Candida Albicans: Necessary and Sufficient Cause of Cancer
When facing the most pressing contemporary medical problem, cancer, the first thing to do is to admit that we still do not know its real cause. However treated in different ways by both official and alternative medicine, an aural of mystery still exists around its real generative process.
The attempt to overcome the present impasse must therefore and necessarily go through two separate phases: a critical one that exposes the present limitations of oncology, and a constructive one capable of proposing a therapeutic system based on a new theoretical point of departure.
In agreement with the most recent formulation of scientific philosophy, which suggests a counter-inductive approach where it is impossible to find a solution with the conceptual tools that are commonly accepted, only one logical formulation emerges; that is, to refuse the oncological principle which assumes cancer is generated by acellular reproductive anomaly.
However, if the fundamental hypothesis of cellular reproductive anomaly is questioned, it becomes clear that all the theories based on this hypothesis are inevitably flawed.
It follows that both an auto-immunological process, in which the body’s defence mechanisms against external agents turn their destructive capacity against internal constituents of the body, and an anomaly of the genetic structure implicated in the development of auto-destruction, are inevitably disqualified.
Genetic influences in the development of cancer processes
Moreover, the common attempt to construct theories about multiple causes that have an oncogenic effect on cellular reproduction sometimes seems like a concealing screen, behind which there is nothing but a wall. These theories propose endless causes that are more or less associated with each other; and this means in reality that no valid causes are found. The invocation in turn of smoking, alcohol, toxic substances, diet, stress, psychological factors, etc., without a properly defined context, causes confusion and resignation, and creates even more mystification around a disease which may turn out to be simpler than it is depicted to be.
As background information, it is important to review the picture of presumed genetic influences in the development of cancer processes as they are depicted by molecular biologists. These are the scientists who perform research on infinitesimally small cellular mechanisms, but who in real life never see a patient. All present medical systems are based on this research, and thus, unfortunately, all therapies currently performed.
The main hypothesis of a genetic neoplastic causality is essentially reduced to the fact that the structures and the mechanism in charge of normal reproductive cellular activity become, for undefined causes, capable of an autonomous behaviour that is disjointed from the overall tissular economy.
Genes
The genes that normally have a positive role in cellular reproduction are, then, imprecisely referred to as proto-oncogenes; those which inhibit cellular reproduction are called suppressor genes or recessive oncogenes.
Both endogenous (never demonstrated) and exogenous cellular factors — that is, those carcinogenic elements that are usually invoked — are held responsible for the neoplastic degeneration of the tissues.
In J.H. Stein (Medicina Interna – Internal Medicine, Mosby Year Book inc.1994, St. Louis, Missouri, 4th edition, Milano, 1995, page 1186 -1187) the following is reported:
The mitogenic signals, from the microenvironment or from more distant areas of influence, are transmitted to the cells through numerous receptive structures that are associated to the plasmatic membrane.
Among these structures, the ones that have been studied most exhaustively are receptors with an external domain for the binder, a transmembranic domain and a cytoplasmatic domain with a thyrosinkinase activity.
Classes of molecules
Besides these, it is thought that at least seven distinct classes of molecules participate in the transmission of the mutagenic signal:
- receptors coupled to G proteins
- ionic channels
- receptors with intrinsic activity guanil cyclase
- receptors for many lymphofokines, cytokines and growth factors (interleukine, eritropoietine, etc.)
- receptors for the phosphothyrosine phosphorilase activity
- nuclear receptors belonging to the supergenic family of the receptor for steroidal estrogenic and thyroidal hormones
- Finally, increasing numbers of tests suggest that the adhesion molecules expressed on the surface of the cells communicate with the microenvironment in ways that produce very important consequences for cellular growth and differentiation.
From a very superficial analysis of this presumed oncological picture, however, it seems to be clear how the assertion of all this unstoppable genetic hyperactivity, generated by elements that almost seem to lurk in the realms of the sinister and the monstrous, and that therefore suggest the existence of God-knows-what abysmal mechanisms that can only be deciphered with equally abysmal conceptual mechanisms — all this can do nothing more that unveil the abysmal stupidity that is at the basis of this way of conceiving things.
What is even more serious is the fact that nobody in the present health establishment seems to question the above-mentioned stupidities. All those who work in the field do nothing but repeat the stale litany of reproductive cellular anomalies on a genetic basis.
Since in this state of affairs the present medical theory shows an impoverishment and a superficiality that are indeed abysmal, it is better to look for new horizons and conceptual instruments that are capable of unearthing a real and unique neoplastic aetiology.
After so many years of failure and suffering it is time to rejuvenate minds with new and productive juices. Arguments for mysterious and complex genetic factors, a monstrous reproductive capacity by a pathologic entity capable of tearing apart any tissue, the idea that there is an implicit and ancestral tendency of the human organism to deviate in an auto-destructive sense — these and other similar arguments, spiced with exponentially multiplying numbers of “ifs” and “maybes” — it all has the flavour more of raving free-association than of a healthy scientific discourse.
Classify successes achieved by official medicine and by alternative medicine
Once the present oncological perspectives have been refuted, however, it is legitimate to ask how the successes achieved by official medicine and by alternative medicine have to be classified.
To this end, it is useful to remember that contemporary epistemology has demonstrated how the contributions to causality of contextual and co-textual elements of a theory, if they cannot be defined, are therefore chancy, especially in ultra-dimensional space, that is, in the microscopic dimension.
In practical terms, this means that data or positive facts that are considered proof when concerning a basic principle (for example, the above-mentioned cellular reproductive anomalies), and therefore obtained by utilising a limited number of variables next to the complexity of human disease, cannot be trusted, since they work only from the initial hypothetical functions.
Where, in fact, we admit the possibility of improvements or cures, it is not admissible from the logical point of view attribute them to this or that method of cure that is more of less official, since it is not possible to specify and include all or the majority of the components that are at play in the object man, in whom conditions of certainty cannot exist.
Paradoxically, the possible positive effect of each therapeutic system could derive from elements that are not foreseen and are unknown to all. Those elements, however, could be influenced by or determined to some extent by one another.
We may find ourselves in a position in which everybody rightfully has the right to promote his point of view, without knowing the real reasons for his successes.
In this case, then, even the most rigorous experimentation takes on a fictional character rather than the function of a true correspondence with reality, and the end result is a continuous sterile petitio principii.
If we then put aside completely the conceptual frame of contemporary oncology with all its interpretative variables of genetic, immuncological and toxicological character, what is left as the only logical, practicable way is the domain of the infectious diseases, to be seen and reconsidered with different eyes that has been the case so far.
Two considerations support such a conclusion. One is of a historical nature, and the other is of an epidemiological nature. The former derives from the fact that, in the therapeutical approach to the patient, the improvement in quality, that is the possibility of a real cure for the patient, has been determined almost exclusively by the development of microbiology. The latter derives from the analysis of life expectancy that has taken place in the last decades which, since it is associated with an inevitable change of the sthenicity of individuals, can be hypothesised as a determining factor in the development atypical infectious pathologies.
In order to find the possible carcinogenic ens morbi on the horizon of microbiology, it appears useful to return to the basic taxonomical concepts of biology, where we can see, incidentally, the existence of a noticeable amount of indecision and indetermination.