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.

Processed with VSCO with f2 preset

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.


Contraceptives, Hormones, and… Depression?

For many years, researchers have been trying to clarify the association between estrogen, progesterone, and depression. We know that women are twice as likely as men to become depressed (likely due to hormones). We know that changes in the level of estradiol (a type of estrogen) are associated with depression. Furthermore, fluctuating hormones in the days before menstruation are believed to be the cause of premenstrual syndrome (PMS) and can even cause its angrier sister, premenstrual dysphoric disorder (PMDD).

Combined oral contraceptives include synthetic forms of both progesterone and estrogen. These hormones (given in specific doses and at certain times during a woman’s cycle) inhibit ovulation and prevent pregnancy. Interestingly, external progestins (more than endogenous progestins) seem to increase levels of monoamine oxidase, leading to more serotonin breakdown. Degrading more serotonin may lead to depression and irritability. [If you’ll remember from this article, one of the major classes of antidepressants blocks monoamine oxidase. External progestins seem to do the opposite.] 1

Looking back, I remember many of my friends taking birth control in college for the first time. Incidentally, many of these same friends also began to take antidepressants for mood changes or anxiety. After I started my first hormonal contraceptive, I too felt uncontrollably moody. I have always been prone to ups and downs, but certain types of contraceptives have made me feel as though I cannot regulate my feelings.

On to the data. Similar to the research on statins and SSRIs, Denmark has published another large study examining the rates of depression in women who use hormonal contraception. Over 1 million women from ages 15-34 were observed for 14 years. Women who had used antidepressants or who had been diagnosed with depression prior to study initiation were excluded. Both the first diagnosis of depression and the initiation of an antidepressant after starting hormonal contraceptives were tracked and were used to estimate the increased risk of depression with hormonal contraceptives.

The relative risks (RR) of first-use of antidepressants for users of hormonal contraceptives versus women not taking hormonal contraceptives are outlined below.

Combined oral contraceptives 1.2
Progestin-only pills 1.3
Vaginal ring (Nuva Ring) 1.6
Implant (Implanon) 2.1
Levonorgestrel IUD (Mirena) 1.4
Medroxyprogesterone depot (Depot-Provera) 2.7

RR can be understood as the number of “times” more likely you are to experience an effect. For example, an RR of 1.2 means that users of combined oral contraceptives are 20% more likely to use an antidepressant for the first time than women not taking combined oral contraceptives.

Clearly the use of hormonal contraceptives was associated with antidepressant use and also a diagnosis of depression. Interestingly, the relative risk decreased with age (i.e. adolescents had significantly higher relative risks: up to an RR of 3.2 for adolescent users of Mirena). For both age groups, the RR peaked at 6 months of hormonal contraceptive use.

This article should be taken with a grain of salt. Hormonal contraceptives play an incredibly important role in many women’s lives and have provided an independence that wasn’t present before. Women have more control over their health than ever and birth control plays a large role in this gain. Regardless, it is important to be aware of the possible side effects and to make informed decisions about your health care [and to seek help should you need it].


In Pop Culture: Is your birth controlling depressing the hell out of you?


  1. External Progestins and MAO
  2. Association of Hormonal Contraception with Depression 


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

Psychiatric Applications of Psilocybin

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:



  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.

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.

  1. Cytokines and Depression
  2. Statins and Depression