The biological Nature of Cancer and its Therapy

"Not who says what, but WHAT who says ... counts."

"Only the message is judged very radically, never the messenger!"

Prolog

At the end of the 19th century, John Beard recognized the biological nature of the cells from which tumors originate, namely the cells of the 'inner cell mass' that form on the 5th day after fertilization and a good 2 weeks later in the early embryonic body immigrate. Nicholas J. Gonzalez 100 years later that these are identical to the adult stem cells, whose origins lie in the dark for science, and that they form our lifelong reservoir of cell renewal. Beard was nominated for the NP in 1903.

Beard also recognized that the “outer cell mass” of the pre-embryonic germ is a tumor that eats its way into the uterus like a malignancy. Not until the 54th-56th post-fertile day, exactly when the embryonic pancreas begins to work, its growth is suddenly ordered, which leads to the later placenta (placenta). With the onset of activity of the pancreas, bicarbonate and the enzymes trypsin and chymotrypsin in addition to the other proteases/peptidases, lipases and amylases) appear in the embryo-trophoblastic complex. The boundary between the endocrine and exocrine function of the pancreas is not an absolute one; there are circulating digestive enzymes in the blood that are activated in an alkaline environment. They represent the antithesis of the cancer cells' feeding enzymes, the matrix metalloproteinases, which perform their gruesome work of destruction most effectively in an acidic environment. With pancreatic enzymes, especially trypsin, he was certain that he had the body's most important weapon against malignant tumors in front of him, and he became the founder of enzyme therapy for cancer.

Otto Warburg discovered the fundamental metabolic difference between normal and cancer cells in the 1920s, Heinrich Kremer many decades later that the difference is not an either or, but a gradual one (normal cells cover 90% of their energy needs with oxygen, cancer cells only 35% or even less). Warburg received the NP in 1931 for his clarification of the energy metabolism of normal cells, for that of cancer cells he should supposedly have received it in 1944, which he was politically denied.

Warburg gradually withdrew the oxygen from a cell culture, which gradually led to the death of the cells. Some survived and became cancerous, these were the stem cells, which of course were not yet known at the time, they epigenetically increased their glycolytic energy production to the vitally necessary level.

However, the latest research shows an even greater flexibility and adaptability, both cancerous (Gonzalez CD et al) and non-cancerous (Caudwell Xtreme Everest Research Group) cells, with regard to the metabolic pathways of their energy production than previously assumed, for example, epithelial cancer cells are capable of glycolysis in neighboring fibroblasts to induce, the high accumulation of tricarboxylic acids (lactate, pyruvate) is used to heat up their mitochondrial oxidative phosphorylation (with upregulation of antioxidant enzymes), which in turn increases the overall ATP yield and tumor aggression (inverse Warburg effect).

Therapy resulting out of the model of what cancer is according to its biological nature and how it functions.

In our body only the germ cells (and a few immune cells) are immortal, i.e. they have no hayflick limit, cancer stem cells are also immortal because they are actually germ cells, because:

There is only one physiological equivalent of the (multiple) chromosome changes in cancer cells (Springer) and that is the premeiotic crossover in the germ cell cycle.

Only one of a decade-long resting latency, the female egg cell after crossing for up to 50 years and even more (Diktyotaene).

Only one unbridled aggressive growth, the germinal vesicle tumor (from the fertilized egg cell), which eats its way into the uterus from the 6th day after fertilization.

Only one for cell migration (metastasis) with colonization (clones), the migration of germ cells from the inner cell mass ('embryonic stem cells') into the early embryo towards the end of the 3rd post-fertile week ('adult stem cells').

Only one for the use of zinc matrix metalloproteinases, the cells of the outer cell mass that eat their way into the tissue of the maternal uterus up to the end of the 8th week of pregnancy.

Only one for active telomerase, just our germ, trophopblast, as well as embryonic and fetal cells up to differentiation (apart from the memory cells).

And finally only one for hCG production, the fertilized egg cell with its complete set of foreign chromosomes (Acevedo)! The crossover of the later cancer cell does not initiate a regular maturity division, but "at best" an incomplete one, there is no halving of the chromosome set e.g.,the ability to divide is retained. After the crossover, mitosis probably occurs in which duplicated chromosomes are separated and not the chromosome pairs, as is usually the case with first meiosis. After all, the average body temperature of 37°Celsius is too high for an orderly meiosis.

In regular I. meiosis, the dividing spindle pulls the chromosome pairs apart (diakinesis) while “opening” the synaptonemal complex and a haploid chromosome set with double chromatids per chromosome is attached to each of the two daughter cells. Disturbances in diakinesis or second meiosis often occur as separation anomalies (non-disjunction), which can lead to trisomy 21, for example.

In the development of cancer cells, the synaptonemal complex probably does not open at all,whereas the centromeres as in normal mitosis, which at least mathematically leads to a cell with a complete set of chromosomes that may immediately divide.

After the crossover, the adult stem cell becomes a new trophoblast cell with all its properties, a perverse fruit imitation, a "foetate". Whether cancer is a solid tumor (e.g. pancreas) or a diffuse appearance in the blood e.g. leukemia), the basis is the chromosomal alteration and activation to the "new" trophoblastic stem cell with its inherent compulsion to divide. This is the initial program that drives the fertilized egg cell to proliferate division and formation of the trophoblast (nutrient germ). In the case of neoplasms of the hematopoietic and reticulo-endothelial system as mentioned leukaemia, a profound change in the chromosome set is obviously not necessary as in solid tumors; the imitation or (more accurate) following of the germ cell cycle does not seem to begin, if at all, with the proliferating of the fertilized egg cell but "later". Only the trophoblast tumor is present up to the 5th post-fertile day, from which the offspring (embryo) only grows from a single cell on the 6th day.

It is just the language of embryology that I use, and not that of genetics, which has to put up with being hit on the nose from an elder venerable subject! Genetics disguises and encrypts truth and knowledge with its bizarre jumble of letters, something only computers can deal with fully.

What is pissed around with surface markers, which probably change like nothing, and still nothing decent comes out of it (apart from extremely expensive detail effects), is a horror! We know from Gilbertt N. Ling that it is the inside of the cell that makes up the cell.

The fact that cancer is a "crippled" germ cell line has been ignored since John Beard (1). If you think about this further, our adult stem cells in their niches are those cells that migrated from the inner cell mass of the early trophoblast into the even earlier embryo (Gonzalez (2)).

When I think this cancerous “crippled” germ cell cycle through to an end, I inevitably arrive at irregular crossovers, diakinesis, meioses and mitoses as the cause of the genetic heterogeneity of cancerous tumor cells and not mysterious spontaneous and secondary mutations.

Crossovers start at chromosomal breaking points, mutations do not. This should be proven in a nifty study with comparative genome analyzes of both tumors and their carriers. We need holistic embryologists, geneticists and oncologists!

(1) Beard, John "The Enzyme Treatment of Cancer", Chatto & Windus, London 1911 (reprinted New Spring Press, New York 2010)

(2) Gonzalez, Nicholaz J. "The Trophoblast and the Origins of Cancer", New Spring Press, New York 2009

The biological Nature of Cancer

page 1

Cancer cells show a high level of incomplete “sugar burning” (with or without the participation of free oxygen in the cytoplasm!) (Kremer), therefore the high lactic acid content must be effectively neutralized intracellularly and this is only possible via a certain enzyme, namely the carbonic anhydrase, this enzyme must be inhibited or overstraining it to cause a metabolic breakdown of the cancer cell.

In order to be able to breathe off continuously produced carbon dioxide, a capillary blood transit time of more than 5 seconds is required, but it happens in one. How does the body do it? In the 1920s, researchers were puzzled. Hemoglobin was "suspected", it wasn't.

Norman Urquhart Meldrum, born in 1907 in Mid Lothian, Scotland, grew up in Bombay, where his father worked as a chemist at what was then the Royal Institute of Science,completed his doctorate in Cambridge in 1931 with a dissertation on glutathione and died suddenly on May 17, 1933. Just in time he had discovered carbonic anhydrase a year earlier and was able to leave this priceless gift to mankind, as if his life had only been there for this task (Chegwidden et al. "The Carbonic Anhydrases - New Horizons", Basel Boston Berlin 2000, Seitze 8).

Meldrum's friend and colleague Francis John Wordsley Roughton (the two of them did research together) in the 30ies (Meldrum had been dead for a few years) once reasoned that carbonic anhydrase in peripheral tissue is more an enemy of the organism than a friend (ibidem) . He referred to the hydration of the CO₂ by the CA to the bicarbonate ion, which he viewed as an "uneconomical", even harmful metabolic detour, compared to the direct passive diffusion of the carbon dioxide (Roughton FJW, Meldrum NU). Similar to the fact that the unstable carbonic acid is highly stable in the cell metabolism and requires carbonic anhydrase (isoenzyme II) to break down into water and carbon dioxide, the cellular metabolic product CO₂ needs the isoenzyme III of carbonic anhydrase (CA III) to diffuse out of the cell. We know from Gilbert N. Ling that the cell is not a sack filled with salt water in which everything swims around, but a gel state (Ling) structured by the interaction of dipole water molecules with fixed ionic peptide charge carriers, which allocates space and dynamics to each molecule involved , this is of course especially true for water, but also for CO₂, which cannot simply "gas away" or diffuses away, but requires CA III, which cannot be inhibited by acetazolamide. Of course, Roughton could not have known that at the time.

Dr. Tullio Simoncini, totally hereticised as a doctor, claims stiffly and firmly that he has cured countless cancer patients by giving high amounts of sodium bicarbonate (baing soda), but this therapy is theoretically entirely conceivable, because high amounts of food overwhelm carbonic anhydrase ...

Simoncini himself thinks that cancer is actually fungus (Candida), and that this would be destroyed by the antifungal baking soda, which is not absurd either, because all tumors are totally streaked with fungus.

Simoncini is not alone.

Page 2

As early as 1948, the pathologist, microbiologist and hygienist, Franz Gerlach, veterinary professor in Vienna and director of the Federal Institute for Animal Disease Control in Mödling / Vienna, after decades of studying thousands of microscopic tumor preparations, advocated the theory that cancer growth was triggered by fungi (Micromyces blastogenes) in "Krebs und obligater Pilzparasitismus" (Cancer and obligatory fungal Parasitism ”(Urban & Schwarzenberg, Vienna 1948). In the summarizing final sentence he states straightforwardly (quote): “No malignant tumor without involvement of the tumor micromycete, on the other hand numerous infections with the tumor micromyte without a tumor becoming manifest! The tumor micromycete, Micromyces blastogenes, is an obligatory parasite in all malignant tumors!"

The solid cancerous growths with through-growing fungal mycelia are not secondary infections but causally responsible for neoplasms; Gerlach had tirelessly studied tumors under the microscope and experimented with them since the beginning of the 20th century. When the fungus cultivated from tumors of patients was transferred to healthy animals, malignant growth arose in 3–4%. Mycoses are facultative precancerous diseases; Gerlach also tried to vaccinate with the fungus 'Micromyces blastogenes' that he had identified.

The fact that microbes cause cancer has also been found among pleomorphists since the 19th century (in the early twentieth, Enderlein). Fungi are considered to be the most highly developed microbes and in the dark field microscop there are clearly visible inclusion bodies on erythocytes in predisposed and cancer patients (Dumrese J, Haefeli B), as well as "coin roll" formations and massive mucus as general acid and fungal signs.

In the last third of the 20th century. Simoncini begins in Italy to treat (predominantly solid) malignant tumors with high doses of sodium bicarbonate enterally and parenterally; intensive iodine brushes are also used for skin cancer. Simoncini attributes the apparently astonishing successes to the "fungal nature" of cancer, because NaHCO₃ is a highly potent antifungal agent due to its alkalinity. He identified Candida albicans as the universal cancer trigger. Candida albicans can be detected in approx. 30% of all people in western industrial nations (sprouting fungi). Gerlach's Micromyces blastogenes was later assigned to mycoplasmas in the 1950s as a group of "pleuropneumonia-like-organisms" (PPLO) between viruses and bacteria Dumrese).

Scientific medicine thinks that this is a secondary infestation. Although fungal and cancer cells cannot be identical due to different sets of chromosomes (e.g. those show very long telomeres, cancer cells mostly very short ones), mutual influence can not be ruled out, perhaps there is even a symbiosis. Fungi could prevent apoptosis of senescent body cells with appropriate signal substances (Dalmasso, Filler) and trigger unbridled cancerous growth, the cancer cell "thanks" by creating extracellular lactic acid milieus. Mushrooms "like it" sour.

Dr. Stan Burzynski discovered as early as in the 1940s that various types of cancers in the blood and urine of their carriers lack certain small organic molecules that are characteristic of each type of cancer. Burzynski identified these molecules and substituted them in his patients with impressive success. Because their effects are directed against neoplasms, he called them antineoplastons (Elias TD).

Page 3

Antineoplastons are substances that are metabolically similar to those active molecules that are “between” glycolysis and the citrate cycle, such as phenyl acetate or butyrate. The much-touted dichloroacetate (DCA) is one of them.

A reference to an anti-carcinogenic effect of such small molecules can also be found in H. Nieper “Auf neue Wegen” (Langenhagen 2000), page 136f (acetaldehyde, benzaldehyde).

The 3.5 billion year old genome A (“archaic” - eating, multiplying, growing), which produces ATP without burning oxygen (at that time no or hardly any free O₂ was available), is still active in all of us, but is later switched over and being dominated by Genome B (“bacterial”) from the phylogenetic point of view , which enables further combustion of pyruvic acid in the citrate cycle and respiratory chain to CO₂ and H₂O (with 19x higher energy yield).

Cancer is dominant genome A (Kremer)

As early aerobic bacteria, our mitochondria entered into a cell symbiosis with the anaerobic primordial cells and thus created the foundation for the evolution of today's life on earth.

Under certain circumstances, it is made impossible for the mitochondria to continue to burn oxygen for energy production, because otherwise the entire cell would be damaged and it is forced to switch back to the old mode (glycolysis with lactic acid as the end product), which economically reduces the energy yield to 1/19 (severe tiredness and exhaustion of the individual, burnout as facultative precancerous condition) and fuels the cellular primal division program that gives birth to the cancer cell (Kremer).

Cancer cells not only show a striking resemblance to embryonic (actually trophoblastic) cells, no, they are, and it is well known in oncology that the following is undisputed: the more immature the embryonic degree of differentiation of a cancerous tumor, the more malignant it is. And: It's not going to have an abortion.

"Cancer is our unrecognized dark parthenogenic brother, a deadly sibling who gives birth to daughters."

Cancer cells show a changed (mutated) set of chromosomes different to the carrier, malignant tumors are cellular individual associations with their own strategy and will to survive, have withdrawn from the community of body cells, adapt to changed environmental situations, so they act sensibly.

In evolutionary terms, tumors correspond to the unicellular associations in the primordial sea (Kremer); if you think a little further in evolution, you will notice a certain similarity between our internal and external sexual organs with sea cucumbers, jellyfish and other molluscs.

page 4

"Cancer Intelligence"

According to Beard, every tumor is its own being (namely the asexual intermediate generation known in botany also exists in animals and humans) with its inherent instinct for self-preservation; In embryology this being is called a trophoblast, in some species there are even beginnings for nerve cells, this nutrient germ develops into a placenta and is specially born. The darkly humorous malevolent bitterly angry statement in our sometimes heartless culture of conversation that one would have better raised one's afterbirth instead of him or her, receives an additional tragicomic echo here.

On the 5th day after fertilization, the egg cell, which is constantly dividing, has already formed an outer cell mass of over 100 cells, enclosing a fluid-filled cavity into which the inner cell mass ('embryonic' stem cells) protrudes at one point. The next day, the human chorionic gonadotropin (hCG) secreting "germinal vesicle tumor" from over 200 cells with a foreign chromosome set embeds itself in the mucous membrane and muscles of the uterus. When connected to the maternal tissue hCG diffuses into the bloodstream (Gravindex pos) and the embryo begins to sprout out of a single inner cell. Cancer is the monstrous development of into the early embryo immigrated germ cells, which are found as adult stem cells in so-called niches everywhere in the body (Gonzalez). Cells, from which a new person normally emerges and which in the course of life constantly renew our damaged and dead body tissue, differentiate into gruesome cancerous tissue. They are distributed throughout the early embryonic body at the beginning of the 4th week after fertilization. They begin a few days earlier in the inner cell mass, that focal elevation of proliferating cells that protrudes into the germinal vesicle from the 5th day onwards. Because the offspring does not begin to sprout from a single cell until the 6th day, in parallel with the better supply, and no other inner cells participate, the immigrated stem cells are not of somatic origin. Except for that one cell of the inner cell mass of the nutrient germ, which forms the basis for the growth of the embryo, all the others stay “apart” until they migrate in the 3rd and 4th week.

Since the inner cells are suitable for growing all types of tissue, the somewhat sloppy term 'embryonic stem cells' has become established for the migrated 'adults'. Since there are signs of foci of the inner cell mass already on the 4th day, the next day the cells are clearly recognizable, and there is still no trace of the embryo, it should correctly be called "trophoblastic stem cells".

The mulberry-like, spherical cell structure of the egg cell, which divides rapidly in the first few days, reflects the phylogenetic aspect of that early phase of cellular life on earth more than 2 billion years ago, when there was no or only small amounts of free oxygen in the atmosphere during this time, before photosynthesis, drift in the primeval ocean, only to eat, grow and multiply, to dew, infiltrate and grow through any usable inorganic and organic material in the neighborhood. Some of these tumors may also enclose germinal vesicle-like cavities and thus set the beginning of the compartmentalization of different milieus. They get their energy from sugar splitting, probably as today with the formation of pyruvic and lactic acid, carbonic acid and its salts, as well as uric acid from the breakdown of ATP will have played a role, as well as the production of energy from inorganic material, chemolithotrophy (Kremer).

page 5

Germ cells in the morula and blastocyst stage are still far from any kind of organic specialization and differentiation, infinitely capable of division, pluripotent in their disposition, they show cellular survival instinct. In the later embryonic development after the 20th week, when after the completion of the differentiation of the organs only size growth begins, the immortality of the body cells is lost when the telomerase is silenced. It remains unchanged and active only in the germ cells of the gonads.

On the 6th day, the embryo sprouts from only one single cell of the 'inner cell mass' (embryonic stem cells) present in the blastocyst from the 5th postfertile day onwards, all other stem cells do not take part in this development, they migrate towards the end of the 3rd week from the 'rear' embryonic intestinal anlage into the transitional yolk sac in order to multiply significantly, is distributed in the 4th week (again over the 'rear' intestinal anlage) in the form of a comprehensive spiral movement throughout the embryo (including the gonads).

In the body, these cells (adult stem cells) serve the whole life the tissue structure and its renewal, only in the gonads do duplicated chromosome pairs sooner or later exchange chromosomes parts of each other (crossover or crossing over) and halve their chromosomal sets (reduction division, meiosis), in principle, after the crossing over, it is actually a question of 'foreign cells', because the changed set of chromosomes no longer corresponds quantitatively and qualitatively to that of the carrier individual. In a controlled gonadal environment, there is normally no immune reaction against sperm and egg cells or their precursors.

On the 6th post-fertile day, nidation in the uterus begins, the hCG seems to play the most important role in preventing rejection, it is produced very early by the trophoblasts (GravIndex test positive even before the rule fails).

Cancer is a 'differentiation disorder of stem cells or their descendants that are still able to divide', embryonic and adult are identical, the latter only divide in adults when tissue renewal is pending, and once an 'asymmetrical' copy is created that it divides 10-15 generations long and thereby gets more and more differentiated, until it only matures further and is no longer capable of dividing. (terminal restriction). The closer the differentiation stop takes place in the generation sequence to the stem cell, the more anaplatic, i.e. more malignant, the tumor. The stem cell itself remains unchanged.

Since stem cells ("cancer stem cells") have meanwhile been found in various cancer tissues, this suggests that the stem cell itself is not "consumed", but its progeny of division. There is one stem cell for every 100 cancerous tumor cells.

Before the war, researchers discovered meioses in tumors, but not since then. It was not until 2007 that similarities with gametes were found again (Kohane et al.). The decisive factor in the development of cancer seems to be a crossing over, the 2nd meiosis does not necessarily have to occur, i.e. the halving of the chromosome set may not occur, but further cell divisions with further crossing overs may follow, hence the chaotic diverse chromosome sets in Cancer cells and hCG production (from crossing over?). If no hCG is produced, it is a so-called benign tumor (Acevedo).

page 6

For some reason, direct descendants of adult stem cells try to form an 'irregular' trophoblast in the body with all the disadvantageous consequences (see ability to migrate in the 3rd / 4th week post-fertile, a kind of physiological metastasis).

