Somatic Biopathies Part II: The Diaphragmatic Segment
Charles Konia, M.D.
Reprinted from the Journal of Orgonomy, Vol. 24 No. 2
The American College of Orgonomy
Classical medicine does not comprehend the medical-historical back-ground of diseases of biopathic origin. Regarding peptic ulcer, for example, Reich wrote, "Obviously, the stomach ulcer with its chemico--physical functions is rooted in a more general functioning principle that is not of a chemico-physical nature" (1).
This wider realm of functioning involves the bioenergetic basis of both psychic and somatic functioning. The general biopathic condition of the organism, as well as the specific segment containing armor, are crucial aspects that have to be considered in the removal of any biopathic illness.
In this section, the question of biopathic differentiation, that is, why individuals with significant armor located in a particular segment develop different somatic biopathies, is investigated.
The choice of organ involvement is related, in part, to the history of armor development, that is, the time and extent of its formation. Obviously, the earlier the armor appears and the greater its severity, the more destructive will be its effects. Other factors include the impulse against which the armor is directed, as well as the defending impulse. In peptic ulcers, for example, there is a great deal of repressed hatred located in the diaphragmatic segment.
This article describes three patients with diaphragmatic armor in whom a somatic biopathy developed in different organs within this segment.
The diaphragmatic segment comprises the diaphragm and all the organs located immediately below it. Armor of this segment may be manifested by epigastric spasm, muscular tension, and tenderness, especially along the xyphoid process, the margin of the lower ribs dorsally to the lumbocostal arches, and a particular respiratory disturbance which consists of a ballooning of the abdomen on expiration indicating that the diaphragm is fixed in the descending position.
The status of armor of this segment may be difficult to evaluate in the earlier stages of therapy. It may have been for this reason that Reich used x-ray fluoroscopy of the diaphragm to determine the biophysical status of this segment. Only when armor in the first four segments is sufficiently eliminated does the true picture of this segment reveal itself. Diaphragmatic armor is characterized by the absence of spontaneous pulsation of this segment (2). With elimination of armor in the upper segments, emotional expression contained in this segment spontaneously surfaces.
Although every diabetic patient is armored in the diaphragmatic segment - most conspicuously manifested by a ring of fat around the waist - this is not a sufficient condition for the development of this biopathy. Many considerations, including the occurrence of insulin-resistant diabetes, suggest there are other bioenergetic factors at work which are necessary conditions in the pathogenesis of this biopathy. In his discussion of diabetes, Dew focuses on the disturbance in the ability of the various tissues of the body to maintain an adequate orgonotic charge (3). The importance of the orgonotic potential (the stronger orgonotic system attracting the weaker) in the process of absorption, assimilation, and digestion of food substances is clear.1 Each tissue, based on its level of orgonotic charge (orgonity) over and above that of the local environment, is capable of drawing off nutrients (chemically broken down food substances) from the bloodstream into the tissue cells. Since nerve tissue (central and peripheral nervous system and the autonomic nervous system) has the highest orgonity, its metabolic requirements are the highest. 2
Dew suggests that diabetes mellitus is a form of shrinking biopathy in which the tissues themselves undergo disintegration, that is, massive catabolism melting down into urine. 3 The common functioning principle in this biopathy seems to be low tissue charge (tissue anorgonia), and the pathogenesis is the inability of tissues of low orgonotic charge to draw nutrients from the blood plasma because of a weakening of the orgonotic potential.
The alterations in the basement membrane capillaries in muscles and the renal glomerulus, which occur long before the detection of abnormalities in carbohydrate metabolism, may be the pathological consequence to tissue anorgonia. In contrast to the cancer biopathy, the charge of the vascular system (blood) remains high, hence the absence of the characteristic blood picture (anemia, etc.) found in this biopathy.
