What is Sport Psychology?

November 12th, 2018

The field of Sport Psychology/Psychiatry broadly aims to optimize performance and well-being by developing a robust mental skillset and addressing mental health needs directly.

     Athletes at all levels confront a unique set of mental health challenges. Beyond the stress of frequent practices and competition, athletes can experience elevated rates of injury/pain disorders, burnout, depression and anxiety, all of which can limit the enjoyment and success of their efforts. Most people deeply engaged in sport spend countless hours honing their physical skills but allocate much less time to working on the mental skills necessary for peak performance or to address psychological symptoms affecting results. The field of Sport Psychology/Psychiatry broadly aims to optimize performance and well-being by developing a robust mental skillset and addressing mental health needs directly. Additionally, the work can explore an athlete’s relationship to his/her sport and motivations for participating.


     Sports work is always tailored to the athlete’s unique circumstances and goals, but often integrates elements of mindfulness, CBT, and visualization training. The focus is placed on the process of training and improvement rather than any specific outcome of a competition. Daily brief homework assignments coupled with pre- and post-workout exercises are used to reinforce the mental skills being developed. For some clients, developing and implementing a mental training routine over 8-10 weeks suffices to set the path an athlete can then follow on his/her own with follow up scheduled as needed. Other clients find their sports work as an entry point into longer-term dynamic psychotherapy which provides insight into other domains of their lives. The flexibility, creativity and shared goals make Sport Psychology a highly rewarding field for both client and therapist.

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.

Genetic Testing for Antidepressants: Voices of Skepticism

October 15, 2018

     Dozens of studies - usually conducted by the manufacturers - purport that they work. And countless excellent psychiatrists - again usually working for the manufacturers - have given their endorsements. But much of the field remains skeptical.

There's been a recent explosion in products that use genetic testing to determine which antidepressant is right for you. Since finding the right antidepressant can be a long process of trial and error, these tests seem very exciting.


Dozens of studies - usually conducted by the manufacturers - purport that they work. And countless excellent psychiatrists - again usually working for the manufacturers - have given their endorsements. But much of the field remains skeptical.  Dr. Allen Francis, chair of the DSM-IV task force, writes that "So far, genetic studies have no proven role in guiding medication choice in psychiatry - except for profits gained by labs doing premature testing." And Daniel Carlat, editor-in-chief of the Carlat Report, reports that "if we were to hold the GeneSight test to the usual standards we require for making medication decisions, we’d conclude that there’s very little reliable evidence that it works."


We agree with these voices of skepticism.


Prediction of drug response falls into two categories - pharmacokinetics and pharmacodynamics. "Pharmacokinetics" means the way your body metabolizes the drug.  For example, whether you're a "fast metabolizer" whose liver destroys the drug before it has time to take action. "Pharmacodynamics" means the way the drug works on your body.  For example, whether an SSRI antidepressant effectively increases your serotonin levels. Most genetic testing products claim to be able to predict both of these domains.


But experts in pharmacokinetics say that the few genes that these products test (usually genes coding for liver enzymes) can reliably predict response to antidepressants. From the Handbook of Pharmacogenomics and Stratified Medicine


"Available data do not support a correlation between [antidepressant] plasma levels and the response of most [antidepressants] (with the exception of [tricyclics]) and this is probably linked to the lack of association between response and CYP450 genetic polymorphisms found for the most part by previous studies. Therefore, evidence does not as yet exist to support the recommendation of CYP genotyping in clinical practice, since the effect of CYP variants on clinical outcomes is still not completely clear for the most studied isoenzymes."


In other words, the plasma level of most antidepressants (the parameter that liver enzymes affect) doesn't really seem linked to how well they work. This is probably because antidepressants don't work through the plasma, rather they work in the brain, which is separated from the plasma by the blood-brain barrier. Although being in the plasma is a necessary first step to getting in the brain, plasma levels themselves, and the liver enzymes that help determine them, are not robust predictors of response. Studies investigating the link between genes coding for liver enzymes and antidepressant response have uniformly come up negative.