The physiological trophoblast grows 'cancerous' up to the 8th week of pregnancy (54th day) in the maternal uterus; With the onset of the secretory activity of the embryonic pancreas, the external trophoblast ceases to aggression and begins to differentiate in an orderly manner from the later placenta. According to J. Beard, the endopeptidases trypsin and chymotrypsin are responsible for this, which are also endocrine-disruptive and can dissolve cell clusters. This control of the 'nutrient germ' remains necessary until birth, because if the placenta is incomplete after the placenta has passed, there is a risk of potentially fatal chorionic carcinoma, which can metastasize within hours.

According to Beard, teratomas are only so harmless because they contain pancreatic tissue in addition to trophoblastic tissue.

The rapidly dividing fertilized egg cell has already divided 58 times on the 4th day after fertilization and surrounds a fluid-filled cavity, the blastocyst, as the outer cell mass, with a focal elevation inside it, the inner cell mass.

Up to the 5th day after fertilization, only the trophoblast (nutrient germ) with 107 cells is present, it shows a blastocyst (germinal bubble) with a focal cell accumulation on the inside at the edge, which is clearly thickened at this point by the inner cell mass. This inner cell mass consists of the embryonic stem cells, which are much discussed today, and any type of tissue can be grown from them.

On the 6th day, a large tumor of over 200 cells had already formed and began to implant in the lining of the uterus. On the 6th day the implantation in the uterus begins and at the same time the embryo ("inner sprout") begins to sprout from a single cell of the inner cell mass as an embryoblast ("sprout germ"). The embryo gives rise to the trophoblast (Gonzalez). The sudden improvement in the diffusion supply of the cell structure with nutrients goes hand in hand with the sprouting of the embryo (inner sprout) from a single cell, which divides quickly and selectively, and whose offspring change more and more and differ from one another (differentiate). Via an outer (ectoderm) and inner cotyledon (endoderm) with yolk sac, and finally a middle one (mesoderm), at the end of the 3rd week the sprout already shows a clearly recognizable shape with an eye / head area, body with intestine and yolk sac and the lower end of the body with coming Genital ridge, from which the gonads (ovaries and testicles) of the internal sex organs later develop.

The other cells of the inner cell mass stay apart and do not take part in this process. Strictly speaking, one cannot speak of an embryo before the 6th day, because none is there yet, but only that undifferentiated or hardly differentiated cluster of cells that gives the nourishing soil for the sprout to sprout and nourishes it, the nutrient germ (trophoblast). Later the placenta (placenta or chorion).

Page 7

All other trophoblast cells of the inner cell mass stay “to the side” and do not take part in the formation of the cotyledons and further differentiation of the embryo the temporary yolk sac, in which they feed and multiply considerably; At the beginning of the 4th week it goes back into the intestine and finally colonizes the entire embryo (migrating germ cells), including the later gonadal area (primordial germ cells), in a spiral-like migration. In the gonads they cross over with the reduction division in the course of life and thus lay the genetic foundation for the next living being; in the body they are responsible for tissue renewal throughout life (adult stem cells). These cells are not somatic but trophoblast cells and have the ability to form an accumulation of trophoblast cells (tumor).

Only towards the end of the 3rd week does this cell association suddenly become active and embark on its migration to distribute itself throughout the body of the embryo, a third of the migrants end up as germ cell precursors in the lower end of the body, where the genital ridge soon forms.

Externally, the fetus eats its way into the uterus like cancer, the same growth and inhibiting substances are used, above all the zinc matrix metalloproteinases. This process lasts until the 8th week of pregnancy (54th day), then suddenly the aggressive growth stops and the outer trophoblast begins to develop in an orderly manner into a placenta (chorion, placenta). On the 54th day, the embryo's pancreas begins to work, especially the endopeptidases trypsin and chymotrypsin seem to play an important role. This “termination” of the trophoblast by foeto-embryonic factors is necessary until birth, because if an incomplete placenta follows after the umbilical cord, a fatal metastatic chorionic carcinoma can develop within hours.

It is well known that humans have 23 pairs of chromosomes (diploidy), and when the egg cell is fertilized by the sperm, each of the two produces 23 unpaired chromosomes (haploidy), which then result in 23 pairs. But before that, the set of chromosomes must be halved during the development of the egg and sperm cell, that is, the meiosis or reduction division (meiosis).

On the genetic level, our life does not begin with the fertilization of the egg cell, but a crucial period before that, namely when the genes (or their carriers, the chromosomes) of the future living being rearrange themselves in a mysterious way, namely in the random distribution of homologous partners in the chromosome pairs on the two daughter cells and the cross-wise exchange of chromosome segments (crossover) in the development of our germ cells as part of the development process that is referred to as maturity or reduction division, because only when the normal diploid chromosome set is reduced by half (haploidy) , the cell is ripe to later serve as a fertilizing sperm or fertilized egg cell. The process consists of 2 cell divisions in a row (I. and II. Meiosis).

After the chromatid doubling, the partner chromosomes arrange themselves spatially parallel, with 4 double nucleotide strands (chromatids) lying next to each other, whereby the telomeres adhere to the inside of the nuclear membrane over their entire length in order to ensure a stable starting position for the upcoming dynamics of the crossover. The end pieces clearly do not take part in the genetic mix, which would also make no sense, since they all consist of identical base sequences.

In the exchange round of crossing over, maternal and paternal chromosome parts are vigorously exchanged and new, mixed genetic material is created, during the subsequent division the pairs are separated and each of the two daughter cells receives 23 double chromosomes, each with 2 chromatids (I. meiosis).

page 8

It is only during the subsequent 2nd division that the actual reduction to half occurs, as the chromatids of the chromosomes are separated from one another. Now 23 unpaired chromosomes fall on each of the two daughters (II. Meiosis). Because 2 cells arise from the 1st meiosis, there are a total of 4 daughter cells (gametes) after the 2nd meiosis.

In the crossover of the germ cells, the paternal and maternal chromosome parts are exchanged for each other after duplication and lateral aggregation (synapse pairing of the homologous chromosomes) and a "new" paternal-maternal genetic material is created, which through the subsequent cell division on both daughter cells is "normal", but unpaired, is distributed (I. meiosis), because there are 2 cells with each "doubled" haploid chromosome set, which is only subsequently halved by the actual reduction division (II. meiosis), in which the now mixed 23 "double chromosomes" are definitely separated and opened the two daughter cells are divided. Each of them is given a set of 23 unpaired chromosomes.

Through this reduction, half the foundation stone is laid for the genetic makeup of the future human being.

About 99% of what and how we are physically and have been based on the information program that is stored in each of our trillion cells in the cell nuclei and is permanently active, because it is not only the blueprint of our body, but also the helmsman for all that run continuously Metabolic and regeneration processes in the organism. The nucleus contains the core or nucleic acids, which consist of a sugar, a phosphoric acid residue and a base; this group of three is called a nucleotide, without the phosphoric acid residue the group of two is called the nucleoside.

Many substances dissolve in aqueous solution as particles with excess charge, the ions. Those with positive are cations, those with negative anions.

Whether a substance reacts alkaline or acidic depends on how the dissolved hydrogen atoms or H⁺ + ions change in their concentration (pH value) in aqueous solution when they are added, if a pH above 7 shows the substance is basic (alkaline), under 7 acidic. Since the pH value or the pH is defined as the negative decadic logarhythm of the hydrogen ion concentration, a low pH indicates a strong acid. In the human organism this only affects gastric acid with a pH of 1-1.5 when fasting and 2-4 when the stomach is full, otherwise in human nature (physiology) the metabolic processes do not take place around the chemical neutral point of 7.0, that would be far too acidic, but rather the pH value that prevails in human blood with values between 7.38 (7.35) - 7.43 (7.45), the biological neutral point of 7,4. The differences in concentration on the pH scale are so huge that it was decided to write the pH value as an exponent (power) of the number 10 (decadic logarhythm) and pH of 7 means 10⁷, but because it is, however, about the negative decadic logarhythm, the concentration increases downwards, i.e. a concentration of 1/10⁷ writes 10^-7, which corresponds to a ten-millionth, a pH of 6 would be 1 millionth, pH 5 1 hundred-thousandth, and so on.

Page 9

The pH value or the pH is therefore the negative decadic logarhythm of the hydrogen ion concentration, it relates exclusively to the concentration of the H⁺ -ions in a solution. Strictly speaking, every free H⁺ cation "attaches itself" to a water molecule and forms H₃O⁺, the hydronium or oxonium ion. Since it is a information on concentration, the pH is a ratio number.

Acids give off their positive hydrogen cations (H⁺ -ions) in aqueous solution, they dissociate. Strong acids such as hydrochloric acid (HCl) do this to a large extent, while weak acids to a low one. The ratio of the concentration of dissociated to undissociated molecules of an acid in aqueous solution is the dissociation constant K, and as with pH it is written as a pK value as an exponent of 10 in the denominator (the numerator is again 1), i.e. also as a negative logarhythm.

Bases, on the other hand, take up H⁺ -ions in aqueous solution, the more pronounced this circumstance, the greater the alkalinity of the base or lye.

Apart from the notation as negative logarithms, the pH value as a concentration specification is a ratio, the pK value is the ratio of the product of two concentrations (ratios) to the third, i.e. a ratio of a total of 3 ratios, which is why the pH and pK of acids in biological Systems are mostly in a similar range, but are never exactly the same, unless the concentration of the negative acid anion (e.g. lactate ion) and that of the undissociated "mother acid" (e.g. lactic acid) are the same, which interestingly in the case of the pK of 6.5 of the carbonic acid applies. The buffering or neutralization of the free positive H⁺ -ions means nothing else than that the natural low dissociation state of the weak (mostly organic) acid is spontaneously produced from negative and positive ions by gathering, which means that too much acid is withdrawn from circulation depending on metabolic requirements.

The pK value or the pK is the negative decadic logarhythm of the dissociation constant. If the hydrogen ion of one acid is replaced by another in aqueous solution (in metabolism mostly Na⁺, K⁺, Mg⁺⁺, Ca⁺⁺, Zn⁺⁺, etc.), the salt of this acid is present, which usually shows completely different properties. The best-known example is strong hydrochloric acid (HCl), a sometimes highly aggressive substance, which is whereas its sodium salt (NaCl) is an elixir of life , also known as table salt, which is converted into sodium (Na⁺) and chloride ions (Cl^-) dissolving in water. Salts are basically (like strong acids) dissociated, which sets them in contrast to their weak “mother acids”, which show only slight dissociation. Ions are elements (single atoms) or molecules (several elements) with excess charges, cations with positive, anions with negative, mostly in aqueous solution.

However, the low tendency of weak acids to dissociate is sufficient in biological systems to maintain the meticulous dynamic equilibrium between slightly dissociated “weak” organic and strong inorganic acids and their completely dissociated salts. Since salts of hardly dissociated acids are able to neutralize H⁺ -ions in solution, to buffer them as it is, a large number of which are active in the organism, one speaks of the buffer system of acids and their salts in the body.

Only a salt of a weak acid can buffer, because the positive hydrogen ion (cation) can only form a non-dissociated chemical compound with the negative ion (anion) of a salt of a weak acid, thus neutralizing it and rendering it "acidicly" ineffective. Not, however, with the salt of a strong acid, because there cannot be a non-dissociated complex, because the corresponding acid would be a strong one and therefore retain dissociated, the H⁺ would remain free and effective.

Page 10

When a dissociated buffer salt of a hardly dissociative weak acid is added, the sudden excess of hydrogen cations in the solution and the negative salt anions collide and fuse in no time, because the natural state of non-dissociation is created spontaneously. The free negative anions of the buffer salt are gradually consumed by the absorption of the positive hydrogen cations, forming the solid, undissociated molecules of the weak mostly organic acid, and when the distribution and concentration ratios of the dissociation constant K or the pK value are reached the buffering process stops. The lactate anion has now hardly become dissociated lactic acid, acetate has become acetic acid, citrate citric acid, etc.

So that the consumption of all buffer capacity, which would lead to acid death, does not occur so easily, nature has taken impressive precautions by the highest possible level of the salt of carbonic acid in the 1st dissociation stage, the hydrogen or bicarbonate anion (HCO₃^-), which is mostly present as a dissolved sodium salt.

If the bicarbonate anion spontaneously combines with the hydrogen cation in the buffer reaction, carbonic acid is formed which, outside of the metabolism, e.g. in an open vessel in a laboratory, quickly breaks down into carbon dioxide and water. Because carbonic acid occurs as an unstable acid, it is referred to as free and bound, the former relates to dissolved carbonic acid and carbon dioxide, the latter to hydrogen carbonate (and carbonate, being negligibly small under metabolic conditions).

However, the spontaneous decomposition of carbonic acid under laboratory conditions does not actually take place in the metabolism (or slows down to such an extent that it comes to the same effect). The carbonic acid appears in the metabolism as a stable acid and must be catalytically forced to decay. Because it has 2 cations to dissociate (H₂CO₃), there is a 1st pK value or a 1st acid constant of 6.5, where only one H⁺ is dissociated, and there are equal amounts of free carbonic acid and bicarbonate, so that would be the case to expect the best buffering effect at the same high pH. (The unbiological relationships of the 2nd acid constant with pK and pH above 10 are only of formal interest.)

On the other hand, an average pH of 7.4 is maintained in human blood. How is that possible?

Perhaps the most effective enzyme in all of nature: carbonic anhydrase. It accelerates the spontaneous (de facto not happening) decomposition of carbonic acid into CO₂ and H₂O by up to 10 million times!

In addition in the legendary textbook of the physiology of Ganong, William F. "Review of Medical Physiology" (German edition, transl. W. Auerswald, page 651, open bicarbonate buffer) 4th edition, Springer Verlag, Berlin Heidelberg New York 1979 Quote: '... If H⁺ is added to the blood, then HCO₃^-, the concentration of which is additionally regulated by the kidneys, decreases, while more H₂CO₃ is produced. If this additional H₂CO₃ were not converted into CO₂ and H₂O and the CO₂ ventilated in the lungs, the H₂CO₃ concentration increases. For example, if the amount of H⁺ added had been sufficient to reduce the plasma HCO₃^- by half, then the pH would drop from 7.4 to 6.0. In reality, however, not only is all of the additionally formed H₂CO₃ removed, but the rise in H⁺ also stimulates breathing; this causes the pCO₂ to drop so that additional H₂CO₃ is removed. The pH would therefore only drop to about 7.2 in the present example (Fig. 40.2). The reaction CO₂ + H₂O = H₂CO₃ proceeds slowly in both directions if the enzyme carbonic anhydrase is not present. Carbonic anhydrase is absent in the plasma, but it is abundant in the erythrocytes ... ‘

Page 11

Garrett Reginald, Charles M. Grisham: Biochemistry. (International Student Edition). 4th edition. Cengage Learning Services, 2009, ISBN 978-0-495-11464-2, p. 394, quote: '… carbonic anhydrase is an enzyme that catalyzes very quickly: it can hydrate up to 10⁶ molecules of carbon dioxide per second and accelerates the reaction 10⁷ times, i.e. 10 million times, Kcat value 1,000,000 per second … ‘

Karlson, Peter "Short textbook on biochemistry for medical and natural scientists" (page 311, open bicarbonate buffer) 11th edition, Springer 1980 Quote: '... The pK value of carbonic acid (1st stage) is 6.1; ( personal note: in more recent ref. 6.5) with a non-volatile acid, the best buffer effect would be expected in this area. However, since CO₂ is volatile and the carbonic acid hydratase (pers. note: old name of the CA) always sets an equilibrium between CO₂ and H₂CO₃, the effective H₂CO₃ concentration is primarily dependent on the carbon dioxide tension. ... '(pers. note: all underlining by the author)

Because the carbonic acid produced by the buffering of H⁺ is immediately disintegrated by the CA and the carbon dioxide and water produced can be easily exhaled and excreted via the lungs and kidneys, the "open" carbonic acid-bicarbonate buffer system is the most important buffer for absorbing pH - Fluctuations in the blood, consisting of carbonic acid (H₂CO₃) as the acid and the bicarbonate ion (also called hydrogen carbonate ion, HCO₃^-) as the base. The form of transport of CO₂ in the blood is the bicarbonate - anion HCO₃^-, the excretion or retention of which is also regulated by the CA in the kidney epithelial cells. This prevents unnecessary loss of the bicarbonate ion buffer reserve.

The protein buffer is predominant intratracellularly, as the amino and carboxyl groups of the peptide chains are ideally suited to bind H⁺ when too much acid and release OH^-, and release H⁺ or bind OH^- again when too little. This buffer does not use up itself.

This is the essence of buffering excess acid, without which life in this form would be inconceivable. If several molecules are linked together in an acidic compound, as in the case of nucleic acids, this does not mean that the molecules in question also individually react acidic, as shown by the purine and pyrimidine bases, which are very important components of the nucleic acids.

The information program in the cell nucleus consists of two parallel nucleotide chains on the outside, in which sugar and phosphoric acid residues are alternately linked to one another, and which are linked to one another on the inside via the hydrogen bonds of the complementary base pairs. Only adenine with thymine (2 H-bridges) and guanine with cytosine (3 H-bridges) connect, i.e. only one purine with one pyrimidine base (RNA shows uracil instead of thymine). This double chain now also turns in and we get the most famous spiral in the world, the double helix of the cell nucleus. Another well-known term for the entire giant molecule is chromosome. In humans, 6 base pairs are constantly repeated at both ends and give strength and stability to its structure. These sections of the chromosome, which in humans each have a length of 5,000 - 10,000 base pairs, are called telomeres (end pieces, less commonly used: sleeve ends) and are covered by a protective cap made of protein, the shelterin.

page 12

The telomeres control the aging process at the cellular level. The length of the ends (telomeres) of our chromosomes determines the number of cell divisions (cellular aging clock, Nobel Prize 2009) that a body cell can go through in the course of its life (Hayflick limit). With each division, approximately 100-150 base pairs are lost (replication problem, identified and defined by Watson 1973) because the replicating primer (primase) “runs along” the strand to be doubled and “comes to a stand” at the outer end, and those bases, on which “it sits” cannot double. This clearly has no influence on the length of the respective starting strand, i.e. the chromatid before the start of replication, which is why each chromosome has 2 nucleotide chains of different lengths at its ends.

There is an enzyme that returns the chromosome strands to their original length after duplication: telomerase, which is silenced in our somatic cells and adult stem cells yet during the embryonic period and only remains active in the non-somatic germ cells.

If a chromosome is shortened to a telomere length of about 3000 to 5000 base pairs, the whole cell enters the state of senescence ("age rigidity"), which is disadvantageous for the whole organism because this cell (for the time being) no longer divides or renews itself, "remains" in the tissue and possibly produces inflammation mediators (abnormal function).

In the best case, apoptosis is triggered in such a cell, in the worst case it suddenly divides further and forms a tumor. When the telomeres reach a shortness that is only compatible with the indispensable cellular vital functions (dividing, multiplying, growing), and a corresponding "hostile" cancerophilic environment is present, the stem cell follows the path of the germ cell to the first meiosis in a kind of survival reflex . The second does not necessarily have to happen (completely), because the “formal” haploid chromosome set (according to meiosis I) that now exists shows 2 chromatids per chromosome, so it has doubled “diploid” genetic material, which would formally allow unlimited mitoses anyway, such as when the there would be no further furrowing after Meiosis II. Mathematically, one can imagine all possible deviations that contain a crossover, the set of chromosomes changes significantly, but the following cells remain capable of reproduction. Even a fusion of gametes would be conceivable in the context of cellular tumor processes and as soon as the telomere length finally becomes critical, i.e. there is a threat of cell death, the telomerase switches endogenously intracellularly to a maximum. A parthenogenesis. In between, crossovers and irregular, mostly incomplete first meioses are repeatedly performed (by chance? Spontaneously?) And the chromosomal heterogeneity of the tumor continues to increase.

Meiotic-mitotic mixing processes seem to be taking place here.

