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This book cites the most recent scientific findings to provide a radically different approach to the formation and background of cancer, and also lays down the scientific foundations for a new, effective methodology for curing cancer.
The author began his research in the early 1990s while investigating the role that deuterium (heavy hydrogen) plays in regulating biological and physiological processes. A number of leading universities and research institutes worldwide have joined the groundbreaking research.
The book examines the most common conventional treatment methods in oncology and introduces the most effective combinations of treatments while providing detailed instructions on using deuterium depletion.
Also discussed are deuterium depletion’s mechanism of action, the most important factors affecting effectiveness, and the main considerations when using the method. The method’s therapeutic potential is demonstrated through sixteen types of cancer, results from clinical trials, and specific case studies. One crucially important chapter describes how to use deuterium depletion to foster a healthy lifestyle. The last chapter contains recommendations for use, providing a helpful guide for health-conscious individuals or those struggling with the disease.
This book strives to keep a balance between being easy to read or speaking in laymen's terms while providing a professional introduction of the research and clinical application to researchers and doctors. It discusses the treatment method based on deuterium depletion, which offers a tool for curing cancer and other chronic diseases, while also being more efficient and milder than any other oncotherapy up to now.
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Veröffentlichungsjahr: 2022
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DEUTERIUM DEPLETION
A New Way in Curing Cancer and Preserving Health
Gábor
ISBN 978-615-01-4502-0
All rights reserved
© Gábor Somlyai 2022© ATP Ltd. Cover©123RF Translation Balázs
Table of Contents
PREFACE
CHAPTER ONE GENERAL CHARACTERISTICSOF CANCER
WHAT IS CANCER?
ARGUMENTSSUPPORTINGTHEGENETICTHEORYOFCANCER
ARGUMENTSSUPPORTINGTHEMETABOLICTHEORYOFCANCER
WHATISTHEFOREFRONTNOWINTHETREATMENTOFCANCER, ANDWHEREISITHEADED?
CHAPTER TWO A PARADIGM SHIFTIN BIOLOGY
THECONCEPTOFMOLECULARANDSUBMOLECULARBIOLOGY
DEUTERIUM
DEUTERIUMINNATURE
Water with a lower-than-natural deuterium content: deuterium-depleted water (DDW)
The production of DDW
THEBIOLOGICALEFFECTSOFDEUTERIUM
Biological processes in an environment with a higher-than-natural deuterium content
Variation of the D/H ratio is a natural biological process
The effect of DDW intake on organisms' deuterium levels
CELLPHYSIOLOGYFUNDAMENTALS
Cell membrane
Nucleus
The mitochondrion
THESUBMOLECULARREGULATORYSYSTEM (SMRS)
The evolution of the regulatory mechanism
The submolecular regulatory system (SMRS) and the biochemical processes
The relationship between the submolecular regulatory system (SMRS) and genetic function
The submolecular regulatory mechanism and tumor necrosis
CHAPTER THREE CLINICAL RESULTSOF DDW APPLICATIONIN CANCER PATIENTS
THECONCEPTOF DDW DOSAGE
PROSPECTIVE PHASE II CLINICALTRIALONPATIENTSWITHPROSTATETUMORS
FOLLOW-UP (RETROSPECTIVE) STUDIES
Breast cancer
Prostate tumor
Pancreatic tumor
Lung tumor
Colorectal cancer
Results supporting the anti-cancer effects of deuterium depletion in the entire population
The use of deuterium depletion may prevent and protect against the recurrence of the disease
DYNAMICSOFDISEASERELAPSEINLIGHTOFTHERECENTRESEARCH
CHAPTER FOUR LOW DEUTERIUMASA KEY ELEMENTOFA HEALTHY LIFESTYLE
THEUSEOFDEUTERIUMDEPLETIONINHEALTHYPOPULATIONS
THELIMITATIONSANDCONTRADICTIONSOFSCREENINGTESTS