Attending to this viewpoint, abnormalities in pancreatic (insulin) function could be considered a reaction to chronic tissue anorgonia. A function of insulin is to facilitate glucose and potassium transport into the cell. It also promotes fat and glycogen synthesis and growth. These functions are identical to a parasympathetic effect on the plasmatic system. Anorgonia of the tissues, especially muscle, signifies that the orgonotic potential is not sufficiently high. As a result, insulin function is reduced and plasma levels of glucose increase in proportion. This, in a vicious circle, stimulates the pancreas to produce increasingly greater amounts of insulin finally leading to islet cell failure. At this stage of the illness, the patient becomes dependent on exogenous sources of insulin. This view is supported by the clinical observation that symptoms of di-abetes mellitus are often preceded by a phase of hyperinsulinism. At this late stage in the biopathic process, the manifestations of full-blown dia-betes mellitus appear. Since water and orgone charge attract each other, 1ow tissue orgonity leads to tissue dehydration, electrolyte depletion, as well as all the clinical signs and symptoms that are the hallmarks of this biopathy (polyurea, polydypsia, polyphagia, etc.).
From this perspective, the current medical treatment of this biopathy deals only with the most superficial aspects of the disorder. Giving exogenous insulin to diabetic patients may temporarily mask the signs and symptoms of this illness, but it leaves the underlying anorgonotic process, manifested by progressive vascular and neurological symptoms, untouched.
Since both cancer and diabetes involve a shrinking process, the question arises: What distinguishes these biopathic processes from each other? Perhaps the distinction is determined by the locus of the anorgonotic process in the biosystem. In the cancer biopathy, shrinking (anorgonia) progresses to involvement of the vascular component of the plasmatic system, and shrinking takes place at the very core of the biosystem. In diabetes, on the other hand, the anorgonotic process remains more superficial and confined to other tissues (kidneys, muscular apparatus, etc.) while leaving the plasmatic system intact. In the diabetic biopathy, the orgastic disturbance, a disturbance of tissue pulsation in the form of tissue anorgonia, spares the energy charge of the plasmatic system. A reduction in orgonity of tissues other than the plasmatic system, by lowering the energy charge of the organism, may interfere with the capacity for tumor formation, an explanation for the rare occurrence of primary cancer tumors in the presence of diabetes mellitus. Because of a pre-existing anorgonotic process, diabetics may never have the capacity for deep sexual longing which is a frequent clinical finding in patients who go on to develop cancer. There is nothing for the diabetic individual to resign from.
The frequent observation that diabetics seem to be excessively sweet may be based in part on an inability to express strong rage reactions because of an anorgonotic tendency in the skeletal musculature. As defensive maneuvers, they typically express soft feelings, such as longing and sadness. These defensive tendencies are discouraged in therapy. The question arises: To what extent does increased blood glucose levels contribute to the expression of sweetness?
Clinical experience shows this biopathy can only be treated in the earliest stages of illness. Once the disease has progressed to the point of islet cell destruction, the biopathic process is, for all intents and purposes, irreversible. When this occurs, the individual may be dependent on exogenous sources of insulin.
The following case presentation of a patient who developed biochemical manifestations of diabetes during the end-stage of orgone therapy illustrates some of the clinical events encountered in the treatment of this biopathy. It also sheds light on some of the biophysical and characterological aspects of this disorder.
This 18-year-old, passive-feminine patient had a his-tory of depressive episodes with several serious suicidal attempts. Except for recurrent hemorrhoids, he was in good physical health. Biophysical examination revealed a well-developed, mesomorphic individual. He appeared superficially soft and slightly effeminate. There was severe armoring of the oral segment and moderate armoring throughout the rest of his body. On intial examination, there was no conspicuous armoring of the diaphragmatic segment.
