Acetylcholine ("Vagus Substance") Helps Dopamine Transmission, but Adrenaline (Stress) Inhibits Acetylcholine

Another Way by Which Stress Results in "Low Dopamine"

We have said before that considering imbalances of a single neurotransmitter in isolation, e.g. low dopamine, is overly simplistic and unlikely to yield results, because, in reality, all the different neurotransmitters work together, interact and interplay.

A case in point recently came up when a therapist asked me what is the main neurotransmitter associated with the all important vagus nerve. Recall, the vagus nerve, together with a few of the other parasympathetic cranial nerves, is responsible for anti-inflammation and detoxification of the body. Answering this question led me down a path to discovering some important and very interesting nuggets of knowledge, which, when connected, have a profound implication.

My answer was “acetylcholine”, originally called “Vagus Substance” in German, the first neurotransmitter which was ever discovered. Acetylcholine is the main neurotransmitter for voluntary, fluid movement, as well as some cognitive functions. It is also the main neurotransmitter released when we activate the so called ventral vagus complex of parasympathetic cranial nerves, such as when we engaged in positive social engagement. It is acetylcholine cell receptors that nicotine stimulates.

Indeed:

“acetylcholine is the chemical messenger that allows your body to calm down after a surge of adrenaline occurs — only then can you get in a relaxed state…”

This led me to wonder if the opposite was also true, whether stress, and hence adrenaline release, inhibits or depletes acetylcholine. A quick search found this was the case. So when we are chronically stressed, and producing adrenaline all the time, this infers that acetylcholine levels will be more or less permanently lowered.

It is no wonder the symptoms of low acetylcholine overlap so strongly with those of chronic stress:

• brain fog;

• poor short term memory;

• fatigue and chronic fatigue;

• constipation, gastric issues;

• dry eyes and vision problems;

• hypertension and blood pressure issues;

• emotional instability;

• chronic inflammation.

This then led me, and also my colleague

Lilian Sjøberg

, to wonder, especially based on some personal experiences I have had with Parkinson’s drugs, about the interplay between acetylcholine and dopamine. Again after a quick search, we found that acetylcholine increases the transmissions of dopamine from the parts of the brain which are supposed to be dopamine deficient in conditions like Parkinson’s, implying, conversely, that low acetylcholine means less dopamine activity in the brain.

Putting these two pieces of information together, we see that stress, and hence adrenaline production, has a double whammy effect on dopamine levels. Not only does adrenaline deplete dopamine directly [because adrenaline is actually made from dopamine, and competes with dopamine production for the very same precusor chemicals (phenylanaline, l-tyrosine, l-dopa), gobbling them up so they are not available for dopamine],

Supplementing Dopamine or Feeding Adrenaline?

but also, since adrenaline inhibits acetylcholine, which in turn down-regulates dopamine transmission, stress also lowers dopamine levels indirectly by this route.

To my mind, this once again iterates that many (most?) “dopamine deficient” conditions are really chronic stress conditions. It once again highlights the role of too much adrenaline in these conditions, the vital need for stress reduction, and increasing stress resilience, and for becoming a calmer more relaxed person, in order to reduce symptoms and lower drug burdens.

This also highlight the role of vagus nerve stimulating activities in “low dopamine” conditions. For folks who want specific suggestions and ways to do this, I have developed a pragmatic online course, which now also includes a substantial module on dopamine: