Osmind

Hunter-gatherers who walk 10–14 km per day burn roughly the same number of calories as sedentary Westerners. That finding shocked evolutionary anthropologists. It also exposes a common misunderstanding about exercise. Walking isn’t powerful because it burns calories. It’s powerful because of what it does to glucose, insulin, and mitochondrial function. A short walk after meals activates insulin-independent glucose uptake in muscle, blunts glucose spikes, and creates a metabolic environment that favors lipolysis and ketone production. Why should psychiatrists care? Because brain function is energy metabolism. Glucose variability and metabolic dysfunction influence inflammation, cognition, mood stability, and treatment response. William Sauvé, MD and Annette Bosworth, MD explore this connection in our latest blog. Nancy Sinatra was right: These boots were made for walkin. https://lnkd.in/eHZY5sUs

New real-world data highlights the growing burden of generalized anxiety disorder in the United States. https://lnkd.in/eqwSuek2 A major study analyzing millions of insurance claims from 2020 to 2023 found that the projected annual prevalence of diagnosed GAD rose from 5.4 percent in 2020 to 6.6 percent in 2023. The three-year cumulative prevalence reached 10.3 percent, meaning more than one in ten adults met criteria over that period. Annual incidence remained steady between 2.1 and 2.3 percent. Women were diagnosed at more than twice the rate of men, with most cases occurring among middle-aged adults who were commercially insured. These numbers are substantially higher than those reported in older epidemiologic surveys. They underscore how common and clinically significant GAD remains, particularly given its frequent overlap with depression, chronic pain, insomnia, and other conditions. Despite this clear and increasing public health impact, there remains a dearth of truly effective, well-tolerated new treatments for GAD. Even today, the most reliable path forward for many patients is still the hard way: structured psychotherapy, particularly cognitive behavioral therapy and related approaches that build lasting skills for managing worry, avoidance, and physiological arousal. Isaac Asimov captured something essential about this in his 1957 short story "Profession." In it, society imprints professional knowledge directly into people's brains on Education Day. A small number of individuals cannot receive these imprints. They are set aside and must instead learn the old-fashioned way: slowly, one page at a time, through books and deliberate study. (Hey Brittany Albright MD, MPH, DABOM I haven't called you out on Nerd Credentials in a bit ... 😂) Psychotherapy for anxiety disorders works in much the same manner. It must be done one patient at a time, face to face. There are no shortcuts, no mass-produced tricks, and no technological bypass. Becoming a skilled psychotherapist takes years of training and experience. For patients, particularly those with GAD, the work is often difficult to tolerate. It requires confronting worry, avoidance, and physiological arousal directly, much like the disciplined pain of serious physical training, only more intimate and emotionally demanding. Yet it remains the treatment that builds genuine, lasting skills for managing anxiety. Medications have their place, but they often fall short on durability and come with trade-offs. We urgently need better pharmacologic options and far greater access to high-quality therapy. What are your thoughts on bridging the gap between rising diagnoses and meaningful recovery in anxiety care?

Treatment-resistant depression doesn't have a formal DSM definition. But most psychiatrists know it when they see it—and most of them are seeing it constantly. Osmind CMO William Sauvé, MD and medical advisor Brittany Albright MD, MPH, DABOM joined a Psychiatric Times panel to unpack why depression persists after multiple medication trials, and what full remission actually requires. A few things that stood out: → The majority of patients with MDD in psychiatric practice meet the threshold for TRD: two or more adequate trials at appropriate dose and duration → Many patients who say they've "tried everything" discontinued within days. Distinguishing that from true TRD matters before changing course. → Residual symptoms, even with partial response, significantly increase relapse risk → One panelist reframed TRD as "monoamine treatment-resistant depression"; the medications are failing patients, not the other way around Full remission, not just response, is the goal. Watch here → https://lnkd.in/eABHaUNh

Eli Lilly just launched two Phase 3 trials for a GLP-1 drug. Not for diabetes. Not for weight loss. For alcohol use disorder. 2,200 patients. Principal investigators from UCLA, UCSF, and Penn. Primary completion in 2028. Big pharma does not run trials this size because they think a drug slows down your gut. They run them because they think it rewires reinforcement learning. Here's what most psychiatrists don't know: GLP-1 receptors aren't just in your gut. They're in the VTA, the nucleus accumbens, the insula, and the prefrontal cortex. The exact circuits that run cue salience, reward valuation, and compulsive behavior. This drug class is acting on the brain. Directly. Whether psychiatry is paying attention or not. Last week I sat down with Dr. Annette Bosworth to talk through what the evidence actually show: the addiction trials, the anhedonia concern (and why it might be a dosing problem, not a drug problem), and the scope-of-practice question psychiatrists keep asking me. My answer to that last one: if you have a license to prescribe, you can prescribe everything. The question isn't permission. It's whether you understand what you're prescribing well enough to use it well. These drugs are already showing up on your patients' medication lists. Better understand them before someone else's prescribing decisions become your clinical problem. https://lnkd.in/eMhg2MeH

