Cause of Cancer

From Theresa Dale, CCN…

The causes of cancer have been reviewed, previewed and discussed for a very long time and yet there is no cure in the traditional medical model.

I have always known through working with clients/patients for 30 years that Candida Albicans and other types of fungus and parasites are usually present when Cancer is present.

In Europe there are Cancer treatments that include homeopathic formulas to kill fungus (Candida Albicans), molds and parasites. I want to empower you to follow the methods that you feel are right for you. Moreover, I am offering information to help you make new choices and offer harmless and thorough methods of detoxification, which is so very important in healing any health condition.

Our formulas that help with any health condition follows:

  • Candida-Ease
  • Lymph Detox Plus
  • Whole Body Deep Cleanse
  • Para Pro
  • Hormone Saliva test

Is the Cause of Cancer a Common Fungus?
According to this hypothesis based on years of scientific and clinical research, the cause of cancer is infection by a common fungus, Candida albicans.

Extracted from Nexus Magazine, Volume 14, Number 5 (August – September 2007)
PO Box 30, Mapleton Qld 4560 Australia.
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381

by Dr Tullio Simoncini ©2007

My idea is that cancer doesn’t depend on mysterious causes (genetic, immunological or auto-immunological, as the official oncology proposes), but it results from a simple fungal infection whose destroying power in the deep tissues is actually underestimated.

The present work is based on the conviction, supported by many years of observations, comparisons and experiences, that the necessary and sufficient cause of the tumour is to be sought in the vast world of the fungi, the most adaptable, aggressive and evolved micro-organisms known in nature.

I have tried many times to explain this theory to leading institutions involved in cancer issues (the Ministry of Health, the Italian Medical Oncological Association, etc.), elaborating on my thinking, but I have been brushed aside because of the impossibility of setting my idea in a conventional context. A different, international audience represents the possibility of sharing a view about health which differs from what is widely accepted by today’s medical community, either officially or from the sidelines.

There is an opposition between the allopathic and the Hippocratic medical ideal. The position that I promote represents instead a meeting point of these two conceptions of health, since from the conceptual point of view it sublimates and adds value to both, while highlighting how they both are victims of a common conformist language.

The hypothesis of a fungal aetiology in chronic-degenerative illness, able to connect the ethical qualities of the individual with the development of specific pathologies, reconciles the two orientations (allopathic and holistic) of medicine. The hypothesis is a strong candidate for being that missing element of psychosomatics that was sought but never found by one of the fathers of psychosomatics, Viktor von Weiszacker.

In considering the biological dimensions of the fungi, for instance, it is possible to compare the different degrees of pathogenicity in relation to the condition of organs, tissues and cells of a guest organism, which in turn also and especially depend on the behaviour of the individual.

Each time the recuperative abilities of a known psycho-physical structure are exceeded, there is an inevitable exposure, even considering possible accidental co-founders, to the aggression–even at the smallest dimensions–of those external agents that otherwise would be harmless. In the presence of an indubitable connection between patient morale and disease, it is no longer legitimate to separate the two domains (allopathic and naturopathic) which are both indispensable for improving the health of individuals.

Flaws in mainstream theories on cancer causation

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, cancer has an aura of mystery that 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,1 only one logical formulation emerges: to refuse the oncological principle which assumes that cancer is generated by a cellular 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.
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 reasons, capable of an autonomous behaviour that is disjointed from the overall tissular economy. The genes that normally have a positive role in cellular reproduction are, then, imprecisely referred to as “proto-oncogenes”; those that 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…

>From a very superficial analysis of the presumed oncological picture, however, it seems to be clear how the assertion of all this unstoppable genetic hyperactivity can do nothing more that unveil the abysmal stupidity that is at the basis of this way of conceiving things. All those who work in the field do nothing but repeat the stale litany of reproductive cellular anomalies on a genetic basis. It is better to look for new horizons and conceptual instruments that are capable of unearthing a real and unique neoplastic aetiology.

Back to taxonomy
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.