The pharmacodynamic picture is even more complicated. Most consumer genetic tests only look at one pharmacodynamic gene related to efficacy - SLC6A4. While two meta-analyses (linked here and here) have found it matters for antidepressant response, two other meta-analyses (linked here and here) have found that it doesn't, leaving its status questionable. Even the positive studies find it only explains about 3.6% of antidepressant response - not really enough to significantly matter. But this is the only pharmacodynamic gene linked to efficacy that most of these products test. So these products probably have little ability to predict pharmacodynamic response either.


Another issue with these tests, is that so many genes are involved in the antidepressant response, that likely, no gene in isolation has a huge impact on the efficacy of these drugs. Tansey et al found that no single chromosome explained more than 5% or so of antidepressant response.  But chromosomes have thousands of genes on them, and each gene can have hundreds of relevant sites. They warned that antidepressant response was likely to be "polygenic", ie involve very many genes of small effect. A well-validated genetic test, the massively polygenic score for heart disease, looks at 6.6 million variants. Most antidepressant tests look at between ten and twenty. If the trait really is polygenic, the tests may be useless.


Representatives of genetic testing companies have noted that all public research on gene-response correlation has been disappointing, but claim to have done their own proprietary research. Since this research is not released, we cannot be sure one way or the other. Given these companies are unregulated, there is literally nothing stopping them from potentially reporting biased information. The current claim is that their in they have solved this previously unsolvable problem of linking genes to antidepressant response.  However, they are keeping their solution secret, even as public study after public study comes up negative. The only evidence they provide is from in-house studies by scientists they hired purporting to show their product works. These studies are usually open-label, not placebo-controlled, and otherwise violate the rules of good research.


As a result, we may not recommend these tests to our patients. Instead, we recommend careful titration of and experimentation with antidepressants.


Right now, the best test for antidepressant response is through trial and error.  The best test for your personal metabolism of antidepressants is to take antidepressants at different doses and see which one works for you. We realize this is not a lot of comfort for patients who have had to try many different antidepressants are are tired of constant experimentation. A good psychiatrist can sometimes use features of the patient's condition or family history, as well as response from prior psychotropics to make predictions about which medication to try next.

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.


Beef & Bipolar: New Data Suggests Surprising Link 

September 11, 2018

     In 2007, scientists at John Hopkins started asking inpatients at local psychiatric hospitals about their diets, to determine whether there were any links between specific foods and psychiatric disorders. After ten years of work, they found primarily a single, striking effect: people who eat dry cured meats (like beef jerky) were much more likely to develop bipolar mania

    More specifically, researchers asked people in the hospital with four different conditions - depression, bipolar mania, bipolar depression, and schizophrenia - whether they had ever eaten various groups of foods. They compared the answers to a control population of healthy people without known psychiatric disorders. In most cases, the hospital patients’ answers more or less lined up with the healthy controls. But patients in the hospital with bipolar mania - though not bipolar depression - had an odds ratio of 3.5x of eating dry cured meat, suggesting a major connection between these products and mania.

     Is this due to some sort of socioeconomic connection - for example, bipolar patients might be less well-off, and so more likely to eat cheap meat products? The researchers tried to control for a number of factors, including age, sex, socioeconomic status, and other health issues; none of these seemed to be the source of the finding. Further, it would be surprising if a spurious correlation like this only showed up in bipolar mania, and not depression, bipolar depression, or schizophrenia. 

     To further investigate the association, they gave jerky to lab rats in a series of experiments. The lab rats who ate jerky seemed to show mania-like hyperactivity, tending to run around their cages for longer than the rats eating regular rat food, suggesting that this might be a real causative effect.

     Why might dry cured meats have this effect? Most contain nitrates, chemicals resulting from the preservation process. The scientists aren’t exactly sure why nitrates should cause mania, but one theory is that they get metabolized to nitric oxide, a neurotransmitter known to be involved in some cases of bipolar disorder. Another possibility is that the cured meats somehow affect gut bacteria in a way that activates or modulates the immune system. The researchers admit further research is needed for the process to be understood.

