Should GLP-1 agonists be added to the drinking water?

For starters GLP-1 agonists are drugs like Ozempic and Weygovy.  See this post for a current list.  It is hard not to hear about them since they are heavily hyped in just about every form of media. They are being touted as a cure for just about everything.  Various celebrities are either promoting them or denying that a dramatic weight loss was associated with their use.  Some in the weight loss and exercise industry are pushing back with statements about side effects and rapid weight gain if you ever stop taking them.  The sales of these drugs is a windfall for the pharmaceutical industry and current pricing means that other businesses that make money from rationing access to medical care and medications will be trying to prevent their use.  I thought I would post a contrast today between the latest review of conditions these medications have been researched for and a new paper that suggests they may increase the frequency of psychiatric disorders.

The rest of the title comes from my experience in many medical settings over the decades.  Any time a medication is commonly prescribed you can count on someone saying “We should just put it in the drinking water.”  Examples over the years have been amoxicillin, H-2 blockers like ranitidine, statins, beta blockers, lorazepam, and even haloperidol.  It all depends on the prescription frequency in a particular setting. At the rate GLP-1 agonists have been hyped - somebody is saying it somewhere.  The irony in that statement is that many medications are now in the water supply and not doing anything for anybody.

When I describe this group of drugs as hyped that is exactly what I mean.  The only comparable hype has been for cannabis and psychedelics/hallucinogens.  Typical newspaper headlines about GLP-1s say they are wonder drugs and go on to describe them as indicated for several conditions ranging from addiction to Alzheimer’s disease.  Currently 5.4% of all medication prescriptions in the United States are for GLP-1 agonists.  These drugs have been around for 20 years and during that time transitioned from use primarily for Diabetes Mellitus Type 2 to weight loss. Despite all the clinical trials and experience with them I do not think the final verdict is in and the main papers relevant to this post will illustrate why.    

The first paper (1) is a large observational study using databases from the Veterans Administration (VA) health care system (1).  The authors describe the rationale of their study as looking at the real-world outcomes of the use of GLP-1 agonists – both the positive effects and adverse outcomes. They had an N of 1,955,135 followed for a median of 3.68 years looking at 175 health outcomes.  The authors use an interesting methodology.  Patients were recruited based on incident use of a medications for Type 2 diabetes mellitus (T2DM) between October 1, 2017 and December 31, 2023.  That created 4 groups based on the medical treatment of T2DM)  including GLP-1 agonists (N= 232,210), sulfonylureas (N= 247,146), Dipeptidyl peptidase-4 (DPP-4i) inhibitors (N= 225,116), and SGLT2i inhibitors (sodium-glucose cotransporter 2 inhibitors) (N= 429,172).  There was also a treatment as usual (TAU) group (N= 1,513,896) with Type 2 DM who took non-GLP-1 antihyperglycemics between the study dates of October 1, 2017 and December 31, 2023.  As a point of reference, I have included a table of the medications in each class used for T2DM. 

Glucagon-like peptide 1 (GLP-1) agonists	exenatide (Bydureon) exenatide (Byetta) liraglutide (Victoza) liraglutide (Saxenda) dulaglutide (Trulicity) semaglutide (Wegovey) semaglutide (Ozempic) semaglutide (Rybelsus) tirzepatide (Mounjaro) tirzepatide (Zepbound)
Sulfonylureas	Glipizide Glimepiride Glyburide
dipeptidyl peptidase 4 (DPP4) inhibitors	alogliptin (Nesina, Vipidia) sitagliptin (Januvia) saxagliptin (Onglyza) linagliptin (Tradjenta)
sodium−glucose cotransporter-2 (SGLT2) inhibitors)	bexagliflozin (Brenzavvy) canagliflozin (Invokana) dapagliflozin (Farxiga) empagliflozin (Jardiance) ertugliflozin (Steglatro)

 

This study was designed to assess groups on 175 health outcomes from these treatment cohorts compared with two control groups.  One control group was a composite of equal numbers of diabetic subjects using oral hypoglycemics and the other control groups was diabetics who continued GLP-1 agonists that they had already been started on.  Results varied but generally the health outcomes measured were significantly improved on the GLP-1 agonists compared with the controls and across categories.  For example, when GLP-1 agonists were compared with the sulfonylurea, DPP4, and SGLT2 classes outcomes were improved in 13.14%, 17.14%, and 11.43% of the outcomes respectively. 