And the quantitative outlook of a single crossover process is enormous, after all there are 222 different possibilities (around 4.2 million) of chromosomal recombinations (Love J). 16 different sets of chromosomes (i.e. 16 crossovers!) have already been found in malignancies (Hiddemann et al.). Well over 100 years after Beard, the treating doctors also notice this:

Page 13

Just recently, on November 7, 2013, at the congress of the Austrian Society for Hematology and Oncology (ÖGHO): "Mutation heterogeneity as a central characteristic in malignant tissues presents researchers and clinicians in oncology with new challenges." (Springer Medizin Onkologie 07.11.2013)

Cancer is the crossover of an irregular meiosis, the birth of the immortal cancer cell. In contrast to random mutations, the crossover adheres to predetermined chromosomal breaking points (Panizza et al. 2011).

The often heterogeneous and chaotic sets of chromosomes in cancer cells are not the result of “mysterious” mutations, but of a repeated anomalous crossover, which is preceded by the lateral aggregation and docking of the chromosomes with duplicated chromatids (synapse pairing); 4 chromatides are arranged parallel to each other in the room, with their sleeve ends (telomeres) fixed to the inner nuclear membrane, and form a tetrad, including those in the crossover would make no sense, since all telomeres show identical base sequences.

Now the first meiotic division takes place with the result of two haploid cells with doubled chromatids ("formal diploidy"), which do not necessarily have to go into the further actual reducing 2nd meiosis, but can easily be going into unlimited mitotic and also further incomplete meiotic (cancerous) Divisions can occur, which explains the occurrence of several different sets of chromosomes in malignant tumors (chromosomal heterogeneity). Both in primary tumors and metastases.

The lateral aggregation and synapse pairing (after pair doubling) with the crossover, in which chromosome parts under the 4 chromatid strands are vigorously exchanged, represents the most significant difference to normal mitosis, which activates the nucleic spindle immediately after the doubling (i.e. no lateral aggregation with crossover ).

Cancer is a cell differentiation disorder, it occurs in the context of (attempted or failed) tissue renewal (Wicha et al.); E.g. epithelial cells of the entire digestive tract renew themselves every 10 days, which is not surprising in view of the frequency of colon cancer. Another example is the prostate cells compared to those in the seminal vesicles; the former show a known high proliferation tendency with a high cell turnover. In contrast, the active cells of the small intestinal mucosa almost never show cancer, although large intestinal cells with the high cancer incidence regenerate significantly less often. The pancreatic enzymes, which are active in the duodenum, jejunum and also yet the ileum, make the difference.

Already in his 1911 book "The Enzyme Treatment of Cancer" (Chatto & Windus, London 1911, reprinted New Spring Press, New York 2010), John Beard points out on page 103 the noticeable reduction in chromosomes in malignancies (the term meiosis of the primordial germ cells was already known at that time, but had not yet been established itself) and cited the work of Farmer, Moore and Walker (Lancet, Dec 26, 1903, p. 1830); It is not until the 3rd millennium that one remembers J. Beard and sees common genetic programs in tumor cells and gametes (Kohane et al.) (Scientific American Magazine, April 23, 2009).

Page 14

The primordial migrant germ cells of the inner cell mass of the blastocyst (germinal bladder, 5th day), which are distributed throughout the embryo during the 4th post-fertile week, are identical to the later adult stem cells that are found in all body tissues forming the lifelong (non-somatic) cell reservoir for tissue renewal and substitute (NJ Gonzalez "The Trophoblast and the Origins of Cancer", New Spring Press, New York 2010).

Since humans age due to shortening telomeres (switched off telomerase), the adult stem cells (in contrast to the embryonic ones) are not immortal and therefore only have a limited number of possibilities for cell division in their genetic program (Hayflick limit).

Humans are born with an average telomere length of about ten thousand base pairs, in the course of their life each dividing cell loses about 100 - 150 (Blasco M) with each division, and with a telomere length of about 5000 gets into a physiological state called Senescence ("old age") is called.

The cell is (for the time being) no longer able to divide and remains “lying” in the tissue, possibly producing disruptive inflammatory mediators, i.e. having a disturbed function. In the best case, apoptosis is triggered, in the worst case a cancer cell arises, possibly "creeping" over (many) years. In the meantime, stem cells ("cancer stem cells") have been found in various cancer tissues, all of them are the product of irregular meioses, with extremely high upregulated telomerase, are immortal in contrast to the adult stem cells from which they derive and do not need each other. There is one stem cell for every 100 cancerous tumor cells (Gonzalez).

Carcinogenesis

The current “official” cancer theory assumes that we all have so-called proto-oncogenes in our genes, which are held in check by so-called suppressor genes, which does not always (as is well known) work; If a suppressor gene is switched off by a carcinogen and a proto-oncogene becomes an oncogene, this oncogene can switch off another suppressor gene and thus turn another proto-oncogene into an oncogene, and if this happens at least 6 times, we (possibly) have a cancer cell with its unpleasant properties.

So it is not a single gene that is mutated, but an entire signaling path that has mutated!

A project is currently underway to sequence all mutated signaling pathways of all cancers, the Human Cancer Genom Project (HCGP) to compile the genetic cancer atlas (The Cancer Genome Atlas, TCGA), in contrast to Venter's HGP in the nineties (Mukherjee S); it should take about another 10 years, which is why at the last Cancer Forum in Alpbach in 2012 (zur Hausen, Wintermantel) it was said that cancer would now be surely curable in about 10 years. Each tumor will then be genetically blocked individually; an obvious fallacy, because defined tumors are not based on a common genetic program, but the number of possible genetic combinations (read: signal pathway aberrations) that tumors can use is (almost) infinite. Even with normal meiosis, the number of possibilities for crossover of the double chromosome pairs is 4,194,304 (2²²). In view of the completely unpredictable extent of the heterogeneity even with tumors of the same type, a hopeless Sisyphean task.

Page 15

That is, you genetically block a tumor (temporarily), which after a certain time shakes new signal pathway aberration (s) or crossovers out of its sleeve and ... grows again, you determine the new aberration (s), fight them again, etc. , with that cancer has finally turned into a chronic disease, the permanent management or maintenance of which brings permanent business ...

And once again, this time for another 10 years, we are put off ...

Cancer (senescent cell proliferation) occurs as part of natural periodic or forced post-traumatic tissue renewal, which does not (or no longer) succeeds (Wicha et al.). An adult stem cell divides once and its “asymmetrical” copy divides “horizontally” and “vertically” (cloning) 10-15x until the division stops (terminal restriction), after which differentiation processes only occur until the complete tissue cell is produced. However, we know that the telomere is shortened by 100-150 base pairs (Blasco M) with each division, and with a stem cell telomere length of around 6500 (older patient) we may come to the Hayflick limit even before the terminal restriction in the case of the “daughter cell clone”, which means the sudden appearance of senescent cells in the middle of the tissue regeneration process; if apoptosis does not succeed, these are optional “cancer time bombs” in the organism, because the stem cell that does not receive a stop signal from the terminal restriction clearly “pushes in”. The closer to the terminal restriction, the more differentiated the possible tumor, the closer to the stem cell, the more undifferentiated ...

With "appropriate" therapy, which always only affects the offshoots of the adult stem cell, their telomeres in the cell line become shorter and shorter, and finally the resting stem cell is forced to divide permanently. Other clone members may remain quiet for years (Ärzte Zeitung, January 24, 2012). If there is a corresponding (slimy, acidic, hyp / anoxic, oxidized, 'disinformed', low-photon, hypothermic) environment, toxins, mutagens, deep UV radiation, infectious viruses, bacteria and other microbes (e.g. trichomonads) and above all fungi (Simoncini, Gerlach , Dumrese), the (archaic) division program is restarted in the senescent stem cell and after chromosome duplication (repeatedly) it is driven into abnormal lateral aggregation and crossing over (genome A, irregular trophoblast cell, hCG production).

It is well known that male sperm cells need a slightly lower temperature to mature than normally prevails in the body, which is why the male sex glands are positioned in the scrotum outside the pelvic area. In the body, as part of the renewal of tissue, mitoses take place continuously in abundance, in the gonads, however, meioses occur in a “cooler environment”. From old reports from the South Seas we know that in the formerly sexually liberal tribal communities the men sometimes wore their testicles in bast suspensors to prevent unwanted conception.

Page 16

The only conceivable molecular biological process which, in contrast to mitosis, can be dependent on the reduced ambient temperature, are crossover and diakinesis in thecontext of the reduction division. But shouldn't the woman's ovaries also be located outside the abdominal cavity?

Not at all.

In contrast to men, in whom spermatozoa with the preceding reduction divisions are continuously formed throughout their entire fertile life, the thematically often neglected oogenesis of women is far more interesting and highly fascinating; in her very early own embryonic period there is a halt in development in the diplotaen stage of meiosis I after chromatid duplication and lateral aggregation or synapse pairing with crossover. This development stop is an arrested diplotene and is called a dictyotene. This cell pool of a few hundred thousand remains at rest until menarche, whereby it has been reduced to a few tens of thousands over the years due to natural cell failure. Some cells rest for 50 years and longer The first menstrual period leads to the first ovulation, and that is the decisive moment and the beginning of the, from now on, mostly single cyclic egg cell maturation up to menopause.

When the egg cell (still not yet mature) is thrown out of the ovary into the abdominal cavity, a drop in temperature and diakinesis of the first meiosis occur, while the germinating egg cell is caught by the fimbriae of the fallopian tube. One daughter cell becomes stunted and becomes the first polar body and the other one returns to rest. If fertilization does not occur, the unfinished egg cell is excreted with menstruation after the first meiosis. If, on the other hand, this happens, the docking of the sperm cell triggers the second meiosis, a daughter wither away as the second polar body. And after the two unpaired sets of chromosomes have been united, the familiar process begins, the inexorable cell division begins.

One must keep in mind that there is a slimy (sometimes fungal), acidic, hypoxic, hypotrophic, photon-poor, hypothermic, “disinformed” oxidized environment in the fallopian tube; it is “cold, acidic and dark.” The proliferating tumor is looking for food and a place to flourish, he finds it on the 6th day in the uterine lining and inside it begins to sprout ...

Adult stem cells, by nature nonsomatic trophoblastic cells, change their chromosome set through such milieu-related influences with the help of irregular crossovers and diakinesis during irregular pseudomeioses, which creates a cell individual independent of the organ system with the ability to divide, a thoroughly misdirected fruit imitation, a "foetate" with the power of division of the fertilized egg cell, which also produces human chorionic gonadotropin (Acevedo et al.).

So it is not nonsensical to do a GravIndex in cancer patients, it can also be used for early detection.

According to Kremer, when cells divide, the mitochondria are shut down or switched off (protection against oxidation) in order to then start again (from terminal restriction?), In cancer they do not.

As soon as the telomeres of the cancer cell threaten to become too short for their primitive program, the telomerase is maximally activated intracellularly.

An irregular, fungal, hCG-secreting trophoblast with active genome A (commonly known as cancer) is born. The designation genome A stands for the original program (archaic) and genome B (bacterial) for that coming from the bacterial mitochondria, which about 2.1 billion years ago was "switched" dominantly over the former (Kremer) ..

Page 17

In Cancer appeared on October 15, 1995; 76 (8): 1467-75 a work (Acevedo HF, Tong JY, Hartsock RJ), which proves the secretion of hCG-beta in all embryonic / fetal and malignant cells, benign tumors do not produce hCG!

The antineoplastons discovered by Stan Burzynski in cancer-free individuals appear to be the expression of the restrained “trophoblastic” genome A, they possibly represent something like “negative” tumor markers.

"QUOD ERAT DEMONSTRANDUM"

Cancer cells get around two thirds of their energy from incomplete “sugar combustion”, which, unlike normal cells, leads to a high level of lactic acid, which requires sophisticated mechanisms that neutralize the acid storm sufficiently so that vital processes can be maintained. These neutralization mechanisms are to be therapeutically impaired and vulnerable. Since the incomplete sugar burn is only about 10% in normal cells, this is harmless for normal cells.

The ability to migrate (metastasis) is exclusively one of the early trophoblast cells of the inner cell mass.

The cancer cell receives a third of its energy from complete burning of sugar with the participation of oxygen, which leads to the well-known accumulation of water as the end product. This metabolic pathway, known as the respiratory chain, can be blocked therapeutically.

A metabolic peculiarity, which finds its explanation in the ancestral old age of the cancer cell, allows an exclusive blockade of the respiratory chain and poisoning of the tumor cell without affecting normal cells. The combination of both methods ideally leads to cell death of the cancer cell.

Therapy

The selective acidification of tumor cells

Kremer definitely says that the cells treated by chemo are forced into the highest possible dedifferentiation and thus the ultimate malignant tumor stem cells are created that "differentiate" (according to latency) into all possible types of cancer.

Cancer cells are acid machines, they cover more than 65% of their ATP requirements from glycolysis with the end product L-lactate. Healthy cells only cover 10% of their ATP requirements from glycolysis. In cancer cells, too, 35% come from the citric acid cycle and substrate chain phosphorylation (respiratory chain with oxygen combustion) (Guppy et al.), in healthy cells this accounts for 90%. For every 2 moles of ATP from “anaerobic” glycolysis, 18 moles come from the “aerobic” respiratory chain. (Those 35% 'oxidative' ATP also contain the 'upstream' glycolytic amount of ATP, measured in this work at 20%, which increases the total glycolytic proportion to over 70% and even more).

page 18

The two systems do not exist side by side, but are connected in series; the “anaerobic” glycolytic system is, as I said, the more inefficient and phylogenetically much older one, it was there before. The more recent, efficient “aerobic” system became dominant over 2 billion years ago (Kremer).

Since the end product of glycolysis is L-lactate and more than 65% of the ATP requirement is met from it (Guppy et al.), Enormous amounts of lactic acid ("acid machine") are created that are not fed into the citric acid cycle via pyruvate, which is what healthy people do. Cells keep the electron and proton transfer in the respiratory chain.

Although lactic acid is considered a weaker acid in organic chemistry, too much can very well pose a serious problem for the organism, similar to "unstable" carbon dioxide, which is clearly stable in the metabolism, i.e. does not break down by itself.

The cancer cell first has to withstand this immensely high intracellular acid storm! That is why it is strongly alkaline calibrated or “fixed” inside the cell (according to Kremer 7.47 - 7.60)! To do this, the cancer cell uses an ion exchange mechanism ‘by shoveling lactate ions out of the cell via the monocarbolate transporter and bringing in bicarbonate ions for this. Bicarbonate immediately buffers H⁺ and carbonic acid (H₂CO₃) is formed, the decomposition of which into water and carbon dioxide is catalytically accelerated up to 10 million times by the carbonic anhydrase. The bicarbonate buffer is therefore a so-called open buffer, because the dynamic reaction equilibrium is always on the "left" side of the reaction, so there can never be a product inhibition.

Second, the cancer cell exports massive amounts of H⁺ into the tumor interstitium and brings in Na⁺, partly also K⁺, but mainly the former, which is why it is so full of it. Which is why the intercellular space in tumors is significantly more acidic than the tumorous intracellular space and healthy tissue. Because of the old methods of measurement, it used to be assumed that tumors were acidic through and through.

The decay of the carbonic acid resulting from the buffer reaction into CO₂ and H₂O is the decisive process!

This spontaneous reaction of the unstable carbonic acid is 10 million times too slow for the (patho)physiological requirements, while the pH of the buffer area would adjust to the pK value of the 1st dissociation stage of 6.5 of the carbonic acid, and even with a corresponding bicarbonate consumption at pH 6 (Karlson, page 311, open bicarbonate buffer, 11th edition, Springer 1980), which would be incompatible with the life of the tumor cell.

Studies and citations show that both bicarbonate and acetazolamide inhibit cancer cells, so this strange parallelism can only be explained by the inhibition of carbonic anhydrase (Xue-Jun Li et al.). This leads to (respiratory and metabolic) acidosis and an increase in CO₂, as in CO₂ poisoning (Casarett and Doull's Toxicology, 4th Edition 1991, Pergamon Press).

Page 19

Since the cancer cell can use O₂ much poorly or not at all, it produces these enormous amounts of lactic acid, the H⁺ ions are shoveled on the one hand into the tumor's interstitial space and on the other buffered immediately by inshoveled NaHCO₃^-. The product H₂CO₃ breaks down immediately by means of carbonic anhydrase into H₂O and CO₂, which "diffuses" out (the latter by CA III).

When large amounts of bicarbonate are supplied, the CA is obviously "overwhelmed" (substrate inhibition) and the cancer cells become carbonic acid. Of course, I also achieve the same effect with selective inhibition of CA by acetazolamide.

Carbonic acid-loaded cancer cells are clearly very sensitive to heat, cold, oxygen radicals, ionizing radiation, etc. A variety of mutually supporting therapeutic measures opens up here.

The enzyme carbonic anhydrase (CA) accelerates this decay by up to 10 million times, which is why the cancer cell, together with the export of H⁺, can maintain its internal alkaline pH and thereby create a strongly lactic acid environment extracellularly!

It eats its way into the surrounding healthy tissue with the help of the zinc matrix metalloproteinases and these enzymes love it sour!

The therapy model is now very simple, one inhibits the CA with acetazolamide and creates carbonic acid poisoning in the cancer cell, because then the pH (with a 50% reduction in the HCO₃ concentration even to about 6.0) drops (Ganong), which is incompatible with cancer life.

As an accompanying measure, we inhibit the H⁺-export with amiloride, thereby holding H⁺ in the cancer cell and thus acidifying it intracellularly.

With L-lactate infusions (also subcutaneously in the tumor area) we buffer acid in the interstitium of the tumor and thus achieve an impairment or perhaps even inhibition of the acid-loving zinc matrix metalloproteinases.

Since L-lactate is exported by the cancer cell (monocarbolate transporter), there is no risk that it will "misuse" the L-lactate supplied to the tumor interstitium for intracellular alkalinization. The administration of K^-Mg^-aspartate (e.g.Tromcardine) is also indicated in order to prevent K⁺ and Mg⁺⁺ loss due to the diuretics and, on the other hand, to offer more Mg⁺⁺ and K⁺ to the cancer cell, as this significantly reduces the tumor threshold pressure. In addition, Mg⁺⁺ is said to have a direct anti-tumor effect.

The additionally supplied L-lactate leads to an increased occurrence (due to the lactate buffering) of undissociated lactic acid, which is resynthesized to glucose in the liver leads to further increased carbonic acidification, so that the death of the cancer cell by acid occurs all the faster.

Never give bicarbonate or sugar to cancer patients without prior CA inhibition!

Page 20

Many “biologically” oriented doctors give sodium bicarbonate infusions to cancer patients, this leads to the support of the intracellular alkalization of the cancer cells. So it's counterproductive! Unless the doses are so high that the CA is no longer able to accelerate the decomposition of all the carbonic acid produced, the CA must be “overwhelmed”, so to speak (substrate inhibition), but this can already have systemically unpleasant effects.

It is just as contraindicated to give sugar in any form (as supposedly problem-free calories), you only feed the cancer cell with it. Unless there is reasonable hope that the cancer cell will eat its way to death.

The blockade and / or forced activation of the oxidative "thigh"

Overload of the aldehyde bottle neck

In amygdalin, the two active ingredients benzaldehyde and hydrocyanic acid are in a beta-glycosidic bound to a hexose (usually glucose).

Cancer cells reflect very early unicellular organisms from the time before photosynthesis occurred, cells from this period express beta-glucosidase on their surfaces, which on the one hand releases benzaldehyde from Amygdalin, which creates "backwater" and collapse in the aldehyde bottle neck of the P-450 detoxification system, and on the other cyanide, which is to block the cytochrome c in the respiratory chain. Hydrocyanic acid is only (fully) effective if the cancer cell requires he oxidative energy metabolism to a vital extent, and not (that effective) in case when it's glycolytically dominated. (Although a carbonic anhydrase inhibition in vitro was also proven by Meldrum and Roughton for HCN.) (Chegwidden, page 8)

On the other hand, it is advisable to “force-breath” the inactive, frozen mitochondria (Kremer) with cucurmin and/or dichloroacetate, which causes ruptures in the mitomembrane and subsequently triggers apoptosis via caspase activation.

Since the respective extent of both the glycolytic and the oxidative metabolic component of a tumor cell is not known a priori (Guppy et al.), Combination therapy is recommended.

It is also possible that the energy metabolism of the cancer cell can adapt to the requirements (epigenetically). After all, this is known from facultative aerobic microbes, and this seems to be possible even with normal body cells under extreme conditions (Caudwell Xtreme Everest Research Group).

