Dr. Jason Winkelmann

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Dr. Jason Winkelmann Let's learn about chronic pain I treat chronic pain completely naturally, without side effects, with a program that is 100% customized to YOU!

If operations, injections, and medications have not worked, or are not for you, click the link below to get out of pain and get your life back!

10/15/2026

Part 8: How chronic inflammation drives chronic pain

Normal thyroid labs and feeling completely run down can both be true at once, and the standard test is part of why it gets missed.

Your thyroid mostly produces T4, a storage form that does very little until tissue enzymes convert it into T3, the version that actually runs your cells. Chronic inflammation interferes with that conversion. Cytokines like IL-6, TNF-alpha, and IL-1 slow those enzymes down and activate a different one called D3, which reroutes T4 into reverse T3, an inactive form that does nothing useful. A standard screen usually only checks TSH, a brain hormone, not a thyroid hormone, so everything can read normal while your tissues are starved of active T3. Repair slows, muscles ache, and recovery drags.

S*x hormones take a similar hit. The same inflammatory cytokines switch on aromatase, which converts testosterone into estrogen, especially in fat and inflamed connective tissue, while also dampening the brain's signal to produce testosterone, a hormone with pain-dampening effects of its own.

Replacing a hormone helps when it's genuinely low, but if inflammation is the reason conversion is clamped down, replacing the end product without addressing that leaves the underlying loop still running. Upstream, selenium is a key nutrient for these conversion enzymes, alongside enough calories and protein, good sleep, and cooling inflammation itself.

Normal labs don't always mean normal function. Has that gap between "your labs are fine" and how you actually feel ever been dismissed by a provider?

10/14/2026

Part 7: How chronic inflammation drives chronic pain

High inflammation with normal, or even high, cortisol shouldn't be possible. Cortisol is supposed to shut inflammation down. Here's why it stops working.

Cortisol normally enters an immune cell, binds the glucocorticoid receptor, and carries it to the nucleus to tell NF-kB, the master inflammation switch, to stand down. But with prolonged chronic inflammation, the reverse starts happening. Cytokines like IL-1, IL-6, and TNF-alpha tag that receptor so it can't reach the nucleus, and raise a decoy receptor called GR-beta that soaks up cortisol and makes it useless. This is glucocorticoid resistance.

It compounds from there. Your brain's stress thermostat, the HPA axis, uses those same receptors to decide how much cortisol to make. If the receptors aren't responding, because cortisol got absorbed by the decoy, the brain thinks levels are too low and produces more. That extra cortisol converts stored glucose into active glucose, and without enough movement to use it, that glucose becomes inflammatory itself, feeding right back into your pain.

Steroid medications hit this same receptor harder, so if it's resistant, relief can be weaker or shorter, and higher doses carry real risk. That's not a reason to avoid them when needed. It's a reason to ask why the receptor isn't answering. Upstream, it's the unglamorous stuff: consistent sleep, steady blood sugar, and calming the signals jamming the receptor in the first place.

Has a doctor ever told you your cortisol or hormone labs looked "normal" even though you felt anything but?

10/13/2026

Part 6: How chronic inflammation drives chronic pain

Feeling flat and unmotivated but also wired and on edge, at the same time, sounds like a contradiction. It isn't. Both come from the same source.

Start with dopamine. Your brain builds it using an enzyme that needs a helper molecule called BH4. Chronic inflammation destroys BH4. Less BH4 means less dopamine, and dopamine isn't just about pleasure. It's part of motivation and part of your body's natural pain-dampening system, so when it drops, you get flatness and a lower pain threshold.

Now the wired half. Glutamate pushes pain signals up to your brain, and astrocytes are supposed to clean it up afterward. Inflammatory cytokines like TNF-alpha interfere with that cleanup. Quinolinic acid, the same byproduct from last video's serotonin pathway, blocks it further, opens the NMDA receptor, and triggers microglia to release even more glutamate. Everything gets through, the signals that matter and the ones that shouldn't.

Medications for dopamine or excitability, like gabapentin, work downstream. They can't rebuild BH4 and they can't stop glutamate production at the source. Upstream means lowering oxidative and inflammatory load. Vitamin C and folate help keep BH4 usable, and magnesium acts as a natural NMDA blocker. Supportive, not a cure, but that's how chronic conditions tend to work. Multiple small levers, not one fix.