Risk of adverse outcomes were 8%, 7.43%, and 16.57% in the same order.  Those adverse events in aggregate included: nausea and vomiting, gastroesophageal reflux disease (GERD), sleep disturbances, bone pain, abdominal pain, hypotension, headaches, nephrolithiasis, and anemia. 

When comparing the addition of GLP-1s to treatment as usual (the composite control) better outcomes were observed in 24% and increased risk of adverse outcomes in 10.86% of outcomes.

The reduced risk of several CNS disorders were estimated by hazard ratios and they were modestly decreased for alcohol use disorder, cannabis use disorder, stimulant use disorder, opioid use disorder, suicidal ideation of self-injury, bulimia, schizophrenia, seizures and neurocognitive disorders.  Risk reductions were in the 10-16% range. 

The authors of this paper use several graphing techniques to present their data.  They graphed hazard ratios for both improved and adverse outcomes and made negative log transformed Manhattan plots as a measure of statistical robustness as alternate graphing technique.  The paper is open access and I encourage reading the paper to see these data presentations.  I included a partial Forest plot at the top of this post to illustrate some of these graphs and the outcomes they measured. The blue dots indicate reduced risk relative to controls and the orange dots indicate increased risk (calculated as hazard ratios (3).

The strength of this study is that it summarizes a large amount of data across a VA database.  Since it is administrative data it is collected in nonstandard way and the diagnoses are not necessarily made by experts - this data may not be as robust as a prospective randomized clinical trial.  The population was older white veterans and that may be a factor when considering pleotropic effects.  The authors conclude that the GLP-1 agonists had broad pleotropic effects based on the spectrum of positive results and preclinical work.  They emphasize the positive results for neuropsychiatric diseases and disorders.  They discuss the issue of suicidal behavior and point out that earlier studies raised concerns to the point that the European Medicines Agency investigated and found no evidence for causality.  This study showed decreased suicidality and possible antidepressant effects.  The results generally showed significant positive effects on outcomes across major disease categories with a clear group of adverse effects.   

For comparison there is a recent large retrospective cohort study (2) that uses deidentified data on patients from 66 different health care organizations.  This appears to be a database with a commercial purpose, but I cannot identify what that purpose might be based on their web site.  In their rollover map, most of the deidentified patients in this database are Americans.  The study was approved by an IRB in China and I assume that is where the analysis takes place.  The study was focused on examining the effects of GLP-1 agonists on patients being treated for obesity.  Subjects were selected for a diagnosis of obesity and incident use of a GLP-1 agonist. It was a retrospective cohort analysis similar to the first study but propensity score matching was done to pair treatment subjects more closely with controls. Exclusion criteria included use of any other weight loss drug and any psychiatric diagnosis or significant symptom like suicidality.

The main results of this study are summarized in 3 tables in the body of the paper (Tables 2, 3, and 4).  Psychiatric outcomes were measured over a period of 5 years and the percentage of patients with major depression, any anxiety, any psychiatric disorder and suicidality (ideation or behaviors) we measured at 6 months, 1 year, 3 years, and 5 years.  The cumulative incidences of disorders and suicidality increased over these intervals.  Hazard ratios were calculated compared with the control population and they were generally doubled.  

Results stratified on demographic factors and GLP-1 agonist potency showed that both sexes had higher than expected psychiatric morbidity associated with GLP-1 agonist use but that women had significantly higher hazard ratios across all categories. Age was inversely correlated with older populations having lower risk of psychiatric comorbidity. Finally, the potency of the GLP-1 agonist directly correlated with potency of the GLP-1 agonist and time of exposure.  The authors discuss the limitations of their study and implications for future use and study.