     Although this is all very preliminary, bipolar patients at risk of mania might want to consider cutting back on dry cured meats, or eliminate them from the diet entirely. These would include things like bacon, jerky, “meat sticks”, “Slim Jims”, and hot dogs. Uncured meats like chicken breast or hamburger do not appear to increase risk. If you can find a version of your favorite cured meat produced by a process that does not create nitrates, those should be safe too.

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.


To Supplement or Not to Supplement

July 24th, 2018​

Most modern antidepressants act on serotonin, one of the neurotransmitters in the brain. While depression is much more complicated than a simple "serotonin imbalance", increasing serotonin certainly seems to help in many cases of depression.

This is the intuition behind the popularity of L-tryptophan and 5-HTP, two dietary supplements that target the serotonin pathway. L-tryptophan is an amino acid found in various foods. The body converts it to an intermediate, 5-HTP, and finally to serotonin itself. It makes sense that supplementing either L-tryptophan or 5-HTP would increase serotonin in the body, and various studies have confirmed this to be true. So, is this a good solution to depression?


Studies have been contradictory and shown generally small effects - but this is true of almost all research into depression treatments. A review by the Cochrane Collaboration states that "the available evidence suggests these substances were better than placebo at alleviating depression...however, the evidence was of insufficient quality to be conclusive" and adds that "because alternative antidepressants exist which have been proven to be effective and safe the clinical usefulness of 5-HTP and tryptophan is limited at present."


Right now it is unclear whether L-tryptophan is more effective, less effective, or as effective as standard antidepressants. Aside from it being a gamble, one has to consider side effects and convenience. The side effects of conventional antidepressants are generally well-known. The side effects of L-tryptophan are still unclear. In 1989, thousands of people developed a dangerous immune condition called eosinophilia-myalgia syndrome from a contaminated batch of L-tryptophan. Since then manufacturing processes have improved, but there continue to be sporadic reports of a few L-tryptophan users developing this condition each year. There are also theoretical reasons to think L-tryptophan might contribute to liver disease, hypertension, and other serious conditions. In terms of convenience, most good studies of L-tryptophan supplementation have recommended doses between 3 and 6 g daily; since L-tryptophan usually comes in 500 mg capsules; a proper dose would require taking 6 to 12 capsules per day unless you can find a more efficient way to ingest the bulk powder (maybe a smoothie)?


The situation is similar with 5-HTP. Evidence is poor, with the Cochrane analysis showing a possible effect, and other studies failing to find one. There are some theoretical reasons to expect side effects, based upon excessive supplementation with one neurotransmitter causing deficiencies in others; for this reason, most 5-HTP supplements come with warnings suggesting not to use the substance for more than three months at a time. Both L-tryptophan and 5-HTP can cause drowsiness, nausea, and GI discomfort.


The question on most people's mind is - are these a good alternative to SSRIs? For most people, the answer is probably not. There's better evidence for SSRIs in treatment of depression. Although SSRIs have their share of side effects, they're generally well-known and unlikely to spring any surprises on you. And because SSRIs mostly work in the brain, compared to the effects of taking chemicals that increase serotonin everywhere, there's a theoretical reason to think they will have fewer long-term side effects in the cardiovascular, GI, and other systems. All of these substances are so poorly studied that for all we know this could be inaccurate, and their long term effects could be minimal,  whereas those of SSRI’s might end up being worse than we currently believe. But right now this is the state of our understanding.


Who might want to try L-tryptophan and 5-HTP? People who have tried antidepressants and found they didn't work. People who have too many side effects on antidepressants. People who have financial or other reasons to prefer non-prescription medication. People with relatively mild conditions who are willing to experiment and won't be too upset if the experiment fails.


A final consideration: both of these substances are used for sleep, with much better evidence than for depression. Although we always recommend people try non-chemical solutions to sleep problems first, L-tryptophan and 5-HTP are probably safer than most prescription sleeping pills. Although there are a few antidepressants that also help with sleep (for example mirtazapine), these tend to have their own set of side effects (for example, mirtazapine causes weight gain). An Individual who has problems with both mild depression and insomnia, and who wants to avoid weight gain, (both L-tryptophan and 5-HTP are sometimes marketed as weight loss supplements, though not especially effective ones) might be an ideal candidate for one of these supplements. We would recommend L-tryptophan as a first choice over 5-HTP; because its an earlier substrate in the metabolic pathway, your body has ultimate control over how much it converts to 5-HTP or serotonin.


