Flashlight adrenal test and a glutathione connection

[Guest guest]

Hi, all.

Dr. L. , in his book " Adrenal Fatigue, the 21st Century

Stress Syndrome, " describes a flashlight test for adrenal fatigue on

pages 77-79, based on work published by Arroyo in 1924. By " adrenal

fatigue " Dr. is referring to a deficient secretion of

cortisol by the adrenal cortices.

In this test, a person goes into a darkened room and shines a

flashlight across one eye from the side of the head, while watching

the eyes in a mirror. The size of the pupils is observed while doing

this for two minutes. In a normal, healthy person, the irises of

both eyes will contract when the light is shined across one of the

eyes, so that the pupils become small in size, and they will remain

small for the entire two minutes. If a person with adrenal fatigue

runs this test, the pupils will become small at first, and then will

dilate before the two-minute period is over. After about 30 to 45

seconds, they will contract again.

No explanation was given by Dr. for the physiological basis

of this test. I have been puzzling over what goes on in this test,

and now I think I understand it, so I want to share this

hypothesis.

It is known that the dilation of the iris (mydriasis) involves a

part of the autonomic nervous system that uses norepinephine as a

neurotransmitter, acting on alpha-1 adrenocepters. The contraction

of the iris (miosis), on the other hand, makes use of acetylcholine

and its receptors (Ganong, W.F., Review of Medical Physiology, 21st.

edition, Lange, 2003, p.229).

In a person with adrenal fatigue, it appears to me that what is

going on in this test is that there is a tendency toward dilation of

the irises, which the effort to contract (in response to light

input) is not fully able to overcome, and this gives rise to the

oscillating behavior of the irises. I think that what is causing

this is an elevated level of systemic adrenaline (epinephrine), to

which the alpha-1 adrenoceptors are also sensitive. I suspect that

what is going on in a person with adrenal fatigue is that their

adrenal cortices (as part of the HPA or hypothalamus-pituitary-

adrenal axis) are not putting out enough cortisol, and that their

adrenal medullas (as part of the hypothalamus-sympathetic-adrenal

medulla system) are attempting to compensate by putting out excess

adrenaline. (Note that cortisol and adrenaline produce some of the

same effects in the body.) This stimulates the various

adrenoceptors in the body and produces a variety of effects, one

(which is produced by adrenaline but not cortisol) being difficulty

in contracting the irises of the eyes.

In a healthy, normal person, adrenaline is secreted mainly in highly

stressful, fight-or-flight situations. In such situations, the

function of adrenaline in dilating the irises is probably intended

to ensure maximum ability to see, even in low-light situations.

However, in a person with adrenal fatigue, this apparently goes on

more or less continuously, and probably causes the photosensitivity

and problems with headlights when driving at night that many PWCs

report.

This hypothesis still does not explain why the HPA axis is

dysfunctional in CFS, which is what usually produces the so-called

adrenal fatigue in CFS (Note that there is a paper in the literature

reporting shrinkage of adrenal glands in PWCs. This most likely

occurs because of lack of sufficient drive by ACTH secreted by the

pituitary. This in turn probably results from lack of sufficient

CRH from the hypothalamus, and it isn't yet understood why this

occurs in CFS.) However, this hypothesis does suggest that PWCs who

show up with adrenal fatigue on this test may be running more or

less continuously at higher than normal levels of adrenaline

secretion. The likely resulting formation of adrenochrome from

autoxidation of the excessive adrenaline can be expected to place a

demand on glutathione, which is needed for its Phase II

detoxification, and this may constitute one of the vicious circle

mechanisms tending to hold down glutathione in CFS. This in turn

emphasizes the need to decrease the level of stress in PWCs in order

to lower the secretion of adrenaline and thus relieve this vicious

circle.

It would be interesting to know if there is a positive correlation

between positive results on this flashlight test and elevation of

the metabolite of adrenaline (vanilmandelic acid) in the urinary

organic acids test. This hypothesis would suggest such a

correlation.

As always, comments are welcome.

Rich