Macular Degeneration :: Pineal Gland theory & eye disease, sleep disorders

The pineal gland — which regulates the cycles of sleep and
waking — appears to have evolved as an indirect way to
improve vision, by keeping toxic compounds away from the
eye, according to a new theory by a researcher at the
National Institute of Child Health and Human Development at
the National Institutes of Health.

The theory has implications for understanding macular
degeneration, a condition causing vision loss in people age
60 and older.

The theory is described in the August “Journal of
Biological Rhythms” and represents the work of David Klein,
Ph.D., Chief of NICHD’s Section on Neuroendocrinology. Dr.
Klein studies melatonin, the pineal hormone that regulates
sleep and wake cycles.

Briefly, the theory holds that melatonin was at first a
kind of cellular garbage, a by-product created in cells of
the eye when normally toxic substances were rendered
harmless. Roughly 500 million years ago, however, the
ancestors of today’s animals became dependent on melatonin
as a signal of darkness. As the need for greater
quantities of melatonin grew, the pineal gland developed as
a structure separate from the eyes, to keep the toxic
substances needed to make melatonin away from sensitive eye

For sight to be possible, Dr. Klein explained, a form of
vitamin A (also called retinaldehyde) must chemically
attach itself to rhodopsin, a protein found in the light
detecting cells of the retina (the photoreceptors). When
struck by light, the retinaldehyde-rhodopsin combination
undergoes physical changes that begin a series of chemical
reactions. These reactions ultimately generate an
electrical signal that travels into the brain, making
vision possible.

This is a one-time event for each retinal-rhodopsin
combination. In the process, light also renders the
retinaldehyde inactive and frees it from rhodopsin. The
free, inactive retinaldehyde is then recycled within the
retina to an active form, so that it can again participate
in light detection.

Roughly 500 million years ago, animals acquired the ability
to make an enzyme known as arylalkylamine N-
acetyltransferase (AANAT). Earlier this year, Dr. Klein
and his colleagues presented evidence that animal cells may
have acquired this ability by incorporating bacterial DNA
into their own DNA.

AANAT chemically alters arylalkylamines to prevent them
from combining with retinaldehyde. AANAT alters serotonin
by changing it to a compound known as N-acetylserotonin.
However, N-acetylserotonin is still toxic to the cells of
the retina, although less so than is serotonin. A second
enzyme, hydroxyindole-O-methyltransferase (HIOMT) further
changed N-acetylserotonin, converting it into melatonin,
which is relatively harmless to the eye. In the earlier
paper, Dr. Klein and his coworkers also provided evidence
that, like AANAT, HIOMT originated in bacteria. He
believes that these enzymes — both of which are essential
for melatonin synthesis — were acquired by the ancestral
eye to increase sensitivity to light. The enzymes
presumably were acquired before the evolution of the pineal

Dr. Klein points out that as humans and other primates
evolved, melatonin production was lost in the retina and
became restricted to the pineal gland. Although melatonin
is no longer manufactured in the primate retina, AANAT
still is. Dr. Klein suspects that the enzyme plays a role
in protecting the human retina. Arylalkylamines
(tryptamine, phenylethylamine, and tyramine) are likely to
be made in cells of the retina, and AANAT may function to
convert them to less harmful forms.

Accordingly, AANAT may play two roles — in the retina it
would have a detoxification role whereas in the pineal
gland it would have a role in melatonin synthesis It’s
possible, Dr. Klein said, that low levels of AANAT might
lead to the deterioration of the retina seen in macular
degeneration; and, perhaps it might be possible to prevent
this disease by increasing AANAT levels.

Leave a Comment