If you're on any other medication, especially antidepressants, please don't try either of these supplements until you talk to your doctor and make sure there are no drug interactions.

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.


"How Do I Know if I Have an Anxiety Problem?"

July 6th, 2018

People often present to us wondering whether they may have an anxiety problem. Often they find themselves bogged down in their personal or professional lives with stress. Family members or loved ones may encourage them to seek help with anxiety.  

How much anxiety is normal?


Anxiety exists on a spectrum. On one end, there may be those with little to no anxiety. This in itself can be problematic, in that they may struggle with motivation to get things done or to be productive. Alternatively, they may also act as though everything is fine even when it is not.


In the moderate range, anxiety can lead one to perform when the pressure is on. When there are upcoming deadlines or potential negative outcomes, anxiety can trigger one to get things done. In these cases, however, an individual is able to “turn off” the anxiety when it is no longer needed.


Further along the spectrum, is the realm of “too much” anxiety. One may find themself ruminating or being preoccupied by various issues in one’s life. This may start to interfere with the ability to be “present” or to problem solve. This level of anxiety often feels as though one simply can’t “relax” or slow down one’s thoughts. It can lead to feeling easily overwhelmed or “frozen” when faced with challenges. It is also the most common cause of difficulty focusing or concentrating. This may lead to problems not just with productivity, but also to problems in interactions with others.  Individuals can appear inflexible or unable to emotionally engage. It may also lead to significant challenges with sleep, including problems falling and staying asleep, as well not feeling rested in the mornings. This level of anxiety can lead to avoidance of tasks or issues, in effect having the opposite effect as moderate levels of anxiety.


Signs and Symptoms


  • Constant and unsubstantiated worry that causes significant distress and interferes with daily life


  • Feeling wound up, on edge or restless


  • Feeling easily fatigued


  • Increased irritability


  • Finding it difficult to concentrate, or finding one’s mind goes blank when trying to do tasks


  • Avoiding social situations for fear of being judged, embarrassed or humiliated


  • Seemingly out of the blue panic attacks and preoccupation with the fear of having another one


  • Irrational fear or avoidance of something that poses little to no threat of danger


  • Sleep problems


  • Recurrent nightmares, flashbacks, or emotional numbing related to a traumatic event




Anxiety disorders are generally treated with psychotherapy, medication, or both.  Ask your doctor if you think you may be struggling with an anxiety disorder.


Learn More

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.


Decoding the Data on Anti-Depressant Discontinuation

June 8th, 2018

What percent of people coming off antidepressants really get a discontinuation syndrome? This question is hard to answer accurately.

A recent front-page article in the New York Times noted that Many People Taking Antidepressants Discover They Cannot Quit. It pointed out that the SSRIs and SNRIs, the most commonly used antidepressants, often have a "discontinuation syndrome" where people feel sick after stopping them.  They describe symptoms like headaches, chills, mood swings, and tingling feelings. The article includes interviews with people who were disabled for months by the discontinuation syndrome, or who had to give up altogether on quitting the medications because of the syndrome.


The article's claims were concerning, but many of the nation's top psychiatrists wrote in to say they were exaggerated and irresponsible. A letter by 35 psychiatrists and professors of psychiatry affiliated with Columbia University stated that the Times' claims about discontinuation were "simply not the case" and that "the clinical consensus is [antidepressant withdrawal] is real, rare and always treatable.” Ronald Pies, a Tufts psychiatry professor, wrote that "based on my experience over 25 years of treating depressed patients, fewer than 10 percent will experience severe withdrawal symptoms when the antidepressant dose is tapered over three to six months." Another professor, Michael Serby, wrote that "withdrawal symptoms are readily avoided or minimized by careful tapering over a number of weeks."


