Subject: Dopamine Precursors and Anhedonia: The Raw Materials Everyone’s Missing
From: Derek from Research Radar <[email-masked]>
To: [email-masked]
Date: Thu, 14 May 2026 16:08:59 +0000
List-Id: <derekpruski.substack.com>

View this post on the web at https://derekpruski.substack.com/p/dopamine-precursors-and-anhedonia

Why the flatness people are blaming on GLP-1s, BPC-157, and half the peptides on the market might have less to do with the compound and more to do with what’s on the plate.
Read this first: Everything below is for research and educational purposes only. Research-use only, not for human consumption. Nothing here is medical advice or a dosing recommendation. If you’re navigating this personally, that’s a conversation for a qualified clinician — not a Substack post.
What led me down this line of thinking
I’ve been thinking a lot about anhedonia lately. It’s the word that keeps showing up around GLP-1s, around BPC-157, around half the peptides people are scared of right now. Scroll through any forum and you’ll find someone convinced their compound flattened them out — that they used to feel things and now they don’t, and it’s the compound’s fault.
I’m not dismissing that. The pharmacology is real. GLP-1s genuinely turn down the dopamine signal in the reward circuit — that’s the part of the brain that says “this thing is worth wanting.” When that signal gets turned down, everything flattens. Food, music, social interaction, the lift that used to hit — all of it pings less hard. That’s anhedonia, and it’s been written up extensively.
But the more I sat with it, the more I started thinking there’s a bigger problem at play. Something that doesn’t get talked about almost at all. And the more I dug into the research, the more obvious it became.
The brain builds dopamine from raw materials that come almost exclusively from food. Specific amino acids. Specific cofactor nutrients. And when food intake drops by 30 to 50 percent — which is what these compounds reliably do — the raw materials drop with it.
So it’s not just the compound flattening people. It’s the compound PLUS a quiet nutritional shortage that nobody is tracking. The pharmacology suppresses the dopamine signal. The diet suppresses the dopamine supply. They stack on top of each other.
Today I’m going to walk through what’s actually happening in the brain when dopamine gets built, which raw materials matter most, which foods carry them at the highest density, and why this matters so much more than the fearmongering would suggest. The flatness gets a lot less mysterious when you understand the chemistry.
How the brain actually makes dopamine
Dopamine isn’t pulled from a reservoir. It’s built in real time, one step at a time, from food you ate. Here’s the chain:
L-phenylalanine (an amino acid you can only get from food) converts to L-tyrosine in the liver
L-tyrosine travels through the blood and crosses into the brain
An enzyme called tyrosine hydroxylase converts L-tyrosine into L-DOPA (this is the slowest, most important step — the bottleneck)
Another enzyme converts L-DOPA into dopamine
Dopamine gets packaged up so it’s ready to release when a neuron fires
Dopamine can also get converted into norepinephrine, the alertness chemical
Every step in that chain needs the previous step’s raw material to be there. There’s no buffer. No warehouse of pre-made dopamine sitting around waiting. Each neuron makes what it needs roughly when it needs it. If the tyrosine isn’t in the blood, the chain stops.
The bottleneck enzyme is the whole story
Tyrosine hydroxylase is the gatekeeper. And the research established something crucial about it decades ago: how much dopamine it produces depends directly on how much tyrosine is sitting in front of it.
This is unusual. Most enzymes in the body have way more raw material than they need, so their output stays steady — give them more material and nothing changes. Tyrosine hydroxylase doesn’t work that way. More tyrosine in the blood means more dopamine being made. Less tyrosine means less. Linear, real-time, no buffer.
This is why food intake matters so much for mood. It’s not loose correlation. It’s the actual biochemistry.
The transport competition problem
Tyrosine doesn’t have a private door into the brain. It uses a shared transporter — think of it like a single elevator — that also carries phenylalanine, tryptophan, and the three branched-chain amino acids (leucine, isoleucine, valine). They all compete for the same ride.
Translation: how much tyrosine actually reaches your brain doesn’t just depend on how much tyrosine you ate. It depends on the ratio of tyrosine to its competitors. If a meal is heavy in branched-chain amino acids and light in tyrosine, the tyrosine loses the elevator fight at the brain’s door — even if your total protein looks adequate on paper.
The practical implication: a diet built mostly on whey shakes or chicken breast (both high in branched-chain amino acids), while skipping tyrosine-dense foods like eggs, hard cheese, or fish, can end up with worse brain tyrosine availability than a diet with less total protein but better-balanced sources. It’s the ratio, not just the gram count.
Firing neurons burn through raw material faster
Here’s the part that ties directly to GLP-1 flatness. The substrate-sensitivity of tyrosine hydroxylase is most pronounced in neurons that are actively firing. A resting dopamine neuron uses raw material slowly. A neuron being asked to fire — to respond to a reward cue, to produce the burst of dopamine that registers as pleasure or motivation — burns through tyrosine fast.
On a GLP-1, the medication is dampening dopamine release. The brain is essentially trying to fire harder to produce the same downstream signal. That’s higher demand for raw material at the exact moment supply is collapsing because food intake is down.
You feel this as flatness. The reward circuit is functionally trying to do its job. The valve is being held partially closed by the medication. And the raw material the circuit needs to push against that valve isn’t there. The result is a system that fails to produce the dopamine signal that would otherwise register as pleasure, motivation, or anticipation.