Already in the last century, a German biologist, Ernst Haeckel (1834-1919), departing from the Linnaeian concept that makes for two great kingdoms of living things (vegetable and animal), denounced the difficulties of categorising all those microscopic organisms which, because of their characteristics and properties, could not be attributed to either the vegetable or the animal kingdom. For these organisms, he proposed a third kingdom, Protista (protists).
“This vast and complex world includes a range of entities beginning with those that have sub-cellular structure–existing at the limits of life–such as viroids and viruses, moving through the mycoplasms to, finally, organisms of greater organisation: bacteria, Actinomycetes, Myxomycetes, fungi, protozoa and perhaps even some microscopic algae.”2

The common element of these organisms is the feeding system, which, being implemented (with very few exceptions) by direct absorption of soluble organic compounds, differentiates them both from animals and vegetables. Animals also feed as above, but especially by ingesting solid organic materials that are then transformed through the digestive process. Vegetables, by utilising mineral compounds and light energy, are capable of feeding by synthesising the organic substances.
The contemporary tendency of biologists is once again to pick up, though in a more sophisticated way, the concept of the third kingdom. One goes even further, however, arguing that within that kingdom, fungi must be classified in a distinct category.

O. Verona3 says that if we put multicellular organisms provided with photosynthetic capabilities (plants) in the first kingdom and the organisms not provided with photosynthetic pigmentation (animals) in the second kingdom–and organisms from both these kingdoms are made of cells provided with a distinct nucleus (eukaryotes)–and, furthermore, if we put in another kingdom (protists), those monocellular organisms that have no chlorophyll and have cells that are without a distinct nucleus (prokaryotes), the fungi can well have their own kingdom because of the absence of photosynthetic pigmentation, the ability to be monocellular and multicellular, and, finally, their possession of a distinct nucleus.

Additionally, fungi possess a property that is strange when compared to all other micro-organisms: the ability to have a basic microscopic structure (hypha) with a simultaneous tendency to grow to remarkable dimensions (up to several kilograms), keeping unchanged the capacity to adapt and reproduce at any size.

>From this point of view, therefore, fungi cannot be considered true organisms, but cellular aggregates sui generis with an organismic behaviour, since each cell maintains its survival and reproductive potential intact regardless of the structure in which it exists. It is therefore clear how difficult it is to identify all the biological processes in such complex living realities. In fact, even today, there are huge voids and taxonomical approximations in mycology.

Fungi characteristics
It is worthwhile to examine more deeply this strange world, with such peculiar characteristics, and try to highlight those elements that somehow may be pertinent to the problems of oncology.

1) Fungi are heterotrophic organisms and therefore need, as far as nitrogen and carbon are concerned, pre-formed compounds. Of these compounds, simple carbohydrates, for example monosaccharides (glucose, fructose and mannose), are among the most utilised sugars. This means that fungi, during their life cycle, depend on other living beings which must be exploited in different degrees for their feeding. This occurs both in a saprophytic way (that is, by feeding on organic waste) and in a parasitic way (that is, by attacking the tissue of the host directly).

2) Fungi show a great variety of reproductive manifestations (sexual, asexual, gemmation; these manifestations can often be observed simultaneously in the same mycete), combined with a great morphostructural variety of organs. All of this is directed toward the end of spore formation, to which the continuity and propagation of the species is entrusted.

3) In mycology, it is often possible to observe a particular phenomenon called heterokaryon, characterised by the coexistence of normal and mutant nuclei in cells that have undergone a hyphal fusion. Nowadays, phytopathologists are quite worried about the creation of individuals that are genetically quite different even from the parents. This difference has taken place by means of those reproductive cycles, which are called parasexual. The indiscriminate use of phytopharmaceuticals has in fact often determined mutations of the nuclei of many parasitic fungi with the consequent creation of heterokaryon–and this is sometimes particularly virulent in its pathogenicity.4

4) In the parasitic dimension, fungi can develop from the hyphas more or less beak-shaped, specialised structures that allow the penetration of the host.

5) The production of spores can be so abundant as to include always, at every cycle, tens, hundreds and even thousands of millions of elements that can be dispersed at a remarkable distance from the point of origin5 (a small movement is sufficient, for example, to implement immediate diffusion).

6) Spores have an immense resistance to external aggression, for they are capable of staying dormant in adverse conditions for many years while preserving unaltered their regenerative potentialities.