CHAPTER FIVE USEOF DEUTERIUM DEPLETIONIN BENIGN TUMORS
CHAPTER SIX DEUTERIUM DEPLETIONASA SUPPLEMENTARY TREATMENTFOR MALIGNANT TUMORS USED ALONGSIDE ONCOLOGICAL TREATMENTS
A PARADIGMSHIFTINCURINGCANCER
A comparison of conventional and submolecular treatment strategies
Deuterium depletion may influence tissue pathology
The dilemmas of histological sampling
The alignment of deuterium depletion with imaging tests, their sensitivity and influence on the results of the tests
Deuterium depletion may affect tumor marker levels
The correct definition of DdU and the principle of dosage
CHAPTER SEVEN THE APPLICATIONOF DEUTERIUM DEPLETIONBEFORE DIAGNOSISUPUNTILTHE STARTOF ONCOLOGICAL TREATMENTS
INDICATIVESIGNSBEFOREDIAGNOSIS
THEDIFFICULTIESOFDIAGNOSTICTESTS
THEAPPLICATIONOFDEUTERIUMDEPLETIONINBORDERLINECASESWHENITISREASONABLETOSUSPECTCANCER, BUTNODIAGNOSISANDTREATMENTISAVAILABLEYET
ESTABLISHINGADIAGNOSISANDCOMMUNICATINGITTOTHEPATIENT
PLANNINGATREATMENTAFTERDIAGNOSIS
Difficulties in planning conventional treatments
CHAPTER EIGHT ADDITIONAL USEOF DEUTERIUM DEPLETION ALONGSIDE ONCOTHERAPIES
THETIMINGOFDEUTERIUMDEPLETIONANDCONVENTIONALTREATMENTSAREDIFFERENT
The conventional treatment according to the protocol has not started yet
Chronic lymphocytic leukemia (CLL)
The patient has not consented to conventional treatment as prescribed by the protocol
Prostate cancer
Breast cancer
Lung cancer
Conventional treatment options have been exhausted
Stomach cancer
Liver cancer
Conventional treatments are completed
THECOMBINEDUSEOFSURGERYANDDEUTERIUMDEPLETION
The preoperative use of deuterium depletion
Picking the ideal time for a surgery
Head and neck cancers
Bladder cancer
Breast cancer
The postoperative use of deuterium depletion
THECOMBINEDUSEOFDEUTERIUMDEPLETIONANDCHEMOTHERAPY
General advice for the complementary use of deuterium depletion alongside chemotherapy
The use of deuterium depletion following chemotherapy
The simultaneous use of chemotherapy and deuterium depletion
Deuterium depletion is started after or at the same time as chemotherapy treatment producing partial results
THECOMBINEDUSEOFDEUTERIUMDEPLETIONANDHORMONETHERAPY
General guidelines for the combined use of deuterium depletion and hormone therapy
Hormone treatment prior to deuterium depletion
Deuterium depletion and hormone therapy are used simultaneously
Deuterium depletion should be started following a hormone therapy
SYNCHRONIZINGDEUTERIUMDEPLETIONANDRADIOTHERAPY
FITTINGDEUTERIUMDEPLETIONTOCONVENTIONALTREATMENTS
Using deuterium depletion after surgery and alongside radiotherapy
The use of deuterium depletion during pre-operative radiotherapy and following a surgery
Rectal cancer
Breast cancer
Brain tumor (not glioblastoma)
Using deuterium depletion after a surgery alongside conventional treatments
Using deuterium depletion combined with post-operative chemotherapy
Adjuvant chemotherapy following a successful surgery
Using deuterium depletion alongside chemotherapy preceding a surgery
Chemotherapy is used to achieve operability
Using deuterium depletion alongside chemotherapy and (subsequently) radiotherapy
The tumor is not operable, due to its location, staging, or classification
Using deuterium depletion alongside conventional treatments in recently diagnosed stage III patients
The use of deuterium depletion combined with oncological treatments in stage III patients receiving conventional treatments
Use of deuterium depletion alongside or following targeted therapies
Herceptin/Breast cancer
Gefitinib/Lung cancer
Sutent/Kidney cancer
The combined use of deuterium depletion and immunotherapy
CHAPTER NINE FACTORS AFFECTING DOSAGEANDTHE EFFICACYOF DEUTERIUM DEPLETION, FINDINGS CONCERNINGTHE USAGEOF DEUTERIUM DEPLETION
