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

The Uterus and Heredity: The Biopathic Process and Intrauterine Development

Classical medical science has amassed a wealth of statistical information on genetic factors in the incidence of various diseases. It would be a grave error to brush this aside as so much mechanistic wishful thinking. To be sure, to some degree, the preoccupation with genetics in the biopathies (particularly cancer) reveals a certain deep feeling of futility, and certainly has been responsible for carrying modern research up blind biochemical alleys. Nevertheless, there are, clearly, enough examples of genetic diseases in the literature, e.g., phenylketonuria and various other metabolic and hematologic disorders, to warrant this line of approach even if only for purposes of exclusion. To my knowledge, however, none of the biopathies has been conclusively demonstrated to follow the pattern of Mendelian genetics. There is no death of documentation for the familial incidence of certain of the biopathies, e.g., thyrotoxicosis, diabetes mellitus, and rheumatoid arthritis. From the literature, one gets the distinct impression that the word "familial" is more or less intended to convey the supposition that a genetic mechanism does exist, but it simply has escaped elucidation until now. The concept of genetic "penetrance" was evolved to explain the discrepancies observed. I prefer to use "familial" in its strictest sense; it at least puts us on factual grounds.

Character analysis has clearly related the emotional atmosphere of the family to the structure and function of the individual. In The Function of the Orgasm and the Mass Psychology of Facism, we see how character attitudes are anchored in each succeeding generation. Since character attitudes are biophysical, the theoretical basis for the familial incidence of biopathic disease would seem to be on solid ground. Reich also touched upon the intrauterine factor in the biophysical fate of human beings (1: pp.339-40). We can only guess at the consequences to the fetus of spending nine months in a chronically spastic, characterologically "disgusted" uterus. It is reasonable to assume that the vitality of the placenta and fetus will suffer or prosper along with any other organ of the mother’s genital system. Inasmuch as embryonic development must involve lumination, streaming, and superimposition, it is entirely possible that congenital malformations are in part uterine in origin. The deleterious effects of drugs, viruses, and certain bacteria on embryogenesis would seem to bear this out. Likewise, we may conclude that, since character structure is the result of environment and the raw material (biosystem) upon which it works, the foundation for a particular biopathy or group of biopathies is laid in the uterus.

Here, again, I should like to return to the problem of genetics. There is probably as much evidence for the existence and behavior of genes as there is for subatomic particles, e.g., nuclear physics and animal husbandry both work. Furthermore, there is a mass of cytochemical and morphologic data which irrefutably links genes to reproduction and development. Yet, since all structure in nature is ultimately derived from orgone energy, so must the genes. It is apparent from cytologic observations that chromosomal division and segregation in mitosis and meiosis are subject to a more fundamental order of regulation than is inherent in the genes themselves. We would point out, in this connection, the similarities between the orientation of iron filings in a magnetic field and the chromosomal disposition in the metaphase of mitosis. Thus, viewing the organism’s environment as beginning in the uterus, we can understand the familial epidemiology of the biopathies. It is interesting that, in this light, the previously abandoned idea of Lamarck, i.e., the inheritance of acquired characteristics, appears to have some basis in fact.

It may seem premature to introduce a specific disease entity at this point in a general survey of the biopathies. However, diabetes presents us with some difficult theoretical problems which are relevant to the problem of biopathic differentiation.

Reich expressed the belief that diabetes mellitus was a biopathy based on a disturbance of pancreatic function due to a diaphragmatic block. There is reason to believe, however, that the problem is some what more complex than that. For one thing, the incidence of diabetes in the general population is roughly two percent, rising to as high as ten percent in the sixty-and-over age group. Even these high figures indicate that there are undoubtedly fewer cases of diabetes than there are severe diaphragmatic blocks. For the moment, though, let us hold this possible objection in abeyance. Does the disease have the general features of the biopathies which we outlined above?

1. The cause of diabetes is as yet unclear. The earlier assumption that it is due simply to a failure of the pancreas to produce adequate insulin has not withstood the scrutiny of more recent investigations. At the present time, as one authority observes, "The biochemical and physiologic explanation of the mechanism of diabetes is undergoing intensive reexamination" (2: p. 1175).

2. There is a "psychosomatic component." The factor of emotional stress in modifying the course of the disease is well known and needs no further documentation here.

3. The disease may be characterized by a long course with exacerbations and remissions leading to irreversible morphologic changes.

4. Diabetes is a generalized disorder with no recognizable local nidus of origin. [Reference 2]

Except for one final criterion, then, diabetes mellitus seems to fit the picture generally associated with the biopathies. The difficulty arises in identifying the specific functional disturbances preceding the gross morphological changes.

At one time, the disease could be divided into a "latent" phase in which no biochemical abnormality could be demonstrated; a "pre-clinical" phase when a biochemical abnormality, e.g., glucose tolerance test, could be shown, but no clinically apparent derangement of carbohydrate metabolism is present; and, lastly, the "clinical" phase when polyuria, polydypsia, glucosuria, etc., are there for all to see. It would have been a fairly simple matter to regard the abnormality in carbohydrate metabolism as the functional disturbance antedating the morphologic changes of early and clinical diabetes. Recent work has shown, however, that changes in the basement membrane of the capillaries in muscle and renal glomerulus may occur long before the most sensitive tests of carbohydrate metabolism can detect any abnormality. A similar angiopathy has been demonstrated in women with so-called idiopathic edema of the extremities. There is a high incidence of diabetes in the families of these women and a significant number go on to develop diabetes. One currently proposed explanation for these capillary changes is that they are due to the deposition of a glycoprotein derived from glucose which has been shunted away from a normal metabolic pathway because of a specific pyruvate kinase deficiency.

