Why it's called "borderline"

If you've been close to someone with BPD, you probably know the moments I mean. They were certain you were cheating. Certain you said something you never said. Certain an event happened a way it demonstrably didn't. Not suspicious. Absolutely certain. Even within a single conversation, reality would shift, as if what had happened twenty minutes earlier no longer existed. No amount of evidence, calm explanation, or receipts could touch it. I walked away from those conversations questioning my own memory because of how certain they were in their version of things, and because of how much I trusted them.

Sharp explained where the word "borderline" actually comes from. It's not describing a person who is borderline-anything in the casual sense. It's a clinical border, the term originated to describe patients who sat between neurosis and psychosis.

The history is worth a minute. For most of early psychiatry, patients went into one of two bins. Neurotic meant anxious, depressed, conflicted, but in contact with reality. Psychotic meant a break with reality. In 1938, a psychoanalyst named Adolph Stern described a group who fit neither bin. In the office they looked neurotic, but under stress (often the stress of the therapy itself) they would slide toward paranoid, reality-distorted states, and then come back. They lived on the border line, so that's what he called them.

The concept got sharpened over the next forty years. One analyst famously described these patients as "stably unstable" — the instability was the consistent feature. Otto Kernberg formalized it in 1967 as a level of personality organization sitting between neurotic and psychotic structure, researchers led by John Gunderson turned it into measurable criteria in the 1970s, and the DSM-III made it official in 1980.

By then the name was a fossil. It describes a 1930s sorting problem rather than the disorder's actual content, which is why other diagnostic systems have preferred names like "emotionally unstable personality disorder." The fossil nonetheless preserves a real observation. Under enough emotional load, these patients drift toward the psychotic side of the border.

That drift is what Sharp is describing. Her words: a person in full psychosis is certain they're seeing an image that doesn't exist. That's the most extreme form of what researchers call psychic equivalence (when whatever is in your mind feels identical to reality, with no gap between "I feel it" and "it's true.")

People with BPD typically don't have that in a full-blown, fixed way. But Sharp is direct that in severe presentations, under enough emotional intensity, they can edge toward that place. This is what I encountered.

Two things this understanding has helped me with:

  1. Trust in my memory. The gaslit feeling — where you doubt what you know happened — makes a different kind of sense when you realize the other person was reporting their internal state with the full confidence of their perception being accurate.
  2. It drew a line. Understanding the mechanism is not the same as accepting what it produced. The certainty had a cause, the damage was still damage. Both are true, and you don't have to pick one. And there's variance. Some people with BPD are more intentional in the harm they do, the same way cruelty and altruism vary in the general population. The mechanism explains a pattern. It doesn't adjudicate every act.

Eighty years ago, clinicians watched people cross back and forth over a border between shared reality and private certainty. I didn't know the term's history, but I spent too much time staring at someone walking that border without understanding what was happening.

u/wizbanger — 1 day ago

Why it's called "borderline"

I'm a former partner. The relationship left me with PTSD, and part of how I've processed it is trying to understand the mechanics of what I lived through — reading the research, listening to the people who study this. Recently that led me to an interview with Dr. Carla Sharp, one of the world's leading BPD researchers.

If you've been close to someone with BPD, you probably know the moments I mean. They were certain you were cheating. Certain you said something you never said. Certain an event happened a way it demonstrably didn't. Not suspicious. Absolutely certain. Even within a single conversation, reality would shift, as if what had happened twenty minutes earlier no longer existed. No amount of evidence, calm explanation, or receipts could touch it. I walked away from those conversations questioning my own memory because of how certain they were in their version of things, and because of how much I trusted them.

Sharp explained where the word "borderline" actually comes from. It's not describing a person who is borderline-anything in the casual sense. It's a clinical border, the term originated to describe patients who sat between neurosis and psychosis.

The history is worth a minute. For most of early psychiatry, patients went into one of two bins. Neurotic meant anxious, depressed, conflicted, but in contact with reality. Psychotic meant a break with reality. In 1938, a psychoanalyst named Adolph Stern described a group who fit neither bin. In the office they looked neurotic, but under stress (often the stress of the therapy itself) they would slide toward paranoid, reality-distorted states, and then come back. They lived on the border line, so that's what he called them.

The concept got sharpened over the next forty years. One analyst famously described these patients as "stably unstable" — the instability was the consistent feature. Otto Kernberg formalized it in 1967 as a level of personality organization sitting between neurotic and psychotic structure, researchers led by John Gunderson turned it into measurable criteria in the 1970s, and the DSM-III made it official in 1980.