Both studies generally illustrate some of the advantages and problems of conducting large clinical trials. The numbers in the hundreds of thousands or million plus range would be very difficult if not impossible to conduct randomized clinical trials on.  It is manageable using the naturalistic retrospective designs employed here commonly referred to as real world designs.  The obvious limiting factor is expense and the methodological problem of drop outs over time.  In these specific cases the first study is selecting a subject cohort based on a diagnosis of diabetes mellitus type 2 (DMT2) and the second obesity.  Both are heterogeneous populations with some overlap.  If I was influenced at all by some of the current psychiatric literature, I might suggest transdiagnostic features common to both but the importance of that term seems inflated relative to common medical diagnostic formulations.  Instead - I will use the parlance of medical trials and point out that there are signals in both papers.  Those signals are both good and not so good.  In the first paper there were clearly improvements in many medical outcomes when T2DM was treated with GLP-1 agonists in about 25% of the conditions studied and adverse outcomes in about 10%.  Improvement occurred in conditions outside of the endocrine/metabolic sphere including some psychiatric conditions. In the second study, significant increases in psychiatric conditions were noted to occur associated with GLP-1 agonist potency and total exposure in a population selected for obesity treatment.  The authors are careful to point out that obesity and metabolic syndrome may be a risk factor for mood disorders and they provide an excellent discussion of how trial design and patient selection may have affected these results.  

When these trials are reported in the news, they are generally not reported as showing modest results.  Side effects are typically ignored.  I have not heard anything about the study that showed that increased rather than decreased psychiatric morbidity may be a possible outcome.  The media generally reports them as miracle drugs and patients with the best possible results are given as examples.

GLP-1 agonists are clearly serious medications with potentially serious adverse effects.  The prescription of these medications requires close monitoring and thorough patient education.  If I was prescribing these medications today - in the informed consent discussion I would include the potential for modest outcomes, potentially increased psychiatric side effects, the general potential for side effects, and why outcomes may be variable.  I would also make sure to let people know that long term outcomes at this point are not known with any degree of certainty.    

   

George Dawson, MD, DFAPA

 

References:

1:  Xie Y, Choi T, Al-Aly Z. Mapping the effectiveness and risks of GLP-1 receptor agonists. Nat Med. 2025 Jan 20. doi: 10.1038/s41591-024-03412-w. Epub ahead of print. PMID: 39833406.

2:  Kornelius E, Huang JY, Lo SC, Huang CN, Yang YS. The risk of depression, anxiety, and suicidal behavior in patients with obesity on glucagon like peptide-1 receptor agonist therapy. Sci Rep. 2024 Oct 18;14(1):24433. doi: 10.1038/s41598-024-75965-2. PMID: 39424950; PMCID: PMC11489776

3:  Spruance SL, Reid JE, Grace M, Samore M. Hazard ratio in clinical trials. Antimicrob Agents Chemother. 2004 Aug;48(8):2787-92. doi: 10.1128/AAC.48.8.2787-2792.2004. PMID: 15273082; PMCID: PMC478551.

4:  Sam AH, Salem V, Ghatei MA. Rimonabant: From RIO to Ban. J Obes. 2011;2011:432607. doi: 10.1155/2011/432607. Epub 2011 Jul 6. PMID: 21773005; PMCID: PMC3136184

Graphic credit:

Table at the top of the post of form Reference 1 and it is not copyrighted. The comparison Table was made by me.

Romantic Love and SSRIs

 

A paper came out this week that examined the relationship between selective serotonin reuptake inhibitors) SSRIs and romantic love. The lead author is a PhD candidate in anthropology with an interest in romantic love.  At first glance, the paper seems to run counter to a lot of sensational papers on the sexual side effects and possible persistent sexual side effects of SSRIs, because it found no differences between romantic love as assessed by a standardized scale and SSRI use. 

That is contrary to well-known sexual sides effects of these medications and the more recent controversy that SSRIs may cause persistent sexual dysfunction as either PSSD (Post SSRI Sexual Dysfunction) or PGAD (Persistent Genital Arousal Disorder). I have written about this controversy in the past and have not seen any useful advance in that literature.  Since that writing my information has been posted somewhere and I continue to get emails from people requesting my assistance in either assessing or treating PSSD.  I am no longer treating patients and therefore must decline. I am interested in researching this topic but do not have the resources on my own and my suggestions to various research entities have not produced any results.

This study looked at an N of 810 adults (48% women) from an original study of 1,556 adults from 33 countries who were defined as being in romantic love (Romantic Love Survey (RLS)).  The Passionate Love Scale (PLS-30) was used to identify romantic love.  The PLS-30 is a 30-point scale of descriptors of romantic love. Each item is rated on a scale of 1 (not true) to 9 (definitely true).  The scale is available at the above link.  This is an example of a typical item:

3. sometimes my body trembles with excitement at the sight of ____________

               not at all true 1 2 3 4 5 6 7 8 9 definitely true

 

By my inspection the 30 items of this scale are all cognitive and emotional features of love.  There are no items specific to sex or sexual fantasy.  The maximum scale score is 270 and participants in the RLS had to score a 130 or above and be in love for 23 months or less.  The authors of the scale suggest that a score of 106 -135 on the shortened version (15 items and a max score of 135) means – “Wildly, even recklessly, in love.”