7) The development coefficient of the hyphal apexes after the germination is extremely fast (100 microns per minute under ideal conditions) with ramification capacity, thus with the appearance of a new apex region that in some cases is in the neighbourhood of 40-60 seconds.6

8) The shape of the fungus is never defined, for it is imposed by the environment in which the fungus develops. It is possible to observe, for example, the same mycelium in the simple isolated hyphas status in a liquid environment or in the form of aggregates that are increasingly solid and compact, up to the formation of pseudoparenchymas and of filaments and mycelial strings.7

9) By the same token, it is possible to observe in different fungi the same shape whenever they must adapt to the same environment (this is called dimorphism). The partial or total substitution of nourishing substances induces frequent mutations in fungi, and this is further proof of their high adaptability to any substrata.

10) When the nutritional conditions are precarious, many fungi react with hyphal fusion (among nearby fungi) which allows them to explore the available material more easily, using more complete physiological processes. This property, which substitutes co-operation for competition, makes them distinct from any other micro-organism, and for this reason Buller calls them social organisms.8

11) When a cell gets old or becomes damaged (e.g., by a toxic substance or by a pharmaceutical), many fungi whose intercellular septums are provided with a pore react by implementing a defence process called protoplasmic flux, through which they transfer the nucleus and cytoplasm of the damaged cell into a healthy one, thus conserving unaltered all their biological potential.

12) The phenomena regulating the development of hyphal ramification are unknown to date.9 They consist of either a rhythmic development or in the appearance of sectors which, though they originate from the hyphal system, are self-regulating,10 that is, independent of the regulating action and behaviour of the rest of the colony.

13) Fungi are capable of implementing an infinite number of modifications to their own metabolism in order to overcome the defence mechanism of the host. These modifications are implemented through plasmatic and biochemical actions as well as by a volumetric increase (hypertrophy) and numerical hyperplasy of the cells that have been attacked.11

14) Fungi are so aggressive as to attack not only plants, animal tissue, food supplies and other fungi, but even protozoa, amoebas and nematodes.
Fungi hunt nematodes, for example, with peculiar hyphal modifications that constitute real mycelial criss-cross, viscose or ring traps that immobilise the worms.
In some cases, the aggressive power of the fungus is so great as to allow it–with only a cellular ring made up of three unit–to tighten its grip, capture and kill its prey within a short time, notwithstanding the desperate struggling of the prey.

>From the short notations above, it therefore seems fair to dedicate greater attention to the world of fungi, especially considering the fact that biologists and microbiologists constantly highlight large deficiencies and voids in all their descriptions and interpretations of fungi’s shapes, physiologies and reproductions.

So the fungus, which is the most powerful and the most organised micro-organism known, seems to be an extremely logical candidate as a cause of neoplastic proliferation.
Imperfect fungi (so called because of the lack of knowledge and understanding of their biological processes) deserve particular attention, since their essential prerogative sits in their fermentative capacity.
The greatest disease of mankind may therefore hide within a small cluster of pathogenic fungi, and may after all be located with just some simple deductions able to close the circle and provide the solution.

Candida albicans: a necessary and sufficient cause of cancer

Considering that among the human parasite species the Dermatophytes and Sporotrichum demonstrate an excessively specific morbidity, and that experience shows that Actinomycetes, Toluropsis and Histoplasma rarely enter the context of pathology, the Candida albicans fungus clearly emerges as the sole candidate for tumour proliferation.

If we stop for a second and reflect on its characteristics, we can observe many analogies with neoplastic disease. The most evident are:
1) ubiquitous attachment–no organ or tissue is spared;
2) the constant absence of hyperpyrexia;
3) sporadic and indirect involvement of the differential tissues;
4) invasiveness that is almost exclusively of the focal type;
5) progressive debilitation;
6) refractivity to any type of treatment;
7) proliferation facilitated by multiplicity of indifferent co-founders;
8) Symptomatological basic configuration with structure tending to the chronic.

Therefore, an exceptionally high and diversified pathogenic potentiality exists in this mycete of just a few microns in size, which, even though it cannot be traced with the present experimental instruments, cannot be neglected from the clinical point of view.