1. Daily DDW intake
2. Deuterium concentration of DDW
3. The body's response to deuterium depletion
4. Body weight
5. The type and histological classification of the tumor
6. The tumor mass
7. The shape of the tumor and the impact on the surrounding tissues
8. The location of the tumor
9. Sensitivity of the tumor to deuterium depletion
10. Treatment of the primary tumor and/or metastasis
11. Classification of the tumor stage at the beginning of deuterium depletion
12. General physical condition of the patient
13. Other treatments
14. Complete blood count
15. Time elapsed since the start of deuterium depletion
CHAPTER TEN GENERAL ADVICEONTHE APPLICATIONOF DEUTERIUM DEPLETION
1. Additional procedures that counteract deuterium depletion
2. How to consume DDW?
3. How does the deuterium concentration of DDW vary when boiled and kept in the open air?
4. On the carbonic acid content of waters
5. For how long should DDW be consumed?
6. Interrupting a deuterium depletion course
7. How to end a DDW course?
8. Long-term positive effects of deuterium depletion
9. Diets supporting deuterium depletion
10. Other additional procedures
CHAPTER ELEVEN THE MOST COMMON ACCOMPANYING SYMPTOMOF DEUTERIUM DEPLETION
Weakness, prostration, drowsiness
Increasing the dosage may also cause increased fatigue and drowsiness
Blushing, increased temperature, and fever spikes
Intermittently increasing pain
Pain management
Swelling and softening of the tumor-affected area
Local warmth of the affected area
Cerebral edema
Pulling and tingling sensation in the tumor
Minor bleeding in the bladder, stomach, or rectum
An improvement of appetite and general health
Weight gain
Exudation and wound healing in ulcerating tumors
An improvement of general comfort
Brick dust urine
Better tolerance of radiotherapy and cytostatic treatments
Transient coughing in lung cancer patients
Tumor necrosis may cause abscesses
CHAPTER TWELVE THE MAIN PHASESOFTHE APPLICATIONOF DEUTERIUM DEPLETION (1992–2020)
CHAPTER THIRTEEN A DEMONSTRATIONOFTHE EFFECTIVENESSOF DEUTERIUM DEPLETIONTHROUGH CASE STUDIES
CASESTUDIES
Lung tumor
Breast cancer
Prostate tumor
Head and neck tumors
Colorectal cancer
Ovarian cancer
Cervical cancer
Melanoma malignum
Liver cancer
Grade I astrocytoma
Grade III astrocytoma
Glioblastoma
Neurofibromatosis
Bone marrow cancer
Myeloma
Acute myeloid leukemia (AML)
Chronic lymphocytic leukemia (CLL)
CHAPTER FOURTEEN ADVICEON ESTABLISHINGTHE DOSAGE
RECOMMENDATIONFORHEALTHYPEOPLE, PREVENTION, ENHANCINGPERFORMANCE
H/1 Protocol
H/2 Protocol
RECOMMENDATIONSFORPEOPLEWHOARENOTYETDIAGNOSEDWITHCANCER, BUTAREEXAMINEDFORTHESUSPICIONOFCANCER
P/D Protocol
RECOMMENDATIONSFORCANCERPATIENTS
RECOMMENDATIONSFORPATIENTSWHOHAVERECOVEREDTOPREVENTTHERELAPSEOFCANCER
RECOMMENDATIONSFORPATIENTSWHOHAVEACHIEVEDACANCER-FREECONDITIONWITHCONVENTIONALTHERAPIESTOPREVENTDISEASERECURRENCE
C/R/1 Protocol
C/R/2 Protocol
RECOMMENDATIONSFORPATIENTSWHOHAVEBECOMECANCER-FREEDURINGTHECOMPLEMENTARYUSEOFDEUTERIUMDEPLETIONTOPREVENTARELAPSE
C/R/3 Protocol
RECOMMENDATIONSFORCANCERPATIENTSTOACHIEVEACANCER-FREECONDITION, TAKINGINTOACCOUNTTHECONVENTIONALTREATMENTSUSED
The patient is about to undergo surgery
C/C/Op Protocol
Inoperable patients receiving chemotherapy
1/C/C/Chem Protocol
Patients receive aftercare with adjuvant chemotherapy following a successful surgery.
