The Endocrine and Metabolic Effects of Alcoholism

Alcohol
addiction is a major health and social problem in the United States.
Close to 18 million Americans are habitual drinkers. Medical
conditions, accidents, and loss of work account for $26 billion in
health core costs. The effect of alcohol on major organs is well
known. Practically, alcoholism damages all organs, the important ones
being the liver, gastrointestinal tract, central nervous system,
pancreas, and heart. However, the effect of alcohol on endocrine and
metabolic systems(1-2)is neither well described nor appreciated by the
general public.
The endocrine effects of alcohol are acute or chronic, and can be
contributed indirectly to be existing malnutritiontion and liver
disease. At the pituitary level, one of the actions of alcohol is to
decrease the release of vasopressin. Vasopressin is secreted from the
hypothalamus, is stored in the posterior pituitary, and it is the
hormone that controls urinary output. In chronic alcoholism, as a
result of a lack of vasopressin, there is a diuretic state leading to
further dehydration.(3-4)
Alcoholics(1)serum calcium and magnesium levels are low because of
malnutrition, malabsorption, diarrhea, and pancreatitis with increased
urinary loss. Serum albumin is also low; therefore, the total calcium
is falsely reduced further. Magnesium and calcium contribute to
alcoholic tetany and cardiac arrhythmia.(5-6)Alcohol can increase
serum triglycerides and VLDL associated with chronic fatty liver and
acute pancreatitis, can cause exacerbation of the primary liver and
acute pancreatitis, and can cause exacerbation of primary
hypertriglyceridemia and diabetic hypertriglyceridemia. There is also
a question of whether it will increase HDL.(7)
There is sodium retention in alcoholics because of increased
aldosterone and estrogen and abnormality of the prostaglandin and
kallikrein/kinin system. There is also a decrease in the naturetic
factor. The cortisol output from the adrenal cortex increases due to
dual action of alcohol on the hypothalamus and pituitary. At the level
of the hypothalamus, it causes an increase in CRF; at the level of the
pituitary, it causes an increase in CRF; and at the level of the
pituitary, it causes an increase in ACTH production.
As a result, pseudo-Cushing's syndrome is not uncommon in alcoholics.
The physical features are very similar to classical Cushing's
syndrome, and it is confirmed with excess corticosteroids both in
serum and urine. However, it suppresses normally on Dexamethasone, and
there is a spontaneous resolution with abstinence.(8)
Alcohol has many effects on carbohydrate metabolism, including glucose
intolerance, alcoholic hypoglycemia, alcoholic ketoacidosis, and
lactic acidosis. The mechanism of alcoholic hypoglycemia includes a
decrease in glycogen storage and decreased production of glucose of
decrease gluconeogenesis. One of the features of alcoholic
hypoglycemia is that it is prolonged and does not respond to glucagon
injections. Therefore, 50% or 10% Dextrose must be used to correct it
until the effect of the alcohol has passed.
Alcohol depresses LH and FSH secretion at the pituitary level, and
there is also a possibility that it might affect LH-RH releasing
hormone at the hypothalamus. The combination of this affects both
testicular and ovarian functions.(9)As a result, the serum
testosterone is decreased, not only because of a lack of gonadotropin
acting on the testes, but also there is an increased clearance of
testosterone and metabolites in the liver. Alcohol may also block LH
receptors at the testes.
Another factor in both decreased testosterone section and decreased
spermatogenesis is malnutrition, which lowers FSH and LH hormones. As
a result of decreased testosterone formation, there is a decreased
libido, gynecomastia, atrophied testes, and impotence. Therefore, the
myth of alcohol being an aphrodisiac is broken by actually causing
more permanent damage on the gonadal system. Not only is there a
decrease in testosterone level, but there is also an increased
estradiol-testosterone ratio, increased LH and FSH due to decreased
feedback and a decreased sperm count.
In women, alcohol can cause oligomenorrhea, amenorrhea, and decreased
fertility by acting directly on the ovaries or decreasing LH and FSH
to the pituitary. Also, malnutrition in alcoholics affects LH-RH
secretion in the hypothalamus, and LH-FSH section from the
pituitary.(10)
Some of the features of hypermetabolism are seen in alcoholics with
proptosis of both eyes, plethora, tachycardia, warm and sweaty palms,
and tremors. Thus, the question is, is there any thyroid dysfunction
in alcoholism? Indeed, serum T4 is decreased in cirrhosis with a
decrease in thyroid-binding globulin. However, there is an increase in
the reverse T3 level in liver decreases and acute illness as a
compensatory phenomenon. The firee T3 level actually may also
increase, explaining some of these hypermetabolic features of
alcoholism.(11)
In summary, alcohol, in both acute form and in chronic cirrhosis,
affects the endocrine and metabolic systems by acting directly or
through malnutrition, affecting hormone releasing secretions. We hope
that the above information will be understood and passed on to
patients by the physicians so that they will practice abstinence or
enter into a treatment program and not wait for end-stage liver
disease, pancreatitis, or GI bleeding.