The authors cite previous data suggesting the 2-year timeframe is necessary for romantic love and they removed 2 cases of high scorers because they were at the 4-year mark.  They deemed that 4 years of romantic love was improbable.

In their analysis the independent variable was SSRI use and they examined biological sex, mental health problems, intensity of romantic love, obsessive thinking, commitment, and frequency of sex as the dependent variables.  No specific details were given about the antidepressants – it was an SSRI or not binary.  At the time of the study only 9% of the sample (76 subjects out of 810) were taking SSRIs. Obsessive thinking was measured by a single question using a Likert rating.  Commitment was measured by adopting an item from another scale and changing the rating from 5 points to 9 points.  Frequency of sex was open to interpretation.  The question was “How often do you have sex on a weekly basis?” and a 50-point scale was used.  The mapping of responses to that scale is unclear from the description in this paper.  Mental health problems were measured with the Assessment of Quality of Life 4D (AQOL-4D) and distilled down to 1 question that looked at a anxiety, depression, or a combination ( “I do/do not feel anxious, worried or depressed). Any endorsement of these symptoms was considered a positive score of 1.

Binary logistic regression was done to see if any of the variables of interest predicted SSRI use and none was noted.  The authors confirm that none of their hypotheses about SSRI use correlating with less intense romantic love, less obsessive thinking, less commitment, and less frequency of sex were confirmed.  They conclude: “The results from this study demonstrate SSRIs use is not significantly associated with features of romantic love in our sample of young adults experiencing romantic love.”

I note that there was some reaction to this paper on social media.  Some were surprised by the results and some saw the result as a call for celebration. There are some people who claim that SSRIs have damaged their capacity for sex irreparably and the sexual side effects of the medication are well known.

The authors are more measured in their assessment of results. They comment on the discrepancy between their results and the literature on sexual side effects and consider several explanations.  The first has to do with selection bias.  Some people on SSRIs may have met exclusion criteria due to sexual side effects and for that reason would have been excluded from study.  Their demographic of young college age students may have been limiting. Is it possible that youthful vigor can counter known SSRI side effects? Specific drug, dosing and duration were also not specified.   

Any observational study like this one can be confounded by many factors.  As the authors mentioned selection bias can be primary. The original selection criteria may have selected out any persons with sexual dysfunction on or off SSRIs.  Interestingly the same phenomenon may occur in psychiatric practice.  Any psychiatrist who has been in practice for more than a few years has patients being seen on a long-term basis who are probably satisfied with treatment. Any medication being used may be well tolerated with few side effects.  Psychiatrists in that setting who routinely inquire about sexual side effects and relationship problems are not likely to hear about any.  The opposite selection bias occurs in some studies of these problems where subjects are recruited based on side effects.  In either scenario the true prevalence is likely to be over or underestimated.  

The authors advance several neurobiological explanations about brain substrates and serotonin that are highly speculative. Emotional blunting by antidepressants is discussed as a possible factor along with the potential brain substrates, but significant evidence against this occurring is not mentioned (3).   Several discuss the importance of the serotonin system and its up-regulation in romantic love.  Serotonin is a very important neurotransmitter in the human brain. Unfortunately, measuring it in vivo over time is very difficult.  Methods for accurate measurement in pre-clinical setting have only recently become available (5). One of the interesting findings is that serotonin can be increased in the extracellular space by several medications, therfore any serotonin-based mechanisms are not specific to SSRIs. I tried to capture the basic findings from this paper in the graphic at the top of this post.  The striking finding from Hashemi Lab is that antidepressants that purportedly have different up front mechanisms all increase extracellular serotonin. The discussion of serotonin is clouded by a lack of precision.  Terms like up regulated, down regulated, increase, and decrease are all meaningless unless it is relative to a specific location or structure and mechanism.   This finding needs to be incorporated into any discussion of how brain structures are involved.  Any interested reader can find the referenced studies to see if that is happening.  In my experience it is not. 