These considerations may create some anxiety; we feel ourselves on the brink of a mechanistic biochemical morass. Recalling some of the features of diabetes may help guide us past these muddy waters. First of all, the description of diabetes (by Artaeus in the 1st century A.D.) as "a melting down of the flesh and limbs into urine" is to my view, a functionally accurate one. In essence, the plasmatic system is literally "melting away" and being excreted through the kidneys. The kidneys, beside their functions of maintaining acid-base and water balance, etc., normally excrete the "waste products" of metabolism, e.g., the products of tissue breakdown: catabolism. Might we not then regard the polyuria, ketonuria, hyperkaluria, and negative nitrogen balance (i.e., catabolism) of diabetes to some extent as a pathologic exaggeration of a normal process? If, for the moment, we accept this premise, we must go on to explain just what prompts this unique "exaggeration."

The basis of all the biopathies is more or less chronic sympatheticotonia. In the shrinking cancer biopathy, there is a gradual loss of energy through the bionous disintegration of the red blood cells. I would suggest that diabetes mellitus is another form of shrinking biopathy in which the tissues themselves undergo disintegration, i.e., a massive catabolic "melting down." The red blood cell system is not directly involved, hence anemia is not a characteristic concomitant of the disease. The features of shrinking are certainly there. Autonomic and peripheral neuropathy (which is recently receiving much attention in clinical cancer disease) is a long recognized complication of diabetes. I believe it is identical functionally to what is seen in cancer. The predilection for furunculosis, "premature" atherosclerosis, and indolent ulcerations of the lower extremities, all indicate low tissue charge, shrinkage of the plasmatic system and bioenergetic core. The poor handling of infection suggests impaired luminating capacity, as well. The extreme frequency of maturity-onset diabetes further supports the idea that this is closely related to the shrinking biopathies.

Let us return, now, to the biochemical aspects of this disease. We know that there is not necessarily a primary underproduction of insulin. It has been shown that in "latent" and even clinical phase diabetics there is increased insulin-like activity (ILA) in the serum. Radioimmuno assays (RIA) of insulin are also elevated. It is generally agreed that there is, at least initially, an overproduction of insulin, very probably in response to an increased requirement, and that the histologic morphologic exhaustion of the islet cells seen later on is a result of this. Why the increased insulin requirement?

One of the earliest observations in bion research was that the stronger orgonotic system attracted the weaker. The importance of this phenomenon in the process of absorption and assimilation is obvious. The removal of nutrients, e.g., amino acids, fats, carbohydrates, etc., from the bloodstream by the tissue cells, is a further manifestation of this. Insulin is presumed to work at the cell membrane aiding the transport of glucose across to the cell interior. Insulin also promotes fat and glycogen synthesis and growth, and it effects the movement of potassium into the cells. In short, insulin exerts a parasympathetic effect on the plasmatic system: it has a life-positive action. 3 If the assumption that tissue cell charge is low is correct, then the primary energetic drive (or pull) in glucose transport would be blocked.

As a consequence, glucose piles up in the blood plasma and the stimulus for increased insulin production and release would result.

This mechanism would also explain other metabolic and morphologic derangements seen in diabetes, hypertriglyceridemia and hypercholesteroleinia, for example. These substances are known to be implicated in atherogenesis. The failure of undercharged tissue cells to take up these materials from the blood plasma could account for the increased concentration and eventual deposition in the walls of the vessels. Our hypothesis carries us further. Water and orgone energy mutually attract one another. If the tissue cells are losing charge, then water would tend to leave the tissues and enter the capillaries (carrying with it potassium and other electrolytes) where there is a relatively higher charge owing to the presence of erythrocytes and abnormally increased concentrations of unassimilated nutrients. 4 This would account for the poor tissue turgor, the "hypokalemia" evidenced on the ECG, and the normal or near-normal serum potassium not infrequently encountered in diabetic acidosis.

For the present, our discussion of the biochemical derangements of diabetes need go no further. If our theoretical assumptions are correct, then the chemical sequelae of the disease as described in the text-books would make complete sense once the low tissue charge set them in motion. The functional disturbance in diabetes, in my view, is an imbalance in the relative charge of tissue cells and blood plasma which interferes with nutrient transport. This is "interpreted" by the endocrine system as a "shortage" of insulin. Apparently the successful treatment of the biochemical disturbance in diabetes with exogenous insulin occurs as a result of an overwhelming effect on the tissue cell membrane charge. The fact that the underlying biopathic process is untouched is borne out by the relentless advance of vascular, neurological, and other complications in the face of "good control" of blood glucose and glucosuria. Our hypothesis, however, gives rise to two difficult questions:

1. If the basic disturbance in diabetes is bioenergetic shrinking, should we not see a much higher incidence of cancer in diabetics?

2. Or, conversely, why don't cancer patients routinely develop diabetes?

There are no data, to my knowledge, which suggest an unusual correlation of cancer and diabetes. In fact, in the period 1914 to 1963, cancer as a cause of death in diabetes rose only from 4 to 9.5 percent, a rise which is easily attributable to the decrease in deaths due to coma and infection and the well-known increase in the incidence and diagnosis 5 of cancer itself. Deaths due to cardiorenal, i.e., non-neoplastic, causes in diabetes have more than tripled. There are isolated syndromes such as cancer of the uterine body and diabetes in which the two occur together with a higher than expected incidence; however, the frequency of this is not sufficiently high to provide much support for our thesis. How, then, can we account for the fact that what we call a shrinking biopathy does not especially enhance the cancer process? I cannot give a clear answer to this question any more than I can explain why biophysical resignation and shrinking give rise to a cancer tumor in one patient and leukemia in another. The pathological behavior of these diseases suggests that they may occur at different energy levels. That is, we may postulate a (quantitatively) descending order of energy states, as follows:

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