Therapy level steps plan

Page 21

The best thing is to take Supuran, Claudiu T .; Scozzafava, Andrea; Conway, Janet; "Carbonic Anhydrase - It's Inhibitors and Activators", CRC Press, Boca Raton, London, New York, Washington D.C. 2004 at hand and turn to page 269 (possibly also 261) and consider the graphic scheme of a tumor cell:

pHi = pH intracellular, pHe = pH extracellular

1. Due to the export of the lactate-ion and H⁺ (both from glycolysis) into the tumor interstitium, the pHi of 7.2 is significantly more basic than the pHe of 6.8 (a)

2. Intracellularly, CA II splits the "buffered" carbonic acid accelerated (10 million x) into H₂O and CO₂ which "diffuse" out of the cell (e)

3. The membrane-based CA IX / XII recycle the HCO₃^- from H₂O and "diffused" CO₂, which goes back into the cell in an anion exchange with Cl^-, of course, Cl^- is also exchanged for bicarbonate occurring in the EZR (e ')?

4. The cell throws out H⁺ in the antiport and brings Na⁺ in (b)

5. Furthermore, the vacuolar H⁺ -pump is used for intracellular pH stabilization and the Na⁺/K⁺ - ATPase to cover the potassium requirement (c) (d)

6. Simoncini: Offer HCO₃^- abundant, overwhelming CA II, which leads to an increase in H₂CO₃ due to the (instantaneously spontaneous) buffering, and because the accelerated splitting into H₂O and CO₂ does not actually occur and the pH adjustes itslf in accordance with the natural dissociation of the carbonic acid, which of course requires a cellular HCO₃^- uptake mechanism that is independent of the overstrained CA IX / XII (e ')? 7. Simoncini modified I: In addition, block the CA II (CA IX / XII) (Chegwidden et al., Page 16, Supuran et al., Page 269), for example with acetazolamide (Diamox) or ethoxzolamide, of course more carbonic acid and thus more H⁺ (e '')?

8. Simoncini modified II: additionally block the antiport H⁺ to Na⁺ with amiloride, as far as the epithelial sodium channel is concerned, can no more H⁺ be exchanged for Na⁺, do more H⁺ remain in the cell (b ‘)?

9. By 6.), 7.) and 8.), the cancer cell is largely deprived of the ability to "get rid of" H⁺. It is forced to fall back on ATP-dependent mechanisms, which also leads to an increased increase of another acid, namely Uric acid(from the heated breakdown of the purine bases adenine and guanine from the ATP)

10. Simoncini modified III: If I finally offer the cancer cell, for example, fructose or glucose (with 4 IU old insulin / 500ml glucose 5%) in excess, lactate (possibly also pyruvate), carbonic acid and uric acid increase again strongly, which you theoretically do the death knell, in particular because there is no control of uptake by insulin (fructose is absorbed independently of insulin), but an even stronger coercive hyperalimentaion is to be expected from the administration of glucose + insulin, which could be effective with regard to inactive "sleeping" cancer stem cells by forcibly activating their metabolism and becomes therapeutically vulnerable.

11. From 1 mole of glucose / fructose / galactose, 2 moles of ATP are obtained by glycolytic means

12. 19 mol of ATP are oxidatively obtained from 1 mol of glucose / fructose / galactose, these two chemisms are connected in series, i.e. the normal healthy body cell only gains 10% of its ATP from glycolysis

Page 22

13. The Australian work 'Contribution to different fuels and metabolic pathways to the total ATP turnover of proliferating MCF-7 breast cancer cells' in Biochem J. (2002), May 15; 364 (Pt 1): 309-15 shows (Guppy et al.) that 35% of the total energy of these cells is obtained oxidatively, 65% from an "other source", this 65% can (e.g. according to Heinrich Kremer) only be of glycolytic or non-oxidative origin. (It must be said, however, that the 35% “oxidative” ATP also contains the “upstream” glycolytic, measured in this work at 20%, which increases the total glycolytic proportion to over 70%).

14. This shows that there is practically no risk for the patient when the above measures are carried out at the local level, whereas at the systemic level, the dosages of 6.), 7.), 8.) and 10.) have to be calculated exactly, since those mentioned inhibition and stimulation mechanisms also clearly include normal cells, whereby a significantly lower acidification is to be expected due to the low glycolytic proportion of the cells.

15. For bladder irrigation it would be logical to first use NaCl + xylo + diamox + amiloride, after about 10 minutes a certain amount of 500ml fructose 5% or 500ml glucose 5% + 4 IU altinsulin, after a further 10 minutes finally the bicarbonate 5%.

16. In the case of infiltration, only 5% fructose (plasma iso-osmotic) or 5% glucose (with insulin), and the amount of amiloride must be considered, if ampoules are (still) available.

17. Since hydrochlorothiazide was developed from acetazolamide, the question arises whether the good old combination of amiloride + hydrochlorothiazide could kill two birds with one stone?

18. Amygdalin locally and / or systemically (blockage of the respiratory chain by cyanide and overloading of the P-450 system), DCA (with DMSO?) And / or curcumin (Kremer) for forcing or forced activation of oxidative phosphorylation with apoptosis result.

Views for the Future

Telomerase activation

Studies show that with increasing age, when the telomeres become shorter and shorter, the risk of cancer increases (Kiechl). Humans age at the cellular level due to the increasing shortening of the chromosome end pieces by 100 - 150 base pairs with each cell division of their adult stem cells.

The enzyme that returns the telomere to its original number of base pairs after division has taken place, telomerase, has been silenced since the fetal age.

Telomerase activators have been on the market for a few years, and some demonize them as cancer activators, where telomerase is highly active in malignancies, while others, such as the well-known US doctor and supporter of activation, Ed Park, see them as the biggest event for humanity, ever since Luther proposed his theses to the castle church in Wittenberg.

Page 23

Although this is often referred to in oncology, telomerase is not an oncogene (Harley, Calvin B). Their activation in cancer cells appears to be less of the cause of their malignancy than of a consequence thereof.

The basic requirement for aggressive cancerous growth is the sufficient change (mutation) of the chromosome set, which can hardly be caused by the tragant capsules (astragalus) currently on the market.

In animal experiments, the cancer risk clearly does not increase with a telomerase activator (Harley CB, de Jesus BB).

Should the assumptions prove true, telomerase activation will be THE timely cancer prophylaxis of the future.

The association/induction hypothesis of Gilbert N. Ling

According to Dr. Gilbertt N. Ling www.gilbertling.org all common diaphragm and diaphragm pump theories are incorrect because the energy for them is lacking. When their monophosphates are split off to diphosphates, the energy-supplying adenosine triphosphates do not release the amount of energy that would be necessary for the officially postulated membrane functions.

Because the energy “doesn't work out”, there is a lot of speculation with so-called antiports, which means that one ion (e.g. H⁺) goes out, but another (e.g. Na +) comes in. Thanks to a "rocking effect", the process remains energy-neutral. A large number of such ion swings was devised in order to make the functioning of the cells conceivable according to current ideas.

Cell membranes are much more permeable than assumed, however, the key word for this is 'diffusion', which means that substances that we believe can only be smuggled into the cell interior with (enormous) energy expenditure (e.g. sugar molecules, drugs, salt ions, etc.) diffuse on the other hand very simple (almost passive).

What diffuses in and what does not, have to do with the states of charge, the electron density or distribution inside the cell (protoplasm). Only in the case of interfaces(epithelia) do membranes exercise the barrier function assigned to them. Ling has experimented “meticulously” with frog muscle cells for many decades, studying myoglobin as a “simplified hemoglobin”. It became clear that, for example, large molecules can pass through the membrane meshwork unhindered, while small molecules cannot pass through, because what comes in the cell is “decided” inside the cell and not in the membrane.

The inside of the cell is in a gel state, due to the dipole water molecules, and not a sack of salt water in which everything "swims around", otherwise it would have to "splash" when you cut into a fillet or meat, but it does Not.

The charge state in the protoplasm is determined in the first line by the open ion residues on the peptide chains, the amino and carboxyl groups. By more or less folding of the protein strands, more or less positively or negatively charged “knobs” protrude into the cytoplasm, on which multiple layers of polarized water are deposited, giving the inside of the cell structure.

Page 24

Magnetic resonance imaging is based on the dipolarity of the water molecules

Docking an ATP molecule triggers a 'wandering chain reaction', like the successive fall of dominoes, and the state of charge changes in an instant. These constant changes in the state of charge seem to trigger something like vital inductions and to be the motor of life on a cellular biological level: Gilbrt N. Ling's Association/Induction Hypothesis (www.gilbertling.org homepage, point 9, Zimmerman, Power Point for download) .

In the future, electron donating and electron withdrawing molecules will be precisely calculated to the respective extent, so that drugs can be designed that are tailored to the exact needs.

The biological Nature of Cancer and its Therapy
(fragmentary original thoughts and drafts by the author)

Page 1

By Kremer we know there is an ancient program (still fully active) in our chromosomes or genes reflecting times when there was no or little oxygen on earth, it is burning sugar fuel without oxygen, upon that there is a „younger“ system of burning sugar by oxygen. The latter is much much more effective energetically and positioned upon the former. Both systems are active and the endproduct of the first one (lactic acid) is handled into the other one (into citric acid cycle and oxidative phosphorylation or „oxidative chain“).

If there is no oxygen the first system is active only. In cancer cells 60% of the energy need is covered by this system, the other 40% are covered by oxygen burning (on the average).

Cancerous tumors consists of compounds of unicells reflecting those in the archaic ocean (of anaerobic or facultative anaerobic property), with the only intentions of growing, eating, spreading and multiplicating.

Kremer treats cancer by starting and pushing the main actors of the ‚younger‘ oxygen burning system namely the mitochondrias by means of Resveratrol, Pterostilbene(?), Cucurmin, Vitamin D3 and many other polyphenolic compounds.

By Gonzalez and Beard we know that phylogenetically the period of archaic unicells is embryologically reflected by the trophoblast in mammals and man (vertebrates). And in early pregnancy the foetus, invading the mother’s uterus, is ‚physiologic cancer‘, by exactly the 56th day of pregnancy (in humans) the character of a part of these cells changes dramatically into benign ones and the more outer placed ones are getting into apoptosis. That change of this ‚physiologic cancer‘ into „good“ tissue takes place when the pancreas of the embryo starts to work. The discovery of this was the beginning of the ‚pancreatic enzyme treatment of cancer‘ by means of mainly Trypsin and the other pancreatioc enzymes.

By Beard we know that in nature (plants and animals) in the process of multiplication asexual generations are always followed by sexual ones etc. (this is a rule!), the trophoblast is the asexual generation in mammals and men and when the trophoblast gives rise to primordial germ cells only one (or more than one in case of twins, triplets etc.) of those gives rise to the embryo the other ones travel into the back part of the yolk sac (hypoblast), multiplicating tremendously and go back into the embryonic body in which meanwhile all the organs have been formed basically structured and these ‚vagrant germ cells‘ are being spread all over the embryo’s body and remain there the rest of the individual’s life, also an adequate portion gets into the gonads being bound to meiosis to make way for the following sexual generation on the cellular level.

By Beard we also do know that the (cancerous) trophoblast is growing best in an acidic environment (now we know a tumor’s matrix-metall-proteinases like it acidic), while the upcoming pancreas on day 56th of pregnancy produces pancreatic ferments or enzymes working best in an highly alkaline juice (pH 9!).

Page 2

By Gonzalez we know that these vagrant germ cells remainig all over our bodies are nothing else but the so called adult stem cells whose origin lies completely in the dark according to official science. These cells serve as repair and replacing cells for our tissues and they obnoxiously can occasionally form a „sibling“ of us: a cancerous tumor

By Simoncini we know that cancer behaves very much like fungus and according to him it is even one because he discovered that cancerous compounds dissolve quite well by alkalizing their extracellular interstitial space moreover he states that fungus can represent itself in so many forms science does not know yet. The best natural antimycotic is Sodiumbicarbonate.

Official oncology admitts there is always fungus with cancer but it is a secondary fungal infection. Simoncini maintains the other way, there is always fungus in the first place! I am deeply convinced Simoncini is right because there are so many positive therapeutic reports on cancer on his homepage these can’t all be faked.

Simoncini observed that the links between cancer cells get disrupted easily by alkalinity and the immune system can deal much much better with singular cells but a compound (tumor), here it is at hand to combine alkalinization (Simoncini) with pancreatic enzymes (Gonzalez and Beard).

C O N C L U S I O N OF THE CONCLUSION

Cancer cells are acid machines, this counts first of all for solid tumors (not necessarily in lymphomas) these are producing abundant amounts of lactic acid because 60% of their energy need is fed by sugar burn without oxygen. That acid on the one hand is being exported in the extracellular space right outside the cell membrane and sets a remakable activating stimulus to the matrix-metallo-proteinases that melt away the healthy surrounding tissue of the cancer patient (or the uterus tissue of the mother in case of pregnancy) and on the other the huge acidity is buffered in the cell’s inside very effectively.

The acid export can be blocked amongst other chemicals by commonly prescrib ed Amilorid .

First of all cancer cells do have to stand their own acidity that’s why those are intracellularly calibrated highly alkaline! This is happening through buffering by Sodiumbicarbonate, the crucial point is that NaHCO₃ is a so called ‚open buffer‘ means the carbonic acid molecule which is formed by the buffer reaction (HCO₃^- + H⁺ = H₂CO₃) falls apart immediately into water and carbondioxide and therefore gone thus the buffer can keep a very high alkalinity without being used up too quickly. The falling apart of carbonic acid is actually a spontaneous reaction BUT accelerated by the intracellular enzyme Carboanhydrase 10 000 000 times thus the intracellular pH of the cancer cell is definitely steered by CA.

Page 3

The acid buffering inside the cell can be blocked by inhibiting carboanhydrase by Acetazolamide (Diamox e.g.).

The acidic interstitial space and the further environment of a cancerous tumor has to be alkalized but not mainly by Sodiumbicarbonate but by the salt of a weak organic acid like citrat, lactate, acetate etc.

The strategy implies the cancerous tumor‘s extracellular alkalinization by intake (or iv) of organic salts and acidification intracellularly by inhibition of Carboanhydrase (and ev. the acid exporting membrane carrier).

Eventual additional application of pancreatic enzymes, Resveratrol, Cucurmin, Vitamin D3 (very important) and many polyphenolic compounds (PAC etc.) . Healthy cells are only effected minimaly (acceptable intracellular pH decrease) because they are depending mainly on oxygen burn.

ETC. !!!!???

Gonzalez’ cancer theory is being based on too scientific disciplines, namely Neurophysiology (very logical and very unknown) and Embryology, first we focus on Embryology.

www.dr-gonzalez.com

Already in the fading 19th century the Scottish embryologist Dr.John Beard found out that the embryo or very early fetus invades the maternal tissue like cancer. The fascinating fact about this is that the very early embryo does not only behave like cancerous cells in a way but IS cancer indeed, using e.g. the identical matrix metallo-proteases to dissolve the tissue of the uterus, this is latest research as well, please see:

http://www.scientificamerican.com/article.cfm?id=cancer-clues-from-embryos

Thus we have too accept the weird fact that the early fetus is cancer, it invades the uterus as primary tumor, but this is the way of nature UNTIL the 56. day of pregnancy (in humans), this is when the fetus‘ pancreas starts to work, this is the day when pancreatic enzymes appear in the fetal blood the first time;

From this moment on the development of the „outer“ fetal cells take an orderly differentiating course changing into trophoblastic cells (first Syncytiotophoblast, later the complete placenta) to nurture the fetus.

This tremendous change in the character of the fetal cells must be caused by the newly upcome of pancreatic enzymes!

For Beard it became clear later that it’s the pancreatic enzymes trypsin and chymotrypsin (e.g. trypsin is being used in biology to dissolve strongly linked groups of cell in vitro, moreover in cleansing agents like wash powders etc.). Trypsin (an endopeptidase) splits peptides usually behind the aminoacids Arginine and Lysine which are both known for their antitumorous properties.

In modern physiology it has been known for the longest already that there is no strict functional separation between the exocrine and endocrine pancreas, means there is also a significant amount of trypsin and chymotrypsin circulating in one’s body disarranging probably upcoming ensembles of tumor cells.

Page 4

So first of all cancer seems to be some kind of pancreas insufficiency! Strange, isn’t it?

Why do cancer cells have these embryonic properties because cancer does not exclusively take place in a woman’s uterus only, no, cancer takes place EVERYWHERE in the body!

There are two cell-aggregations in the first days of pregnancy called the inner and outer cell mass.

Out of common morula, followed by blastula, that changes in humans directly into the liquid filled blastocyst which shows on the fifth postfertile day a round convexed herd of cells inside prostating into the cyst, the inner cell mass.

The other cells (called the outer cell mass) tend somehow to becoming a cell arrangement called the trophoblast (the later placenta or chorion) and the „inner“ cells intent being one called the embryoblast, but there is hardly a difference between these ones in the beginning.

The 6th day the embryo sprouts out of a single cell of the inner cell mass, after all the other cell have continuously developed out of the fertilized egg, this fact gives way to the insight that the throphoblast is there from the beginning and the embryo comes out of it. Thus the trophoblast gives „rise to the embryoblast.“ (Gonzalez)

ATTENTION!

When the embryoblast further starts to develop into the epiblast (a complete microcellular arrangement of the later human body) and the hypoblast (e.g. yolk sac etc., bound to degenerate later), the BUNCH OF THE REST OF CELLS OF THE INNER CELL MASS get aside and travel to the „back margin“ of the yolk sac remaining there and multiplicate several days, these cells are so called migrant or vagrant primordial germ cells and these are not somatic because of their coming from the trophoblast.

At the beginning ot the fourth week of pregnancy these primordial germ cells start to move on again, this time in a spirallike motion through the whole of the later human body (Epiblast) finally ending up in our reproductive organs (embryonic stem cells - ESC) being developed into sperms and eggs later.

BUT! During their journey to the genitals through the whole of the later body to be formed, almost everywhere a portion of germ cells STOPS migrating and remain where they are for serving from now on as repair or replacing cells the rest of our life.

AND THESE CELLS ARE OUR ADULT STEM CELLS, nobody in official science wants to know that, but this is the truth. And according to Beard and Gonzalez it’s those cells only that can become cancerous. Again modern science accepts in the meantime that only one or two cells out of several hundreds of tumor cells are definitely responsible for a tumor’s growth, please see:

http://www.cancer.med.umich.edu/news/stemcell.htm

And changes in the milieu around these cells in our body make those vagrant germ or adult stem cells to develop what we call cancer later in life, some strange stimuli drive them into a trial of (pseudo)meiosis (by chronic infection esp. fungal one, mechanical irridation, lack of trypsin, etc.?) with a totally disarranged set of chromosomes (up to 92 ones and even more fractured pieces) to form a trophoblast without success, only able to grow, invade and metastasize …

Page 5

The basic line of Beard and Gonzalez ist that cancer only can come from adult stem cells which are identical with the vagrant embryonic germ cells that are actually trophoblastic cells dwelling in our bodies the whole of life and serving as supply for tissue replacement.

Modern molecular biology says clearly that only undifferentiated cells are able to divide and duplicate themselves.

As you know from university medical studies there is a part of the vagrant germ cells that travels into the gonades as primordial germ cells bound to undergo meiosis to form eggs and sperms (haploid chromosomal setting), and after fertilization a trophoblast in a woman’s uterus, this is their natural healthy way.

AND NOW PLEASE LISTEN!

The other portions of these identical vagrant germ cells that remain in the early embryonic body outside the gonades are n o t supposed to undergo meiosis to form new life, as mentioned above thea serve as source for tissue renewing the whole of our life. BUT for some reason(s) some of those are trying in abundant cases an

UNSUCCESSFUL UNDERTAKE OF FORMING A TROPHOBLAST

outside the gonades at the wrong place and at the wrong time, and

THIS IS CANCER !

