Part 5. Making a Laboratory of My Own Body

After taking medication for a long time, at some point this thought comes to mind.

Same medication — so why is today different?

Yesterday I moved well; today it’s late. Some days the same dose brings on dyskinesia; other days it doesn’t come up enough at all.

At first I thought all of this was just the disease’s unpredictability. But the longer I kept records, the more a different picture began to emerge.

The drug was the same, but the conditions were not.

Was I fasting or had I just eaten. Might some of the previous day’s dose still be in my system. How had I slept. Was I constipated. Did the next dose arrive while some effect from an earlier dose was still on board.

In the end, I couldn’t understand my body without looking at the drug, and I couldn’t understand the drug without looking at my body.

So at some point, my records stopped being a simple diary and became a small observational experiment.

Chapter 30. What I Mean by “Experiment” Here

First, I want to make one thing clear.

What I call an “experiment” is not recklessly changing medications, or telling other patients to try the same thing.

I have taken the same class of medication for a long time, and I have continued to observe how ON and OFF, dyskinesia, delayed ON, and incomplete ON appear in my own body. What I have tried to do is check, through records, the questions that arose along the way.

This article is not a treatment guideline. It is one patient’s record of placing the changes in his own body on a time axis and trying to interpret them.

I share the observation, but I do not recommend the experiment. I explain the process, but I do not offer a prescription. My experience is data — but it is not a treatment for anyone else.

Chapter 31. What Five Days Showed Me

Over the five days from August 29 to September 2, 2026, I recorded similar conditions again and again.

At first these could have been days that ended with nothing more than “the medication worked well today.” But once I wrote down the time, the dose, the first sign, and the time ON began, the days became comparable to one another.

The first thing that caught my attention was the morning.

When I took the extended-release formulation (Perkin CR 100 mg) around 6:00 AM, then took immediate-release 75 mg on an empty stomach around 7:20 AM, a similar pattern appeared on two occasions.

First sign between 8:00 and 8:20 AM. ON between 8:15 and 8:30 AM. Then a relatively stable stretch of about 5 hours. No clear dyskinesia in the record.

Two repetitions alone cannot be generalized. But at least in my own body, a similar pattern appeared twice — too similar to simply write off as coincidence.

This was the starting point of the record.

Chapter 32. The Same Drug Behaves Differently Starting From Empty Versus From a Body Already Risen

Watching how the extended-release drug responded, I learned one more thing.

Looking only at the dose itself is not enough. A state where some drug effect is already on board is different from a state close to complete OFF.

In my records, when I took Perkin CR 100 mg starting from nearly empty, the first sign took about 85 minutes, full ON needed about 215 minutes, and even that ON broke down in a little over 30 minutes.

By contrast, on evenings when some of the daytime dose’s effect was still on board and I used the same CR 100 mg, there were days when the effect held for close to 6 to 7 hours.

It was the same pill.

A drug’s effect is not decided by the properties of the pill alone. Where the body was before it received that pill decides it together.

I came to call this the “initial condition.” Even with the same input, a different starting point produces a different output curve. In Part 4, Chapter 24, I wrote that “medication carries over from the day before” — this is that idea showing up in numbers.

Chapter 33. Are HBS and CR Really Different?

My records also include values comparing Madopar HBS 100 mg and Perkin CR 100 mg.

Starting from empty, the first sign came at about 120 minutes for HBS and about 85 minutes for CR. The time to full ON, on the other hand, was recorded as about 180 minutes for HBS and about 215 minutes for CR. For both, when used alone, full ON was sustained for only about 30 minutes.

Interesting numbers. But look closely and something is off. The first sign came sooner with CR, yet full ON came sooner with HBS. That is a combination that would be hard to produce if the same drug had been measured under the same conditions.

The mismatch itself tells the answer. The conditions on the days I measured were not the same.

Meals. The previous day’s dose. Background medications. The depth of OFF. Sleep. The state of the gut. All of these were different.

So the most important thing these numbers taught me was not which drug is superior.

It was that comparing drugs requires matching the conditions.

Chapter 34. The Day Fasting and Post-Meal Were Different

On September 1, one distinctive event stood out.

The morning was relatively stable. But the response to the immediate-release 50 mg I took as a supplement after a hamburger meal in the afternoon was different. On an empty stomach, this dose usually gave a first sign within 15 minutes and a sufficient ON by 50 minutes. That day, it took about 105 minutes to reach a sufficient ON. The peak was pushed back, and dyskinesia continued for about 2 hours and 20 minutes.

In the moment, it’s easy to assume food was the cause. As I wrote in Part 2, Chapter 7, gastric emptying and amino acid competition can slow a drug’s effect, so this interpretation makes theoretical sense as well.

But that alone cannot fully explain it. The amount eaten. Fat. Protein. The rate of gastric emptying. Drug effect already accumulated in the body. The afternoon’s cumulative dose. Several variables were present at the same time.

So it is more accurate to leave it in my record like this:

Under post-meal conditions, the peak was delayed and dyskinesia lasted longer. The cause is not yet known.

That one sentence matters more than it seems. It leaves a distance between observation and interpretation.

Chapter 35. The Hypothesis of a Residual Ongentys Effect

On August 29, I considered the possibility that the effect of the Ongentys I took the night before had carried over into the morning.

That morning I had focal dyskinesia, and in the afternoon generalized dyskinesia appeared for more than 40 minutes. A few days later, on a day when I did not take Ongentys, dyskinesia of the same degree did not appear.