In terms of the study design, metrics for anxiety, depression, and sexual side effects would provide additional comparisons.  Many psychopharmacological investigations use the Arizona Sexual Experience Scale (ASEX) to measure the sexual side effects of medications in a more detailed way.  The ASEX is a 5-item list that assesses sex drive, sexual arousal, erections/vaginal lubrication, orgasm ease and orgasm intensity using a 6-point scale.  It would also allow for the study of dissociations of romantic love from sexual behavior – as an example asexual adolescent crushes on one end of the spectrum and sexual behavior in the absence of romantic love on the other.  

In the end this study is reassuring that at least some people can take SSRI medications and it does not affect their love-life. But large questions linger at this point. The authors call for additional research. but it would also benefit from consultation with psychopharmacology researchers for additional design elements.  One interesting consideration is whether there is any dissociation of adverse effects between romantic love and sex and whether romantic love may be protective.  Like all complex human behavior precise mechanisms require more precise phenotypes and methodologies. 

Romantic love is no different.

 

George Dawson, MD, DFAPA

 

References:

1:  Bode A, Kowal M, Aghedu FC, Kavanagh PS. SSRI is not associated with the intensity of romantic love, obsessive thinking about a loved one, commitment, or sexual frequency in a sample of young adults experiencing romantic love. J Affect Disord. 2025 Jan 21:S0165-0327(25)00100-4. doi: 10.1016/j.jad.2025.01.103. Epub ahead of print. PMID: 39848471.

2:  Bode A, Kavanagh PS. Romantic Love and Behavioral Activation System Sensitivity to a Loved One. Behav Sci (Basel). 2023 Nov 10;13(11):921. doi: 10.3390/bs13110921. PMID: 37998668; PMCID: PMC10669312.

3:  Dawson G, Pies RW.  Antidepressants do not work by numbing emotions.  Psychiatric Times.  September 26, 2022.  https://www.psychiatrictimes.com/view/antidepressants-do-not-work-by-numbing-emotions

4:  McGahuey CA, Gelenberg AJ, Laukes CA, Moreno FA, Delgado PL, McKnight KM, Manber R. The Arizona Sexual Experience Scale (ASEX): reliability and validity. J Sex Marital Ther. 2000 Jan-Mar;26(1):25-40. doi: 10.1080/009262300278623. PMID: 10693114.

5:  Witt CE, Mena S, Holmes J, Hersey M, Buchanan AM, Parke B, Saylor R, Honan LE, Berger SN, Lumbreras S, Nijhout FH, Reed MC, Best J, Fadel J, Schloss P, Lau T, Hashemi P.  Serotonin is a common thread linking different classes of antidepressants. Cell Chem Biol. 2023 Dec 21;30(12):1557-1570.e6. doi: 10.1016/j.chembiol.2023.10.009. Epub 2023 Nov 21. PMID: 37992715.5:  (Open Access)

Levels of Physician Accountability

 

I thought I would start the new year out with a post that looks at the factual basis of physician accountability and satisfaction with care provided by psychiatrists.  Apart from the usual irrational and conflict of interest derived criticism of psychiatry – there appears to be a significant number of people promulgating the myth that there are many people with complaints about psychiatrists.  One of them suggested that the numbers were in the millions.  That number sounds large, but if there are roughly 40,000 psychiatrists treating 1,000 patients a year that is 40M people.  I did ask for that reference but there apparently was none.

I have written about this issue many times on this blog.  My position could not be clearer, but to restate it – I have no doubt that problems arise during clinical care in medicine that result in suboptimal care, dissatisfied patients, and in the extreme angry, offended, concerned, or injured patients.  I do not think that happens more often in psychiatry than any other specialty and have recorded a few examples of my experience with specialty care that was clearly suboptimal.  I do not think that complaining about these incidents in social media, suggesting that all psychiatrists learn from isolated incidents that they were not involved in, or criticizing the entire field based on these anecdotes is either productive or useful. What is useful is presenting these problems as soon as they occur to the various entities charged with monitoring physician professional standards, behavior, and qualifications.