The American Journal of Psychiatry published its own response by Dr. Roy Perlis, a leading psychiatrist. Dr. Perlis argued that psychiatrists have been aware of the discontinuation syndrome since these medications started being widely used, but that with a careful taper most patients will not encounter major problems. He also notes that many of the descriptions of "discontinuation syndrome" are unfair because they include anxiety, depression, and irritability as discontinuation symptoms. Since individuals that stop a working antidepressant are likely to relapse, this is not an avoidable problem or something that can be held against the medication. He accuses the Times of "refram[ing] a mental health success story into a conspiracy theory".


We have found that our clinical practice generally supports the psychiatric consensus, with a few caveats. The Times is right that many patients coming off antidepressants will have a few days or weeks of mildly unpleasant symptoms, and a few can have more severe symptoms that last months. But Perlis and the other experts are right when they say that if doctors and patients work together to stop an antidepressant in a gradual and well-considered way, most will not encounter anything like the Times' horror stories.


It's worth looking at the Times' evidence to see why they came to a conclusion so much different from Dr. Perlis' and our own. They present three studies which they purport show that "many" people who come off the drugs "often" encounter debilitating withdrawal symptoms.


First, they cite Ostrow et al. This is a study of 250 patients coming off various psychiatric medications. 54% described their withdrawal symptoms as "severe". However, the study did not give any information about whether any of the patients with severe withdrawal symptoms were on antidepressants. The New York Times tries to spin this away by saying the patients were "most commonly" on antidepressants, but this is meaningless given that many patients in the study were on multiple psychiatric medications. For example, 56% were on anxiolytics, likely benzodiazepines, which have a much more serious withdrawal syndrome than antidepressants. It's entirely possible that all 54% of people with severe withdrawal symptoms were benzodiazepine users, and that no patient rated their withdrawal from an antidepressant as severe. Using this study to estimate antidepressant withdrawal is inappropriate. Further, there is limited information about how the patients performed their taper, high risk of selection bias, and almost half the patients discontinued the medication without telling their doctor or against their doctor's advice.


The second study, Cartwright et al, looks at 180 current or former users of antidepressants. The Times says that "withdrawal symptoms were reported by over 130". But only 29 patients in the survey were off antidepressants; the large majority of people who said they had withdrawal symptoms were still on the drugs. While it is possible that some people's withdrawals were so bad that they restarted the medication, most likely this is describing people who forgot to take their medication for a few days, or who lost access to a prescription. This is different from a proper psychiatrist-assisted taper. And like the other study, this one has high risk of selection bias - people who have side effects are more likely to take an online survey on antidepressant side effects.


The third study, Rosenbaum et al 1998, avoided selection bias by being a randomized controlled trial, where researchers withdrew volunteers from their antidepressants under controlled conditions. The trial was placebo controlled, so patients did not know whether they were getting their real antidepressant or a placebo that would induce withdrawal. The study found no withdrawal symptoms from Prozac (ie no difference from placebo), but some withdrawal symptoms from Zoloft and Paxil. Once again, this was stopping the medication without any taper, which is not generally recommended.


What percent of people coming off antidepressants really get a discontinuation syndrome? This question is hard to answer accurately. Almost everyone will at least feel some mild change; what percent of people have a significant problem depends on where one puts the cutoff for "significant problem". But various researchers using standardized definitions of "discontinuation syndrome" have gotten a rough picture of rates for different antidepressants. The general consensus is that Prozac is about 10% (1), Lexapro is about 20% (1, 2, 3), and Paxil is 40% (1, 2). About 10% of people in placebo trials who think they are withdrawing from their antidepressant, but who are actually receiving it as usual, report a discontinuation syndrome.


Some of the responses to the Times claim that antidepressant discontinuation never happens with a proper taper. Unfortunately, that isn't entirely true. Studies are inconsistent in exactly how much a taper helps (1, 2), but it seems clear that some patients develop discontinuation even with the recommended few weeks of tapering. Tapers as long as Dr. Pies' recommended three to six months have rarely been fully investigated. There does seem to be some evidence that longer tapers are better than shorter ones, although even a short taper will be enough to prevent most patients from having serious problems.


