More Than You Wanted to Know about Bird Flu and Chickens...

 

Are chicken flocks only culled in the US?

I ran into typical MAGA disinformation on the Internet the other day.  The post stated "not a single chicken" had been killed in Canada or Mexico due to the bird flu compared to millions in the US.  Since all the social media sites have been captured by MAGA I decided to debunk the claim that only flocks of chickens with avian influenza in the US are culled and not chickens in Canada or Mexico.  After reading pandemic misinformation for the past 5 years – it seemed like this was going to be an easy task and I was not wrong.

The latest North American bird population estimates were about 7 billion birds in 529 species in 2019 (1,2).  That represented a decline of about 3 billion birds since 1970.  Habitat loss, ecosystem destruction, and climate change were considered significant factors according to these authors. Anthropogenic threats like collisions with vehicles and other manmade structures, poisoning, and predation by domestic animals was also estimated to be a significant factor. Domestic cats kill roughly 1.3 to 4 billion birds annually (3). By comparison the estimate of bird deaths from contact with windmills is about 140,000 – 328,000 annually (4).      

Considering the chicken population in all 3 countries – the US has a total of 1.53 billion chickens annually that includes 1.2 billion broiler chickens alive at any one time and about 350,000 egg laying chickens. The total chicken population in Canada is 173.94 million.  In Mexico the total chicken population is 611.2 million.

Meat, poultry, and egg production in the US is regulated by the USDA and the Poultry Products Inspection Act (PPIA).  That includes other poultry like geese, ducks, guinea hens, and other more exotic domesticated birds.  In Canada it is the Canadian Food Inspection Agency (CFIA).  In Mexico it is the Ministry of Agriculture and Rural Development.  The culling of domestic chickens because of avian influenza has become a contentious political issue and a source of right wing misinformation. Additional misinformation has included blaming the Biden administration for culling chickens and driving up egg prices. The question of how these decisions get made, especially when large numbers of infected chickens are euthanized has been answered by experts in the past.  Here is one quote from CBS News when asked about the loss of 148M poultry since 2022:

"It's a staggering number, there is no doubt," said Jodie Guest, a professor of epidemiology with Emory University's Rollins School of Public Health in Atlanta. "But it is, and always has been a policy across administrations, with the USDA, that this is how they handle infections like this among poultry. And as we've seen bird flu move [across] species, it becomes even more important to try to contain that infection in the flocks that it's in, so that we don't continue to see spread."

The USDA has an infographic on measures to contain avian influenza outbreaks.  From that page “Birds are destroyed usually within 24–48 hours of detecting the disease. USDA pays for birds that must be destroyed.”  The cost of a live chicken can range from $5 to $20.  There seems to be a question about whether infected birds need to be euthanized.  This is the rationale provided by the American Veterinary Medical Association (AMVA):

“Recovery of poultry from HPAI is extremely rare. Infected poultry typically are euthanized and poultry products destroyed when HPAI infection is confirmed. The outcome also may be influenced by the producer’s participation in secure food supply plans. If regulatory officials authorize you to treat, keep in mind that the FDA prohibits extralabel use of adamantine and neuraminidase inhibitor classes of antiviral drugs in chickens, turkeys, and ducks.”

HPAI in this case is Highly Pathogenicity Avian Influenza defined as causing high mortality in poultry and are H5 and H7 influenza viruses.  Not all viruses belonging to those classes are highly pathogenic.  There are also Low Pathogenicity Avian Influenza (LPAI) viruses that may not cause any symptoms in affected birds.  There is the possibility that LPAI viruses can mutate into HPAI viruses and they are monitored for that reason. In the US – ill or deceased domestic birds are typically reported at the state level to animal health officials. They decide what level of analysis needs to be done and recommend protective measures.  Any casual historical search of previous outbreaks in avian populations will also reference significant culling of domestic fowl in all three countries. 