Eli Lilly just launched Phase 3 trials for a GLP-1 drug in alcohol use disorder. Not diabetes. Not weight loss. Addiction. GLP-1 receptors sit in the VTA, nucleus accumbens, insula, and prefrontal cortex, the brain regions that run reward, craving, and compulsion. In a study of 142,000+ patients published this month in Frontiers in Psychiatry, GLP-1 RA users had 75% lower odds of any substance use disorder. William Sauvé, MD, Annette Bosworth, MD, and Brittany Albright MD, MPH, DABOM break down what psychiatrists need to know: → Why the addiction trial data is stronger than most clinicians realize → How anhedonia on GLP-1s may be a dosing problem, not a drug problem (and a ziprasidone parallel that hits close to home) → What low-dose tirzepatide combined with a ketogenic diet looks like in real patients One clinician on the call shared a case: a 42-year-old woman with alcohol use disorder whose PHQ-9 dropped from the twenties to 2 in seven weeks on tirzepatide. If you treat reinforcement dysregulation, you can't afford to outsource this drug class to primary care. Read the full breakdown here → https://lnkd.in/ek7bhtPq

A little over ten years ago, Gregory O'Shanick MD sent me what he calls his “index case.” Greg is dear friend and psychiatrist who specializes in brain injury — Medical Director of the Center for Neurorehabilitation Services and former Medical Director of the Brain Injury Association of America — and at the time I had just started an interventional psychiatry practice in Richmond. The patient had suffered a traumatic brain injury decades earlier and had spent years struggling with depression, cognitive symptoms, and an inability to return to work despite extensive treatment. The plan was simple: treat the depression with TMS. Six weeks later her depression was gone. But on the way out the door she added something neither of us expected: "By the way… my memory is better." That moment turned into a collaboration that has now lasted more than a decade. Over the years Greg has referred well over a hundred patients with traumatic brain injury to me for TMS — mostly for treatment-resistant depression, which is by far the most common psychiatric complication after brain injury and often responds poorly to medications. Which brings us to this week. This morning at the North American Brain Injury Society (NABIS) conference in Arlington, Greg and I presented outcomes from 73 of those patients. For me, now serving as CMO at Osmind, it was also a chance to think about how real-world clinical observations like these can be captured, studied, and shared at much greater scale. The depression results were strong: about a 57% reduction in PHQ-9 scores, with a 63% response rate and 32% remission rate — essentially the same outcomes we see in the general treatment-resistant depression population treated with TMS. For patients with TBI, who often struggle for years with depression that medications fail to touch, that alone is a meaningful result. But what really caught our attention were the broader changes. Across a range of post-concussive symptoms we saw significant improvements in cognitive fog, slowed processing, concentration, irritability, emotional regulation, fatigue, and memory. Importantly, these patients were not enrolled in a TBI neuromodulation trial. More than 90% were simply receiving insurance-covered TMS for depression. The improvements in broader neurobehavioral symptoms were essentially a side effect. Which makes you wonder: if treating depression alone can move the needle this much after brain injury, what might happen if neuromodulation were actually designed with neurorehabilitation in mind? I have a feeling this is a conversation that is just getting started. Very grateful to Greg for a decade of collaboration and friendship — and to NABIS for the opportunity to share the story.

Tomorrow! Register here and get the recording after if you can't make it live: https://lnkd.in/eUhDen6P

Register here: https://lnkd.in/eNNaCEGi

Your most treatment-resistant patients need more options. This webinar shows you how to deliver them. Considering VNS Therapy™ for your patients with difficult-to-treat depression? This webinar covers what happens after you decide it's the right clinical option. Karen Giles, MD, MS joins William Sauvé, MD discuss the practical side of VNS Therapy implementation. From identifying candidates to understanding the surgical procedure and dosing, they'l walk through the essential knowledge for both new and experienced prescribers. March 12, 2026 | 11am PT / 2pm ET Can't make it live? Register and we'll send you the recording. https://lnkd.in/eQwprrbs Webinar selected by Osmind | Sponsored by LivaNova, PLC More information about VNS Therapy for Difficult-to-treat Depression (DTD) is available at https://lnkd.in/gH7WAE_s The VNS Therapy™ System is indicated for the adjunctive long-term treatment of chronic or recurrent depression for patients 18 years of age or older who are experiencing a major depressive episode and have not had an adequate response to four or more adequate antidepressant treatments. The most commonly reported side effects from stimulation are voice alteration or hoarseness, increased coughing, sore throat, paresthesia, dyspnea, and pain. Infection is the most commonly reported complication of the surgical procedure. Important safety information is available at https://lnkd.in/gtEr6-aV us/hcp-safety-information DEP-2600029 #VNSTherapy #Depression #DifficultToTreatDepression #DTD #TRD