If a discontinuation syndrome does develop, Fava et al report it as usually lasting only a few weeks. This doesn't mean that a few unlucky patients won't get a very serious discontinuation syndrome lasting months or more, but in our clinical experience this is quite rare.


The Times claims that "the medical profession has no good answer for people struggling to stop taking [antidepressant] drugs - no scientifically backed guidelines, no means to determine who's at highest risk, no way to tailor appropriate strategies to invididuals." This is false. There are plenty of good evidence-based guidelines, for example Guidance For The Discontinuation Or Switching Of Antidepressant Therapies In Adults and Antidepressant Discontinuation Syndrome: Consensus Panel Recommendations. There are plenty of treatments for discontinuation syndrome - the most common is to go back up to a comfortable dose that stops the symptoms, and then taper down more slowly. Other possibilities include converting the offending medication to Prozac, which very rarely causes discontinuation, and going off that one instead.


If you're worried about antidepressant discontinuation, please talk to your psychiatrist. They can guide you towards medications with low discontinuation risk, like Prozac, and avoid ones with higher discontinuation risk, like Paxil and Effexor, or help you investigate non-medical means for dealing with your depression.


When the Times cited the Cartwright survey of antidepressant users, they didn't mention one of its other findings - 85.5% of users said that antidepressants had improved their quality of life (54% "greatly" improved), and 89.4% said they reduced depression. Like the discontinuation numbers, these findings are certainly confounded by selection bias. But this underlines that the same people reporting withdrawal symptoms are also saying they are generally happy they went on the medication.


Antidepressants, like all drugs, are potentially dangerous chemicals with serious and real risks. But if you're depressed or anxious, there is a lot of evidence they are well worth taking.

Disclaimer: The posts on this blog are for informational purposes only and do not replace direct care from your mental health care provider. Contact your mental health care provider for specific questions or concerns about your own mental health. All posts are copyrighted, and the views expressed on this blog are representative of the opinions of Pacific Coast Psychiatric Associates (PCPA) as an organization.


Antidepressants: Balancing Trade-offs

  May 10th, 2018

In February, The Lancet-- a British medical journal-- published the largest study on antidepressants ever: Comparative Efficacy And Acceptability Of 21 Antidepressant Drugs For The Acute Treatment Of Adults With Major Depressive Disorder: A Systemative Review And Network Meta-Analysis. What did it find?










First, antidepressants work. The study found antidepressants had odds ratios from about 1.5 to 2, which means people on antidepressants were more likely to recover from depression than people who were not on antidepressants. 


Second, the effect size was generally small. In terms of a statistic called “Cohen’s d”, it only reached 0.32 for the average antidepressant. What does that mean in real life? It depends on the exact distribution being looked at; but for comparison, a diet pill with an effect size of 0.32 would equate to about 9 pounds. It’s not zero, but it’s not miraculous either.


Third, some antidepressants did better than others. Here’s the table from the paper:

































In terms of efficacy (how well the medicine worked), the older antidepressant amitriptyline seemed most effective, followed by newer antidepressant mirtazapine. In terms of tolerability (how few side effects there were), the leaders were agomelatine (a European antidepressant not available in this country), and fluoxetine (better known as Prozac). Few medications did well in both categories simultaneously, although a few of the SSRIs like escitalopram (Lexapro) and paroxetine (Paxil) had generally respectable performances. But the error bars (the uncertainty on each result) are so wide that it’s hard to really draw any firm conclusions about one being better than another.


How does this study change how we treat depression? The relatively small effect size should be disappointing to people who expect antidepressants to work miracles. But it’s important to remember that these are averages. Each drug worked very well for some people, didn’t work at all for others, and on average had a small positive effect. We know that people respond to medications differently. An antidepressant trial is always just an educated guess on what will work for any particular patient. If one doesn’t work, another one might. So the effect size for a rational regimen of trying drugs-- rejecting the ones that don’t work, and continuing the ones that do-- will be higher than the effect size for any individual drug. So the first lesson from this study is to be willing to try different things.


