50 Hz, continuously (24 hr) or intermittently (6.5 hr/day for 7 days) (20). In both instances, an insulin
insufficiency was produced. Blood glucose was not affected by the continuous exposure but it was
increased by 37% following the intermittent exposure.
Summary
Adrenal corticoid production can be influenced by EMFs, and the dynamics of the effect depend
on many factors: field strength, frequency, duration of exposure, whether the exposure is continuous or
intermittent, the ratio of the exposure to the nonexposure period in intermittent exposures, and the
organism's predisposition. Since the adrenal-cortical response to EMFs is the same as that caused by
known stressor agents (2), it follows that EMFs can also be biological stressors. Other endocrine organs
that can be triggered by EMFs include the thyroid, pancreatic islets, and the adrenal medulla.
There are many important but unanswered questions. Where within the organism does the EMF-
tissue interaction occur? What is the level of the interaction-organ, cellular, or molecular? What is the
temporal sequence of events and the factors which influence it? Are the thyroid, adrenal, and pancreas
particularly sensitive to certain types of EMFs, or are the changes in these organs reflective of an EMF
interaction with more central structures-or both? Suppose, for example, that the thyroid is sensitive to a
particular EMF: an EMF-induced change in thyroxine production would alter pituitary production of
TSH, but measurements of thyroxine and TSH would not, in themselves, tell us either the location,
level, or sequence of the interaction. Indeed, given the pervasive changes that can be induced by EMFs
in the nervous system and the endocrine system-and in view of the intimate interconnection and
synchronization of the two-there is a serious question concerning whether it is methodologically
possible to demonstrate a specific causal sequence in many instances. The diversity of the reported
effects suggests that EMF-induced changes in the endocrine system are mediated by the CNS.
However, until now, most investigations have focused on the need to demonstrate an EMF impact on
the endocrine system, and thereby to lay the foundation for more in-depth studies. Only Udinstev has
even approached what might be called a systematic study of a particular EMF (200 gauss, 50 Hz).
When other EMFs are studied systematically, perhaps it will be possible to delineate the sites and the
level of the interaction (see chapter 9).
Most of the endocrine system effects seemed to be compensatory rather than pathological (see
table 6.2 for example). But even though the homeostatic mechanism generally brought the corticoid
level back to normal, it does not follow that the animal became physiologically equivalent to what it
would have been at that point in time if it had not been exposed to the EMF. Animals that have been
exposed to one stressor are known to have a diminished capacity to deal with a second simultaneous or
contemporary stressor. Thus, animals that have accommodated to an EMF would, in general, be more
susceptible to a second stress, compared to animals that experienced only the second stress.
There is, of course, a difference between the existence of an EMF-induced biological effect, and
its detection in a given experiment. In our study, for example, the lack of a consistent statistically
significant difference between the exposed and the sham-irradiated rats in each experiment sugggested
that uncontrolled variables were present in the study. Possibilities include zoonoses, and genetic
predispositions. This can cause individual animals, in an apparently homogeneous population, to react
in completely opposite ways to the same EMF. In such cases there is no average response of the group
to the EMF, despite the occurrence of individual responses. The most sensitive experimental paradigms
for EMF research, therefore, do not rely on the comparison of group averages for the assessment of an
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