Akathisia II – Deep Dive

[redsun]

@redsun


Sure, and perhaps that is the case with pure D2 antagonism, but in my situation there is clear dopaminergic decline, which cannot be explained by that mechanism alone. Also I think there needs to be reduced stimulation in the NAc from the mesolimbic pathway, otherwise, you would get normal arousal by the LC. That is kind of the problem, I never took d2 antagonists, and I have a permanent change (as opposed to a withdrawal period). It's clearly something both specific, and also fundamental. Heck, after a long day's work, I could eat some sugar and get a dramatic increase in akathisia, which to me, implies energy problems.

I recently discovered that if you block calcium influx into SN mitochondria, the SN is unable to maintain normal spiking, and degenerates into irregular patterns (due to energy depletion, from a lack of Ca2+ in the mito). If pushed enough, this turns into a complete block. In fact, some studies propose this as the mechanism of action of antipsychotics, basically, D2 antagonism -> overexcitation -> depleted energy -> low DA (in addition to their D everything blockade). They did say that this effect took a while to develop in rats, though.


I have eaten that amount through collaged for long stretches of time, noticing only mild improvement in gut symptoms. Occasionally I also did small bursts of ~3g for a week or so, and also noticed no improvement.


Well, I think it's mainly my malabsorption that is protecting me. Besides, I have read that zinc can upregulate NMDA in the prefrontal cortex, while downregulating NMDA in the hippocampus (or vice versa), meaning that it's not always clear-cut. In fact, I find that my rumination is almost at a zero when I take enough minerals, especially zinc and copper.

It is definitely partially energy related. But also be aware of the issue of overstimulation. Long day of work enhances norepinephrine activity even if the work is not physical. I don't know if you have seen this thread where it compared the effects of starch and sucrose feeding on norepinephrine levels. Sucrose increases noradrenaline the most.

Norepinephrine Is Not A Stress Hormone

Fromm @Kartoffel Consuming sugar rather than starch raises norepinephrine levels. Peat has spoken very "favorably" about norepinephrine as an important integrator of energy metabolism. Below are two responses I got from him regarding norepinephrine. It increases oxygen consumption and carbon...

raypeatforum.com

Also the B vitamins, though they are needed for energy metabolism also can be too stimulatory and promote blood sugar drops, which then cause spikes in noradrenaline. This is especially an issue at high doses. In my experience, B vitamins unless I take them once in a while at low doses always lead to anxiety, nervousness, restlessness and even physical sensations (heart racing, adrenaline reactions). I even notice this when I take it once in a while, it just amplifies the more I take them. So I don't know how they affect you but this is something keep in mind. Low dose Bs and infrequent supplementation may be less problematic.

The other issue is enhanced methylation from these vitamins. It may actually reduce tonic dopamine excessively by enhancing COMT. Though in the striatum, where the nucleus accumbens and VTA are, DAT transporter proteins are the primary way of regulating dopamine activity in the synapse while in the cortex, COMT is the major player. So it may not matter as much since the issue is in the striatum.

@redsun

I recently discovered that if you block calcium influx into SN mitochondria, the SN is unable to maintain normal spiking, and degenerates into irregular patterns (due to energy depletion, from a lack of Ca2+ in the mito). If pushed enough, this turns into a complete block. In fact, some studies propose this as the mechanism of action of antipsychotics, basically, D2 antagonism -> overexcitation -> depleted energy -> low DA (in addition to their D everything blockade). They did say that this effect took a while to develop in rats, though..

Perhaps the painkiller you took could have made you susceptible to something to this effect because of opioids being effective calcium channel blockers and your health already being in a bad spot for a while before this happened.

 

[gunther]

I haven't tried myself. Its not a dopamine agonist. Its a well known cAMP inducer which indirectly affects dopamine but also other processes in the body. I’m

Noted, thanks.