The Experiment Begins: Why I’m Asking My Doctor for Selincro

Hi. I’m starting this journal because I’ve finally figured out the code to my own destruction, and I’m about to try to rewrite it.

I don’t fit the classic stereotype of an alcoholic. I don’t drink every day. I don’t hide bottles in the toilet tank. But I have analyzed my patterns, and I’ve realized that I have a very specific, likely genetic, neurobiological glitch.

I have decided to stop relying on willpower. Instead, I have booked an appointment with a doctor to request a specific prescription: Nalmefene (brand name Selincro).

Here is the analysis of why I believe this is the only logical solution for my specific brain chemistry.

A Broken Switch & The Glutamate Storm

To understand why I need this specific medication, you have to understand how my brain malfunctions. It comes down to two critical failures:

1. The “All-or-Nothing” Alcohol Priming Effect. 

For many people, a drink is just a drink. For me, it isn’t. The first drink reliably triggers a strong alcohol priming effect: once alcohol enters my system, my brain rapidly increases the motivational value of alcohol itself. Dopamine-driven “wanting” and opioid-mediated reward surge together, while the brain systems responsible for inhibition and long-term planning are temporarily weakened. The result isn’t poor judgment — it’s a predictable neurobiological shift.

In that state, stopping at one or two is no longer a realistic option. The goal of drinking changes almost immediately, from enjoyment to continuation. This isn’t about liking the taste; it’s about a switch being flipped where alcohol becomes the most salient reward available, and my capacity to disengage from it is sharply reduced.

This pattern most likely developed through a combination of biological vulnerability and learning. A family history of alcohol problems suggests inherited differences in dopamine and opioid signaling that make alcohol especially reinforcing. Repeated experiences where drinking led quickly to relief, stimulation, or escape likely strengthened this response over time. Together, these factors mean that my brain updates the value of alcohol very rapidly once drinking begins — faster and more forcefully than average.

Brain shifts from "enjoyment" to "continuation" before you even finish the glass

In other words, the loss of control doesn’t start after several drinks. It starts with the first one, when alcohol temporarily reprograms motivation in a way that makes moderation biologically unrealistic for me. I call it "The Broken Switch."

2. The Kindling Effect (The Aftermath). The drinking is bad, but what comes after is worse. I suffer from the "Kindling Effect." To understand why, you have to look at the two neurotransmitters two dominant opposing systems that largely regulate brain excitation: GABA and Glutamate.

• GABA is the brain's "brake pedal." It calms you down and lowers anxiety.

• Glutamate is the brain's "gas pedal." It is responsible for excitement, alertness, and anxiety.

The Control Loop Failure.  When I drink, alcohol as an external force increases GABA and suppresses glutamate, slowing the system and reducing anxiety.

The Overshoot (The Hunt for Balance). Here is where the disaster happens. When the alcohol wears off the next morning, that external force vanishes instantly. But my brain's controller is still calculating based on the previous error. It it has started to pump out maximum Glutamate and lowered GABA below the minimum. The system rockets past the setpoint into extreme anxiety and panic. The controller then tries to correct this new error, but it’s too aggressive. It becomes unstable. It’s "hunting" for the baseline—swinging between exhaustion and chemical terror—but it keeps missing the mark.

The "Glutamate Storm." Note how the red line (Excitatory Glutamate) spikes dangerously high once the alcohol leaves the system, while the black line (Calming GABA) crashes. This gap is the chemical cause of "The Fear" (hangxiety).

My brain isn't just "anxious"; it is a destabilized system oscillating wildly, trying to find equilibrium and failing. This one I call "Glutamate Storm" also known as "Hangxiety (Hangover Anxiety)."

Why Nalmefene (Selincro)?

I’ve tried "just stopping." I’ve tried promises. But you can’t promise your way out of a chemical reaction. I need a chemical intervention.

Based on my research into The Sinclair Method (TSM), Nalmefene is the missing key. Here is why this specific drug matches my specific profile:

• It targets the Opioid Receptors: Nalmefene is an opioid antagonist. It sits on the receptors in the brain that usually receive the "pleasure rush" from alcohol.

• It keeps the Frontal Lobe online: By blocking that massive opioid flood when I take the first drink, the medication should theoretically prevent the "shutdown" of my decision-making center. It turns a "runaway train" back into a choice.

• It facilitates "Pharmacological Extinction": The goal isn't just to stop drinking today (which usually leads to a relapse later). The goal is to teach my brain that alcohol does not equal reward. Over time—perhaps 6 months to a year—the brain stops craving the poison because the chemical reward is no longer there.

Next Steps

I have the appointment booked. I am going to present this analysis to my doctor not as a confession of guilt, but as a strategy for health.

This isn't a quick fix. It is a long-term process of rewiring my neural pathways. But for the first time, I feel like I have a weapon that actually works against the enemy in my head.

This blog is the log of that experiment. If you have the same "broken switch" I do, welcome. Let’s see if we can fix it. My doctor’s appointment is on January 7th. I’ll let you know if I have any updates.