Wiliam Donald Kelley, the ingenious dentist, in his post mortem edited book ‚Curing the Incurable‘ expresses out of pure clinical observation and knowing Beard’s book of 1911, that the basis for cancerous development are tissue damage, presence of ectopic germ cell(s) and female hormones locally and a pancreas insufficiency generally with reduced amounts of trypsin and chymotrypsin circulating (chapters 3 and 4).

http://www.amazon.de/Cancer-Incurable-Without-Chemotherapy-Radiation/dp/0970429002/ref=sr_1_1?s=books-intl-de&ie=UTF8&qid=1414573496&sr=1-1&keywords=kelley+curing+the+incurable#reader_0970429002

Or putting it in actual terms: ‚Damaged tissue‘ is a fairly oxidized microenvironment, acidic, lacking informing photons, slime, transfected by fungus, in which ‚ectopic germ cells‘ (senescent stem cells) hardly can survive, fungus separates those completely from any infomative connection with the body, the cell is „on its own“, the chromosomal setting changes, the reproductive program starts to secure the survival of the new cellular being. Because of the fungus supporting acidity eventually circulating active proteolytic pancreatic hormones are being inactivated, this circumstance may be accentuated by a general ‚pancreas insufficiency‘. The ‚female hormone(s)‘ human chorionic gonadotropin (hCG), reflecting the luteinizing one (LH) besides others are expressed by the onsetting cancer (Acevedo) to defend rejection by the immune system.

http://www.ncbi.nlm.nih.gov/pubmed/8620425

Page 6

Those adult (later senescent or and possibly precancerous) stem cells are primordial germ cells immigrated from the inner cell mass at the 4th postfertile week. This is the reason why they have to go on trying to deliver new cells for damaged or ageing organs or form new life (by undergoing recombination and chromosomal change). They have developed for that. This is their natural and physiologic mission.

And if they change theit chromosomal setting they have to face the body’s immune reaction to be dispelled thus they produce analogous hormones to avoid this, first of all human chorionic gonadotropin (hCG) reflecting the luteinizing hormone (LH) besides others like FSH or TSH.

These adult stem cells and those (ectopic) vagrant germ cells are identical they serve as tissue suppliers in the whole of the body for the rest of our life. Telomerase is only active until the end of differentiation of the organs in different fetal tissues (e.g. heart 12th week, brain and kidneys 16th week, liver and testicles 21st week).

Thus adult stem cells do have a Hayflick limit (Blasco), their forerunning embryonic ones do not and thus the germ cells of adult males and females as well.

Cancer is trophoblastic cells they feed nobody (except fungus?), there is a philosophic – spiritual link, fungus is philosophically often seen as ‚manifested negativity‘ in our organism, it’s logical that ‚strongest negativity‘ (cancer) could grow out of ‚negative‘ fungus.

I suspect, our adult (senescent) stem cells (vagrant ectopic germ cells) are being enslaved by fungus to support it‘s growth by delivering the (lactic) acidic milieu fungus likes so much to grow …

Neurophysiology, another part of Dr. Gonzalez‘ approach (the basic idea is very simple) refers to our autonomic nervous system, it consists of 2 parts, Parasympathicus or Vagus or 10th brain nerve and the Sympathicus.

All humans are either dominated by one of these parts or in a mixed (more or less balanced) state. The phylogenetic older part is the vagal (parasympathetic) one, inducing relaxation, calmness, sleep, recreation, tissue replacement, low RR and pulse etc. and the other „younger“ one is the Sympathicus mediating activity, aggression, fight or flight, facing problems, high RR and pulse etc.

The system out of this is very simple and correlates widely with old eastern ones.

People being dominated by the sympathetic system develop solid tumors (colon, stomach, esophagus, kidneys, liver, lungs etc.) and

NOW PLEASE LISTEN:

People that are being dominated by the parasympathetic system receive diffuse cancer types (e.g. myeloma, lymphoma, plasmocytoma, leucosis or leukemia, generally spoken these types called ALL, CLL, AML, CML)

And consequently persons having a mixed state of the autonomous nervous system tend to get no cancers but if, they are getting both forms somehow diminished (maybe Hodgkin or Non-Hodgkin?)

This is the simple truth behind cancer disposition but in detail very difficult to figure out.

Page 7

The therapeutical consequence is nothing else but feeding „sympathetic“ cancer patients with solid tumors by energetically soft structured food, means the have to have a pure vegetarian or even better vegan diet!

AND NOW PLEASE READ CAREFULLY AGAIN, THIS IS EVEN SHOCKING!

‚Parasympathetic People having a diffuse type of cancer are born carnivores, they have to have an (almost) pure red meat diet!

If you can’t believe look to Dr. Gonzalez homepage:

www.dr-gonzalez.com

One finds generally enough evidence explaining this (strange) fact. I personally believe this is true because I was engaged in Macrobiotics several years, moreover a person I had been knowing for decades turned (by the influence of his mate, a nurse) into vegetarianism and developed lymphoma!

It’s so weird they have to eat lots of meat, I put it in red, it hurts a little bit the eyes, thus one will be keeping it in mind forever.

As I told in detail it’s not that simple because people are often mixed types but it’s the type of cancer that is guiding the dietary recommendation. The modern name of this kind of medical science and therapy is Metabolic Typing, it’s just another word and Gonzalez (he got it from his teacher Kelley) figured out the deepest therapeutical consequences.

The cells forming normally the orderly placenta are nothing else but those vagrant germ cells taking place in the embryonic gonades during early fetal development, going into recombination and meiosis, later being connected with another gamet (sperm or egg) during and by sex and form the trophoblast of the new fetus and this physiologically „cancerous“ trophoblast turns into orderly development to form the placenta AFTER THE 56th DAY OF PREGNANCY or fertilization (literature not fully clear on that).

The root of the problem ist the continuous ongoing shortening of the adult stem cells‘ telomeres by each division. These are in charge of repairing and replacing impaired tissues whenever necessarry (harm, inflammation, natural cell death by ageing).

In the course of life the shorter a stem cell‘s telomeres get the more incomplete and impaired cellular differentiation of its offsprings in the process of periodic natural cell renewal or damaged tissue repair. By ongoing cell divisions and telomeres‘ shortening the genetic program of celluar renewal is losening ist accuracy more and more, replacement of gone well differentiated proper functioning cells by dys- and further anaplastic ones (e.g. villous polypes, basalioma etc.).

Before this is happening such cells should get apoptotic but for some reason in so many cases they don’t!

Page 8

Further regression leads finally (via irregular recombination as latest step of „differentiation“) to solid cancerous tumors without any signs of differentiation detectable. Cancer is impairment of cellular differentiation. Dividing cells are always on the glycolytic metabolic pathway of ATP-production to prevent oxidative damage of the nucleic spindle by oxygene radicals from respiratory burst in oxidative phosphorylation (usual energy source in metabolic active non-dividing cells) (Brand).

http://www.ncbi.nlm.nih.gov/pubmed/9387096

http://www.ncbi.nlm.nih.gov/pubmed/9141507

Glycolytic pathways imply the production of lactic acid as endproduct to be discharged by the cell (monocarboxylate transporter) causing an acidic interstitial environment fungus likes a lot. So to say while trying to repair something damaged, those cells are feeding the main cause of metabolic damage: fungi. And providing those with lactic acid they turn into glucose or other sugars.

Fungi are the most developed microbial beings, creating communities of cells apparently showing „social“ behavior thus cells helping each other in case of food shortage or if one’s damaged. In cancerogenisis fungi seem to infect and enslave senescent stem cells by blocking their apoptotic triggers and programm (e.g. p53 etc.).

The Italian physician Dr. Tullio Simoncini counteracts this by delivering large amounts of sodium bicarbonate to turn lactic acid into the harmless sodium lactate and neutralizing H⁺ cations to carbonic acid with sodium bicarbonate (buffer reaction).

Fundamentally is valid if you deliver lactate (it’s the anionic salt of lactic acid, normally sodium lactate) you have a buffering effect, if you deliver it as acid, you have an acidifying effect, normally the sodium bicarbonate molecule is automatically delivering its dissociated sodium anion to turn lactic acid into sodium lactate, the acidic H⁺ will be linked via sodium bicarbonate to H₂CO₃ and fall apart by Carboanhydrase into CO₂ and H₂O, better you do not deliver lactic acid but its salt thus the body can spare this reaction. There are certain preparations carrying lactic acid and its salt by adjusted pH (e.g. Canesten).

Concerning uric acid, it has been found out recently that you should not lower uric acid or urate in the blood because it acts with Vitamin C and E and Provitamin A as first-line-free-radical-scavenger-defence! Lower it only if someone has gout attacks! (Mikami et al.)

http://www.ncbi.nlm.nih.gov/pubmed/10625215

http://www.ncbi.nlm.nih.gov/pubmed/10730822

Besides treating cancer patients by pancreatic enzymes and food Doctors Kelley and Gonzalez do have a third therapeutic column namely ‚liver-detoxification‘. Let’s go now to this third basic approach concerning their theory and method:

The 3rd column is (liver) detoxification, whatever has to be broken down being eliminated by the kidneys, sweat out by our skin or breathed out via the lungs, or grown out by our hair … is definitely happening in the liver. So it’s tantamount to support our livers for leading a healthy life. As I told you already the vagus is promoting sleep, recreation, relaxation, detoxification etc.

Page 9

What Gonzalez has gotten by his ingenious teacher the dentist Dr. William Donald Kelley is really incredible: it’s the coffee enema

Yes you did hear rightly, taking coffee up the rectum it has a complete different effect than the oral way, this has to do with the autonomic innervation that differs in the lowest part of the body, you‘re having in your small pelvis (little sidestep: ruled energetically by Muladhara cakra acc. to Hindu cosmology)) a dominating vagal (parasympathetical) innervation because the vagus is the very elder brother of the latter sympathicus (by the way this is the reason why we have to face very archaic feelings when having sex with the lowest body-entrances, it’s actually the lust of jellyfish, molluscs and worms).

By taking rectally (saw a DVD with Gonzalez, he stated he never would take coffee through the mouth because he never wants to get cancer in his life) coffee is stimulating tremendously the parasympathicus, leading to total vagal activation of the liver that is almost immediately dumping all the junk there is into its bile ductuli and the gall bladder and finally via the choledochus into the duodenum.

The coffee enema has been discovered by the magnificent and unforgetable Florence Nightingale in the Krim War (1853 -56), for evident waring reason they had nothing left for treating the wounded but large amounts of coffee beans, there was no intravenous infusion then, so they applied it as enemas and many of the death ridden soldiers improved because it turned on their liver function and this fact turned out to have been life saving in so many cases.

Gonzalez mentions that the coffee enema was in the Merk Manual (American doctor‘s handbook) up until the nineteen-twenties, then it got removed (Gonzalez‘ cancer patients are doing coffee enemas several times a day).

Now we have finished Dr. Gonzalez, next will be Dr. Siomoncini.

Normal oncologists say there is always cancer with fungus because fungus likes being in the environment of cancerous cells, thus cancer patients have usually a so called secondary fungal infection, Simoncine says it’s the other way round, first the fungus and thereafter the cancerous fungus. He proves this by using a very cheap and strong natural alkaline antimycotic substance called sodium bicarbonate, saying cancer cells are fungal cells and NaHCO₃ is doing nothing else but dissolving the loose bounds between these cells that are linking those together and the immune system of the patient can easily deal with singular cancer or fungal cells.

I am deeply convinced Dr. Simoncini believes what he sayse, look at his homepage. Can this all be a lie?

www.curenaturalicancro.com

Thus look at his protocols and see the evidence, Dr. Simoncini states cancer is a fungus and NaHCO₃ a very strong and cheap antimycotic and it destroys the cancer! Not much about, that’s all. But (I believe) the truth behind is on the biochemical level more complicated and so far very fascinating as well. Evidently for Simoncini the most important factor is that it works and the theory is more or less of little importance. He is right NaHCO₃ is a good antimycotic, just make a salve or creme out of it (your pharmacist should puffer it at pH 7,5) and put it on the spots between your toes, the fungus vanishes … But why does it work?

Page 10

We know from studies by Australian scientists that 65% (and above) of a cancer cell’s energetical need is being fed by anaerobic glycolysis in the cytosol (Guppy et al).

http://www.ncbi.nlm.nih.gov/pubmed/11988105

This means a very big lot of lactic acid is being produced all the time, this is the reason why the intracellular pH of a cancer cell is very alkaline for to stand all the acidic outcome of anaerobic glycolysis. The cancer cell is permanatly shufflings lots of Na⁺ and HCO₃^- ions into itself and is putting the equivalent amount of H⁺ ions and lactic ions out of the cell. Thus a cancer cell‘s inside is buffered on a very high alkaline level and because of its very high acidic output a tumor’s interstitial space is very acidic (0,5 lower than inside on the average). Untill recently for technical reasons the pH-values of tumors were taken from the interstitial space only, therefore came the general conviction cancers be through and through acidic by their nature.

But the truth is : Cancer cells are alkaline in the inside and acidic in their nearest vicinity (the so called tumor mass), thus cancerous tumor’s cells are (very) alkaline and a tumor’s interstitial space is (very) acidic.

In the process of acid buffering the cancer cell is acting very clever by achieving buffering of 2 acidic H⁺ ions by 1 molecule of dissociated sodium bicarbonate (Na⁺ HCO₃^-), the 1 Na⁺ ion „in“ is being traded against 1 H⁺ ion „out“ (this happens with potassium also but to a much lower extent compared to normal cells, cancer cells are known to have lots of sodium in the inside).

The putting out of an acidic H⁺ ion is a simple thing compared to that what the inshuffled HCO₃^- ion is doing, immediately after entering the cancer cell’s cytosol it is buffering 1 H⁺ ion forming spontaneously H₂CO₃ (carbonic acid) and H₂CO₃ is being split in H₂O and CO₂ by the enzyme carbonic anhydrase, both molecules are diffusing away (or being transported) and have no longer any acidifying effect and thus the buffering has been completed (too much CO₂ will be finally breathed out by the lungs and H₂O by the kidneys and skin).

Now we have to make a little sidestep , we look into well known textbooks in biochemistry and physiology (Karlson and Ganong)

Karlson (11. Auflage, 1980) Seite 311: (Anm.: bei Säuren ist pK gleich pH, wenn das dissoziierte Anion in gleicher molarer Konzentration vorliegt wie das nichtdissoziierte Molekül)

Zitat : '...Der pK-Wert der Kohlemsäure (1. Stufe), beträgt 6,1; bei einer nichtflüchtigen Säure wäre in dieser Gegend beste Pufferwirkung zu erwarten. Da aber CO₂ flüchtig ist und durch die Kohlensäurehydratase stets ein Gleichgewicht zwischen CO₂ und H₂CO₃ eingestellt wird, ist die effektive H₂CO₃-Konzentration vor allem von der Kohlendioxid-Spannung abhängig. ...'

Ganong (deutsche Ausgabe, 4. Auflage, Springer Verlag, Berlin Heidelberg New York 1979) Seite 651 links unten:

Page 11

Zitat : ‚ … Wird dem Blut H⁺ zugesetzt, dann nimmt HCO₃^-, dessen Konzentration zusätzlich durch die Niere reguliert wird, ab, während vermehrt H₂CO₃ entsteht. Würde diese zusätzliche H₂CO₃ nicht in CO₂ und H₂O übergeführt und das CO₂ in der Lunge abventiliert, so müßte die H₂CO₃-Konzentration ansteigen. Wäre z.B. die zugesetzte H⁺ Menge ausreichend gewesen, um das Plasma-HCO₃^- auf die Hälfte absinken zu lassen, dann wäre ein pH-Abfall von 7,4 auf 6,0 die Folge. In Wirklichkeit wird aber nicht nur die gesamte zusätzlich gebildete H₂CO₃ entfernt, sondern der H⁺ Anstieg regt auch die Atmung an; dies bewirkt einen Abfall des pCO₂ so, daß zusätzlich H₂CO₃ entfernt wird. Das pH würde daher im vorliegenden Beispiel nur auf etwa 7,2 abfallen (Abb. 40.2). Die Reaktion CO₂ + H₂O = H₂CO₃ verläuft in beiden Richtungen langsam, wenn das Enzym Carboanhydase nicht anwesend ist. Im Plasma fehlt Carboanhydrase, in den Erythrozyten ist sie jedoch reichlich vorhanden …‘

Finally see

Garrett Reginald, Charles M. Grisham: Biochemistry. (International Student Edition). 4. Auflage. Cengage Learning Services, 2009, ISBN 978-0-495-11464-2, S. 394,

Zitat : ‚… Carboanhydrase ist ein Enzym, das sehr schnell katalysiert: Sie kann bis zu 10⁶ Moleküle Kohlenstoffdioxid pro Sekunde hydratisieren und beschleunigt die Reaktion auf das 10⁷-fache. Ihr k_cat-Wert liegt bei 1.000.000 pro Sekunde. …‘

Says the bicarbonate-buffer used up by half and left on it‘s own will cause a pH in the blood of around 6,1. But this would be far too acidic and not compliable with life because we know the pH of the blood is being constantly kept between 7,35 and 7,45 (or more exact 7,38 – 7,43), ICUs are normally dealing with between 7,35 and 7,45. If bicarbonate alone only could keep very acidic levels in our body what does happen really in our metabolism or even in cancer cells having a pH far beyond 7,5 (Kremer even says, „cancer cells are somehow fixed in alkalinity“), but how is the bicarbonate-ion doing this?

Just one shall add one and one and one … It’s quite simple, maybe too simple? Nature’s work appears somtimes surprisingly simple.

The solution for the high-pH-buffer-capacity of the bicarbonate-ion (HCO₃^-) lies in the acceleration of the natural splitting or „falling apart“ of the carbonic acid-molecule (H₂CO₃) into water (H₂O) and carbon dioxide (CO₂) by 10 000 000 times this fact is being achieved by a „very old magic“ exclusively intracellular and surface localized bound enzyme called carbonic anhydrase.

Now we have to make another little sidestep into a well known textbook of toxicology (Casarett and Doull’s) on page 244 the action of a carbonic anhydrase inhibitor (acetazolamide) is described and it mimics CO₂ –intoxication.

Casarett and Doull's Toxicology (4th Edition 1991, Pergamon Press), Seite 244:

Zitat : '...In some respects the CO₂ environment mimics the effects of acetazolamide. ...'

If you are blocking the effect of carbonic anhydrase the falling apart of carbonic acid will be 10 000 000 times slower, meaning you are getting a lot of carbonic acid in your cells falling apart definitely slower which is actually a carbonic acid intoxication because (left on it‘s own) the pH might get down to a point which is not compliable with life, if dosaged properly.

Page 12

From my point of view Simoncini is just overwhelming or overdoing the capacity of a cancer cell’s carbonic anhydrase (CA) by putting lots of sodium bicarbonate into the system, the majority of formed carbonic acid (H₂CO₃) is falling apart10 000 000 times slower than it should for „normal“ function and we have a carbonic acid intoxication of the cancer cell (substrate inhibition)!

But there is a firetest, the same effect should be produced by acetazolamide which mimics CO₂-intoxication (see above) because this substance blocks or inhibits carbonic anhydrase (CA), thus we should have through application of acetazolamide (in a way) the same deteriorating effects on cancer cells as while giving high dosages of sodium bicarbonate. And this is definitely the case, I found a Chinese study showing a decrease in growth of primary tumors and metastasis (see attached study) under application of CA with or without NaHCO₃.

Int. J. Mol. Sci. 2007, 8, 229-240, 13 March 2007 http://www.mdpi.com/1422-0067/8/3/229 or www.mdpi.org/ijms/ or http://www.mdpi.org

"Effects of Acetazolamide Combined with or without NaHCO₃ on Suppressing Neoplasm Growth, Metastasis and Aquaporin-1 (AQP1) Protein Expression"

Zitat aus Abstrakt: '...Results showed that acetazolamide alone could sharply reduce the number of lung metastasis and primary tumor growth, and appeared in a dose-dependent manner. Acetazolamide significantly inhibited carbonic anhydrase activity in tumor tissue. ...'

This implies very simple approaches in treating cancer, imagine prescribing daily acetazolamide (Diamox) and Sodiumbicarbonate (iv or also orally), you could check a patients base excess and adjust him to a maximum level, moreover there is eventually additional Amilorid possible that blocks the acidic H⁺ ions output of the cancer cell. A dangerous loss of Magnesium and Potassium could be prevented by daily intake of moderate amounts of Sodium(Na⁺)Potasium(K⁺)-Aspartate (Tromcardin) or K/Mg-Orotate (Magnerot).

There are some things more to say to this because as you know the devil resides in the detail, this is the basics though.

Last step is to formulate a unifying model in theory and therapy

Although the main challenge will be, as I mentioned, to formulate the unifying ultimate model in thinking (theory) and practicing (therapy), e.g. Gonzalez (Kelley, Beard) found out that the enzyme trypsin (ev. Chymotrypsion also) is dissolving and digesting cancerous tumors, by reading textbooks in physiology you see that the pancreatic juice getting into the duodemum has a pH pf 9 (!!) means the more alkaline the environment the better it works. Though we know highly dosed bicarbonate is actually acidifying the inside of tumor cells by overstraining carbonic anhydrase (substrate inhibition) but the outside is getting probably more alkaline and this supports the action of trypsin, consequently Simoncini’s and Gonzalez‘ approaches should be evidently combined (bicarbonate plus digestive enzymes like trypsin etc).