My opinion on this matter goes beyond my personal clinical experience.  I was a physician reviewer for all Medicare hospitalizations in the states of Minnesota and Wisconsin for about 15 years.  My job was to perform top level reviews on both quality and utilization issues that were flagged by standardized criteria.  As an example, one of the many quality markers was any death that occurred on a psychiatric unit. My job was to review all the available documentation and give an opinion on whether the care was substandard.  Reimbursement for the work was trivial and that was intentional so that no reviewer could make a living doing the reviews.  Another requirement for the position was that reviewers had to be employed full time as practicing clinicians in the states where the reviews were occurring. The program was eventually shut down because not enough problems in inpatient care were identified to justify the cost of the program.  That alone is a statement about the general quality of care provided based on standardized criteria.

At about the same time, a billing and coding system was introduced.  It did not take long for the federal government to decide that it could be used for fraud investigations based on documentation and coding mismatches.  In other words, if there was not enough documentation or specific bullet points were missed the physician or clinic could be fined or worse.  They could be barred from billing government insurers (Medicaid or Medicare).  In the worst-case scenario, they could be charged with mail fraud (since the billing was mailed) or RICO (Racketeer Influenced and Corrupt Organizations Act) violations.  I was in an employer seminar where it was suggested that physicians could end up in federal prison if the documentation did not match the billing code! The FBI conducted many of these investigations and large fines were levied against clinics and in some cases teaching hospitals. Some of those rulings had to do with attending physicians countersigning resident notes rather than writing separate notes.  The resulted in a period when attending physicians had to write notes that were redundant with the resident documentation.  That had a significant effect on morale and teaching.  

Eventually both the policing of the billing and coding and the quality reviews were turned over to health care organizations.  That led to a different kind of accountability. The review process was no longer conducted by independent reviewers carefully screened for conflict of interest or law enforcement.  Now the reviewers were employees of health care companies who could profit from their decisions.  That has resulted in a rationed but semi standardized approach to health care. It is harder to see a physician or see them for any length of time, but since most physicians are employees it is easier to report them up the administrative ladder.  

These days the opportunity for filing these reports generally starts early in the process.  You attend a clinic and as part of the paperwork you are given a patient bill of rights. It explains how you should expect to be treated in health care settings and what the complaint process looks like if that fails. Specific contact numbers are usually given for filing complaints. I have noticed that this process can be selective.  For example, in my experience with emergency departments, some departments of surgery, and some departments of cardiology there was no explicit complaint or feedback process. I worked in 4 different psychiatry departments and that was not the case. Patient feedback was always part of the annual review.  My speculation is that high revenue producing centers may be less likely to solicit feedback or complaints.  Either way the process is not foolproof, but there are avenues for filing complaints outside of the medical institution where the incident occurred.

The diagram at the top of this post shows all the feedback loops available for reporting or critiquing physicians. The complaints can be spontaneous or solicited.  Several levels also report to other levels independent of any patient complaint. For example – several of the entities (State Licensing, DEA, Privileging, Law Enforcement) report to the National Practitioner Database.  The rationale for that database was to prevent any state disciplinary action from being hidden by relicensing in another state.

Apart from the mechanics in the diagram there are additional approaches to the problem of accountability.  Ikkos, et al (1) discuss both the physician patient relationship and the formulation as being central to the work of psychiatry. Professionalism is described as the contract of the profession with society.  That includes the fact that complaint procedures are necessary to maintain professionalism.  Some complaints are accurate and others are not.  The authors in this case look at the psychodynamic and systemic factors that may affect complaints and their accuracy.  Although this paper is form the UK, very similar mechanisms in the US through the medical practice boards of each state.  Those boards are political rather than medical agencies and they enforce state medical practice statutes including relicensing.

Another indirect indicator of physician complaints is malpractice cases.  Ideally malpractice in the US is a marker of negligence but the reality is that it is a much more complicated dimension. In any year a significant number of physicians face a malpractice action but only about ¼ result in a payment.  One study (3) documented that  7.4% of physicians across 25 specialties had a malpractice action in one year and 78% did not result in a financial award.  The rate of malpractice actions varied significantly across specialties with surgical specialties at the top and primary care specialties having the lowest risk.  Psychiatry ranked 25^th out of the 25 specialties in terms of malpractice risk.  Specialties were also analyzed by the 5 highest and lowest risk (includes psychiatry) for cumulative risk of a malpractice action by age 65 and those numbers were 71% and 19% respectively. Additionally, psychiatry used to have a two-tiered malpractice premium system in the US that was modified to one premium because of the low incidence of malpractice cases among the psychiatrists doing electroconvulsive therapy.          