Does that flat but wired feeling show up together for you during a flare, or do you notice one before the other?

10/12/2026

Part 5: How chronic inflammation drives chronic pain

Chronic pain and depression aren't just "connected because pain is depressing." There's a shared biological switch behind both.

Serotonin is built from the amino acid tryptophan, but tryptophan is a shared resource. Normally only a small slice of it goes toward serotonin. Most goes down a separate route called the kynurenine pathway. Chronic inflammation tips that balance further. Cytokines like interferon-gamma and TNF-alpha turn up an enzyme called IDO, which drags even more tryptophan onto the kynurenine pathway, leaving less for serotonin.

It doesn't stop there. In the brain, activated microglia push that pathway toward quinolinic acid, which switches on the NMDA receptor we've talked about in this series, the one that's supposed to filter out minor pain signals. In chronic pain, that receptor stays activated, letting everything through.

So one inflammatory switch does two things at once. It drains the serotonin your mood depends on, and it helps keep the exact receptor open that's amplifying your pain.

Antidepressants that preserve serotonin can genuinely help some people, and this isn't a reason to stop one that's working for you. But they don't add tryptophan back to the line, and they don't touch the switch. Upstream, that means gut inflammation, sleep, blood sugar, and stress. Exercise is worth noting too. Working muscle converts kynurenine into a form that can't even cross into the brain.

Have you noticed your mood and your pain flare together, even when nothing else in your life changed that week?

10/08/2026

Part 4: Why is chronic inflammation so bad for chronic pain?

Why would you feel shooting, burning, or zapping pain when nothing is even touching you?

The cell bodies of your pain nerves sit in small clusters next to the spinal cord called the dorsal root ganglia. Those clusters have unusually leaky blood vessels, so immune cells and inflammatory chemicals get right up against the nerve cells, the same chronic inflammation we've been tracing through this whole series. That lowers the threshold for these nerves to fire.

A nerve fires when sodium rushes in through specialized channels. Inflammation increases how many of these channels exist and makes them open more easily. How much does one channel matter? People born without working sodium channels feel no pain at all. People with an overactive version get attacks of burning pain, from a single channel type.

Chronic inflammation can also damage the myelin insulating these nerves, so they start firing spontaneously.

It's a doorbell with corroded wiring and a hypersensitive button. It rings with nobody at the door. You check, nobody's there, and you start doubting whether your pain is even real. But the doorbell is ringing.

Lidocaine blocks these same sodium channels, which is why it helps, but it doesn't ask why there are so many of them. So we look upstream instead: lowering inflammatory pressure on the nerve, keeping blood flow strong, keeping the surrounding tissue moving.
The pain is real because the signal is real. It's just being generated in the wrong place.

Have you ever had pain that came out of nowhere, with no clear trigger, and had a hard time explaining it to someone else?

10/07/2026

Part 3: Why chronic inflammation is so bad for chronic pain

Why would chronic pain spread and get louder when the original problem was small?

Your brain can't process every signal trying to reach it, like the feeling of clothing on skin. Your spinal cord decides what gets through, using an accelerator and a brake. The accelerator is glutamate. The brake is GABA and glycine.

Here's how the brake normally works. GABA opens a channel that lets chloride flood into the neuron, and that negative charge quiets it down. This only works because the neuron keeps its internal chloride low with a special pump called KCC2.

Add inflammation, and microglia (the immune cells of the spinal cord, the same kind of activation we saw with the inflammatory soup two videos back) release a signal called BDNF. BDNF interferes with that pump, chloride builds up inside the neuron, and when GABA opens the channel, the chloride doesn't rush in the way it should. Sometimes it even flows out. The brake pedal does almost nothing, or starts exciting the neuron instead of calming it.

At the same time, inflammatory cytokines like TNF-alpha and interleukin-1 beta make the accelerator (the NMDA receptor) more responsive, letting through signals that would normally get filtered out.

Medications like gabapentin can turn down the accelerator, but they don't touch the microglia driving it. So you look upstream: gut-derived inflammation, poor sleep, chronic stress.

This isn't weakness and it isn't anxiety. It's a spinal cord that inflammation has rewired.

