The Stories We Tell About Dopamine and Norepinephrine | ADHD | Episode 29
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- čas přidán 18. 06. 2024
- Stimulants boost forebrain dopamine and norepinephrine, but the stories we tell about dopaminergic executive function circuits that "decrease the noise" and noradrenergic attentional circuits that "boost the signal" oversimplify what goes on in the brains of those with ADHD, and in the rest of humans.
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Thank you for the lucid explanation. The content around ADHD tends to be dominated by personal accounts or very simple educational content, so it's great to see something more in depth and clear.
Thanks for the feedback, and feel free to share this channel with others who might benefit.
Well written comment
Do you know why some people can eat more on stimulants? If you happen to see this question I want to add you really are much appreciated for your videos. You really help to parse out the differences in disorders and for an over thinker like me that’s very helpful. @@dr.johnkruse6708
Hey, so I have a theory for ADHD. I believe we might be over complicating things and looking over some things. I don’t belive ADHD is purely a deficiency in dopamine or norepinephrine. It’s all based on the individual. A person lacking dopamine can go two ways, either a lethargic, forgetful type that has low desires. And another path is one in which the person tries to self medicate by chasing dopamine. Those types of people can get relief by a stimulant.
Now for the other side some people have low dopamine regulation due to parts of their norepinephrine system not activating enough to regulate their baseline dopamine levels. The people have a very noisy brain, very impulsive, though they are impulsive for a different reason than someone lacking dopamine and trying to self medicate. These people are impulsive because their dopamine isn’t regulated and their desires have no limits. These types of people benifit greatly from drugs like strattera, and Guanfacine.
It’s also possible that a person is really deficient in both. They don’t regulate their baseline dopamine, and their baseline dopamine levels are low. in this case a stimulant works well.
Now it’s not all a box, because the dopamine and norepinephrine systems have different receptors and these receptors have jobs, and don’t do all the same things. So one drug that increases dopamine or norepinephrine in a certain part of the brain might not attack the part that a person is actually deficient in.
Last part I’m going to add is about the equalibrium between norepinephrine, more particularly the Alplha 2A part of the norepinephrine system and dopamine. When you have too much dopamine your desires are rampant, so your gonna be very lustful, bad with money (seek to spend it), impulsive in general. On the other side of the spectrum, a person will become unmotivated and too chilled, it might hinder the life progression of the individual long term due to lack of desires. So when treating adhd, no matter what the person is deficient in, the result needs to end in an equalibrium. Over regulating an impulsive person with Guanfacine or strattera isn’t good, the dose needs to be lowered to an equalibrium, or a small dose of a stimulant needs to be added and tittered to make sure the impulsive person is brought to 100%, not 80% and not 120%. The same goes for people with low dopamine baseline, adding too much will change them to become impulsive.
End note, I am no doctor, I’m just a young man who has a lot of theories and I was able to convince my doctor to get me on drugs I thought would work and I have gotten a lot of relief personally from my own theories.
I’m really interested to understand if there’s a relationship between norepinephrine stimulation and heightened anxiety and stress, and what role α-2-adrenergic agonist (clonidine, guanfacine) play in this situation. Is there ever a place for just stimulating dopamine in patients who have heightened anxiety and stress, whether the origins are neurochemical or caused by circumstances such as CPTSD, etc. It would be great if you could do a video on this topic!
Hey, this might just be me, but Guanfacine has actually helped me with my emotional ups and downs and helped with stress. I care less about bad things and feel less excited for good things. It does more than just that though, it also helped my working memory somehow. I ended up taking vyvanse along with Guanfacine and even though the dopamine I gained from vyvanse brought me back to being more impulsive. I still have the memory benifits from Guanfacine. I don’t know why or how. I initially thought that the memory benefits came from not having an overall stimulated mind and that benefit would be counteracted by vyvanse because it stimulates the dopamine. But nope, the memory benifits have not gone away. The way it works is kind of complicated.
Very helpful info, and coherent explanation/reasoning. Thanks for sharing. Found the strattera -> epinephrine mapping to be informative for me (I’d never looked up how it worked), but tried it and it didn’t work for me at all, suggesting that dopamine is at least part of the story for me
You make exiting video
Thanks
So glad i found you. Listened to 3 presentations on my walk today 😅you are soooo mellow n informative.
Loved atomoxetine worked great til it didn't. Got to 54mg...than added Methylphenidate 10 mg than @20mg also worked great; til it didn't. I think my issue is norepi ONLY.(I get no boost at all from exercise).
DA is suppose to convert to epi through a DBH enzyme.. why is that not happening? Do I have a snp on DBH ? Is there something that just increases NE only ?
TIA Cee
Even if we can find agents that only have direct effects on NE or on DA, the two systems interact and regulate each other in so many areas of the brain that I don't know of any current ways ot just impact one of these systems.
It seems that CBD smooths out the spikes in neurotransmitters activity thus regulating them. Have you combined CBD with those agents?
It has to be full spectrum I think though
Depending where in the brain, d2 d3 and d4 receptors the inhibitory type of receptor is either exitatory or inhibitory vs d1 and d5 are allways hyperexitatory or slighly exitatory again which system
Yes, those are some of the layers of complexity.
I’m starting vyvanse soon it seems like adhd medication helps balance out the levels but how does the medication know to make dopamine and the other one both balance at 50% and not one being at like 80% and one at 30%
Do you have fybromyalgia symptoms or CFS with your adhd
Speak up bro