By then the name was a fossil. It describes a 1930s sorting problem rather than the disorder's actual content, which is why other diagnostic systems have preferred names like "emotionally unstable personality disorder." The fossil nonetheless preserves a real observation. Under enough emotional load, these patients drift toward the psychotic side of the border.

That drift is what Sharp is describing. Her words: a person in full psychosis is certain they're seeing an image that doesn't exist. That's the most extreme form of what researchers call psychic equivalence (when whatever is in your mind feels identical to reality, with no gap between "I feel it" and "it's true.")

People with BPD typically don't have that in a full-blown, fixed way. But Sharp is direct that in severe presentations, under enough emotional intensity, they can edge toward that place. This is what I encountered.

This reframed something for me. Those arguments were never fights over facts. I was arguing with a state, not a claim. My evidence was arriving somewhere it couldn't register.

Two things this understanding has helped me with:

  1. Trust in my memory. The gaslit feeling — where you leave doubting what you know happened — makes a different kind of sense when you realize the other person was reporting their internal state with the full confidence of their perception being accurate.
  2. It drew a line. Understanding the mechanism is not the same as accepting what it produced. The certainty had a cause, the damage was still damage. Both are true, and you don't have to pick one. And there's variance. Some people with BPD are more intentional in the harm they do, the same way cruelty and altruism vary in the general population. The mechanism explains a pattern. It doesn't adjudicate every act.

Eighty years ago, clinicians watched people cross back and forth over a border between shared reality and private certainty. I didn't know the term's history, but I spent too much time staring at someone walking that border without understanding what was happening.

u/wizbanger — 1 day ago
▲ 110 r/funfacts+1 crossposts

Fun Fact: Ozempic exists because of a venomous lizard that eats twice a year.

u/wizbanger — 3 days ago

The drug behind Wegovy exists because of a venomous lizard that eats twice a year.

^(^) Short clip from a podcast

Native GLP-1 has a half-life of about two minutes.

The GLP-1 our bodies make has a half-life of about two minutes. It's gone almost immediately. The first GLP-1 drug didn't come from tweaking that, it came from a venomous lizard called the Gila monster. There's a peptide in its saliva, exendin-4, that does the same job ours does but lasts far longer. The lizard eats only a few times a year and its body is built for that.

Dr. Lorenzo Leggio (NIH) walks through how someone looking at a desert lizard for no commercial reason ended up seeding this entire class of drugs.

youtube.com
u/wizbanger — 4 days ago
▲ 400 r/Ozempic+1 crossposts

The drug behind semaglutide, tirzepatide, and retatrutide exists because of a venomous lizard that eats twice a year.

Short clip from a podcast about how we ended up with drugs like Ozempic!

u/wizbanger — 4 days ago

Hoffa’s Fat Pad Support Needed

I’ve got a friend (20s F) who has been completely debilitated by Hoffa’s Fat Pad. Physically, the injury itself has been classified as mild, but there’s a real disconnect between the pain my friend is experiencing and what’s actually physically wrong.

It’s taken a serious toll beyond the knee. My friend has become isolated, avoidant about addressing the injury, and shut off from being helped. They’re in a dark place with it.

I’m hoping someone who has come through this — who knows both the physical recovery and what it does to your head — might be able to connect with my friend in a way that actually lands. If that’s you and you’d be open to talking with them, please DM me and I’ll share more about the situation.

reddit.com
u/wizbanger — 7 days ago

Does your brain produce its own GLP-1?

GLP-1 gets discussed almost entirely as a peripheral satiety signal — released from intestinal L-cells postprandially, acting on the appetite circuit. That’s the Ozempic/Mounjaro story.

But there’s a separate pool. Neurons in the nucleus tractus solitarius synthesize GLP-1 within the CNS, projecting to regions including the hypothalamus and mesolimbic reward areas.

What was this endogenous central system doing before we started flooding it pharmacologically?

That’s where the addiction angle perhaps gets more interesting. GLP-1 receptor activity in reward circuitry is an active research area for alcohol and other substance use disorders, and the agonists everyone’s prescribing for weight loss are crossing into that territory whether or not that’s the intended target.

I talked through this with Dr. Lorenzo Leggio (Clinical Director, NIDA), who works directly on GLP-1 and addiction. Full conversation is Episode 17 of the Might Ramble Podcast if you want the depth — but mostly curious what this sub thinks about the central-vs-peripheral contribution to the behavioral effects.

u/wizbanger — 11 days ago
▲ 145 r/BPD+1 crossposts

"Certainty is not your friend." A BPD researcher's tool for catching yourself mid-split

"Certainty is not your friend." A BPD researcher's tool for catching yourself mid-split

If you have BPD, you might know this feeling: in the moment, you are completely sure. Sure they're leaving. Sure they're angry. Sure you've ruined everything. Not a guess, a fact. And later, when things settle, the certainty quietly doesn't match what actually happened.

In my conversation with Dr. Carla Sharp, one of the leading personality researchers in the world, she gave that feeling a name: psychic equivalence. It's when whatever is in your mind feels identical to reality and there is no gap between "I feel it" and "it's true."

She doesn't treat it as something broken in you. She points out it's actually a normal early stage of development, using the example of s her toddler in an Elsa costume who doesn't feel like Elsa, she is Elsa. Psychic equivalence is that, switched on by strong emotion. It's human. It just runs hot in BPD.

And then she gives an actual tool. Maybe the most useful thing I've heard said about managing a split?

The intensity of the certainty is the warning sign. If you feel certain at a 10 out of 10, that's exactly the moment to suspect you're in psychic equivalence. She suggests stepping out of the situation, calming down, and bringing the certainty down from a 10 to a 6. Once the intensity of the certainty has dropped, go back and ask for clarification instead of acting on the story in your head.

Distrust the certainty. Get curious instead of sure. Ask before you act.

Maybe it won't feel natural at first. But it's a skill, which means it's trainable, and that's a hopeful thing.

u/wizbanger — 13 days ago
▲ 292 r/personalitydisorders+3 crossposts

Why They're 100% Certain You're the Villain: A BPD Researcher Explains "Splitting"

If you've loved someone with BPD, you know the moment: you go from being the most important person in their world to the worst person alive, and they are completely certain about it. No doubt. No memory of the version where you were perfect.

In my conversation with Dr. Carla Sharp, one of the leading personality researchers in the world, she put a name to what's happening: psychic equivalence. In that state, whatever is in the mind feels indistinguishable from reality. She compares it to a small child in an Elsa costume who doesn't feel like Elsa. She is Elsa. During a split, the all-bad version of you isn't a manipulation tactic. In that moment, to them, it is simply true. They cannot see another perspective.

It doesn't excuse the harm. It won't make you less hurt by it. But it explains why arguing never worked. You were trying to reason with someone whose certainty was running at 10 out of 10, and certainty at that level isn't open to evidence.

The part I found most useful, and that I think helps anyone who's been on the receiving end: Sharp's antidote is to distrust certainty itself. When the feeling is absolute, that's exactly the moment to step back, lower it from a 10 to a 6, and ask for clarification instead of acting on the story in your head. That's advice for the person with BPD. But it's also a quiet gift for the rest of us, because the same trap catches everyone: the more certain we feel about what someone really meant, the less we actually know.

Understanding this doesn't mean staying or that what occurred was okay. It just gives you something most of us never got — an explanation for the thing that made no sense.

Full conversation at the links below. Hope this is helpful!

Spotify: https://open.spotify.com/episode/3xOpFFzjXBBTU0zPn7hqtJ

YouTube: https://youtu.be/xADsXc_YCO8

Apple Podcasts: https://podcasts.apple.com/us/podcast/might-ramble-podcast/id1840386628

Substack: https://mitchellpenningroth.substack.com/p/21-dr-carla-sharp-borderline-personality

u/wizbanger — 1 day ago
▲ 11 r/GLP1microdosing+3 crossposts

GLP-1s Help With Addiction Podcast with Dr. Lorenzo Leggio

Dr. Lorenzo Leggio (MD, PhD) is among the most prominent addiction medicine researchers in the United States.

His current roles at the National Institutes of Health: Clinical Director and Deputy Scientific Director of NIDA’s Intramural Research Program; Chief of the joint NIDA/NIAAA Clinical Psychoneuroendocrinology and Neuropsychopharmacology Section (which he founded in 2012); Chief of the NIDA Translational Addiction Medicine Branch (founded 2020). He holds adjunct professorships at Brown University, Johns Hopkins, and Georgetown.

His research sits at the intersection of addiction neuroscience, endocrinology, and the gut-liver-brain axis. His lab’s work on GLP-1 receptor agonists — the drug class that includes semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro, Zepbound) — as potential treatments for alcohol and substance use disorders is one of the most scientifically and culturally relevant areas in addiction medicine right now. It bridges the Ozempic story with addiction treatment in a way that has genuinely caught the public’s attention, and mine — I’ve been following this space for several years.

Dr. Leggio trained in internal medicine in Rome, completed his postdoc at Brown University’s Center for Alcohol and Addiction Studies, transitioned into a faculty role at Brown, and was then recruited to the NIH, where he has primarily worked since.

A special thanks to Max Dennis for helping coordinate this episode and for lending a hand setting up when I arrived.