In the US, 148M domestic birds have been euthanized due to the latest outbreak of avian influenza including 20M egg laying chickens.  Exact numbers of euthanized poultry in Mexico since 2022 are harder to come by but are in the millions.  In Canada the number is about 14.5M.  I have not found a site that examines the differences in euthanized poultry between countries.  Variability will depend on wild bird exposure, total populations of domestic birds exposed, size of the domestic flock, biosecurity measures, and farm density. 

In summary, there is a consensus about approaches to HPAI in domestic birds. There is really no evidence that either Canada or Mexico does not recommend euthanizing infected birds.  There is no evidence that significant numbers of domestic fowl have not been euthanized in both countries currently and during past HPAI pandemics. From a veterinary medicine standpoint, it does not make sense – because most of the HPAI infected population dies and they act as a source for further mutations and facility contamination. The discrepancies in the total populations euthanized in all 3 countries occur because of policies (reimbursement for dead birds in the US), levels of oversight (state and federal in the US), and varying levels of reporting.  There is no evidence that the culling of birds is due to a political initiative or an initiative to adversely impact the economy.  And why would any rational President want to do that? 

 

George Dawson, MD, DFAPA

 

References:

1:  Pennisi E. Billions of North American birds have vanished. Science. 2019 Sep 20;365(6459):1228-1229. doi: 10.1126/science.365.6459.1228. PMID: 31604214.

2:  Rosenberg KV, Dokter AM, Blancher PJ, Sauer JR, Smith AC, Smith PA, Stanton JC, Panjabi A, Helft L, Parr M, Marra PP. Decline of the North American avifauna. Science. 2019 Oct 4;366(6461):120-124. doi: 10.1126/science.aaw1313. Epub 2019 Sep 19. PMID: 31604313.

3:  Loss SR, Will T, Marra PP. The impact of free-ranging domestic cats on wildlife of the United States. Nat Commun. 2013;4:1396. doi: 10.1038/ncomms2380. PMID: 23360987.

4:  Loss SR, Will T, Marra PP. Estimates of bird collision mortality at wind facilities in the contiguous United States. Biological Conservation. 2013 Dec 1;168:201-9.

5:  Ornelas-Eusebio E, García-Espinosa G, Laroucau K, Zanella G. Characterization of commercial poultry farms in Mexico: Towards a better understanding of biosecurity practices and antibiotic usage patterns. PLoS One. 2020 Dec 1;15(12):e0242354. doi: 10.1371/journal.pone.0242354. PMID: 33259478; PMCID: PMC7707464.

6:  CDC site on Avian Influenza (map of counties affected):  https://www.cdc.gov/bird-flu/situation-summary/data-map-commercial.html

7:  CDC site:  2020-2024 Highlights in the History of Avian Influenza (Bird Flu) Timeline. https://www.cdc.gov/bird-flu/avian-timeline/2020s.html

8: Barman S, Turner JCM, Hasan MK, Akhtar S, Jeevan T, Franks J, Walker D, Mukherjee N, Seiler P, Kercher L, McKenzie P, Webster RG, Feeroz MM, Webby RJ. Reassortment of newly emergent clade 2.3.4.4b A(H5N1) highly pathogenic avian influenza A viruses in Bangladesh. Emerg Microbes Infect. 2025 Dec;14(1):2432351. doi: 10.1080/22221751.2024.2432351. Epub 2024 Dec 9. PMID: 39584394; PMCID: PMC11632930.   

Details of the specific viral analysis for HPAI are included in this paper

 

Addendum:  I currently have an email in to Mexico's Secretariat of Agriculture and Rural Development (Secretaría de Agricultura y Desarrollo Rural) requesting more official numbers on the total numbers of domestic fowl euthanized due to HPAI since 2022. 

Graphic Credit:  From Wikimedia Commons.  Rollover photo or click to see full credit and CC license. This is the original unaltered photo.