Has your pain ever felt like it spread beyond the original area, or started responding to things that never used to bother you?

10/06/2026

Part 2: Why is chronic inflammation so bad for chronic pain?

Why would a shirt, a shower, or your own bedsheets suddenly hurt?

Your pain nerves have sensors on their endings, including one called TRPV1, the same sensor that responds to chili peppers. Normally it only fires around 109 degrees, hot enough to actually burn you. Good design.

Now bathe that nerve ending in what we call the inflammatory soup, the same demolition signals from last week's video. Prostaglandin E2, bradykinin, nerve growth factor, interleukin-1 beta, and more acidic tissue. Each one lands on its own receptor and triggers enzymes that chemically tag TRPV1. A tagged sensor fires at a lower temperature, low enough that normal body heat can set it off. Nerve growth factor goes further and tells the nerve to build more sensors and move them to the surface.

NSAIDs lower prostaglandins, and that's real, but prostaglandins are just one ingredient in a soup with a dozen other players. Bradykinin and nerve growth factor are still in the pot, still wreaking havoc.

So the question becomes what keeps making the soup in the first place. In chronic pain, that's usually not damaged tissue. It's diet, lifestyle, blood flow, and inflammation itself.
You are not oversensitive. Your receptors have been recalibrated to fire at the smallest stimulus.

Has there been a specific everyday touch, like clothing or bedsheets, that started bothering you once your pain became chronic?

10/05/2026

Part 1: Why is chronic inflammation so bad for chronic pain?

Your body doesn't end inflammation by running out of steam. It shuts it off on purpose, with its own dedicated process.

Think of the first responders as a demolition crew. Injury happens, they show up, tear out the damaged tissue. That's the swelling, heat, and pain, and it's completely appropriate. But a second crew has to be called in separately. Early on, immune cells produce prostaglandins and leukotrienes (demolition signals). Then they switch to a different family entirely: lipoxins, resolvins, protectins, and maresins, many built from the omega-3s in your diet. Their job is to stop inflammation and start repair.

Most anti-inflammatory drugs slow the demolition crew down. That can make you feel better, but feeling better and getting better aren't always the same thing. NSAIDs interfere with some of those resolution signals, which is part of why pain can drag on or bounce back.

The real question isn't whether you have inflammation. It's whether your body can call in the cleanup crew at all. Do you have the raw materials? Are you sleeping? Is your blood sugar stable? Is your gut still feeding the demolition crew?

Have you ever noticed your pain flares get worse after a stretch of bad sleep or a rough diet week, even with no new injury?

10/01/2026

Part 16: Chronic pain makes you less active. So why does it leave you stiffer instead of looser?

There are two types of muscles. Stability muscles, the deep ones you've probably never heard of, keep you upright with almost no conscious effort. Power muscles, like your biceps, handle the heavy lifting. Chronic pain tends to make people more sedentary, and sitting or lying down doesn't recruit those stability muscles the way standing and walking does. Over time your body deconditions them, since it won't waste energy on what it doesn't use. So when you do stand and walk, those stability muscles don't show up, and your power muscles step in to stabilize the joint instead by shortening. The longer this goes on, the shorter and more fatigued they become.

No amount of stretching, massage, or muscle relaxers fixes this, because if that power muscle stops stabilizing you, nothing will, and your brain won't allow that. The real fix is reactivating the stability muscles you didn't know existed, so your power muscles can finally rest.

Have you noticed stretching never actually resolves your stiffness for long?

09/30/2026

Part 15: You go to get up off the couch and there's already a knot in your stomach before you've taken a single step. That bracing isn't fear. It's a reflex.

Put your hand near a stove you've been burned on before and it pulls back before you've consciously registered the heat. Your nervous system has built that same reflex around movement in general now. Every time movement led to pain in the past, your brain logged it, and the part of your brain responsible for predicting threat doesn't wait for new data. It pattern matches against everything that's already happened and braces you preemptively, the same way your hand pulled back from a stove you weren't even touching.

Sometimes that bracing is protecting you from something real. But often the fear response is bigger than the actual threat. This isn't about pushing through or ignoring the dread. It's about slowly showing your nervous system that not every motion ends in a crash.

Do you ever feel your body brace or flinch before you've even started to move?

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