The Biopathic Diathesis
Robert A. Dew, M.D.
Reprinted from the Journal of Orgonomy, Vol. 2 No. 2
The American College of Orgonomy

Biopathic Diathesis - TABLE

BASAL ENERGY LEVEL
Total charge
Capacity to hold charge
Capacity to luminate

Likewise, we may postulate a descending hierarchy of conditions (with the latter corresponding to quantitative energy levels and qualitative energy functions), as follows:

CONDITION
Health
Inflammatory biopathies
Hypertensive cadiovascular biopathies
Diabetes
Leukemia
Cancer

The capacity for lumination seems less impaired in leukemia than in cancer. The closer epidemiological alignment of diabetes with the cardiovascular biopathies may indicate that the general energy level at which diabetes appears may lie somewhere between the leukemias and cardiovascular hypertensive disease. The preceding schema is not an answer to the problem of differentiation of the shrinking biopathies; future experiences will doubtless reveal its crudeness, but it may at least provide a theoretical foothold in very difficult terrain. Regarding the failure of cancer patients routinely to develop diabetes: We recall that our hypothesis implicates an energy imbalance between tissue and plasma to explain the metabolic defect. In the cancer biopathy, both tissue and blood plasma with blood cellular elements have a poor charge.

This is evident from tumor cell formation and the T-reaction of the erythrocytes. Thus, we would not expect an imbalance between tissue and plasma comparable to that in diabetes. In other words, both orgonotic systems are decaying at the same rate, and the primary metabolic lesion of diabetes does not routinely develop. It should be remembered, however, that the occurrence of diabetes in cancer patients is not uncommon. Certainly it is no less infrequent than the concurrence of arteriosclerotic heart disease and cancer. As a matter of fact, cancer patients not infrequently will die of some complication of arteriosclerosis rather than their neoplastic disease. This is, of course, particularly true in the older age groups. The overlapping of biopathies in general should remind us that patients may enjoy or suffer (as the case may be) a vertical mobility in their energy status as well as certain "pleomorphism" in their response to contraction.

Let us now reconsider the role of a diaphragmatic block in diabetes. If we can no longer regard diabetes as primarily a defect in insulin production, then what role would the block play in its development?

Obviously, as long as the pancreas can respond to the increased demands upon it, the appearance of clinical diabetes may be forestalled, i.e., increased endogenous insulin production can compensate for the failing energetic "pull" of the tissue cells. A severe diaphragmatic block, then, in disturbing pancreatic function, would hasten the emergence of signs of insulin lack. 6 Thus, the diaphragmatic armoring, like a glucose tolerance test or obesity, would bring out much deeper disorder. Yet, this raises an interesting problem. Why does the diaphragmatic block selectively affect the Islet calls’ function and leave the acinar cells intact? This, again, might cast some doubt on the primacy of the diaphragm armoring in the development of diabetes. But, more important are its much broader implications with regard to the selective behavior of the biopathies in general. To clarify this, one would require a detailed knowledge of the discrete differences in susceptibility of various tissues to changes in oxygen tension and orgonotic charge. In this case, what are the relative capacities of acinar and Islet cells to "do without"? In this connection, we think of the relatively high incidence of cancerous change in rapidly dividing and regenerating epithelial tissues, e.g., gastric, bronchial, and the low incidence in supportive and connective tissue (smooth muscle and cartilage). Clearly, rate of cell growth and division are related to the proclivity for bionous disintegration in the face of hypoxia and hyporgonia. Thus, the needs of the various tissues may be a further factor in the differentiation of the biopathies. This will be discussed more fully elsewhere.

To summarize, the differentiation of the biopathies depends upon:

1. The intrauterine environment, particularly as it affects the vitality of the offspring, e.g., total body charge, capacity for lumination.

2. Character structure; character armor, location and severity.

3. Basic level of orgonotic charge.

4. The basic manner in which the organism reacts against contraction, i.e., lumination versus resignation.

5. The discrete differences in susceptibility of the various tissues to hyporgonia and hypoxia brought about by the armoring, etc. III. Classification of the Biopathies on a Bioenergetic Basis As we have gleaned from the previous material, the lack of accumulated clinical data of a character-analytic and orgone-therapeutic nature in the biopathies has created immense gaps in understanding their differentiation. Except in very general terms, it is impossible, at this point, to relate structure to individual diseases. We do know that, although the fundamental disorder underlying all the biopathies is the same, the energy processes which result from this disturbance may vary. We believe, in addition, that total body charge and capacity for lumination undeniably affect the course of the biopathic process. On these premises, then, we shall construct a classi-fication of the biopathies, including as much relevant factual information as possible. Speculative statements will be followed by a question mark in parentheses.

Because of the lack of detailed knowledge in each case, the number of conditions listed is limited. Also, because of the welter of states involved, no attempt at comprehensiveness is made. We strive here only to indicate some of the lines along which the diseases seem to classify themselves.

CONCLUSION

It is said that the fruitfulness of research depends mainly on asking the right questions. In this general survey, I have alluded to some basic principles, elucidated by Reich in The Cancer Biopathy, in an effort to set in relief possible mechanisms of biopathic differentiation. In the discussion of the metabolic biopathy, I attempted to utilize those principles to explain more fully some of the features of diabetes. Whether or not my handling of these concepts is valid remains to be seen. However, questions have emerged which underscore tremendous gaps in our knowledge of the effects of disturbed orgonotic pulsation on the human organism.

We cannot, as yet, fully account for the selectivity of reaction in the different biopathies, e.g., why, if adrenal tumors are due to abdominal blocks, do they occur either in the medulla or the cortex in a given patient but rarely in both layers simultaneously? Why does one patient get regional enteritis, and another get ulcerative colitis, when the small bowel and colon originate in the same segment? Why does biophysical resignation lead to cancer in one and leukemia in another?

Related to this problem is the question of why certain illnesses involve many segments (e.g., lupus) and others affect only one (e.g., cholelithiasis). The answers to these and other enigmas will doubtless carry us deep into involvement in cellular physiology, embryology, and biochemistry.

The prospect, quite properly, makes us uneasy. Mechanistic science has sailed these same waters and has run aground. Hopefully, the fundamental tool of orgonomic research, functional thinking, will rescue future investigators from this fate.

Footnotes

1. We refer here to "idopathic" diabetes mellitus - not that secondary to sergical extirpation or inflammatory disease of the pancreas, or hemochromatosis, all of which account for very few cases. back to text
2. The idea that the pancreas is the anatomic "nidus" is no longer certain. back to text
3. We recall in this connection the insulin-antagonistic effects of epinephrine. back to text
4. Passive osmotic functions are, of course, also at work here. back to text
5. Cancer is more assiduously sought and more easily diagnosed today than it was fifty years ago. back to text
6. The initial abnormal increases in insulin production seen in the early phases of the disease may in part reflect an over-response of the Islet cells to the suffocating effect of the diaphragmatic armoring. back to text

References

1. Reich, W.: The Discovery of the Orgone, Vol.II: The Cancer Biopathy. New York: Orgone Institute Press, 1948.
2. Bondy, P. K.: Cecil and Loeb Textbook of Medicine, eds., Beeson and Mc-Dermott. Philadelphia: Saunders, 1963.

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