Malaria treatment with IPT
According to the World Health
Organization, one fifth of the world's humans are at risk of malaria
infection. Of these, 300 to 500 million people become ill with malaria
each year, five times as many as become ill with tuberculosis, HIV/AIDS,
measles, and leprosy combined. One to several million people die from
malaria each year, most of them children under five, and most in Africa.
I have only found two references to the use of IPT for treatment of malaria
by Dr. Perez Garcia 1. One is a newspaper article from the time period
"He stated his belief that still further recoveries from
malaria could be accomplished with the combined use of insulin and other
medicines.... Remarkable recoveries have been reported, according to Mexican
medical authorities, including malaria, typhoid fever, syphilis, peritonitis,
and rheumatic fever."
The other is the 1944 Time Magazine article:
"Doctors of the San Diego Naval Hospital went
over to Tijuana to hear Dr. Perez Garcia. They were impressed. They invited
him over to treat a few stubborn cases of malaria and rheumatic fever. A malaria
patient had no more fever after his first shock. (Dr. Garcia's full course of
treatment is usually four shocks, five days apart.)"
These are clues that IPT may be a
dramatically successful and rapid treatment for malaria, one of the major
diseases of the developing world. Millions of people have it, and efforts
to eradicate it have been frustrated. In light of this clue, and the
observed ways that IPT can work, I present the following ideas for
1. A major problem with malaria is that the parasite that
causes it keeps evolving resistance to anti-malarial drugs. Perhaps IPT
will increase the effectiveness of anti-malarial drugs at constant dose, and
allow effective treatment at smaller dose, as it does for antibiotics. And
perhaps it will allow much faster treatment. If so, this may give us a
little headway and breathing room in this race between our drug treatment and
the parasite's drug resistance. Perhaps an IPT strategy could be
devised to deliver larger concentrations of anti-malarial drugs into the
parasites themselves (which may have insulin-like receptors). If the
cellular pumps which eject anti-malarial drugs from the parasites can be blocked
or overwhelmed, then even old anti-malarial drugs like quinine or chloroquine
can be used again.
2. Perhaps it will be easier to ensure patient compliance with a
full course of treatment if that treatment is quick and decisive. (Patient
noncompliance, it is thought, is a major factor in survival and selection of
drug-resistant strains.) If IPT can treat malaria faster and more
effectively, if it can wipe out the parasite in the body completely, then it
will actually help us slow the evolution of drug resistance, by ensuring that
even resistant strains do not survive treatment.
3. In addition to killing the malaria parasite, IPT may aid in
treating many of the effects and complications of the disease.
I.e. restoring electrolyte balance, reducing fever, etc.
4. The most common complication and cause of death in malaria
patients is cerebral malaria, where the disease affects the central
nervous system (CNS). Side effects of large doses of malaria drugs may
actually help cause it or make it worse. If IPT can lower the necessary
dose, side effects could be reduced or eliminated. IPT may also be more
effective at delivering anti-malarial drugs to the CNS. Hypoglycemia
is a common complication of malaria, and care should be taken not to push
hypoglycemia too far with IPT.
5. A quick experiment could show if insulin followed by glucose
can increase uptake of chloroquine and other anti-malarial drugs into
erythrocytes (red blood cells) and hepatocytes (liver cells) within which
malaria organisms dwell. If so, then these drugs may be more effective,
using IPT, and it could represent a temporary reprieve from development of drug
These are just ideas that I place
before the experts on malaria. They will have a better idea of how to
approach this disease with IPT.
Today, June 1, 2000 I had a very
interesting meeting with Stanford molecular pharmacology professor emeritus Tag
Mansour. Among other things, he gave me more details about malaria
infection (apparently Plasmodium vivax, a less harmful species) being
given as a treatment for neurosyphilis patients. The way it worked was not
well understood. Perhaps immune stimulation. At any rate, it worked
well in most patients, except for a few of African descent. This is how
the resistance to malaria of people with sickle cell anemia was