This is an interesting difference. Ongentys is a drug whose COMT-inhibiting effect lasts more than a day even though its plasma half-life is short, so the interpretation that the dose taken at night amplified the levodopa curve the next morning is pharmacologically plausible.

But there is more than one possible conclusion. It might have been a residual Ongentys effect. The afternoon’s cumulative dose might have been different. Absorption might have been different. My condition that day might have been different.

So this record is not a “conclusion” but a hypothesis. How good ON and dyskinesia each change when Ongentys is continued versus adjusted is a question I have left to look at together with my clinician.

Chapter 36. Two Evenings That Looked Similar but Were Not

Looking only at the log, the evenings of August 31 and September 1 looked similar.

I took the same Perkin CR 100 mg at the same time, the sign of the drug’s effect came at a similar time, and I was able to move to some degree until I fell asleep. By the log’s classification alone, both evenings were ON.

But the quality of the two evenings, as I experienced them in my body, was different.

On the first night I could walk, but my legs were stiff. I had to consciously direct myself, step by step. The next night, after I took immediate-release 50 mg when the effect dipped, walking became noticeably more natural. The first night felt like running on battery power, straining to hold on; the next night I could rest while using up less of my body’s reserves.

For a long time I lumped this difference together under the phrase “ON is a bit weak.” But placing the two evenings side by side, I saw that it was not a weak ON — it was a partial response. Some motor symptoms had improved, but the automaticity of walking had not returned. This was exactly the state I named incomplete ON in Part 2, Chapter 9.

It is possible that the small additional dose made a real difference. Because extended-release rises slowly and immediate-release absorbs quickly, the immediate-release 50 mg may have helped reach the needed level faster. But two days of observation alone cannot establish that the 50 mg was directly responsible. Meals, gastric emptying, sleep, activity level, residual effect from the prior dose, and the disease’s own natural variability could all have contributed as well.

So I write it this way:

Hypothesis: On a night when the evening CR 100 mg alone did not achieve sufficient functional recovery, the immediate-release 50 mg may have helped reach the needed level faster.

And one thing is not a hypothesis but an observation. The automaticity of walking and fatigue were important enough outcomes that the mere fact of being able to walk was not enough to call it a sufficient ON.

Chapter 37. A Fast Response from Severe OFF

On September 2, in a state of severe OFF, I recorded the response time to a 50 mg diffusible tablet in detail.

First sign at about 15 minutes after the dose. A stronger sign at 18 minutes. Output recovered around 32 minutes. Automatic walking around 42 minutes.

This was, without question, an impressive record. But the sample is one instance. Responding quickly once does not mean it always responds on the same timeline.

If anything, this single record raised the next question. Does the response time change if the depth of OFF changes? Is it the same after a meal? Is it the same on a night of poor sleep?

As these questions arise, the record leads into the next observation.

Chapter 38. The Idea of a Therapeutic Window

Keeping records for a long time, I came to feel in my body that there is a specific range between ON and OFF.

Too low, and movement is insufficient. Within the right range, automatic walking and flexibility of movement come back to life. But climb higher still, and dyskinesia may appear.

In Part 3, Chapter 13, I called this the therapeutic window. The five days of records showed just how narrow that range is in my body. My response was sensitive enough that even a small difference of about 25 to 50 mg of immediate-release medication could change my state.

That does not mean I can say “my therapeutic window is 25 to 50 mg.” Oral dose and brain dopamine concentration do not correspond one to one. Absorption rate, gastric emptying, food, concurrent medications, and the prior dose all change what the same dose does.

The more accurate statement is this:

Within the range of my current records, my response appeared sensitive enough that even a change on the order of 25 to 50 mg could change my state.

My app (the medication diary) has a feature that displays this range as a number called an “LED-equivalent level.” It is only an estimated unit calculated from dosing time and formulation characteristics — it is not an actual plasma concentration or a standardized clinical measurement. It is a personal model I built to explain my own body’s response.

The purpose of this model is not to decide whether to take more or less medication, but to understand why a very small difference can show up in the body as a large one.

Closing Part 5 — The End of the Experiment Was Not an Answer, but a Question

At first I wanted to find the right answer. Which drug, taken at what time, works best? Which combination lasts longest?

But the longer I kept recording, the less it settled into a single right answer. If anything, the questions grew more precise.

Is the drug coming up late? Is it not coming up enough? Is it climbing too high? Did it overlap with a dose already on board? Was it the meal? Was the depth of OFF different?

Here are the questions the five days left behind.

• Does the response to morning CR 100 mg alone repeatedly come late and last only briefly?
• Does the faster improvement after adding a morning immediate-release dose reproduce consistently?
• How much does the immediate-release response time differ before and after a meal?
• Does dyskinesia after the afternoon CR dose vary with the interval since the previous dose?
• Do evening CR alone and evening CR-plus-immediate-release combinations show a reproducible difference in the quality of walking?
• How do good ON and dyskinesia each change when Ongentys is continued versus adjusted?

Any actual change should be discussed with the treating neurology team and checked one variable at a time.

In the end, treating my own body like a laboratory was not about changing medications on my own. It was about observing the changes in my body more accurately.

This article is one patient’s personal record and interpretation, not medical advice or a prescription. Any change to the dose, timing, or combination of medications such as levodopa, Ongentys, dopamine agonists, or amantadine must be discussed with the treating medical team. Sudden worsening of gait, recurrent falls, severe dyskinesia, hallucinations or confusion, fainting, or severe low blood pressure require immediate evaluation by a medical professional.