As I told already biologists are using trypsin to dissolve links between cells in cellular compounds in vitro, moreover (ironically) trypsin appears in many washing powders but not in cancer medicine …

There are conclusions having been thinking it over for years now, the 3(4) theories (Burzynski runs somehow with the others, he should fit in too):

Page 13

Kremer :

More than 2,1 billions years ago there was no volatile oxygen (or very little) on earth, in the archaic ocean then groups of primitive unicells were floating around, these had only few basic intentions to survive and stay alive namely eating, growing and multiplicate themselves. This behavior is being ruled by probably the first genetic program nature ever developed, it’s an old archaic one, therefore called Genome A and it burns sugar without or very little oxygen;

later when photosynthesis came up oxygen appeared in huger amounts on earth nature developed unicells (predecessors of our bacteries) able to utilize oxygen getting much more energy out of the burning of sugar (later these inclusions were called mitochondrias). This bacterial genetic program is therefore called Genome B.

In a unique creational act the archaic and prebacterial cell joined somehow, these prebacteries entered the cytoplasm of the archaic unicells enabled those to utilize oxygen for burning sugar, but also the archaic Genome A remained active but dominated and overruled successively by the oxygen utilizing Genome B. This is called the act of Cell Symbiosis and laid the foundation to the further development of all life on this planet.

But we do have to be aware of the fact that the chromosomal setting of these early cellular beings might have been quite dissimilar to ours because it is also the basis for nowadays insects‘ ones that are very different from humans.

In all living beings both gentic systems Genome A+B are still present and at work and genome B is the dominating one. What Kremer says is just as this simple, through certain unpleasant influences our mitochondrias get weaker and weaker and when this weakness reaches a certain point Genome A takes over and we have cancer. Cancer cells are not bad they just are doing what they need to do for surviving.

According to Dr. Kremer, living in Barcelona for some reason, cancer is dominating Genome A caused by mitochondriac failure (Mitochondriopathy). All the permanent discoveries of oncogenes is (acc. to him) some kind of bullshit because each newly discoverd oncogene is nothing else but a gene or genes of Genome A.

Therapeutic consequence „GET THE MITOCHONDRIAS BACK TO WORK AGAIN“!

Kremer says, if the mitos get into trouble the cell’s ability to utilize oxygen diminishes more and more (although enough oxygen could be around creating a condotion called „pseudohypoxia“), in fact of the cells need for sufficient ATP these are forced to strengthen the anaerobic path for ATP-production but for the price of worsened energy economics and decreased metabolic complexity, de(!)differentiation of the cell takes place until it reaches the point of being cancerous with full activated and dominating Genome A.

Kremer is being treated by his followers like a guru, he discovered a big part of the truth though not all.

Page 14

There is a fourth guy on the block, Dr. Burzynski in Texas, I put him in parentheses, about him I know the least, according to him, cancer patients have a certain lack of peptides in the blood and urine. That’s why they are getting it (a peptide is an amino acid chain of 2 to 50 AA), Burzynski is replacing the missing peptides (which are part of a „second immune system“) that kills the cancer cells.

In the beginning of a treatment the amino acid and peptide pattern in the patient’s blood and urine is detected, because this reflects the genetical make up of a certain cancer, out of these findings the substitution of the „right“ peptides can be applied orally or intravenously, ideally the uncontrolled divisions of the cancer cells are going to be stopped by blocking the oncogenes that are many in all the different cancer types.

Possibly this treatment is blocking those groups of genes which are belonging to Genome A (Kremer).

www.burzynskiclinic.com

Sympathicus and the immune system are phylogenetically young compared to parasympathicus (vagus) and the ground system and its regulation (Prof. Pischinger) which is called the Extracellular Matrix (ECM) and there is even described an intracellular system of units of life as Association/Induction Hypothesis (Ling).

www.gilbertling.org

Saying peptide chains can be totally folded or unfolded (not more or less), presenting different electrochemical loads (+ or -) to dipolic water molecules and neighbouring ions thus steering the cell’s vital and functional activity by this (in cooperation with ATP and other ‚inducers‘).

Perhaps the Burzynski therapy does work specifically on these systems (Kremer’s method seems more unspecific).

The decisive point is that carbonic anhydrase accelerates the splitting of carbonic acid (H₂CO₃) into Water (H₂O) and carbon dioxide (CO₂) and thus by CA nature can adjust very precisely the required pH, I mean CA can more or less accelerate it and even the other way round (forming H₂CO₃ out of H₂O and CO₂ if necessary), because of this unique property sodium bicarbonate is called „open buffer“, to my knowledge the only one in metabolism (but maybe something similar can happen with H₂SO₃ or H₂S in the process of so called chemolithotrophy).

By inhibiting (acetazolamide) CA or putting huge amounts („overdose“) of sodium bicarbonate the splitting rate of H₂CO₃ decreases because CA cannot do sufficiently its job any longer and thus intracellular acidification takes place (carbonic acid intoxication).

Extracellularly there is acidity anyway because there is no CA in the interstitial space, this is the reason why the intercellular space (interstitium) generally tends to be too acidic, making way to virtually all chronic diseases (incl. cancer).

In my younger doctor years I did these things although not understanding the details then, I saw liver metastatic herds getting smaller (a little bit) by sodiumbicarbonate iv infusions with pancreatic enzymes (very high risk of allergic shock), moreover I made the experience that such patients are being ignored by the specialists in the hospitals and die rather fast after a slight improvement was detected. Nowadays the system has become too rigid to do such things in a relaxed way.

Page 15

By Kremer we know there is an ancient program (still fully active) in our chromosomes or genes reflecting times when there was no or little oxygen on earth, it is burning sugar fuel without oxygen, upon that there is a „younger“ system of burning sugar by oxygen. The latter is much much more effective energetically and positioned upon the former. Both systems are active and the endproduct of the first one (lactic acid) is handled into the other one (into citric acid cycle and oxidative phosphorylation or „oxidative chain“).

If there is no oxygen the first system is active only. On the avereage in cancer cells 65% to 70% and even more of the energy need is covered by this system, the other 30% are covered by oxygen burning (Guppy et al).

Cancerous tumors consist of compounds of unicells reflecting those in the archaic ocean (of anaerobic or facultative anaerobic property), with the only intentions of growing, eating, spreading and multiplicating.

Kremer treats cancer by starting and pushing the main actors of the ‚younger‘ oxygen burning system namely the mitochondrias by means of Resveratrol, Pterostilbene, Cucurmin, Vitamin D3 (very important) and many other polyphenolic compounds.

By Gonzalez and Beard we know that phylogenetically the period of archaic unicells is embryologically reflected by the trophoblast in mammals and man (vertebrates). And in early pregnancy the foetus, invading the mother’s uterus, is ‚physiologic cancer‘, by exactly the 56th day of pregnancy (in humans) the character of a part of these cells changes dramatically into benign ones and the more outer placed ones are getting into apoptosis. That change of this ‚physiologic cancer‘ into „good“ tissue takes place when the pancreas of the embryo starts to work. The discovery of this was the beginning of the ‚pancreatic enzyme treatment of cancer‘ by means of mainly Trypsin and the other pancreatioc enzymes.

By Beard we know that in nature (plants and animals) in the process of multiplication asexual generations are always followed by sexual ones etc. (this is a rule!), the trophoblast is the asexual generation in mammals and men and when the trophoblast gives rise to primordial germ cells only one (or more than one in case of twins, triplets etc.) of those gives rise to the embryo the other ones stay aside and travel after three postfertile weeks into the back part of the yolk sac (hypoblast), multiplicating and feeding themselves tremendously and go back into the embryonic body in which meanwhile all the organs have been formed basically structured and these ‚vagrant germ cells‘ are being spread all over the embryo’s body and remain there the rest of the individual’s life, also an adequate portion of 30% gets into the gonads being bound to meiosis to make way for the following sexual generation on the cellular level.

By Beard we also do know that the (cancerous) trophoblast is growing best in an acidic environment (now we know a tumor’s matrix-metall-proteinases like it acidic), while the upcoming pancreas on day 56th of pregnancy (or postfertile?) produces pancreatic ferments or enzymes working best in an highly alkaline juice (pH 9!). The high alkalinity of the pancreatic juice is caused by the very high content of sodium bicarbonate (sive!).

Page 16

By Gonzalez we know that these vagrant germ cells remainig all over our bodies are nothing else but the so called adult stem cells whose origin lies completely in the dark according to official science. These cells serve as repair and replacing cells for our tissues and they obnoxiously can occasionally form a „sibling“ of us: a cancerous tumor

By Simoncini we know that cancer behaves very much like fungus and according to him it is even one because he discovered that cancerous compounds dissolve quite well by alkalizing their extracellular interstitial space moreover he states that fungus can represent itself in so many forms science does not know yet. The best natural antimycotic is Sodiumbicarbonate.

Official oncology admitts there is always fungus with cancer but it is a secondary fungal infection. Simoncini maintains the other way, there is always fungus in the first place! I am deeply convinced Simoncini is right because there are so many positive therapeutic reports on cancer on his homepage these can’t all be faked. Moreover he has scientific predecessors HR Dr. Franz Gerlach from Mödling and the pleomorphists like Dr. Günther Enderlein in general.

Simoncini observed that the links between cancer cells get disrupted easily by alkalinity and the immune system can deal much more the better with singular cells than a compound (tumor), here it lies at hand to combine alkalinization (Simoncini) with pancreatic enzymes (Gonzalez and Beard).

C O N C L U S I O N OF THE CONCLUSION

Cancer cells are acid machines, this counts first of all for solid tumors (not necessarily in lymphomas) these are producing abundant amounts of lactic acid because 70% and more of their energy need is fed by sugar burn without oxygen. That acid on the one hand is being exported in the extracellular space right outside the cell membrane and sets a remakable activating stimulus to the matrix-metallo-proteinases that melt away the healthy surrounding tissue of the cancer patient (or the uterus tissue of the mother in case of pregnancy) and on the other the huge acidity is buffered in the cell’s inside very effectively.

The acid export can be blocked amongst other chemicals by commonly prescribed Amilorid .

First of all cancer cells do have to stand their own acidity that’s why those are intracellularly calibrated highly alkaline! This is happening through buffering by sodium bicarbonate, the crucial point is that NaHCO₃ is a so called ‚open buffer‘ means the carbonic acid molecule which is formed by the buffer reaction (HCO₃^- + H⁺ = H₂CO₃) IN THE MOMENT is believed to fall apart into water and carbondioxide and therefore gone thus the buffer can keep a very high alkalinity without being used up too quickly. The falling apart of carbonic acid does not happen spontaneously in vital systems BUT is accelerated by the intracellular enzyme carbonic anhydrase 10 000 000 times thus the intracellular pH of the cancer cell is definitely steered by CA. Carbonic acid is chemically defined as instabile acid because of its tendency to fall apart into H₂O and CO₂ spontaneously in labs or open systems like alcolholic fermentation etc. BUT this is not the case in closed vital systems like the human body where ist appears as STABILE ACID.

The buffering of acidity inside the cell can be blocked by inhibiting carbonic anhydrase by acetazolamide (Diamox e.g) and other CA –blockers.

Page 17

The acidic interstitial space and the further environment of a cancerous tumor has to be alkalized but not mainly by Sodiumbicarbonate but by the salt of a weak organic acid like citrate, lactate, acetate etc.

The strategy implies the cancerous tumor‘s extracellular alkalinization by intake (or iv) of organic salts and acidification intracellularly by inhibition of Carboanhydrase (and ev. the acid exporting membrane carrier).

Eventual additional application of pancreatic enzymes, Resveratrol, Cucurmin, Vitamin D3 (very important) and many polyphenolic compounds (PAC etc.) . Healthy cells are only effected minimaly (acceptable intracellular pH decrease) because they are depending mainly on oxygen burn in the mitochondrias.

How Burzynski fits into this is not yet clear.

The highly alkalizing effect of sodium bicarbonate is depending completely on the enzyme carbonic anhydrase, first you have the normal buffer reaction where the carbonate ion (HCO₃^-) associates with the acidic hydronium ion (H⁺) forming carbonic acid (H₂CO₃), this is completely spontaneous, but what comes now is different to other buffers that are used up rather quickly when all the buffer salt has been transformed into its acid (pH sinks dramatically).

Unlike other resulting acids carbonic acid is falling apart after buffering into carbon dioxide (CO₂) and water (H₂O) by action of CA, as mentioned in detail above, this means the acid is gone and this buffer is a so called „open“ one means moreover the stoichiometric balance is remaining on the left side of the chemical reaction therefore the reaction does not switch off itself (no product inhibition).

A buffer is a mixture of a weak (organic) acid and its salt(s) and each of these has its ideal pH-value in adjusting a certain liquid solution, interestingly it would be in our body in case of the carbonic acid/bicarbonate buffer a pH range of around 6,2! This is far too acidic for life! The biologic neutral point is pH 7,4! But a cancer cell’s inside is fixed in a pH range between 7,46 and even 7,60 (Kremer) to stand the tremendous amounts of lactic acid being produced.

This high intracellular alkaline calibration of the cancer cell is only possible because of (1st) the permanent export of lactic acid and H⁺ ions and lactate ions out of the cell and importing Na⁺ and bicarbonate ions into the cell, (2nd) as mentioned, the „open“ bicarbonate buffer which keeps the balance of the reaction on the left side and (3rd) the enzyme carboanhydrase that is accelerating the ‚opening‘, namely the falling apart of carbonic acid into CO₂ and H₂O by 10 000 000 times.

This means if you give to a cancer patient sodiumbicarbonate you are actually supporting the tumor cell‘s inside alkalinity because of the action of carboanhydrase which further means you help the cancer cell staying alive and healthy! And in the interstitial space you produce rather the contrary because carboanhydrase is mainly an intracellular and cell surface enzyme, remember without the action of carboanhydrase the carbonic acid/bicarbonate buffer adjusts nearly at pH 6,2!

I have seen many doctors (including myself) treating their cancer patients naturally having given them sodiumbicarbonate and they all failed … except Dr. Simoncini! Nobody else dares to give these large amounts of Sodiumbicarbonate and by these high dosages you are sometimes riskful to the patient especially in the weak and heavily exhausted ones after chemo (Potassium can get down very quickly).

Page 18

Only by giving very huge amounts of NaHCO₃ you are overruling the enzyme carboanhydrase (substrate inhibition) and this consequently leads to a carbonic acid intoxication of the cancer cell and it dies …

To miknimize the risk for patient you just have to inhibit carboanhydrase by a blocker (e.g. acetazolamide), the acid membrane carriers by amilorid and apply to the patient a pure organic buffer like lactate …

(Also citrate, acetate or succinate could be possible but I believe lactate buffer would be best because it is (probably not being endangered of getting imported to the cancer cell’s inside for buffering).

The basic testimony requires the cancer cell‘s intracellular acidification and extracellular alkalinization as it is stated above.

Never give sodiumbicarbonate alone to a cancer patient but orally for heartburn only! It is most decisive to inhibit the enyme carboanhydrase!

Moreover to make a patent of this is hardly possible because all the suggested substances are in longterm use already (‚off label‘ prescription).

Your idea of injecting sodiumbicarbonate (Simoncini) with or without proteolytic enzymes directly into the tumor is also of value though it should be done at least with some portion of lactate to support the enzymes‘ action and effect.

And generally spoken: Simoncioni’s experiences are still valid although you have to inhibit carboanhydrase first, then you need definitely smaller amounts of sodiumbicarbonate if at all.

Of course also a pure oral therapy has to be put into accountance (just swallowing baking soda, acetazolamide, enzymes etc.).

We know that cancer cells need the so called matrix-metallo-proteinases to desintegrate the surrounding tissue for growth, these enzymes work best in an acidic milieu, the model is to alkalize the tumor’s surrounding to slow down the destructive matrix-metallo-proteinases, I believe this works best by lactate because I think it cannot be „misused“ by the cancer cell for alkalizing itself‘s inside (cancer cells exporting lactate, not importing it!).

There are isotonic (0,85 or 0,9%) and isoionic (same electrolyte concentration Na⁺, K⁺, Cl^- as in the serum of the blood) solutions per 500ml or cc plus a certain amount of lactate on the market (Ringer Lactate with e.g. 15 mval lactate- ion per 500ml)

If we give this 500ml iv by a butterfly needle e.g. by this we do a ‚whole body alkalizing rinse‘ of the interstitial space where alkalinity is needed the most.

The other maybe better way would be to set the butterfly needly subcutaneously in the area of the tumor because there interstitial alkalinity is strongly needed (if it’s in the colon e.g. you use the skin of the epigastrium, if it’s colorectally use the skin of the lower body etc.). If this is burning subcutaneous infiltration of the piercing point by lidocain is indicated before (1-2 ml or cc, 2% concentration, the rest put in the lactate solution)

Page 19

(We don’t use sodiumbicarbonate because it is not alkalizing the interstitial space may be even acidifying it by extracellular lack of carboanhydrase and we don’t use other salts like citrate, acetate or succinate because these might be imported by the cancer cell to alkalize itself intracellularly.)

When you talk of infusion you are referring to a subcutaneous injection?. Here there are terminal cases, but the specialists do not say it and they go on and on until the patient dies. They do not die of cancer, but usually because of strokes or heart attack. The drugs used against cancer harm the patients in a great number of cases by so called side effects.
There are many patients that don‘t want to receive zytostatic toxic treatments. They are potential volunteers for this treatment.

250 mg Acetazolamide (Diamox) in the morning and

1 tablet Potassium/Magnesium-Aspartate (Tromcardin) and 1 infusion 500 ml isoionic solution plus 15mval lactate ion (Ringer‘s solution), could be also given, maybe even better, as palliative infusion subcutaneously in the region of the tumor,

if it’s burning infiltrate

1-2 ml Lidocaine 2% where you set the butterfly needle, ev. put the rest oft he ampoule into the intravenous (IV) infusion.

If this works fine after a few days or week we should give additionally

1 mg Amilorid as monosubstance e.g. in the morning, on the market it’s usually combined with Hydrochlorothiazide (HCT).

If the patient is doing well we can increase the dosage, just 20years ago there were many so called „outtreated“ patients (no more treatment options), medicine did not touch them any longer, they were waiting for dying, now thex are put on palliative care. These would be the fitting ones for this treatment.

This low dosage is on purpose because we only want to reach cancer cells that are much more sensitive (theoretically) to this kind of treatment than normal cells, we want to avoid systemic effects as far as possible.

I fit works well so far there will be sodiumbicarbonate infusion (IV or even subcutaneous) the next option.

The normal procedure is very hard for the patients. But what is true now there are many people that survive a cancer much longer more than before. One thing I have noticed is that some years ago patients were very thin before dying, now they are not. Now they look well and sometimes suddenly they are gone by paraneoplasic incidences (usually letal thromb-emboli).

I never injected SBC into tumors, I gave it iv and the results were not satisfying, many doctors still giving it iv, patients getting short of breath an then they die by the tumor … Once I discovered they are doing immediately better by giving them Ringer Lactate iv (alkalizing), thus I realized they had been acidified by the SBC which was and is actually supposed to alkalize. Here I realized further that by SBC you can „overrule“ the potency of CA (substrate inhibition) and making a patient worse and even die if you are continuing the application (inner suffocation). It’s a question of the right dosage! But I believe to give dangerous dosages of SBC is not necessary if you are inhibiting CA at the same time.

Page 20

But intratumorous injections of SBC seems to be a real good solution if the tumor is accessible!

In the last 15 years when palliative care has come up more and more they developed a method of putting liquid to dehydrated (mostly terminal) patients, to avoid the more or less deteriorated arm-veins of the patient they are positioning the butterfly needle of the infusion subcutaneously (fix it by adhesive band) and let it drop …

This is a very gentle method to bring liquid to the body of the suffering, normally the abdominal wall‘s subcutaneous fat is punctured or the inner side of the thighs, although you can do it on other spots of the body as well.

In my mind we can use this to bring alkalinity to the cancer’s immediate surrounding (you are addressing the interstitial space directly!) by doing this with Ringer lactate, to prevent burning at the needle place we apply lidocain subcutaneously bevor starting, we position the needly where we think alkalinity is most advantageous. If there is no special place to figure out we use abdominal wall or the thighs at the inner side, moreover we can administer it iv nonetheless.

