From a neurotransmitter standpoint, there are several different types of anxiety. I wrote here about the high dopamine/low serotonin variety, largely characterized by obsession and overthinking. High levels of adrenaline (norepinephrine and epinephrine) fit here too, since too much dopamine will spill over into high levels of norepinephrine and epinephrine (its biochemical progeny). These are the people who are in constant “fight-or-flight” mode, and they usually have adrenal fatigue too, because they’re not able to counterbalance high adrenaline levels with cortisol to take them back down to baseline.
The low GABA variety is also addressed in this article, characterized by a more generalized, less clearly defined type of fear.
But what about adrenaline deficiency (norepinephrine and epinephrine)? Where does that type of anxiety fit in the continuum?
How Does Adrenaline Get Depleted?
I covered catecholamine (dopamine, norepinephrine, and epinephrine) depletion in more depth here. But as a quick overview: catecholamine depletion can occur due to low insulin or insulin resistance, lack of building blocks (amino acid precursors or vitamin and mineral deficiencies), too much manganese, 5HTP or melatonin supplementation, hypothyroidism, or (the big one): chronic stress. Again, think the other side of the adrenal fatigue coin.
Primary and Secondary Functions of Adrenaline
We typically think of neurotransmitters in terms of their primary functions. Dopamine is the neurotransmitter associated with focus and pleasure, so too much of it tends to mean obsession. WAY too much of it can mean schizophrenia. Too little tends to mean difficulty concentrating, as well as a particular type of depression: specifically lack of interest in life. (Again, dopamine spills over into its biochemical progeny, so this goes for the catecholamines in general.)
But, surprisingly, studies show that depletion of catecholamines also has another effect: anxiety. This effect is nearly as predominant as the depressive symptoms.
It’s not totally clear why this is, but it appears that catecholamine depletion reroutes cerebral blood flow, increasing it in the general region where the amygdala is located (the brain structure most associated with fear). It also alters glucose metabolism, increasing it in the part of the brain containing the nucleus accumbens (or the pleasure and reward center.) Areas of greater glucose uptake are the more active parts of the brain.
My guess is that this is a secondary (rebound) effect, since both of these brain structures are largely mediated by catecholamines—it’s as if the body is trying to compensate for their low levels with increased blood flow and metabolic activity. This study observes that in these areas, dopamine and norepinephrine actually modulate anxiety–so depletion can have a paradoxical effect.
PEA: An Upstream Regulation Attempt?
Along those lines: patients I have seen with low urinary catecholamines tend to also have high levels of phenylethylamide (PEA), a breakdown product of the amino acid phenylalanine.
(Quick biochemistry interlude here: phenylalanine turns into tyrosine, which becomes the rest of the catecholamines. But phenylalanine can also turn into PEA instead via a different pathway.)
PEA’s purpose seems to be to increase catecholamine release, inhibit calming GABA, and inhibit catecholamine reuptake. This will increase the levels of catecholamines over time, while taking the “brakes” off by blocking the effects of GABA.
My guess is, high PEA is less a cause of, and more of a response to, low catecholamine levels. It’s likely another compensatory mechanism: the body is doing everything it can to get back into balance.
It’s not always easy to tell what the neurotransmitter underpinnings are of anxiety just by symptoms alone. Urinary neurotransmitter testing can really help clarify the problem, and offer treatment direction.