Mouse-to-Mouse Resuscitation

 

A paper came out in Science 2 weeks ago (1) on the behavior of mice toward their unconscious or dead peers.  They have resuscitation-like behavior that consists of biting the face and tongue, clearing the airway, elevating the tongue of the unconscious mouse to revive them. Mice who were the recipients of this behavior recovered sooner than mice who did not receive these efforts.  The authors went on to see if they could localize the behavior in the brain and using modern neuroscience techniques, they able to show that they had localized the behavior to a brain substrate.  These papers have implications for psychiatry both at a theoretical and practical level.

In this experiment researchers used genetically identical mice (cross bred for 20 generations).  They followed their reactions closely across time epochs as they encountered a familiar partner anesthetized and unresponsive or euthanized (dead) mice. When compared with the active partner, mice spend 47.4% of the time interacting with the unresponsive partner compared to 5.8% of the time with the active partner.  They also displayed a specific pattern of behaviors directed facial area, trunk, limbs and head of the unresponsive partner. 31.8% of the time was directed at the orofacial area.  The overall duration of contact was extended with the unresponsive partner and it was more focused on the orofacial area.

To confirm the sequence of events, short acting (isoflurane) anesthesia was used to observe the partner response as the anesthetized mouse became less and then more responsive.  Time spent interacting with the anesthetized partner and the topology of interactions (more targeted orofacial activity correlated with the time anesthetized.  Deceased cagemates caused the same pattern of interaction but not sleeping cagemates because during sleep the directed behaviors led to movements of the sleeping mouse. This suggests that mice can differentiate responsive and unresponsive states in their partners.

The orofacial focused behaviors were studied under a high-speed camera.  It was discovered that in nonresponsive mice the tongue was bitten and pulled out of the mouth by casemates.  A similar tongue protrusion did not occur in unresponsive mice.  Pulling the tongue out resulted in a larger airway and the removal of foreign objects in the mouth. Placing the foreign object in a non-oral orifice did not result in removal. Stimulating the oral mucosa was also a strong stimulus for the righting response and arousal. 

Familiarity was a stronger stimulus for eliciting the grooming and resuscitation like behaviors than sex differences or similarities.  When given a choice between familiar partners – one anesthetized and one not – there was a preference for the anesthetized partner.  That did not persist when both target mice were unfamiliar.  The authors also demonstrated that the time spent with the unresponsive mouse did not decrease over a period of days – it did not show habituation.

After characterizing the unique behavioral aspects of the resuscitation like behavior the authors looked at the neural substrate. One hour after exposure to the unresponsive mice the cagemates were given 4-hydroxytamoxifen to label activated neurons.  Following 2 weeks of exposure several brain structures previously implicated in the observed behaviors including the medial amygdalar nucleus (MEA), paraventricular nucleus of the hypothalamus (PVH), basolateral amygdalar nucleus (BLA), hippocampus, and ventromedial hypothalamic nucleus (VMH) were examined. The number of tdTomato+ cells were noted in mice that had responded to unresponsive mice compared with controls (active partners).  This marker is a sign of the transcription factor c-fos and that neurons were recently active. Using a second set of probes roughly twice as many PVH oxytocin neurons were c-fos + and oxytocin + in the mice exposed to an unresponsive partner. 

An additional optogenetics experiment was done to look at the oxytocin PVH neurons.  Optogenetically silenced PVH neuron had the expected effect of reducing interaction time with the unresponsive partner. Optogenetically activating PVH neurons had the effect of increasing interaction time with an unresponsive stranger mouse.  An oxytocin receptor antagonist has the expected effect of reducing interaction time with the unresponsive mouse.

The authors conclude that they have demonstrated the necessity of both an oxytocin neuronal substrate and oxytocin signaling for very specific interactions and behaviors toward unresponsive mice.  Further, encountering a dead or anesthetized partner is required to elicit this response but it does not occur with a sleeping partner. They point out that rapid responses to an unresponsive partner can reduce the time it takes for recovery and decreases the risk of predation.  They suggest further work needs to be done on defining the neural network and sensory cues necessary for these behaviors.