Sodiumbicarbonate could be of help only in very large dosages because you do need those to overrule intracellular carboanhydrase and on the cell’s surface as well, apatient having undergone chemotherapy and radiation before is very weak, high dosages of sodiumbicarbonate would probably put him or her at risk, I would recommend 1000 cc or 1000 ml isotonic and isoionic solution with approximately 30 mval or mmol L-lactate daily given subcutaneously in a region where patient is having the primary tumor but also in regions of swollen lymphnodes as well.

This solution is called Ringer’s lactate, this would be the first step, there can be no harm.

Next would be just 250mg Acetazolamide (Diamox) in the morning plus Mg- and K-aspartate (morning and evening) very simple.

The only guy who knows how to treat with high dosed NaHCO₃ is Dr. Simoncini, just look on his homepage

www.curenaturalicancro.com

But I did not find any usable information on lymphoma, there is in his book „Cancer is a fungus“ though on page 186 a few words on non-Hodgkin-lymphoma, not vera encouraging.

Evidently Simoncini was not that successful in lymphomas with solely sodiumbicarbonate treatment.

The main point, science has not yet found out that all the lymphomas and leukoses are probably another type of disease as compared to solid tumors.

Or tell to the mother Dr. Gonzalez‘ homepage in New York

http://www.dr-gonzalez.com/lymphoma.htm

Page 21

There is some remarkable case reports of non-Hodgkin-lymphomas.

The third way would be to get in contact with German Dr. Kremer living in Barcelona (!), give his email to the mother cellsymbiosis@telefonica.net

Many doctors and healing practitioners are following his way in Central Europe with remarkable results on cancers and AIDS but I don’t know in particular concerning lymphomas.

There are some most successful cancer doctors in the world, there are other ones too, but these ones I tried to understand means to conclude and combine their different theories.

I.) www.curenaturalicancro Simoncini in Rome: Cancer is Fungus

II.) www.dr-gonzalez.com Gonzales in NYC: Cancer is Trophoblast

III.) http://aliveandwellsf.org/kremer/ Kremer in Barcelona: Cancer is Genom A

IV.) www.burzynskiclinic.com Burzynski in Houston/Texas: Cancer is Deficiency in Negative Tumormarkers (small organic molecules named Antineoplastons)

Upcoming:

V.) (www.lifelength.com Cancer is telomeres shortening, it’s quite probable, there might be successes in the near future by either blocking and even activating telomerase.)

They have totally different theories in explaining the nature of cancer but they have one decisive fact in common: Their therapies work!

So it must be possible to create a theory unifying their cancer models, we share (hopefully) the same reality, well this I have been trying for some time with at least a model that covers all 3(4) of them.

Kremer :

More than two billions years ago there was no free oxygen (or very little) on earth, in the archaic ocean then primitive unicells and groups of unicells were floating around, these had only few basic intentions to survive and stay alive namely eating, growing and multiplicate themselves. This behavior is being ruled by probably the first genetic program nature ever developed, it’s an old archaic one, therefore called Genome A and it burns sugar without or very little oxygen; later when oxygen appeared in huger amounts on earth nature developed unicells (predecessors of our bacteries) able to utilize oxygen getting much more energy out of the burning of sugar (later these inclusions were called Mitochondrias). This bacterial genetic program is therefore called Genome B.

In a unique creational act the archaic and prebacterial cell joined somehow, these prebacteries entered the cytoplasma of the archaic unicells enabled those to utilize oxygen for burning sugar, but also the archaic Genome A remained active but dominated and overruled by the oxygen utilizing Genome B.

Page 22

This act is called the act of Cell Symbiois and laid the foundation for the further development of all life on this planet.

In all living beings both gentic systems Genome A+B are still present and at work and genome B is the dominating one. What Kremer says is just as this simple, through certain unpleasant influences our mitochondrias get weaker and weaker and when this weakness reaches a certain point, Genome A takes over! And we have cancer, cancer cells are not bad they just‘re doing what they need to do for surviving.

According to Dr. Kremer Cancer is dominating Genome A caused by mitochondric failure (Mitochondriopathy). All the permanent discoveries of oncogenes is after him some kind of bullshit because each newly discoverd oncogene is nothing else but a gene or genes of Genome A.

Therapeutic consequence „GET THE MITOCHONDRIAS BACK TO WORK AGAIN“!

Kremer says, if the mitos get into trouble the cell’s ability to utilize oxygen diminishes more and more (although enough oxygen could be around „pseudohypoxia“), in fact of the cell’s need for sufficient ATP it is forced to strengthen the anarobic path for ATP-production but for the price of worsened energy economics and decreased metabolic complexity, de(!)differentiation of the cell takes place until it reaches the point of being cancerous with full activated and dominating Genome A. Kremer is being treated by his followers like a guru, he discovered a big part of the truth but not all.

These four physicians have described their methods years ago. this is why they do not mention telomerase maybe in new editions of their books or articles. Nobody can talk about cancer not to mention telomerase today. It is basic information though in fact it doesn‘t matter as long as their methods work.

Another important new information is the discovering of Resveratrol. It is a substance coming from the red wine. Researches are still discussing it, but it seems Resveratrol inhibits telomerase, reversing cancer tumors.

Sugar has also something to do with Resveratrol, because the fermentation of wine needs sugar.

So, it seems crazy, but we are taking TA-65 to activate telomerase, the enzyme of inmortality, and at the same time oncologists are trying to inhibit telomerase in cancer cells. I believe telomerase is good. I believe it is really the fountain of Youth and the prove is that they are active in babys, children and young people. But there must be a mechanism that pushes telomerase cells out of control. So, lets rule out telomerase as well. It seems it prevents cancer. So the "detonant" must be something else and telomerase start acting to heal it, but somehow there is something that obstaculize the work.

I would like to know your opinion on it and also on Resveratrol. By inhibiting telomerase, cells stop mitosis and they -in my opinion-, get "momified". Resveratrol is sold like making cells life longer, but if they can t reproduce themselves... What is the benefit?.

I am expecting the book by the italian doctor. I ll let you know when it arrives. I like Kremer very much. He seems "solid" to me.

Page 23

Well, there is a quite simple thinking; cancer cells are archaic cells (the same as floating in the archaic ocean), they cannot not utilize oxygen (or a limited amount only) to burn sugar(s) that is not sufficient for surviving, so they have to burn very large amounts of sugar(s) to generate enough ATP-energy.

Our cancer cells need much much more sugar than our healthy ones (18 – 32 times!) and because there are not enough mitochondrias to change oxygen into water, it‘s even very toxic to them.

Conclusion : Sugar feeds cancer cells, oxygen kills them. Never give extra sugar(s) to cancer patients, except you have reason to believe that the cancer cells will be overeating themselves to death.

Let’s take the great mystery of terminal anorexia or cachexia of a cancer patient, they oncologists telling you, we don’t know really what actually leads to this tremendous loss of weight in the final state.

This is actually not true, the mystery of terminal cachexia has been solved for the longest by a physician named

Dr. Gold(!) http://en.wikipedia.org/wiki/Hydrazine_sulfate (look for BACKGROUND) or Dr. Gold’s Institute http://scri.ngen.com/ or himself http://www.hydrazinesulfate.org/

If you take 1 mol glucose you get 2 mol ATP, if you burn it by oxygen you get additional 18 or 32 mol ATP ( wheter it’s 18 or 32 or even yet more, literature is formally nor fully clear on that), the more metastasis or primary tumor masses the patient grows the more sugar the cancer cells need, the body starts the only way to get full supply because the patient cannot eat so much sugar or anything else, it starts Gluconeogenesis massively.

Normally Gluconeogenesis starts if the body’s blood sugar level ist getting under 60mg% (by the average), the abundant cancer cells in a terminal patient only burn oxygen up to 30% of their total energy need, the rest of 70% has to be covered by anaerobic glucolysis, means the body’s blood sugar level is permanently in the onset of getting under 60mg%, means Gluconeogenesis is being permanently switched on.

The forming os sugar has to be tremendously switched up in order to hang on or keep up with the 30% aerobic burning

First of all the patient’s cancer cells are putting all the lactic acid, that is produced by anaerobic glycolysis, out of themselves into the bloodstream which carries lactic acid to the liver that changes it into glucose again and the blood brings the newformed glucose back to the cancer cells, this is repeatedly going on and on. Moreover the body is changing all fat that is possble into glucose and all protein that is not of vital function, first total blood protein is reduced to a minimum and then the muscles and so on and on …

Dr. Gold’s method of treatment is as simple as this; he found out in experiments that there is a substance being able to block Gluconeogenesis and this is hydrazine sulphate!

Page 24

HS is a MAO-blocker as being (formerly) used in depressive patients, in the moment you give this to a patient he is gaining weight almost immediately and of course the general condition improves as well.

You start with 60 mg capsules, first 1 cap in the moring after 3 days you go to 2 and after 3 days further you go to the maximum dosage of 1 cap 3 times daily, in case the patient has already a body weight under 40 – 60 kg you are going to do this by 30mg capsules.

Side effects like those of MAO-blockers, because of a certain neurotoxicity, you make a one-week-break after 4-5 weeks of intake, so the onset of neurological symptoms may be postponed.

The problem is, this substance never got approved because of its (rather acceptable) neurotoxocity (I think this was an ‚official lie‘ and does not bear the refusion), but you can get it probably somehow via the internet, there is also a number to call, I mean in case you know someone who is in the urgent need of taking it.

By this treatment there is a real chance to starve the cancer cells to death because healthy cells use oxyygen for much more effective sugar burning thus these remain untouched by the treatment.

A special ‚devilish‘ property of cancer cells relies to the fact that there is (even in cancer cells) a certain ‚oxygenic portion‘ of katabolic burning, this works like a ‚pace maker‘ forcing the anaerobic part to maximal activity.

Gonzalez

Moreover for the moment I am trying to read this book (first published 1911) by Dr. Beard (died 1924+), the other mentor of Dr. Gonzalez‘ the real pioneer of enzyme therapy and discoverer of cancer’s real cause (being germinal in origin and asexual-throphoblastic in it‘s nature).

Gonzalez did a great job by republishing it nowadays again, look www.dr-gonzalez.com http://www.newspringpress.com/beard.html or via amazon.

There is something really magnificent on Dr. Simoncini’s method in fact how it works, there is something probably he himself has not found out yet.

Resveratrol is activating some genes called silent regulators (type I and II?) and therefore called ‚sirtuins‘, there should be it‘s structural formula on wiki?

Resveratrol comes from wine and has been been used to inhibit telomerase expresion in cancer cells. Cycloastragenol is a substance coming out from astragalus and we are taking it with TA-65.

Basically everything being able to turn on the primary germ cell programm in senescent stem cells can cause cancer. Besides fungus also other microbes can do this e.g. viruses (recently a US study indicates people having oral sex quite often show more throat cancers, the scientists see viruses as cause) moreover radiation and toxins might also be able to start this devastating programm in senescent stem cells.

Page 25

TA Sciences (selling TA-65) does not advice people not to take Resveratrol any longer, they did it in the beginning because of its potential telomerase inhibition effect, now they say it’s ok, there was a similar concern with cucurmin. Moreover first shortly they don’t people advice not to take TA-65 MD if they are having cancer or have had it within the last 5 years.

From my point of view, telomerase activation does not force a cell to switch on Genome A (Kremer), moreover it does not force a cell into a form of fake meiosis (Gonzalez/Beard) and it does not cause a fungal infection (Simoncini) or activate telomerase in fungal cells because these are active already. TAS says this study changed everything:

http://www.ncbi.nlm.nih.gov/pubmed/20822369

What theoretically can happen is that a benignom might eventually become a little bit larger because of the increased Hayflick limit in proliferating adult stem or persisting vagrant germ cells (fibroma, myoma, naevus, hyperostosis, meningioma, cysts, mucinoma, teratoma etc.) but these tumors don’t try to form a chorion or placenta (no need to invade the neighbouring tissue).

BTW there are several chlorine-oxygen derivatives that could eventually release Oxygen and/or its derivatives into the tissues, mostly known is ‚sodium chlorite‘ NaClO₂ and its acidified form ‚chorine dioxide‘ ClO₂, e.g. being used against cancer by American Biologics (Bob Bradford’s company for biologic remedies against various diseases).

Cachexia (cancerogenic slim disease) or anorexia (latin marasmus) is the final state of cancer when a patient sometimes has a body weight of 30 kg or even less in the end …

Hydrazinesulfate is a MAO-inhibitor and blocks especially glyconeogenesis.

Oxygen is very useful (by several companiey e.g. Oxychlor, MMS, Oral Oxygen etc.) remedy actually for (almost) everything, but this is a side step in our communication, we’ll be focusing on Gonzalez.

What only a few people know, O₂ is the first defence against free electrons, then it’s getting degraded step by step into water, sodium bicarbonate is the main defence against free protons, then it’s degraded into CO₂ and water.

Therapie mit NaHCO₃ modifiziert nach Dr. W. Zöch (Theorie) & Dr. W. Surböck (Praxis)