Certainly, its present nosological classification cannot be satisfactory because, if we do not keep the possibly endless parasitic configurations in mind, that classification is too simplistic and constraining.
We therefore have to hypothesise that Candida, in the moment it is attacked by the immunological system of the host or by a conventional antimycotic treatment, does not react in the usual, predicted way but defends itself by transforming itself into ever-smaller and non-differentiated elements that maintain their fecundity intact to the point of hiding their presence both to the host organism and to possible diagnostic investigations.

Candida’s behaviour may be considered to be almost elastic. When favourable conditions exist, Candida thrives on an epithelium; as soon as the tissue reaction is engaged, it massively transforms itself into a form that is less productive but impervious to attack: the spore. If, then, continuous subepithelial solutions take place, coupled with a greater areactivity in that very moment, the spore gets deeper into the lower connective tissue in such an impervious state that colonisation is irreversible.

In fact, Candida takes advantage of a structural interchangeability, utilising it according to the difficulties, e.g., in feeding, to overcome its biological niche. In this way, Candida is free to expand to maturation in the soil, air, water, vegetation, etc.–that is, wherever there is no antibody reaction. In the epithelium, instead, it takes a mixed form, which is reduced to the sole spore component when it penetrates the lower epithelial levels, where it tends to expand again in the presence of conditions of tissular areactivity.

The initial mandatory step of an in-depth research endeavour would be to understand if and in which dimensions the spore transcends, what mechanisms it engages to hide itself or, again, to preserve its parasitic characteristic, or if it has available a neutral quiescent position which is difficult or even impossible to detect by the immunological system.

Unfortunately, today we do not have the appropriate means, either theoretical or technical, to answer these and similar questions, so the only valid suggestions can come solely from clinical observation and experience. While not providing immediate solutions, these sources can at least stimulate further questions.

Assuming that Candida albicans is the agent responsible for tumour development, a targeted therapy would take into account not just its static and macroscopic manifestations but even the ultramicroscopic ones, especially in their dynamic valency, that is, the reproductive. It is very probable that the targets to attack are the fungi’s dimensional transition points in order to perform a decontamination with such a scope as to include the whole spectrum of the biological expression–parasitic, vegetative, sporal and even ultradimensional and, to the limit, viral.

If we stop at the most evident phenomena, we risk administering salves and unguents forever (in the case of dermatomycosis or in psoriasis), or clumsily attacking (with surgery, radiotherapy or chemotherapy) enigmatic tumoural masses with the sole result of facilitating their propagation, which is already heightened in the mycelial forms.

Why, one may ask, should we assume a different and heightened activity of Candida albicans, since it has been abundantly described in its pathological manifestations? The answer lies in the fact that it has been studied only in a pathogenic context, that is, only in relation to the epithelial tissues.

In reality, Candida possesses an aggressive valency that is diversified in function in the target tissue. It is just in the connective or in the connective environment, in fact, and not in the differentiated tissues, that Candida may find conditions favourable to an unlimited expansion. This emerges if we stop and reflect for a moment on the main function of connective tissue, which is to convey and supply nourishing substances to the cells of the whole organism. This is to be considered as an environment external to the more differentiated cells such as nervous, muscular, etc. It is in this context, in fact, that the alimentary competition takes place.

On the one hand, we have the organism’s cellular elements trying to defeat all forms of invasion; on the other hand, we have fungal cells trying to absorb ever-growing quantities of nourishing substances, for they have to obey the species’ biological imperative to form ever larger and diffused masses and colonies.

>From the combination of various factors pertinent to both the host and the aggressor, it is possible to hypothesise the evolution of a candidosis.
First stage: Integer epitheliums, absence of the debilitating factors. Candida can only exist as a saprophyte.

Second stage: Non-integer epitheliums (erosions, abrasions, etc.), absence of stage debilitating factors, unusual transitory conditions (acidosis, metabolic disorder, and microbial disorder). Candida expands superficially (classic mycosis, both exogenous and endogenous).

Third stage: Non-integer epitheliums, presence of debilitating factors (toxic, stage radiant, traumatic, neuropsychic, etc.). Candida goes deeper into the subepithelial levels, from which it can be carried to the whole organism through the blood and lymph (intimate mycosis).12

Stages one and two are the most studied and understood, while stage three, though it has been described in its morphological diversity, is reduced to a silent form of saprophytism. This is not acceptable from a logical point of view, because no one can demonstrate the harmlessness of the fungal cells in the deepest parts of the organism.

