I have attempted to explain the concepts of clinical ecology in terms of adaptation to environmental exposures—a framework borrowed from physiology. In biology, when an organism comes into contact with a new element in its environment, it often responds in three stages: first, there tends to be an immediate acute reaction; this may be followed by an adapted stage in which there is a suppression of reactive symptoms; and finally, the organism may become maladapted, and perhaps later, nonadapted to repeated exposures by again presenting immediate, acute symptom responses.
Since new patients usually first come to their physicians midway in this process, they tend to present quite a different clinical picture than observed in laboratory animals. Instead of the sequence noted above, patients are first seen by their physicians as their adaptation to that to which they are susceptible is petering out. To what and for how long they had been adapted to such a frequently repeated exposure, which had maintained a relatively stimulatory phase, remain unknowns. Indeed, such a substance often appears to agree with an adapting person very well. But sooner or later—largely depending on the degree of individual susceptibility—such a person slips into a withdrawal phase for longer and longer periods. In other words, he completes this transition (usually called the onset of the present illness) and is now maladapted (badly adapted).
Such a transition from an adapted and relatively symptom-free existence to chronic illness often involves many side trips, including various levels. The speed with which this transition takes place is also partially dependent on the patient’s awareness of his problem. If he remains totally unaware of the environmental cause(s) of his symptoms, the transition may take place fairly rapidly, If he is aware that eating in general, for instance, agrees with him, he may be able to slow the onset of maladaptation, although he may become progressively obese in the process. And finally, if the patient is aware of the particular food(s) related to his symptoms, he may be able to delay his ultimate downfall by a judicious intake of the particular culprit. Eventually, however, most patients lose their symptom-suppressed adaptation to such substances and wind up in a doctor’s waiting room. Unfortunately, there is another outcome which may occur at any stage of this adaptation process to food(s). Some patients, suspecting that all food and/or food additives and contaminants make them ill, simply stop eating. This may lead to a marked loss of weight and hazardous undernutrition.
For the reader interested in greater detail, adaptation is defined as the ability of an organism to be modified in its function by the impingement of its environment. In the specific and individualized sense employed here, adaptation is limited to observed clinical manifestations resulting from the impingement of given environmental exposures to which individuals are highly susceptible.2,3 Adolph also observed similar effects in animals.4
Environmental features contributing to specific adaptation are the following: a) Given exposures must be cumulative and preferably intermittent. Those substances, such as common foods, retained in the body temporarily are most effective in inducing and maintaining specific adaptation. b) Specific reexposures should be approximately the same size, and rate of absorption through a common portal of entry. c) Given environmental exposures may be harmless (foods) or alleged to be toxic in greater concentrations, although thought to be safe in the lesser amounts encountered (chemicals).
Bodily features contributing to specific adaptation include: ability of an individual to adapt; this probably depends on: a) inherited tendencies, b) adequacy of apparent physiologic mechanisms,5-8 and c) variations in the degree of specific susceptibility, inasmuch as a heightened susceptibility seems to enhance the impact of lesser dosage and accelerates the advancement of the adaptation process.
Because of these environmental and bodily (individual) variants, adaptation to given environmental exposures develops and advances more rapidly in some individuals than in others. For instance, one person may present only a few localized syndromes from only a few environmental exposures, whereas another person may manifest many apparently different physical and more advanced cerebral and behavioral syndromes from multiple exogenous exposures. More over, such lesser and advanced responses may alternate in a given person at different times.9 This alternation of what later were called allergies (rhinitis, asthma, eczema, and headache) with psychoses was apparently first pointed out in 1884 by George Savage, an English psychiatrist. In contrast to this highly individualized interpretation of adaptation to specific environmental exposures, traditionally physiological adaptation has been presented elsewhere in respect to its general features and common bodily mechanisms.5-7 Since a given individual is adapting not only to common foods and lesser chemical exposures, but also to many other environmental stimuli— such as infection, cold, heat, radiation, etc.—the ability to adapt or maladapt must also be considered in a broader context. For instance, it is known that virus infections frequently induce or precipitate maladapted allergic responses to other materials. The same relationship holds for systemic yeast infections,11 and sometimes other infectious processes. Adequate treatment of a concomitant infection in the management of allergies must always be considered. It is also well known that sudden exposure to cold in some persons may be generally deleterious. Although the relationship of these secondary factors in adaptation is important, a detailed discussion of them is beyond the scope of this popular presentation.
*7\110\2*