The second lesson is to pay attention to each individual patient’s needs when looking for a tradeoff between medication strength and side effects. Amitriptyline, the antidepressant which this study found to be most effective, isn’t for everyone. While it’s undeniably a powerful medication, it can also cause weight gain, sleepiness, dry mouth, and a host of other side effects. And even though this study found fluoxetine was well-tolerated and rarely caused major problems, it wasn’t very optimistic about its ability to treat the toughest depression cases. The point is less “here’s the best antidepressant” and more “here are the tradeoffs that each antidepressant involves”. This study helps us quantify those tradeoffs better, but it’s still a question of how many (and which) side effects any given patient is willing to accept.


People who are trying their first antidepressant medication and worried about side effects may want something more tolerable, like fluoxetine. And people who haven’t done well on antidepressants before, aren’t worried about side effects, and just want whatever’s most likely to work may want something more like amitriptyline. If you have a preference like this, talk to your doctor about your concerns and what you want out of medication to see if you can make a treatment plan that balances your needs.



  April 6th, 2018

A recent investigation by Clinical Psychiatry News discovered that a month’s supply of Abilify costs $750 at CVS and $13.75 at HealthWarehouse. The narcolepsy medication Provigil costs $724 at Walmart and $35 at Costco. Insurance companies, pharmacies, and middlemen negotiate complicated deals among themselves that can lead to dramatic variation in medication costs. But a little bit of work navigating this system can sometimes save you hundreds of dollars on expensive medications.



GoodRx.com (goodrx.com) is a pharmacy price comparison website for cash-only purchases. If you enter your prescription, it will tell you where you can get it at the lowest cost. Sometimes even if you have insurance, GoodRx’s cash-only price will be less than your insurance co-pay. You’ll need to print out their coupon or get a GoodRx benefit card from your doctor before you can make it work. This is probably the easiest way to save money on medications and should be the first thing you try.



Some medication costs vary with dose. A month's supply of doxepin 6 mg costs $446; a month's supply of doxepin 10 mg costs $10. If you notice your medication costs much less at a different dose, ask your doctor whether that dose might be appropriate for you, or if you could compensate by taking it on a different schedule.


Sometimes you can save money by cutting down on pills. Instead of taking three Cymbalta 20 mg tablets each morning, ask if you can take one 60 mg tablet - it will bring your costs from about $60 a month to about $20. Instead of taking a drug two or three times a day, see if there's an extended release version you only have to take once. Effexor 25 mg three times a day costs $40; Effexor XR 75 mg once per day costs $10. Consider asking your doctor if there's a way to make this work with your medication.



Some insurances charge a certain co-pay per prescription you pick up, regardless of the price of the prescription or the number of pills you get.


If you're in that situation, consider asking your doctor for a 90-day supply at a time instead of a 30-day supply. You'll still pay the same co-pay, but you'll only have to pay it a third as often.




Most big pharmaceutical companies have patient assistance programs to help customers who can’t afford their drugs. For example, Trintellix is made by Takeda Pharmaceuticals, whose site includes an application for patient assistance. Generally, people are eligible if they have no/limited insurance and an income less than four times the poverty line. Trintellix’s US site also offers “TAccess”, a savings card program that promises $100 off Trintellix prescriptions.


There are lists of the different patient assistance programs available at the Partnership For Prescription Assistance, and NeedyMeds.



Many patients need very specific medications to help with their condition, and there isn’t much that their doctor can do.


But sometimes, if your doctor knows you’re having trouble affording your medications, they can help switch you to a different medication that is better covered and less expensive. For example, although a month’s supply of the antidepressant Trintellix costs $350, a month’s supply of the older antidepressant Prozac can cost as little as $5; there is no evidence that Trintellix will work better than Prozac for the average patient.


Your doctor may also have other ideas for how to help you with medication cost issues. Most importantly, try not to go off medications or decrease the dose unilaterally because of cost. If you find something is unaffordable, ask your doctor if they have ideas for how to make it work.


© 2019 by PCPA, Inc.