Literatur

Acevedo HF , Tong JY, Hartsock RJ „Human chorionic gonadotropin-beta subunit gene expression in cultured human fetal and cancer cells of different types and origins.“ Cancer. 1995 Oct 15;76(8):1467-75. http://www.ncbi.nlm.nih.gov/pubmed/8620425 Ärzte Zeitung, 24.01.2012 „Krebsstammzellen: Die tödlichen Schläfer im Blut“ http://www.aerztezeitung.de/medizin/krankheiten/krebs/mamma-karzinom/article/802445/krebsstammzellen-toedlichen-schlaefer-blut.html?sh=7&h=543734413 Ärzte Zeitung, 28.03.2014 „Erfolge der Forschung zu Stammzellen - Tumorstammzellen liegen in Nischen und teilen sich nur selten. Durch sie kehrt der Tumor nach scheinbar erfolgreicher Therapie oft zurück oder metastasiert.“ http://www.aerztezeitung.de/medizin/krankheiten/krebs/article/857937/jubilaeum-hi-stem-erfolge-forschung-stammzellen.html?sh=1&h=543734413 Beard, J. „The Enzyme Treatment of Cancer“, pg 103 (auff. Chromosomenreduktion bei Malignomzellen) Chatto and Windus, London 1911, wiederaufgelegt New Spring Press, New York 201 www.dr-gonzalez.com Bihn, Detlev „Oxidative Schäden an Membranlipiden und –proteinen in Abhängigkeit von körperlicher Belastung“ 03_kapt4.pdf (Harnsäure Antioxydans), Diss. zum Dr.med. 2010, Freie Universität Berlin, Humanmedizin http://www.diss.fu-berlin.de/diss/servlets/MCRFileNodeServlet/FUDISS_derivate_000000000455/?hosts Casarett and Doull's Toxicology (4th Edition 1991, Pergamon Press), Seite 244, Zitat: ‘...In some respects the CO2 environment mimics the effects of acetazoamide. ...’ Caudwell Xtreme Everest Research Group , Grocott MP,Martin DS,Levett DZ,McMorrow R,Windsor J, Montgomery HE; „Arterial blood gases and oxygen content in climbers on Mount Everest.“ N Engl J Med. 2009 Jan 8;360(2):140-9. doi: 10.1056/NEJMoa0801581. http://www.ncbi.nlm.nih.gov/pubmed/19129527 Chang W. Song , John C. Lyons,Robert J. Griffin, Carol M. Makepeace, and Edward J. Cragoe Jr. „Increase in Thermosensitivity of Tumor Cells by Lowering Intracellular pH“ CANCER RESEARCH 53, 1599-1601, April 1, 1993 http://cancerres.aacrjournals.org/cgi/content/abstract/53/7/1599 Chegwidden, W.R., Carter, N.D., Edwards, Y.H. (Editors) “The Carbonic Anhydrases - New Horizons”, Seite 101, Zitat: ‚… Warburg (1926) suggested many years ago that acidification was a property of maligant cells. Others have argued that extracellular pH of human tumors is, on average, more acidic than that of normal tissues (Griffiths, 1991). …‘ Verlag Birkhäuser, Basel Boston Berlin 2000 http://www.amazon.com/The-Carbonic-Anhydrases-Experientia-Supplementum/dp/3764356707/ref=sr_1_1?ie=UTF8&qid=1396458797&sr=8-1&keywords=Chegwidden+New+Horizons#reader_3764356707 Chlebowski, R.T., Heber, D., Richardson , B. and Block, J.B. „Influence of hydrazine sulfate (HS) on carbohydrate metabolism in cancer cachexia: a randomized, placebo-controlled trial.“ Proc. Am. Soc. Clin. Oncol. 1:59, 1982. http://www.hydrazinesulfate.org/ Chlebowski, R.T., Heber, D., Richardson, B., et al. „Association between improved carbohydrate metabolism and weight maintenance in hydrazine sulfate treated patients with cancer cachexia.“ Proc. Am. Soc. Clin. Oncol. 2:95, 1983. http://www.hydrazinesulfate.org/ Chlebowski, R.T., Bulcavage, L., Grosvenor, M., et al. „Hydrazine sulfate in cancer patients with weight loss: a placebo-controlled experience.“ Cancer 59:406-410, 1987. http://www.hydrazinesulfate.org/ Chlebowski, R.T., Bulcavage, L., Grosvenor, M., et al. „Influence of hydrazine sulfate on survival in non-small-cell lung cancer: a randomized, placebo-controlled trial.“ Proc. Am. Soc. Clin. Oncol. 6:175, 1987. http://www.hydrazinesulfate.org/ Cosentini E.P., Bischof G., Hamilton G.,Teleky B., Riegler M., Feitl W.,Wenzl E. und Schiessel R., “Bedeutung des HCO3-CO2-Puffersystems für die Homöostase des intrazellulären pH in SW620-Kolonkarzinomzellen” European Surgery, Kategorie Chirurgische Forschung, Vol. 26, No. 5/Oktober 1994, Seiten 320-325, ISSN 1682-8631 (Print) 1682-4016 (Online), DOI 10.1007/BF02620674, SpringerLink Date Mi, 2.5.2007, Springer Verlag http://www.springerlink.com/content/40r18m8708347437?print=true Cui W., Liu L., Peschke P., Haberkorn U., Mason R.P. „Transmembrane pH Gradients in Tumor Cells: Observations Using 19F NMR of Promising New Reportermolecules” http://www.utsouthwestern.edu/vgn/images/portal/cit_56417/59/0/319105Cui-ISMRM06.pdf Magn. Reson. Med., 39, 551-556 (1998), Curr. Med. Chem. 6, 533-51 (1999) Dalmasso Guillaume, Loubat Agnès,Dahan Stéphanie, Calle Gustavo,Rampal Patrick,Czerucka Dorota „Saccharomyces boulardii prevents TNF-α-induced apoptosis in EHEC-infected T84 cells“ Research in Microbiology, Volume 157, Issue 5 , June2006,Pages 456–465 http://www.sciencedirect.com/science/article/pii/S0923250806000027 Dumrese J, Haefeli B „ Pleomorphismus – Blutsymbionten Blutparasiten Blutpilze“ (Seite 114) Haug 1996 Elias TD „The Burzynski Breakthrough“, Lexikos, Nevada City (Kalifornien) 2001 http://www.theburzynskiclinic.com Farmer JB, Moore JES, Quarterly Journal of Microscopic Science 48:489 (1905) as quoted in the Oxford English Dictionary, Third Edition, June 2001, „We propose to apply the terms Maiosis [sic] or Maiotic phase to cover the whole series of nuclear changes included in the two divisions that were designated as Heterotype and Homotype by Flemming.“ Filler SG , Sheppard DC „Fungal invasion of normally non-phagocytic host cells.“ PLoS Pathog 2006 Dec; 2(12):e129 http://www.ncbi.nlm.nih.gov/pubmed Gadisseu et, 1984, zit. nach Braverman ER, Pfeiffer CC, „The Healing Nutrients Within – Facts, Findings and New Research on Amino Acids“ Seite 55, Keats Publishing, Kanaan, Connecticut 1984 Ganong, William F. „Review of Medical Physiology“ (deutsche Ausgabe, Übers. W. Auerswald, Seite 651, offener Bikarbonatpuffer) 4. Auflage, Springer Verlag, Berlin Heidelberg New York 1979 Garrett R, Grisham CM: Biochemistry. (International Student Edition). 4. Auflage. Cengage Learning Services, 2009, ISBN 978-0-495-11464-2, S. 394. http://www.amazon.de/Biochemistry-Edition-Garrett-Reginald-Grisham/dp/B00BUW3Z72/ref=sr_1_3?ie=UTF8&qid=1398859565&sr=8-3&keywords=Biochemistry+%2F+Reginald+Garrett%2C+Charles+Grisham . Gerlach, HR Franz „Krebs und obligater Pilzparasitismus“ (Seite 202), Urban & Schwarzenberg, Wien 1948 Genz, Anne-Katrin „Maintenance and regulation of the proton activity at the surface of the apical membrane of guinea pig colonocytes“ „Aufrechterhaltung und Beeinflussung der Protonenaktivität an der apikalen Membranoberfläche der Enterozyten des Meerschweinchencolons“ Diss. Dr.med.vet. 1996 (summary page 89, Zusammenfassung Seite 93), University of Veterinary Medicine Foundation, Stiftung Tierärztliche Hochschule Hannover, http://elib.tiho-hannover.de/dissertations/96genz-a.pdf Gold, J. „Proposed treatment of cancer by inhibition of gluconeogenesis.“ Oncology 22:185-207, 1968. http://www.hydrazinesulfate.org/ Gold, J. „Inhibition of Walker 256 intramuscular carcinoma in rats by administration of hydrazine sulfate.“ Oncology 25:66-7l, 1971. http://www.hydrazinesulfate.org/ Gold, J. „Cancer cachexia and gluconeogenesis.“ Ann. N.Y. Acad. Sci. 230:103-110, 1974. http://www.hydrazinesulfate.org/ Gold, J. „Inhibition by hydrazine sulfate and various hydrazides of in-vivo growth of Walker 256 intramuscular carcinoma, B-16 melanoma, Murphy-Sturm lymphosarcoma and L-1210 solid leukemia.“ Oncology 27:69-80, 1976. http://www.hydrazinesulfate.org/ Gold, J.“ Enhancement by hydrazine sulfate of antitumor effectiveness of Cytoxan, Mitomycin C, Methotrexate and Bleomycin, in Walker 256 carcinosarcoma in rats.“ Oncology 31:44-53, 1975. http://www.hydrazinesulfate.org/ Gold, J. „Potentiation by Clofibrate of in-vivo tumor inhibition by hydrazine sulfate and cytotoxic agents, in Walker 256 carcinosarcoma. Cancer Biochem. Biophys. 3:41-45, 1978.“ http://www.hydrazinesulfate.org/ Gold, J. „Hydrazine sulfate and cancer cachexia.“ Nutr. Cancer 1:4-9, 1979. http://www.hydrazinesulfate.org/ Gold, J. „Inhibition of gluconeogenesis at the phosphoenolpyruvate carboxykinase level, as a means of cancer chemotherapy.“ Proc. Am. Assoc. Cancer Res. 14:9, 1973. http://www.hydrazinesulfate.org/ Gold, J. „Inhibition of gluconeogenesis at the phosphoenolpyruvate carboxykinase and pyruvate carboxylase reactions, as a means of cancer chemotherapy.“ Oncology 29:74-89, 1974. http://www.hydrazinesulfate.org/ Gold, J. „Hydrazine sulfate in non-small-cell lung cancer.“ J. Clin. Oncol. 8:1117-1118, 1990. . http://www.hydrazinesulfate.org/ Gold, J. „More about: biology of cachexia.“ J. Natl. Cancer Inst. 90:1101, 1998. . http://www.hydrazinesulfate.org/ Gonzalez, Nicholas J. “The Trophoblast and the Origins of Cancer” (page 66, Meiosis) New Spring Press, New York 2009, www.dr-gonzalez.com Guppy M , Leedman P,Zu X, Russell V. „Contribution to different fuels and metabolic pathways to the total ATP turnover of proliferating MCF-7 breast cancer cells”Biochem J. (2002), May 15;364(Pt 1):309-15) http://www.ncbi.nlm.nih.gov/pubmed/11988105 Gutteridge JM , Halliwell B. .“The measurement and mechanism of lipid peroxidation in biological systems.“Trends Biochem Sci. 1990 Apr;15(4):129-35 http://www.ncbi.nlm.nih.gov/pubmed/2187293 Gonzalez, Nicholas J. “The Trophoblast and the Origins of Cancer” New Spring Press, New York 2009 www.dr-gonzalez.com Greider, Carol W., Blackburn, Elizabeth H. „Telomere, Telomerase und Krebs“ Spektrum der Wissenschaft, April 1996 http://www.spektrum.de/alias/dachzeile/telomere-telomerase-und-krebs/822939 Greider, Carol W., Autexier, Chantal „Telomerase and cancer: revisiting the telomere hypothesis“ TIBS, Volume 21, Issue 10, p387–391, October 1996 http://www.cell.com/trends/biochemical-sciences/abstract/S0968-0004%2896%2910042-6 Grune Tilman, Schröder Peter, Düsseldorf, und Siems Werner, Bad Harzburg „Niedermolekulare Abwehrtruppe“ (Harnsäure etc.) Pharmazeutische Zeitung 2005/16 http://www.pharmazeutische-zeitung.de/fileadmin/pza/2005-16/titel.htm Tilman.Grune@uni-duesseldorf.de Harley, Calvin B. „Telomerase is not an oncogene“, Oncogene (2002) 21, 494-502 http://www.nature.com/onc/journal/v21/n4/full/1205076a.html Harley CB, Liu W, Blasco M, Vera E, Andrews WH, Briggs LA, Raffaele JM. “A natural product telomerase activator as part of a health maintenance program.“ Rejuvenation Res. 2011 Feb;14(1):45-56. doi: 10.1089/rej.2010.1085. http://www.ncbi.nlm.nih.gov/pubmed/20822369 Harley CB 1 , Liu W,Flom PL, Raffaele JM. „A natural product telomerase activator as part of a health maintenance program: metabolic and cardiovascular response.“Rejuvenation Res. 2013 Oct;16(5):386-95. http://www.ncbi.nlm.nih.gov/pubmed/23808324 Hayflick L, Moorhead PS 1961 „The limited in vitro lifetime of human diploid cell strains.“ Exp. Cell Res. 25:585-621 Hiddemann W, Roessner A, Wörmann B, Mellin W, Klockenkemper B, Bösing T, Büchner T, Grundmann E. „ Tumor heterogeneity in osteosarcoma as identified by flow cytometry.“ Cancer. 1987 Jan 15;59(2):324-8. http://www.ncbi.nlm.nih.gov/pubmed/3467822 Jaskelioff M , Muller FL,Paik JH,Thomas E,Jiang S,Adams AC,Sahin E, Kost-Alimova M , Protopopov A,Cadiñanos J, Horner JW, Maratos-Flier E , Depinho RA. „Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.“ Nature. 2011 Jan 6;469(7328):102-6. doi: 10.1038/nature09603. Epub 2010 Nov 28 http://www.ncbi.nlm.nih.gov/pubmed/21113150 Jesus, BB de, and Blasco, MA 2011 „Aging by telomere loss can be reversed.“ Cell Stem Cell 8:3-4 Jesus, BB de, Schneeberger, K., Vera, E, Tejera, A., Harley, CB and Blasco, MA 2011 „The telomerase activator TA-65 elongates telomere and increases health span of adult/old mice without increasing cancer risk.“ Aging Cell: 4:604-621 Jiang X, Gwye Y, Russell D, Cao C, Douglas D, Hung L, Kovar H, Triche TJ, Lawlor ER. „CD133 expression in chemo-resistant Ewing sarcoma cells.“ BMC Cancer. 2010 Mar 26;10:116. doi: 10.1186/1471-2407-10-116. http://www.ncbi.nlm.nih.gov/pubmed/20346143, Tsuda N , Goto M,Konishi H, Yamashina H. „Effect of IV hydration with sodium bicarbonate on high-dose methotrexate disposition kinetics.“ (Article in Japanese) Gan To Kagaku Ryoho. 1984 Apr;11(4):873-80. http://www.ncbi.nlm.nih.gov/pubmed/6326682 Karlson, Peter „Kurzes Lehrbuch der Biochemie für Mediziner und Naturwissenschaftler“ (Seit 311, offener Bikarbonatpuffer) 11. Auflage, Springer 1980 Kelley DW „Cancer: Curing the Incurable Without Surgery, Chemotherapy, or Radiation“ New Century Promotions, Bonita, CA 2000 http://www.amazon.de/Cancer-Incurable-Without-Chemotherapy-Radiation/dp/0970429002/ref=sr_1_1?ie=UTF8&qid=1397045400&sr=8-1&keywords=kelley+donald+william Kiebish , Michael A., Han, Xianlin†,Cheng, Hua† ,Chuang, Jeffrey H. and Seyfried, Thomas N., Journal of Lipid Research, Vol. 49, 2545-2556, Dec 2008 “Cardiolipin and electron chain abnormalities in mouse brain tumor mitochondria: lipidomic evidence supporting the Warburg theory of cancer”http://www.jlr.org/content/49/12/2545.abstract http://www.ncbi.nlm.nih.gov/pubmed/18703489 Kiechl S ., Willeit P,Willeit J,Mayr A, Weger S, Oberhollenzer F , Brandstätter A , Kronenberg F, „Telomere length and risk of incident cancer and cancer mortality.“ JAMA. 2010 Jul 7;304(1):69-75., http://www.ncbi.nlm.nih.gov/pubmed/20606151 Kohane IS ., Naxerova K,Bult CJ,Peaston A,Fancher K,Knowles BB, Kasif S, „Analysis of gene expression in a developmental context emphasizes distinct biological leitmotifs in human cancers.“ Genome Biol. 2008;9(7):R108. doi: 10.1186/gb-2008-9-7-r108. Epub 2008 Jul 8. http://www.ncbi.nlm.nih.gov/pubmed/18611264 Kremer, Heinrich „Das Konzept der Cellsymbiosistherapie – Der Ausweg aus der therapeutischen Sackgasse“, Aufsatz Seite 3, Om und Ernährung, Juli 2007, Zitat: … Die funktionelle Störung der Regulationsebene der aeroben O2-Nutzung zur ATP-Produktion über das enzymatische Oxidase-System in den Mitochondrien erzwingt eine protektive Umschaltung auf die Regulationsebene der fakultativ aeroben O2-Nutzung zur ATP-Produktion über das enzymatische Oxygenase-System im Zellplasma. …“ http://www.ummafrapp.de/skandal/heinrich/kremer_das_konzept%20der_cellsymbiosistherapie_1.pdf Kremer, Heinrich “Die stille Revolution der Krebs- und AIDS-Medizin” Ehlers Verlag, 6. Auflage 2006 www.ummafrapp.de Link H, Bokemeyer C, Feyer P (Hrsg.) „Supportivtherapie bei malignen Erkrankungen – Prävention und Behandlung von Erkrankungssymptomen und therapiebedingten Nebenwirkungen“ (Seite 75) Zitat: „… Standardmäßig wird zu diesem Zweck der Hydrierungslösung (z.B. 5%ige Glukoselösung und 0,9%ige NaCl-Lösung im Verhältnis 1 : 1, mindestens 3000 ml/Tag), die bereits 12 Stunden vor der Gabe von HD-MTX verabreicht wird, Natriumhydrogenkarbonat zugesetzt (Endkonzentration: z.B. 40 mmol Natriumbikarbonat pro Liter Hydrierungslösung). Bei ungenügender Alkalisierung des Harns kann der Carboanhydrasehemmer Acetazolamid (Diamox) p.o. oder zusätzlich i.v. verwendet werden, wobei im Fall einer gleichzeitigen Natriumhydrogenkarbonatgabe 2-mal 250 mg/Tag verabreicht werden. Bei Verzicht auf eine Natriumbikarbonatgabe sind 500 mg Acetazolamid alle 6 Stunden erforderlich (Shamash J et al. 1991).“ Deutscher Ärzte – Verlag GmbH, Köln 2006 Ling, Gilbert N. „What is Life ANSWERED – In terms of the properties and activities of microscopic assemblies of molecules, atoms, ions and electrons called nano–protoplasm“ Author’s Edition Gilbert N. Ling 2013 www.gilbertling.org Ling, Gilber N „Life at the Cell and Below-Cell Level – The Hidden History of a Fundamental Revolution in Biology“, Pacific Press, New York 2001 www.gilbertling.org Love J „Meiosis“ 2002 (‚Principles of Genetics‘ is a series of five self-paced, self-learning courses in Genetics) http://www.synapses.co.uk/genetics/gene.html Maulbetsch, Christoph: Das Hydrogencarbonat-Puffersystem im menschlichen Blut, Praxis der Naturwissenschaften Chemie 2/61, März 2012, S. 26-30, Aulis Verlag Meldrum,N.U.and F.J.W.Roughton.J.Physiol.(London),80:113,1933. Mikami T , Kita K,Tomita S,Qu GJ,Tasaki Y, Ito A. „Is allantoin in serum and urine a useful indicator of exercise-induced oxidative stress in humans?“ Free Radic Res. 2000 Mar;32(3):235-44 http://www.ncbi.nlm.nih.gov/pubmed/10730822 Mikami T , Yoshino Y, Ito A. „Does a relationship exist between the urate pool in the body and lipid peroxidation during exercise?“ Free Radic Res. 2000 Jan;32(1):31-9. http://www.ncbi.nlm.nih.gov/pubmed/10625215 Mukherjee S, „Der König aller Krankheiten“ (Übers. Schaden B, Seite 555), DuMont, Köln 2012 (amerikanische Originalausgabe „The Emperor of all Maladies“, Scribner, a Division of Simon & Schuster, New York 2010) www.dumont-buchverlag.de Nieper, H. „Auf neuen Wegen“ (Seite 136, Benzaldehyd, Acetaldehyd), Langenhagen 2000 Panizza S , Mendoza MA,Berlinger M,Huang L,Nicolas A,Shirahige K, Klein F, “Spo11-accessory proteins link double-strand break sites to the chromosome axis in early meiotic recombination.“ Cell. 2011 Aug 5;146(3):372-83. doi: 10.1016/j.cell.2011.07.003. http://www.ncbi.nlm.nih.gov/pubmed/?term=21816273 Robey , Ian F., Baggett, Brenda K., Kirkpatrick, Nathaniel D., Roe, Denise J.,Dosescu, Julie,Sloane, Bonnie F., Hashim, Arig Ibrahim, Morse, David L.,Raghunand Natarajan, Gatenby, Robert A. and Gillies, Robert J. “Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases” Cancer Res 2009; 69: (6): 2260-8, March 15, 2009 http://cancerres.aacrjournals.org/cgi/content/abstract/69/6/2260 Roughton FJW, Physiol.Rev., 15:241,1935 (zit.n. Kararli Tugrul T „Kinetics and Inhibition of CA III: Comparison with CA II“, Dissertation University of Florida 1984, Seite 83ff,Zitat: chapter ‚History , Distribution and Physiological Function of CA III‘ – The presence of CO2 hydration activity in the watery extracts of mammalian muscles which we perfused well with sodium solution to remove the blood was reported as early as in 1933 by Meldrum and Roughton(60). Despite this observation Roughton stated that „in such a location CA would be an enemy to the organism, rather than a friend: in its absence the CO2 is able to diffuse away rapidly without loitering appreciably by the wayside in the form of HCO3- ions(59)“ This statement perhaps delayed fot several decades the discovery of CA III in muscle. Another factor which also contributed to such a delay was the expectation that the hydration of CO2 catalyzed by CA should be inhibitable by 10-7 to 10-8 M concentration of sulfonamide inhibitors such as acetazolamide. We now know that CA III is rather resistent to inhibition by several sulfonamide inhibitors. Lack of inhibition by 10-7 to 10-8 M of acetazolamide was interpreted as the absence of Ca inn muscle. https://ia600701.us.archive.org/12/items/kineticsinhibiti00kara/kineticsinhibiti00kara.pdf Scientific American Magazine – April 23, 2009 „Cancer Clues from Embryonic Devlopment Rethinking cancer by seeing tumors as a cellular pregnancy“ by Christine Soares http://www.scientificamerican.com/article/cancer-clues-from-embryos/ Shamash J , Earl H, Souhami R. „Acetazolamide for alkalinisation of urine in patients receiving high-dose methotrexate.“Cancer Chemother Pharmacol. 1991;28(2):150-1. http://www.ncbi.nlm.nih.gov/pubmed/2060085 Shay, JW and Wright WE. 1996 „The reactivation of telomerase activity in cancer progression.“Trends in Genetics 12:129-131 Supuran, Claudiu T.; Scozafava, Andrea; Conway, Janet; „Carbonic Anhydrase – It‘s Inhibitors and Activators“, CRC Press, Boca Raton, London, New York, Washington D.C. 2004 Seite 269 (261) graphisches Schema Tumorzelle Simoncini, Dr. Tullio “Cancer is a Fungus”, Edizione Lampis 2005 www.curenaturalicancro.com Springer Medizin Onkologie 07.11.2013, Österreichische Gesellschaft für Hämatologie und Onkologie (ÖGHO), Austrian Society of Haematology and Medical Oncology „2013: Sturm im Elfenbeinturm - Mutationsheterogenität als zentrales Charakteristikum in malignen Geweben stellt Forschende wie Kliniker in der Onkologie vor neue Herausforderungen.“ http://www.springermedizin.at/fachbereiche-a-z/io/inneremedizin/onkologie/?full=37528 Tayek, J.A., Heber, D. and Chlebowski, R.T. „Effect of hydrazine sulphate on whole-body protein breakdown measured by14 C-lysine metabolism in lung cancer patients“ Lancet 2:241-244, 1987. http://www.hydrazinesulfate.org/ Wall Street Journal, November 28, 2010 „Aging Ills Reversed in Mice“ by Gautam Naik http://online.wsj.com/news/articles/SB10001424052748703785704575642964209242180?mg=reno64-wsj&url=http%3A%2F%2Fonline.wsj.com%2Farticle%2FSB10001424052748703785704575642964209242180.html Wicha MS, Liu S, and Dontu G „Cancer Stem Cells: An Old Idea—A Paradigm Shift“ Cancer Res. February 15, 2006 66; 1883 ,http://cancerres.aacrjournals.org/content/66/4/1883.short Wicha MS , Dontu G1 , Al-Hajj M,Abdallah WM, Clarke MF, „Stem cells in normal breast development and breast cancer.“ Cell Prolif. 2003 Oct;36 Suppl 1:59-72., http://www.ncbi.nlm.nih.gov/pubmed/14521516 Wikipedia (abgefragt am 27. 03. 2014): Carboanhydrase http://de.wikipedia.org/wiki/Carboanhydrase, Wu X, Amos CI, Zhu Y, Zhao H, Grossman BH, Shay JW, Luo S, Hong WK, Spitz MR. 2003 „Telomere dysfunction: a potential cancer predisposition factor.“ J Natl Cancer Inst. 95(16):1211-8 Xue-Jun Li , Yang Xiang ,Bing Ma and Xiao-Qiang Qi “Effects of Acetazolamide Combined with or without NaHCO3 on Suppressing Neoplasm Growth,Metastasis and Aquaporin-1 (AQP1) Protein Expression" Int. J. Mol. Sci. 2007, 8, 229-240, 13 March 2007 http://www.mdpi.com/1422-0067/8/3/229 Yehezkel S 1 , Rebibo-Sabbah A , Segev Y,Tzukerman M,Shaked R,Huber I,Gepstein L,Skorecki K, Selig S. „Reprogramming of telomeric regions during the generation of human induced pluripotent stem cells and subsequent differentiation into fibroblast-like derivatives.“ Epigenetics 2011 Jan;6(1):63-75. doi: 10.4161/epi.6.1.13390. Epub 2011 Jan 1., http://www.ncbi.nlm.nih.gov/pubmed/20861676 Zimmerman, J „The Associaation/Induction Hypothesis by G.N. Ling“, Power Point zum ownloaden, hp Startseite Pkt. 9 www.gilbertling.com Zur Hausen H, Wintermantel M (chair) „Kampf gegen den Krebs – Durchbrüche und Erwartungen“ Plenary, Panel 23.08.2012, Europäisches Krebs Forum Alpbach 2012,http://www.alpbach.org/de/vortrag/kampf-gegen-den-krebs-durchbruche-und-erwartungen/

© Copyright Dr. Wolfgang Zöch, geb. 11.11.1955, Drinkweldergasse 7, 3500 Krems

Dr. Wolfgang Zöch
Drinkweldergasse 7, A-3500 Krems, Austria, EU - ph +43 (0)676 ‐ 936 74 75
e-mail: wolfgang@drzoech.com   Internet: www.drzoech.com