What do I hope people have learned from this post?  First – the first line of approach can a direct discussion of the problem with your physician. Misunderstandings, disagreements, systems problems, and bad days are common and they do not have to be catastrophic. Psychiatrists should be more attentive to the relationship aspects of encounters making that discussion easier.   Second - if you have a complaint against a psychiatrist or any other physician there is an option to take it to one of the many channels in place to hear and act on those complaints.  Posting on social media and attempting to create the impression that your problem is widespread will not address it.  If you are really interested in a solution follow the designated channels. This suggestion does not diminish the problem you are experiencing at all – it is focused on an effective solution. Third – do not expect that all psychiatrists or physicians that you complain to will accept your suggestion that the problem is common or that they need to change based on your problem.  Most physicians practicing get constant feedback from all these accountability measures and none of their work is flagged.  Further – in some cases these same mechanisms are used by administrators to get physicians to do what they want.  There are also cases where complaints are made to harass physicians using these same mechanisms.  Fourth – in acute care psychiatric settings it is common to encounter patients who resent, complain about, or threaten psychiatrists on sight.  In other words – even if they are meeting a psychiatrist for the very first time, they exhibit aggressive behavior. It is the nature of some forms of severe psychopathology and in some cases, it can persist and form the basis of a complaint about that physician. Fifth -   much of the unfounded criticism from both outside and inside the field is based on the assumptions that there is massive wrongdoing, error-making, ignorance, malfeasance, etc on the part of psychiatrists.  There is absolutely nothing to back that position up. Many of those critics seem to be making a career out of criticizing the psychiatrists who are doing the work and have limited to no knowledge of how those psychiatrists work or the stressors they are under.  Sixth – there are no guarantees that any dispute will be resolved to your satisfaction. The number of malpractice cases resulting in a financial payment may be the best indication because it is a rigorous contested dispute where the plaintiffs’ interests are represented and over ¾ do not result in a financial settlement.  Most complaints and disputes do not require that degree of contentiousness.

If you have finally seen a psychiatrist, and there is a problem with the interaction or treatment – use your judgment and try one of the many ways to address that problem. Don’t hesitate to get a second opinion. 

George Dawson, MD, DFAPA

References:

1:  Ikkos G, McQueen D, St. John-Smith P.  Psychiatry’s contract with society: what is expected?  Acta Psychiatr Scand 2011: 124: 1–3

2:  Ikkos G, Barbenel D. Complaints against psychiatrists: Potential abuses, Psychoanalytic Psychotherapy 2000, 14:1, 49-62, DOI: 10.1080/02668730000700051

3:  Jena AB, Seabury S, Lakdawalla D, Chandra A. Malpractice risk according to physician specialty. N Engl J Med. 2011 Aug 18;365(7):629-36. doi: 10.1056/NEJMsa1012370. PMID: 21848463; PMCID: PMC3204310.

Graphic:

Done by me using Microsoft Visio.  Click directly on the graphic to enlarge and see a clearer graphic. 

Dry January? Why Not the Rest of the Year?

 

Every January one of the frequent pledges is to not use alcohol for the month.  In my capacity as a psychiatrist – I have had patients tell me that if they could do it was a sign that they were not an alcoholic because it shows that they can control their drinking.  Never mind the excessive drinking and adverse consequences the rest of the year.  I saw an exchange between a sober bartender and a stress drinker portrayed in a new TV series just today.  It went something like this:

Patron: “I stopped drinking whisky because I am an alcoholic – so I just stick with beer.”

Bartender: “Well you know there is alcohol in beer.”

Patron: (motioning to his light beer) “There is more alcohol in orange juice than there is in this”

Bartender: “I’m just saying…”

Patron: “I’ll tell you what – let me drink 6 of these beers and 6 whiskeys and you tell me which one has more alcohol.”

And so, it goes. If you have a problem with alcohol or any other substance (or behavior) that reinforces its own use – there are endless rationalizations to keep using it and never enough deterrents.  Studies have shown that it often takes a life-threatening problem or major life event to quit - but even that may not be enough.  I am witness to many people who kept drinking despite end stage liver disease in some cases fully supported by their family: “It’s his choice – if he wants to drink, he is free to drink.”   It seems that the only advocates for sober living are in Alcoholics Anonymous or other 12 step recovery groups.  I did post on the Curious Sober movement in the younger generation but that has either not caught on or it is not being adequately covered if it has.