As I read this paper I had a few thoughts:

1:  The hypothalamus is underemphasized in psychiatry.  We spent a couple of decades studying neuroendocrinology that was primarily focused on the pituitary gland. In clinical work, this is also an important system to be able to assess. But in much of the work about the theoretical basis of behavior – not much is said about the hypothalamus.  One example is the proximity of neurons underlying aggressive and sexual behavior in the lateral hypothalamus. 

2:  Social behavior versus the neurobiological substrate – psychosocial reductionists frequently treat the brain like a tabula rasa - not much is there until some kind of social learning or adverse event occurs.  In this case, adaptive complicated behavior is observed without any training.  The experiment illustrates both an anatomical and neurochemical basis for the behavior. Why would we expect anything to be different in humans?  And further - given the general case of biological diversity why wouldn't we expect this behavior to be absent in some and overdeveloped in others?  Even though the authors did not demonstrate this - why would we not expect that it could also be a learned behavior in individuals where it was not present or very robust?

3:  The measurements of activity in both the resuscitation-like and non-resuscitation behaviors were interesting.  Even though the overt behaviors were easily observed as occurring or not occurring – the neurons involved always had some level of activity. In other words – no target behavior did not equate to no neuronal activity.  It is not simply a case of networks being on or off. This has implications for how we attempt to correlate networks with behavior and the meaning of networks having a certain level of baseline activity.

All things considered; I thought this was a great paper. It reminded me of my biochemistry and pharmacology seminars in medical school where we would have spent a lot more time on the experimental methodology in this paper.  I did check my latest copy of The Molecular Biology of the Cell (7^th edition) and found that the discussion of optogenetics relative to this paper was very brief, but I suppose that makes sense.  From the standpoint of animal behavior this also recalls so-called altruistic behavior of some animals.  I have a file of that behavior observed in Humpback whales (Megaptera novaeangliae) interfering with killer whales (Orcinus orca) and hope to post something about that as well.

 

George Dawson, MD, DFAPA

 

References:

1:  Sun W, Zhang GW, Huang JJ, Tao C, Seo MB, Tao HW, Zhang LI. Reviving-like prosocial behavior in response to unconscious or dead conspecifics in rodents. Science. 2025 Feb 21;387(6736):eadq2677. doi: 10.1126/science.adq2677. Epub 2025 Feb 21. PMID: 39977514.

2:  DeNardo L, Luo L. Genetic strategies to access activated neurons. Curr Opin Neurobiol. 2017 Aug;45:121-129. doi: 10.1016/j.conb.2017.05.014. Epub 2017 May 31. PMID: 28577429; PMCID: PMC5810937.

Image Credit:

Generated by ChatGPT based on my parameters.  The original paper has a great image of the specific behaviors mentioned in this post. 

What happened to the Serotonin Hypothesis?

 

Biogenic amine hypotheses of depression date back 60 years at this point.  Ron Pies and I reviewed a couple of the key papers by Kety, Schildkraut and others that were some of the first to apply what was known about biogenic amine neurotransmitters to depression. These papers were elegantly written, keenly aware of the dangers of biological reductionism, and very clear that much more study needed to be done to either accept or reject the biogenic amine hypotheses.  Those hypotheses eventually extended to the specific neurotransmitters -  norepinephrine, serotonin, and dopamine.  Much has been written about the Chemical Imbalance Theory and more recently a Serotonin Theory of depression even though they do not exist.

