Dr. Jason Winkelmann

09/15/2026

Part 6: Twenty minutes before your body feels like it belongs to you. Or feeling a storm coming before the news does. Both jokes point to a real chemical pattern.

Inflammatory molecules like the IL-1 beta we covered last week don't stay constant through the day. They run highest overnight and into early morning, right as your natural cortisol curve, which normally suppresses inflammation, hits its daily low. That combination of peak inflammation and minimal suppression is why mornings are the stiffest window, not because your joints seized up overnight. The weather piece works differently. Joint capsules hold fluid at a balanced pressure, but when barometric pressure drops before a storm, that balance shifts and the tissue expands, triggering pressure sensing receptors nearby. In a nervous system already sensitized the way we covered a few weeks back, that signal gets amplified into real pain.

Morning stiffness and weather sensitivity both get dismissed as things you just live with, but reducing baseline inflammatory load and improving cortisol rhythm are documented ways to actually shift them.

Does your body predict the weather before you check a forecast?

09/14/2026

Part 5: Nothing changed from yesterday to today. Same food, same sleep, same activity. And yet today is a bad day. There's rarely a clean trigger to point to, and that's not in your head.

Your immune system has a built in mechanism that produces exactly this pattern, no new injury required. It lives in a structure inside immune cells called the NLRP3 inflammasome, and it works like a two key system. The first key primes it: nutrition, hormones, mitochondrial dysfunction, gut health, autonomic nervous system dysfunction, the underlying contributors most people never hear about. The second key can be almost anything, one less hour of sleep, a blood sugar swing, a stressful interaction. Once both keys turn, the inflammasome floods your system with inflammatory molecules like IL-1 beta. That's a bad pain day at the chemical level.

Chasing the second key is the wrong move, since triggers are unavoidable in their entirety. The first key is where you have actual control, and stacking small changes there is what starts moving the needle.

Have you ever had a flare with zero identifiable trigger, and been asked what caused it anyway?

09/10/2026

Part 4: Random twitches with no cramp, no exertion, nothing that should have caused them. This closes the loop on everything we've covered this series
Everything so far has been about the sensory side of the nervous system, the pathways bringing information in. But there's also a motor side, the pathways telling your muscles what to do, and they run through many of the same sensitized circuits. When the motor cortex is working alongside a chronically sensitized sensory system, its own firing threshold drops too, making it more likely to trigger a muscle contraction spontaneously. That's the twitch: one sensitized nervous system, showing up on a different pathway.

These twitches often lead to neurological workups looking for a structural cause, which frequently come back clear, because the twitch isn't originating in the muscle. As overall sensitization comes down through the same nervous system regulation we've discussed all series, motor pathway excitability comes down with it, and the twitching typically eases on its own.

Have you had unexplained muscle twitches near the same area where your chronic pain lives?

09/09/2026

Part 3: Constantly checking in on every twinge isn't a personality flaw. It's the felt experience of the same nervous system changes we've covered the last two weeks.

The expanded receptive field and allodynia happen mostly below conscious awareness, in the spinal cord. But the spinal cord sends its amplified output up to the brain, specifically to the salience network, the system that decides what deserves your attention. When that network is fed a constant stream of amplified signals, it starts treating your body as an ongoing threat, which makes it harder to shift attention away from pain and toward anything else.

That scanning and hypervigilance is often labeled anxiety and treated on its own, but the brain is still receiving the same threatening input underneath. Calming the sensitized spinal cord signal at its source reduces the raw material the salience network has to work with, which is what actually quiets the checking behavior.

Have you ever been told your body scanning was "just anxiety," when it felt more like your brain reacting to real signals?

09/08/2026

Part 2: A shirt seam. A light touch. Something that used to register as nothing now genuinely hurts, and that's confusing to everyone around you.

This is the same sensitized alarm system from last week, but now we're looking at its volume dial. Touch and pain normally travel on separate nerve pathways that meet at a relay station in your spinal cord. When that relay station becomes sensitized, those channels start bleeding into each other, and touch signals start triggering the pain pathway instead. This is called allodynia, a real and measurable feature of central sensitization, not exaggeration or overreaction.

Because allodynia comes from the same sensitized source as last week's spreading pain, the fix is the same too: calm the amplification at the spinal cord rather than trying to desensitize every nerve ending on your skin. As that volume comes down, allodynia is often one of the first symptoms to visibly ease.

Have you ever had a normal touch, like clothing or a hug, genuinely hurt, and struggled to explain it to someone else?

09/07/2026

Part 1: Your pain spreading to new areas doesn't usually mean new damage. It means your nervous system changed how it processes pain.

When pain sticks around, the neurons in your spinal cord that process it become more sensitive, a process called central sensitization. Picture a smoke detector that used to go off only for real smoke, now triggering on shower steam. These sensitized neurons also start picking up signals from surrounding areas they used to ignore, a phenomenon called receptive field expansion. That's why a scan of the newest painful spot often comes back clean. The tissue isn't the problem. The alarm system monitoring it just got bigger.

Chasing each new site individually rarely works, because the real target is the sensitized nervous system driving all of them. Calming that system through reduced inflammatory load, better sleep, and nervous system regulation is what shrinks the territory back down.

Has your pain ever moved to a new area, only for imaging there to come back normal?

09/05/2026

https://www.mytruehealthcenters.com/post/can-emotions-really-cause-pain

Chronic pain flares aren't random. Learn the brainstem circuit, inflammatory cascade, and brain network changes that explain why emotion amplifies pain, and what you can actually do about it.

09/03/2026

Part 4: Pain that flares for no clear reason isn't dramatic or imagined. There are two real mechanisms behind it.

The first is neural. Your default mode network (self-focused thinking) and salience network (threat detection) become more strongly connected during pain in people who catastrophize. That means threat signals from your pain get woven directly into your ongoing internal narrative instead of staying a passing sensation. That's your brain rewiring, not a personality flaw.

The second is hormonal. Chronic stress makes glucocorticoid receptors less responsive, so cortisol keeps circulating without being able to shut inflammation down. The result is a pro-inflammatory state that rises and falls with your stress load, even when nothing physical has changed.

Standard treatment plans target the physical pain generator, the joint, the nerve, the tissue, but not network connectivity or receptor sensitivity. That's part of why two patients with the same diagnosis can have very different day to day experiences. CBT reduces cortisol output and shifts these patterns. Mindfulness and yoga measurably affect both the sympathetic response and HPA axis output.

09/02/2026

Part 3: A genuinely good day can take the edge off your pain, and it's not just distraction. It's physiology.

Positive emotion activates the ventral tegmental area, increasing dopamine, which feeds directly into the same PAG-RVM pathway from earlier in this series, this time pushing it in the pain-inhibitory direction. That triggers release of your body's own opioids, beta-endorphins and enkephalins, which bind to the same mu and delta receptors that prescription opioids target. Positive states also boost parasympathetic activity and lower the sympathetic stress response.

This isn't a claim that positive emotion replaces medication when it's clinically necessary. Prescription opioids flood these receptors directly and reliably, which matters for acute or severe pain, and positive emotion doesn't override every dimension of pain, including learned avoidance behaviors.

But meaningful connection, movement you enjoy, and structured mindfulness have been linked to increased natural opioid release in research settings. Authentic positive emotion is doing real neurochemical work on your behalf.