Human gut bacterial enzyme ingests L-dopa and converts it to dopamine | Hacker News Reader

Human gut bacterial enzyme ingests L-dopa and converts it to dopamine

elifesciences.org

48 pointsbookofjoe21 comments

Interesting.

L-dopa appears to have L-Tyrosene as a precursor, which can be found in Casein (present in cheese) or synthesized from Phenylalanine (a metabolic byproduct of Aspartame).

https://en.wikipedia.org/wiki/L-DOPA

https://en.wikipedia.org/wiki/Tyrosine --casein in intro pgh

https://en.wikipedia.org/wiki/Tyrosine#Biosynthesis --phenylalanine

Edit: The phe->tyr connection in the context of a gut biome capable of converting l-dopa to dopamine is dubious, though, because I'd assume phe->tyr synthesis would likely not take place in the gut, rather beyond it, in mammals. So uh, maybe just cheese?

Anyway, I'm not an organic chemist. I can't even remotely pretend to be qualified to connect those dots. But if my anecdotal/personal experience says anything: breaking my aspartame habit has been an utter nightmare when I switched to keto, and I still love cheese. I drank well over two liters of diet coke a day for years, and I still go through cheese like air.

I invite corrections from the experts here. Dead certain I got something wrong. All I know is I have a hideous addiction to certain foods and anything minting dopamine in my gut would surely invite my curiosity.

Dopamine doesn’t cross the blood brain barrier— sorry to burst the bubble of a lot of the posts here. In fact, for the dopamine deficient disease, Parkinson’s, L-dopa is the treatment because it does cross and is the converted to dopamine after crossing.

This doesn't rule out the effect of dopamine on the rest of the nervous system, including the hundred million neurons wrapping the gut as well as the neurons modulating heart function.

The question is: what foods are rich in L-Dopa? Should we therefore avoid them, eat them in moderation, or bulk up on them?

You should do neither right now. Just focus on normal healthy eating habits.

That begs the question of course: What are normal healthy eating habits?

Our eating habits have been formed by mass marketing for many decades so I would not call them normal. Even the fresh fruit and vegetables I see in the supermarkets (Coles and Woolworths in Australia) do not look normal.

Greens - spinach, kale, swiss chard, beet greens, parsley, watercress, mustard, turnip, cress, dandelion

Seeds - sunflower, pumpkin, *

Seafood - Salmon, sardines, mussels

Reds - Tomato, red peppers

Insects - Crickets

Everyone can debate the merits of livestock, cereals, roots, legumes, extracted seed oils, saturated fat, cholesterol, refined sugar, top feeding fish, alliums, brassicaceae. But the other things listed above are about as universally and unequivocally considered healthy with the understanding of food we have, with regard to commonly available foods in a western diet.

* almond, peanut, walnut, pistachio, pecan, cashew, macadamia too if fodmap issues arent a concern. Same with alliums, brassicaceae, legumes.

Velvet and fava beans seem to be the ones mentioned most. I don't think going all in on an L-Dopa 'diet' would be a good idea unless you consult with your doctor first, as is standard. Either way, no point in rushing to eat more beans, just eat healthy.

We massively overestimate what a normal doctor knows.

Eat food. Not too much. Mostly plants.

I wonder how many drug studies we'll end up having to eventually re-do to account for metabolic interference by microbes.

Everyone without this microbe was non-responsive to Drug A. Everyone with this microbe had negative outcomes from Drug B.

Likely none.

The paper describes finding an enzyme that can cleave catecholamine precursors. OK? There's literally only one catecholamine precursor that's used medically, and that's L-DOPA.

We know Parkinson's medications work, and very effectively. L-DOPA is used effectively, despite being metabolized by gut flora.

I think many. Maybe not a negative effect but no effect.

Taking a pill is a somewhat poor way of getting substances into the body because it must go through the liver anyway. It does have the advantage of slowly leaking into the body though.

If you read into this subject to avoid processing by the liver or other problems like this you want an injection, sublingual administration or rectal administration or a patch/cream. For want of a better word "sensitive" parts of the body such as the scrotum are more permeable to patches/creams. You could probably get tipsy by dipping your balls in a drink similar to boofing.

Huh, that's interesting. I wonder what effect this has on the gut and what advantage this confers to the bacterium. AFAIK, dopamine doesn't cross the blood-brain barrier, so it can't (directly) have an effect on the brain's dopaminergic pathways, but who knows what it does to the gut, or follow-on effects on the brain.

Eli5?

The "feel good" chemical in your brain is put together from a building block version of it.

But sometimes it doesn't get that far, because special types of bugs in your gut get to the building block version first. They do the same thing your brain does to it, but it's unclear what the effects are, because it's happening in your gut before it gets to your brain.

This is a paper confirming and isolating one of those special types of bugs. The implications could be pretty big: Are these bugs affecting medications? Moods? Are they stealing our brain's supply of feel good chemical? Can we use their powers for good?

Major nitpick: Dopamine isn't the "feel good" chemical.

Endorphins are more accurately "feel good" chemicals.

Dopamine is involved in motivation through reward reinforcement, movement, and cognition in the human nervous system.

Another nitpick: L-DOPA isn't a building block of dopamine. It's dopamine with an extra molecule attached to it that makes it "inactive." This molecule gets snapped off by the AADC enzyme, which "activates" it. L-DOPA is the precursor to dopamine.

Third nitpick: We can understand how these gut flora affect ingestion of L-DOPA, and neurotransmitter precursors, by looking at how it's used in medical treatments. Most notably, Parkinson's patients. Suffice to say, it really makes no fucking difference, and orally-administered L-DOPA (with a dehydroxylaze inhibitor) is effective.

Whatever L-DOPA is stolen by gut-flora, can be augmented with a higher dosage. If for some strange reason, the converted L-DOPA -> Dopamine gets released into the digestive tract, and absorbed by the body, it's readily broken down in the blood. L-DOPA converts to dopamine in the blood-stream anyway, so it makes absolutely no difference.

I wanted this paper to be novel, but after reading it, it's not.

Gut flora have AADC-like enzymes, cool?

If we're nitpicking, endorphins act on opioid receptors of GABAergic neurons, inhibiting the release of GABA, which in turn disinhibits the release of dopamine in reward pathways.

That dopamine release is what is directly responsible for pleasure and euphoria associated with endorphin release.

That's more "Explain like I'm five years into my PhD"

So not Eli5

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