This isn’t theoretical. Controlled human studies that strip phenylalanine and tyrosine from the diet for just 24 hours produce measurable drops in alertness and reward sensitivity. Animal studies of longer depletion show drops in brain dopamine in specific regions and behavior changes that look a lot like anhedonia. A GLP-1 protocol runs a softer version of the same depletion for months at a time, on top of the medication’s own suppression.
The flatness isn’t “in your head.” It’s in the raw materials.
Why GLP-1s make this worse than a regular diet
Three reasons the raw-material problem hits uniquely hard on these compounds:
Total intake collapses. Going from 2,800 calories a day to 1,400 roughly cuts tyrosine intake in half without even trying. Less food in means less of everything, including the specific amino acid the brain needs to make dopamine.
The dopamine system is already being held down by the medication. The brain is pushing against a partially closed valve, and not having the raw materials makes the push fail. It’s like trying to run an engine with both the air intake restricted and the fuel tank half empty.
The foods that survive an appetite cut are usually the wrong ones. Easy carbs and small portions of bland protein become the default. Eggs get skipped for texture. Red meat gets skipped because it sits too heavy. Organ meats vanish entirely. The most dopamine-dense foods on the planet are the first to leave the rotation.
The dopamine raw materials map
Ranked by tyrosine density per 100 g (USDA data). When stomach capacity is the limiter — and on any appetite-suppressing protocol, it is — what matters is how much raw material you can pack into each bite:
Dried egg whites — roughly 3.4 g tyrosine per 100 g. The highest concentrated source on the planet.
Soy protein isolate — around 3.2 g per 100 g. Easy to mix into anything.
Spirulina (dried) — about 2.6 g per 100 g. Useful in a smoothie when appetite is the limiter.
Parmesan and aged hard cheeses — about 2.3 g per 100 g. Those white crystals on aged Parmesan are literally crystallized tyrosine.
Defatted peanut flour — about 2.1 g per 100 g.
Pumpkin and sesame seeds — 1.0 to 1.5 g per 100 g. Bonus zinc and magnesium.
Lean beef, pork, chicken, turkey — 0.9 to 1.2 g per 100 g cooked. The everyday workhorses.
Salmon, tuna, cod — 0.8 to 1.1 g per 100 g. Tyrosine plus omega-3s plus choline.
Tofu, tempeh, edamame — 0.6 to 0.9 g per 100 g.
Almonds, peanuts — 0.5 to 1.0 g per 100 g.
Whole eggs — about 0.5 g per 100 g, mostly in the white.
For phenylalanine (the upstream amino acid that converts to tyrosine in the liver), the same ranking holds. The body uses them interchangeably to build dopamine, norepinephrine, and epinephrine — the whole “alertness and reward” family of brain chemicals.
The cofactors nobody talks about
Tyrosine alone won’t do it. The enzymes that convert tyrosine into dopamine are like factory machines — and they need specific helper nutrients (cofactors) to function. Anyone running a low-food-intake protocol is likely running short on several of these at the same time the tyrosine itself is going short:
Iron — needed by tyrosine hydroxylase, the bottleneck enzyme. Sources: red meat, liver, shellfish, spinach.
Vitamin B6 (P5P is the active form) — needed for the step that converts L-DOPA to dopamine. Sources: pistachios, salmon, chicken, chickpeas, potatoes, bananas.
Copper — needed to convert dopamine to norepinephrine (the alertness chemical). Sources: beef liver by a wide margin, oysters, shiitake mushrooms, cashews, sesame seeds.
Vitamin C — also needed for the dopamine-to-norepinephrine step. Sources: bell peppers, citrus, kiwi, strawberries, broccoli.
BH4 (a helper molecule the body builds itself) — built from folate, B12, and methyl donors. Sources for those building blocks: leafy greens, eggs, liver, clams, sardines, beef.
Beef liver is the single most concentrated source of multiple cofactors in one food. 3 oz covers iron, copper, B12, folate, and choline simultaneously. It’s also the food most likely to get left out of the rotation. Worth flagging.
The research framework
The published research on raw material adequacy converges on a few principles worth flagging:
Protein floor first. Targets in the literature for people on appetite-suppressing protocols converge on 0.7 to 1.0 grams of protein per pound of goal body weight. Drop below that floor and the body starts pulling amino acids out of muscle to keep critical functions running — which means circulating tyrosine drops even further. The floor is the foundation. Nothing else matters if it’s not there.
Density over volume. When stomach capacity is the rate-limiter, what matters is how much raw material packs into each bite. Egg whites, hard cheese, protein isolates, spirulina, salmon, sardines, Greek yogurt. The formats that survive small portions.
Spread it across meals. Roughly 25 to 40 grams of protein per meal keeps amino acid availability steady through the day, instead of one big spike and a long valley.
Cofactors come from the same foods. Eggs, liver, red meat, shellfish, leafy greens, and seeds cover most of the raw material AND cofactor map together. The system is designed to work as a package — eat the package.
The clean framing
The flatness people are blaming on these compounds isn’t depression, and it isn’t necessarily even the compound itself doing all the work. The medication suppresses dopamine release, sure. But the appetite suppression also quietly strips out the raw materials the brain needs to keep making dopamine in the first place. Both effects are real, both stack, and both are addressable.
The raw material side is the part that almost nobody is tracking. The research on what to do about it is unambiguous: enough protein, dense enough sources, with the cofactors that let the dopamine-building enzymes actually work.
Eat the package. The flatness gets a lot less mysterious — and a lot less flat — when the raw materials are actually there. And maybe, just maybe, the next time someone blames a peptide for their anhedonia, the first question is what they’re actually eating.
Research-use only. Not for human consumption. Work with a qualified clinician on anything you’re actually putting in your body.
— Derek

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