The history of using intoxicants is long and detailed. The two dominant evolutionary theories are that the substances are used because of a mismatch of currently abundant intoxicants on a reward and endogenous opioid system originally there for other reasons or as a form of self-medication that can be observed in other primates. The latter idea is that primates learn that there are certain plants that contain compounds that can treat ailments.  Both of those theories leave out the cultural elements that include social settings, celebrations, religious ceremonies, traditions, and local customs that use intoxicants as part of the event. There are cultural portrayals in movies and television showing alcohol and other intoxicants as necessary to alleviate daily stress.  In more modern times, some of these substances are imbued with magical qualities like being vehicles for mind expansion or even cures for mental illnesses.

The reality of substance use for practically all of the people I have talked with who do not have a substance use problem comes down to using alcohol of drugs to get an enjoyable “buzz”, to get a heightened sense of social competence from the initial relaxation, or just going along with the crowd.  In many crowds there is intense peer pressure to not be the one who is not drinking or smoking cannabis. That is a major source of binge use in the late teens and early 20s. Even in those social situations it is common for people to experience excessive use, intoxication with impaired judgment, and bad outcomes.  I have talked with too many people who sustained severe legal consequences from a single night of excessive drinking. I have also talked with too many people to remember who were admitted to my acute care psychiatric unit based on something that happened when they were acutely intoxicated.

I have covered this issue in the past and will link that post here without having to repeat it.  The basic issue for me is why use intoxicants at all?  Considering just alcohol - it is a neurotoxin, a carcinogen, and a direct toxin to the pancreas, the heart, and the liver. For years it was promoted as a “heart healthy” drink despite methodological problems with studies that put subjects with significant alcohol exposure in the control group.    

There are both informal and professional advocates for getting high. One of the most well-known advocates estimates that 70-90% of people can use intoxicants and they do not become problematic.  He describes his own use of heroin as useful because it results in a “happy and stress-free feeling”, helps him “maintain work-life balance”, and should be legal for everybody.  He also describes the pain of heroin withdrawal but apparently does not see that as a deterrent.  A key question is whether it is possible to get to that “happy and stress-free feeling” without using heroin?  How many people are operating under this premise today as they use various intoxicants some of which are excessively hyped as being good for your mental health? American culture is promoting the idea that you can fine tune your brain by using intoxicants even though there is no evidence this works.  To promote that idea, we have been exposed to 20 years of intoxicants advertised as medical treatments beginning with cannabis.  As the dust settles this idea has little to substantiate it, adverse effects have been minimized, and commercial conflicts of interest have not been disclosed.

The basic consideration comes down to the values you have established for yourself and whether those values can be affected by intoxicants.  There are many approaches to values that apply to intoxicant use. There are several religions, philosophical approaches, and recovery movements that value not using alcohol or other intoxicants as well.  You may value your short term and long-term health and consider not using intoxicants on that basis.  You may have had a close call while intoxicated and decided that you did not want to take that chance again. You might even survey the damage done to your family by intoxicants and decide they are too risky to sample.  On the other hand, you can walk into any small-town bar in the Midwest and people will be joking about the effects of alcohol and in some cases about who has developed cirrhosis or died as a result. They may also be joking about the associated behaviors of excessive intoxication.  Gallows humor is an easily observed adaptation.  There are subcultures that value alcohol use – no matter what.  I would argue that extreme position is a direct result of the reinforcing effects of alcohol rather than any de novo philosophical position. 

In the final analysis this is not about whether intoxicant use is a disease or whether you can control the use or even gain something from it.  Most of the popular discussion comes down to political arguments. In other words – I have a particular belief system about intoxicants and I will marshal every possible bit of evidence to support my position. I will be the first to acknowledge that as an acute care and addiction psychiatrist – selection bias was certainly in effect. I would see the worst possible scenarios.  But I have also seen people in real life who were clearly not doing well at all varying from an intoxicated man I tried to help at 7AM in northern Wisconsin to a young woman my wife and I tried to help in Boston.  You can argue that those folks still had a substance use disorder and most people using intoxicants do not.

In that case – I would offer the personalized evidence.  If you are having a Sober January and things are unchanged, going well or even better than usual – why change that?  

Keep it going.

 

George Dawson, MD, DFAPA

 

 

Graphics Credit - click photo for all details:

1:  

2: