CONCERNING THE CAUSE OF GWI

On April 12, MAGNU96196 posted a statement saying “the cause of GWI is
the many internalized toxins that set off the immune cytokine process.” That
is, Gulf War Illnesses are the results of dysfunction of the human immune
system and the resulting inability to protect our bodies against poisons.
I believe MAGNU96196 is correct in this. That is, the multiple conditions
we know as Gulf War Illnesses are all diseases related to upsets in our
immune systems. In this, they are similar to health problems related to
exposure to Agent Orange in Viet Nam, as well as autoimmune diseases
occurring in the general population such as rheumatoid arthritis, juvenile
(type 1) diabetes, multiple sclerosis, systemic lupus, and probably ALS. All
of these are chronic diseases which are difficult to manage, and often
impossible to cure.
The question then becomes, what are the exposures that cause these
illnesses and how do they do so? The exposures appear to relate primarily to
chemicals introduced into our environment since World War II. These include
industrial solvents such as trichlorethylene, plasticizers such as PCBs
(polychlorinated biphenyls), organophosphate nerve gases such as Sarin and
DFP, insecticides ranging from DDT and other chlorinated materials to
organophosphates, carbamates, and pyrethroids, and chlorinated herbicides
such as 2,4-D and 2,4.5-T used in Agent Orange and also, mixed with
fertilizers in “weed and feed” lawn use combinations. In addition, exposures
to vaccines containing adjuvants such as squalene and to depleted uranium
which acts on the lymph system are also suspect and may produce similar
effects, apparently by overloading the ability of the immune system to defend
against them.
The next question is how do these exposures upset the immune system? The
answer is they poison the process of making and/or transporting the key
hormone involved in regulating the immune system. That hormone is retinoic
acid, also known as vitamin A hormone. Normal levels of this hormone are
required to manage activity in our immune system. Too high or too low levels
of retinoic acid can result in too high or too low levels of immune system
proteins and it is these effects that cause autoimmune diseases.
At the time of the first Gulf War, the importance of retinoic acid
hormone in controlling the immune system was just becoming understood.
Scientists measured susceptibility to acute effects of environmental poisons
only. Long term (chronic) effects were not studied in humans and not required
to be measured in relation to use of these chemicals. Long term effects were
best known in wildlife. Poisoning of reproduction in fish-eating birds such
as the American eagle was the prime example. Occasional cases of chronic
poisoning of humans were occurring in Viet Nam vets and in civilians exposed
to some of these chemicals, but these were not recognized as a major health
problem. It was the appearance of GWI in the mid 1990’s that forced the
realization of these chronic ailments as a serious health problem.
How do these chemicals cause these chronic ailments? Chlorinated
chemicals such as Agent Orange and PCBs poison a transport protein,
transferrin, which moves thyroid hormones and vitamin A from place to place i
n the human body. Most commercial chlorinated herbicides and insecticides
may do the same thing, but so far, their ability to do this has not been
tested. The organophosphate, carbamate, and pyrethroid insecticides
apparently poison the enzymes that activate vitamin A (retinol) and vitamin A
hormone from precursors stored in fat. Exposures to these chemicals, either
as nerve gas agents as at Kamisayah, or as clothing protectants against
insects, are a likely source of GWIs. Certainly, these exposures have p
oisoned farm workers, and also, individuals who use or reside in
farming communities where the chemicals are widely used. And as with the
chlorinated poisons, the effects of these chemicals on vitamin A have not
been measured.
These effects don't occur only in humans and wildlife. They also occur in
insects exposed to pesticides. This writer studied this problem in house
flies during a 45 year career as an entomologist and pesticide chemist. When
flies become resistant to insecticides, they did so because they had an
unusually high level of a hormone known as juvenile hormone (JH). JH is the
insect equivalent of retinoic acid in terms of regulating the immune system
which in turn regulates protein synthesis. When JH levels were high, the
insects had high levels of enzymes that degraded insecticides. These high
levels are what made them resistant.
JH in insects and retinoic acid (vitamin A hormone) in humans are very
similar in function. The high levels of JH caused resistance to insecticides
while low levels were associated with susceptibility. In humans, high levels
of retinoic acid are associated with tolerance to insecticides and other
poisons while low levels are associated with sensitivity. Most people have
high levels of retinoic acid while some, those with high photosensitivity
have lower levels and as a result are more sensitive to poisons and more
likely to have autoimmune diseases. In addition, individuals exposed to
poisons described above may also come down with autoimmune disease. Such
exposures are the likely cause of most Gulf War Illnesses.
Can these disease be treated? So far, the outlook is not good. Quite
possibly, eating diets rich in vitamin A and/or taking vitamin supplements at
the time of exposure may protect against chemical poisoning. Sad to say, once
poisoning has taken place and once illness has occurred, it may be too late
to effectively treat these illnesses.
Prevention is also a possibility. This may be achievable by reducing
exposures to chemicals which produce autoimmune disease. To do so would
require changes in uses of chemicals which produce these problems.

Frederick W. Plapp, Jr., Professor emeritus, Texas A&M University

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