I decided to study the transition in hypotheses over the course of my career by looking at major psychiatric diagnosis and counting the number of hypotheses in the literature for each diagnosis.  For the purpose of this post I will be posting a list of hypotheses about depression and discussing the implications. In general, there are many hypotheses about disorders that seem to linger in the literature. I have not found any solid evidence that hypotheses are accepted or rejected. There is also the possibility that they can be combined to produce new comprehensive hypotheses.  At this point I have not been able to identify any solid theories based on the development of hypotheses.  But before I get into that a brief discussion of definitions is in order to add some consistency to the rest of this essay. 

I will be using definitions from a book written in 1986 (1) because I think they are the clearest. The logical place to start is with a definition of a theory.  Theory is commonly mistaken for a hypothesis.  The best case in point that I can think of is the Serotonin Theory or Chemical Imbalance Theory.  By definition, a theory is a group of related principles that can explain and predict phenomenon in a restricted domain. The domain will vary according to the discipline. Medicine and psychiatry depend on empirical theories that in turn are proven or disproven based on observation and evidence. That demarcation extends to biology in general.  Examples of theories include Evolution, Thermodynamics, The Periodic Table in chemistry, and Germ Theory.  Any casual look at the biogenic amine hypotheses with respect to serotonin, norepinephrine, or dopamine will clearly show an elaboration of the neurochemistry and molecular biology of these systems. It will also show that the research is ongoing and that levels of prediction are not generalized enough for any marker to be used for prediction. At that level, biogenic amine theories do not exist and never have. There is additional confusion added by the common term conspiracy theories because in science they are really pseudo-theories and do not satisfy the general definition of a theory.  They provide false explanations and predictions.

Scientific laws explain how any branch of science organizes observations and explains them.  A good example would be the First, Second and Third laws of thermodynamics.  They are taught in physical science and engineering courses and do predict observations in physical systems at the macro level.  There are some specific laws in biology like mitochondrial DNA being inherited only from the mother and both parents contributing equal amounts of genes to offspring in sexual reproduction.

And finally, a hypothesis is a first step in developing laws and theories.  It consists of speculation about experimental observations at a more fundamental level.  The Serotonin Hypothesis for example was proposed since multiple observations about serotonin in depression were converging to suggest it played a central role in the disorder. It also occurred at a time when there was much active research on neurotransmitters and synaptic function. If it had been more widely accepted and there was a more comprehensive formulation that would have happened.  It did not and in at least one authoritative source – the American College of Neuropsychopharmacology – the Serotonin Hypothesis disappeared after the Fourth Generation of Progress in 1995.

I have included that transition in the four slides that follow.  I decided to include material from Goodwin and Jamison's Manic-Depressive Illness because it includes a commentary from the pathophysiology section of their book on bipolar disorder:

 

 

 

A comparison of dedicated chapters on serotonin between the 4th and 5th generations is also useful.  In the 4th generation there were 12 serotonin focused chapters and in the 5th there was one general chapter.

 As noted in the final summary of serotonin (last slide) , the research emphasis transitioned from strictly neurochemistry to the associated neurobiology and macro observations of brain networks.  At the same time current literature continues to emphasize the importance of serotonin systems in psychiatric disorders.  Although the ACNP Generation of Progress texts stopped with 5th edition I searched for evidence of the serotonin or any biogenic amine hypothesis in a recent comparable text (5).  There were no neurotransmitter centric mechanisms with a more primary focus on imaging receptors and transporter proteins and how neural circuitry was impacted.  Suggested mechanisms for depression converged on neurotrophic, immune, and neuroendocrine pathways (see table of contents below). 

While there has been no overt rejection of the serotonin hypothesis – people remain interested in it and it is useful to consider why.

1:  The search for the underlying pathophysiology of psychiatric disorders has continued emphasis.  The speculative mechanisms are broad and there are numerous hypotheses carried forward – much like the serotonin hypothesis. It seems unlikely that there will be a single basic mechanism leading to disorders based on the heterogeneity and polygenic nature of studied populations (see number of variants for major depression in the Polygenic Score (PGS) Catalogue.      