In fact, the assumption that Candida can behave in the same saprophytic manner that is observed on integer epitheliums when it has successfully penetrated the lower levels is at least risky, because the assumption would have to be sustained by concepts that are totally aleatory (i.e., dependent on chance).

In fact, we are asked not only to accept a priori that the connective environment is (a) not suitable to nourish the Candida, but also at the same time to accept (b) the omnipotence of the body’s defence system towards an organic structure that is invasive but that then becomes vulnerable once lodged in the deeper tissues.

As for point (a), it is difficult to imagine that a micro-organism so able to adapt itself to any substrata cannot find elements to support itself in the human organic substance; by the same token, it seems risky to hypothesise that the human organism’s defence system is totally efficient at every moment of its existence.

As for point (b), the assumption that there is a tendency to a state of quiescence and vulnerability in the case of a pathogenic agent such as fungus–the most invasive and aggressive micro-organism existing in nature–seems to carry a whiff of the irresponsible.

It is therefore urgent, on the basis of the abovementioned considerations, to recognise the hazardous nature of such a pathogenic agent which is capable of easily taking the most various biological configurations, both biochemical and structural, regardless of the conditions of the host organism.
The fungal expansion gradient in fact becomes steeper as the tissue that is the host of the mycotic invasion becomes less eutrophic and thus less reactive.

Benign tumours
To that end, it seems useful to consider briefly the “benign tumour” nosological entity. This is an issue that always appears in general pathology but is brushed aside most of the time too easily, and it is overlooked because it usually doesn’t create either problems or worries. It constitutes one of those underestimated grey areas seldom subjected to rational, fresh consideration.
If the benign tumour, however, is not considered a fully fledged tumour, it would be advantageous, for clarity, to categorise it in an appropriate nosological scheme.

If it is thought that, instead, it fully belongs to neoplastic pathology, then it is necessary to consider its non-invasive character and consequently to consider the reasons for this. It is in fact evident how in this second scenario, the thesis based on a presumed predisposition of the organism to auto-phagocytosis, having to admit an expressive graduation, would stumble into such additional difficulties such as to become extremely improbable.

By contrast, in the fungal scenario, the mystery of why there are benign and malignant tumours is exhaustively solved, since they can be recognised as having the same aetiological genesis.
The benignity or malignancy of a cancer in fact depends on the capability of tissular reaction of a specific organ expressing itself ultimately in the ability to encyst fungal cells and to prevent them from developing in ever-larger colonies. This can be achieved more easily where the ratio between differentiated cells and connective tissue is in favour of the former.

Situated between the impervious noble tissues, then, and the defenceless connective tissues, the differentiated connective structures (the glandular structures in particular) represent that medium term which is only somewhat vulnerable to attack because of an ability to offer a certain type of defence.
And it is in these conditions that benign tumours are formed; that is, where the glandular connective tissue is successful in forming hypertrophic and hyperplastic cellular embankments against the parasites. In the stomach and in the lung, instead, since there are no specific glandular units, the target organ, provided with a small defensive capability, is at the mercy of the invader.

Furthermore, it is worth mentioning how several types of intimate fungal invasion do not determine the appearance of malignant or benign tumours but a type of particular benign tumour (specific degenerative alterations), as is the case with some organs or apparatuses that do not have peculiar glandular structures but nevertheless are attacked in their connective tissue, although in a limited way.

In fact, if we consider multiple sclerosis, SLA, psoriasis, nodular panarthritis, etc., the possible development of the fungus in a three-dimensional sense is actually limited by the anatomic configuration of the invaded tissues, so that only a longitudinal expansion is allowed.

Going back to the precondition of areactivity that is necessary for neoplastic development in a specific individual, it is permissible to affirm how in the human body each external or internal element that determines a reduction of well-being in an organism, organ or tissue possesses oncogenic potentiality. This is not so much because of an intrinsic damaging capability as much as a generic property of favouring the fungal (that is, tumoural) flourishing.

Then the causal network so much invoked in contemporary oncology, which involves toxic, genetic, immunological, psychological, geographical, moral, social and other factors, finds a correct classification only in a mycotic infectious perspective where the arithmetical and diachronic summation of harmful elements works as a co-factor to the external aggression.

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