During most of his therapy, considerable amounts of rage, especially from the oral and anal levels, were expressed. As a reaction to discharged rage from every layer of armor, there developed an intensification of his passive-feminine tendencies which were expressed as soft feelings, feelings of weakness, pleading, and helplessness. From a biophysical stand-point, the patient reacted to a sudden increase of charge, accompanying the emergence of intense rage, with a sudden depletion of energy charge (anorgonia). As each layer of armor was eliminated, both the intensity of the rage and the anorgonotic reaction against it increased in severity. These reactions gradually assumed greater significance as therapy progressed. Mobilization of rage from the oral segment, for example, yielded to intolerable sadness and then briefly to hopeless resignation. These anorgonotic biophysical reactions were viewed as being distinct from his passive-feminine defenses, although both acted in the same direction to immobilize the patient and render him helpless. Another emotion, which gradually began to assume greater defensive significance because of its premature appearance, was deep infantile longing for his mother. This emotion, accompanied by preorgastic melting sensations, appeared regularly whenever the strength of his aggressive impulses began to overwhelm him. The expression of these feelings was also treated as defensive.
As noted earlier, there was no indication at the onset of therapy that mobilization of the diaphragmatic segment was going to be difficult. However, as later events clearly revealed, this was not the case at all. In fact, this segment proved to be the most tenacious and was only less difficult to work through than the pelvic segment. The onset of mobilization of this segment was ushered in by a strong intensification of all his passive-feminine defenses, including the emergence of a significant amount of genital anxiety with premature ejaculation and episodes of erective impotence. This was evidence that a great deal of energy was being immobilized in this segment. His diaphragm became tense and his abdomen bloated. Pressure on the abdominal muscles produced intense squeezing rage followed by relief with a brief, strong generalized increase in orgonotic charge, manifested also by a lumination of his field. He then experienced stabbing pains in his genitals and began to grovel, pleading with me not to hurt him. Typical signs of orgasm anxiety appeared: He lost all interest in getting well, communications became superficial, and he had thoughts of dying.
With partial mobilization of the diaphragmatic segment, I was able to proceed with pelvic mobilization because the upper four segments remained open.
The sudden, sharp increased charge of his biosystem produced by mobilization of pelvic rage was regularly followed by syncopal attacks (anorgonia). Because of the severity of these biophysical reactions, I became concerned about the possible occurrence of a somatic biopath. This concern was based on the observation that his biosystem was neither able to bind energy in the armor nor to retain a strong orgonotic charge. Instead, his biosystem reacted with collapse (anorgonia). Despite this possibility, it was imperative to take a chance and assist his fight for health.
Deep disappointment at being rejected by his mother surfaced, and he developed suicidal thoughts. Overwhelmed by his misery, he repeatedly became syncopal.
Further mobilization of the diaphragm by pressing along the right costal margin produced gagging followed by strong convulsions of the torso. Pressure over the epigastrium which was exquisitely tender, produced large quantities of murderous rage and a sudden jump in his energy followed by a loss of consciousness for about 8-10 seconds with rotation of the eyes upward and to the right. With repeated exposure to this procedure, he gradually became able to tolerate the build-up of energy resulting from diaphragmatic, abdominal, and pelvic mobilization with no tendency to lose consciousness.
At this point, he developed biochemical signs of diabetes mellitus. Blood studies revealed elevated fasting blood sugar (138) and glucose tolerance curve reaching a maximum value of 155.
This somatic biopathic reaction was accompanied by feelings of resignation and suicidal ideation. A deep fear of death surfaced to which he reacted, not with his typical passive-feminine submissiveness, but with a strong desire to fight and not submit to his fate. Rejecting his entire passive-feminine way of coping with life, he both expressed and tolerated strong outbursts of rage without losing consciousness. This was accompanied by strong sensations of well-being which indicated his organism was restructuring and capable of sustaining a high level of orgonotic charge. This capacity to maintain strong orgonotic charge over a period of time and effectively discharge energy in the genital embrace eliminated both his passive-feminine structure and his diabetic tendency.
The significant biophysical events in this case, in which symptoms of diabetes mellitus appear in the end-stage of therapy, are the following:
© 2008 The American College of Orgonomy. All rights reserved.
