Denmark followed 872,216 SSRI users (of whom 113,108 (13.0%) used a statin concomitantly) over the course of 15 years 2. It found that patients who took SSRIs while on a statin had fewer depression-related hospital visits and depression-related hospitalizations. As such, the article concluded that “concomitant treatment with SSRIs and statins resulted in robust advantages compared with SSRIs alone.”

So does this prove the cytokine hypothesis of depression? Should you be taking a statin if you’re depressed? Not quite. Statins are not benign drugs, and the evidence isn’t there yet to recommend augmenting antidepressant treatment with a statin. Regardless, this study represents one more step in the right direction. Here’s to eventually finding a cure (and a satisfying explanation) for the millions of people worldwide who are afflicted with depression.

References:
  1. Cytokines and Depression
  2. Statins and Depression