Aging is characterized by a wide variety of defects, particularly in the cardiovascular and immune systems.
Cyclic AMP levels fall, especially in lymphocytes.
Delta-6-desaturase (D6D) levels have been found to fall rapidly in the testes and more slowly in the liver in aging rats. D6D is an
enzyme which converts cis-
linoleic acid to
gamma-linolenic acid (GLA). Other factors which inhibit D6D activity are diabetes, alcohol and radiation, all of which may be associated with accelerated aging. In meat eaters or omnivores which can acquire
arachidonic acid from food, the main consequences of D6D loss will be deficiencies of GLA, dihomogamma-
linolenic acid (DGLA) and
prostaglandin (PG) E1.
PGE1 activates T lymphocytes, inhibits smooth muscle proliferation and
thrombosis, is important in gonadal function and raises
cyclic AMP levels in many tissues. It is a good candidate for a key factor lost in aging. Moderate food restriction, the only manoeuvre which consistently slows aging in homoiotherms, raises D6D activity by 300%. Other factors important in regulating D6D and the conversion of GLA to
PGE1 are
zinc,
pyridoxine,
ascorbic acid, the pineal
hormone,
melatonin, and possibly
vitamin B3. GLA administration to humans has been found to lower blood pressure and
cholesterol, and to cause clinical improvement in patients with
Sjogren's syndrome, scleroderma and
alcoholism. These diseases are associated with some features of accelerated aging. The proposition that D6D loss is not only a marker of aging but a cause of some of its major manifestations is amenable to experimental test even in humans. The blocked
enzyme can be by-passed by giving GLA directly.