Concepts Referenced in This Episode

GLP-1 (Glucagon-like peptide-1) — A hormone produced in the gut and certain brainstem neurons that regulates appetite, blood sugar, and insulin secretion. The basis for the current generation of obesity and diabetes drugs, and the central molecule in Dr. Leggio’s addiction research.

GIP (Glucose-dependent insulinotropic polypeptide) — A related gut hormone and the other major incretin. Tirzepatide (Mounjaro, Zepbound) targets both GLP-1 and GIP receptors simultaneously.
Incretin — The class of gut-derived hormones, including GLP-1 and GIP, that stimulate insulin release in response to food. The incretin concept is the pharmacological foundation that all of these drugs are built on.

Nucleus tractus solitarius (NTS) — A brainstem region that serves as a primary relay station for signals from the gut, cardiovascular system, and lungs. GLP-1 is produced by neurons here, and it plays a key role in how these drugs affect the brain.
Blood-brain barrier — The selective barrier separating the brain’s circulation from the rest of the body. Relevant here because one of the open questions in GLP-1 research is exactly how and where these drugs act on the brain, and whether they cross this barrier directly or work through other pathways.

GCG gene — The gene encoding proglucagon, the precursor protein that gets cleaved into GLP-1, GLP-2, glucagon, and related peptides depending on which tissue is doing the processing.

Gila monster / exenatide — The origin story of the first GLP-1 drug. In the early 1990s, researchers discovered that the Gila monster’s saliva contained a peptide (exendin-4) structurally similar to human GLP-1 but far more stable. That peptide became exenatide (Byetta), the first FDA-approved GLP-1 receptor agonist, approved in 2005.
Liraglutide — A second-generation GLP-1 receptor agonist (brand names Victoza and Saxenda) developed by Novo Nordisk. Once-daily injection; a major step forward from exenatide in terms of clinical manageability and efficacy.

Ghrelin — A gut hormone often called the “hunger hormone.” Dr. Leggio’s lab has also studied ghrelin as a potential target in alcohol use disorder, making it part of the broader gut-brain axis story.

Spotify: https://open.spotify.com/episode/7yv4i0bul5a3rtY5UR8VWQ (audio / video)

Substack: https://mitchellpenningroth.substack.com/p/17-dr-lorenzo-leggio-glp-1s-and-addiction (audio / video)

Apple Podcasts: https://podcasts.apple.com/us/podcast/might-ramble-podcast/id1840386628 (audio)

Youtube: https://youtu.be/qj8fEoALsXM (audio/video)

Story behind the episode: https://mitchellpenningroth.substack.com/p/behind-the-episodemight-ramble-podcast

u/wizbanger — 16 days ago

Podcast about Schizophrenia with Dr. Aislinn Williams

Aislinn Williams, MD, PhD is an Associate Professor of Psychiatry at the University of Iowa and Associate Director for Research at the Iowa Neuroscience Institute. Her lab uses transgenic mouse models and patient-derived induced pluripotent stem cells (iPSCs) to study how psychiatric risk genes (particularly voltage-gated calcium and sodium channels) alter neurodevelopment and behavior, with relevance to bipolar disorder, schizophrenia, depression, and autism. She is a board-certified psychiatrist who sees patients in the inpatient hospital and supervises residents in psychotherapy. She earned her MD and PhD (Neuroscience) at the University of Iowa, and completed psychiatry residency at the University of Michigan.

Spotify: https://open.spotify.com/episode/47wTOOLJRCYhveTp2HBjUV

u/wizbanger — 17 days ago
▲ 7 r/BPD+1 crossposts

Podcast with Dr. Carla Sharp about BPD

Carla Sharp, PhD, is the John and Rebecca Moores Professor of Clinical Psychology and Associate Dean for Faculty and Research at the University of Houston, where she directs the ADAPT Center and the Developmental Psychopathology Lab. She holds adjunct appointments at University College London and the University of the Free State in South Africa, and completed her PhD at the University of Cambridge. She has published more than 300 peer-reviewed papers and eight books, serves as an associate editor of Personality Disorders: Theory, Research and Treatment, and is a member of the workgroup updating the American Psychiatric Association's practice guidelines for borderline personality disorder.
Dr. Carla Sharp has spent two decades proving two things the field resisted: that you can diagnose personality pathology in adolescents — as early as 12 or 13 — and that "borderline" may not be a separate box at all, but the clearest window we have into the core of personality dysfunction itself. We get into both, plus the question underneath all of it: what does it actually mean to have a coherent sense of who you are, and to make yourself understood by another person?

Spotify: https://open.spotify.com/episode/3xOpFFzjXBBTU0zPn7hqtJ

YouTube: https://youtu.be/xADsXc_YCO8

u/wizbanger — 17 days ago