2:  Studying biological systems requires an appreciation of complexity – particularly when prediction is a dimension of theories. It is well known for example that biologically identical or nearly identical organisms can produce different physical and behavioral outcomes and until all of those mechanisms are appreciated and incorporated into hypotheses and theories – widely accepted overall theories are unlikely.

3:  There are imperfect classifications in biology, medicine, and psychiatry. One of the basic tenets in medicine is that no two people with the same diagnosis are alike.  There are obvious differences in biology, psychological and sociocultural factors.    

4:  Physical theories are not perfect.  There is active debate about theories that seem to be settled science and whether or not they are complete.   Many of those theories are predictive up to a point and useful for many applications - but deficient in some ways.  This is all part of the active process of science.

Despite these considerations – obvious questions about the serotonin hypothesis persist.   Why are medications with a high affinity for serotonin receptors and serotonin transporter (SERT) effective medications for several disorders?  Why in a recent preclinical study (6) was elevated extracellular serotonin  a common signal for several treatments – some of which did not target serotonin systems?  And – is it possible that serotonin signals are just the initial sequence of a larger series of events that leads to an antidepressant or anxiolytic response?

I would be remiss to not remind readers of the importance of analyzing the rhetoric in any scientific paper you are reading on psychiatric topics. On the issue of theories for example, my original source makes the following observation:

“What is a theory” is not as hard to answer as jesting Pilate’s “What is truth?”.  Indeed, one difficulty with our question is that there are so many accepted answers, not that there is none.  That is, the term theory is used in several distinct and legitimate ways in science and medicine, and an explanatory catalogue of those uses would fill many pages.  

“We will limit ourselves to the concept of a theory that suggests understanding, reliability, and grounded belief.” (p. 113)

If you find yourself suddenly reading about theories, hypotheses, or laws in psychiatry or any other branch of medicine look for the author's definitions of those terms.  Most textbooks in medicine and biology may mention brief definitions and references to thermodynamics and evolution but beyond that the terms are missing.  These terms are much more common in physical sciences where the studied objects are more easily classified and experimental observations are clearer.   

So what is the answer to "When did the serotonin hypothesis of depression disappear?"  One short answer is "between 1995 and 2002."  But the reality is that it is still with us despite active campaigns against it and several proclamations in the press that it is "dead".  At this rate it may outlive its detractors.

 

George Dawson, MD, DFAPA

 

References:

1:  Albert DA, Munson R, Resnick MD.  Reasoning in medicine: an introduction to clinical inference.  Baltimore, USA:  The Johns Hopkins University Press, 1988: 112-149.

2:  Pies R, Dawson G.  The Serotonin Fixation: Much Ado About Nothing New. Psychiatric Times. 2022 Aug 22

3:  Goodwin FK,  Jamison KR.  Manic-Depressive Illness.  New York: Oxford University Press, 1990. 

4:  Bloom, F.E. and Kupfer, DJ. Neuropsychopharmacology: The Fourth Generation of Progress. New York: Raven Press, 1995.

5:  Davis KL, Charney D, Coyle JT, Nemeroff C. (2002) Neuropsychopharmacology: The Fifth Generation of Progress. Philadelphia: Lippincott Williams & Wilkins, 2002.

6:  Charney DS, Gordon JA, Buxbaum JD, Picciotto MR, Binder EB, Nestler EJ.  Charney and Nestler's Neurobiology of Mental Illness.  New York: Oxford University Press, 2025.

7:  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.

Supplementary 1:  I contacted several experts involved in this research over the years.  So far none of the researchers I have contacted have responded to my questions that were specific to the serotonin hypothesis. 

Supplementary 2:  The book cover images and quotes are all property of their copyright owners and do not imply any connection to this blog. They are used here for illustrative and educational purposes. I encourage any readers of this blog to do their own research by reading the reference materials.  The ACNP 4th and 5th Generation of Progress are both available to read free online at the ACNP web site.

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 strictures 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:

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