2/C/C/Chem Protocol
Recommendations for patients with glioblastoma, fitted to the Stupp protocol
3/C/C/Chem Protocol
C/C/Horm Protocol
Patients are inoperable and receive hormone treatment
Patients receive radiotherapy
C/C/Radther Protocol
SPECIALADVICE
CHAPTER FIFTEEN RECOMMENDATIONSFOR PATIENTS DIAGNOSEDWITH METABOLIC DISORDERS (M PROTOCOLS)
M Protocol
CHAPTER SIXTEEN RECOMMENDATIONSFOR ATHLETESAND HEALTHY PEOPLE, TO ENHANCE PHYSICAL PERFORMANCE
APPENDIX
SUMMARYTABLEOFTHEDEUTERIUMCONCENTRATIONSINDIFFERENTNUTRIENTS
BIBLIOGRAPHY
ACKNOWLEDGMENTS
Preface
I completed this book twenty years after my book, Defeating Cancer!, was published. Twenty years is a rather long period, not only in someone's life but also in the timeline of history and the history of science. In these two decades, many changes and events took place that we couldn't have even imagined at the end of the 1990s; it is highly likely that we will continue to face many unforeseeable challenges and changes now and in the future. The world was left speechless with the terror attack of the World Trade Center in New York in 2001, it survived a global economic crisis in 2008, was facing a significant migration crisis in 2015, and in 2020, the SARS-CoV-2 pandemic forced mankind to its knees and made it rethink its ways. The pandemic paralyzed the economy, streets became empty for months and the free movement, employment and pastime activities of people have been restrained in a way that has never been seen before. By the time this book was published, more than fifty million people had contracted the disease, resulting in the death of more than a million people. We don't know what the next twenty years will bring us, but in retrospect, we can already consider the changes that took place in curing cancer. Between 1999 and 2015, a 36% increase in new cases was recorded worldwide and in 2018, statistics showed 18.1 million new cases. It is predicted that by 2040, cases will increase to 29.5 million. This also implies that without significant changes to prevention and therapy, the number of those dying of cancer will grow from 9.6 million to 15.6 million in twenty years. The ongoing pandemic alerts the world's attention to the fact that we are facing important changes and decisions to preserve the environment and human life quality. This book aims to contribute to the better understanding and efficient treatment of cancer and other chronic diseases by introducing a new, submolecular approach that opens up a way for mankind to implement an efficient and sustainable therapeutic method devoid of harmful effects.
November 2020
Gábor Somlyai PhD
CHAPTER ONEGeneral Characteristics of Cancer
WHAT IS CANCER?
Considering its many causes and clinical presentations, cancer is a complex medical condition, therefore it is hard to provide a brief, yet professional definition for this group of medical conditions. In a strictly professional sense, the expression "cancer" (carcinoma) only applies to malignant tumors, but people commonly use this expression to refer to any kind of malignant tumor. A common trait of malignancies is that a group of cells forms from a single cell during a given time (in a few weeks, but mostly in three, five, or up to ten years). This group of cells significantly differs from the surrounding healthy tissues in their functioning and morphology. A characteristic property is uncontrolled cell division, resulting in the tumor outgrowing its surroundings and spreading to the adjacent tissues. Cells breaking off of the tumor enter the blood and the lymphatic system to be carried further away in the body. Once they attach to the tissues there and continue growing, they create a new tumor (metastasis). In the case of hematopoietic malignancies, a mass of blastoid cells is released into the bloodstream.
On average, it takes four to five years until a single cell reaches a tumor of 0.5 to 1 centimeter in size that is detectable using current technology. By this time, the number of cells in the tumor is already over ten million. The "treacherous" nature of cancer can be traced back to this fact, as in the first four to five years the tumor stays below the detectable size threshold, with the patient experiencing no symptoms or complaints, during which time a great number of cells can break off of the tumor. If they manage to make it to other parts of the body, it takes another four to five years to create metastases, even if the primary tumor was removed years ago. (This is why we consider a five-year period to be crucial for cancer. If within these five years no new tumors appear in the body, then it is likely that the combined effect of conventional treatments and the body's immune system has destroyed all tumor cells.)
A tumor is therefore the "end product" of a complex, prolonged and multiphase process. We can demonstrate this process with the example of a marble resting in a pit on a slope. Imbalances of the cell's genetic and metabolic processes occasionally cause "a loss of balance" which may dislodge the marble from its position, overcoming the minor obstacle holding the cell back to roll down the slope. Certain "fixing" mechanisms can help the cell find a way back to a safer point in the pit. In healthy cells, forces acting in the direction of the slope are in balance with the forces holding the marble back. The first event in the course of tumor formation is when a cell overcomes this obstacle. Once a cell "has broken loose", another pit may impede it on its way down, but if the forces acting in the direction of the slope outweigh others, it rapidly overcomes this obstacle as well. The more obstacles a cell "overcomes", the easier the next one will be to overcome, with the incline of the slope also increasing. If processes of imbalance cannot hold the cell back anymore, the cell goes tumbling down the slope and it is impossible to prevent it from starting an uncontrollable cell division.
Figure 1The multi-phase process of malignant cell degeneration, as demonstrated with a marble temporarily resting in a pit on a slope, on its path rolling down. It is apparent how a healthy cell becomes increasingly malignant during the years until nothing else stands in the way of uncontrolled cell division.
One generally accepted theory asserts that the primary cause of tumor formation is a sequence of errors in the genetic code [1]. During a person's lifetime, approximately 1016 cell divisions take place in the human body from fertilization to death. In every cell (apart from a few exceptions) of our body is a genetic code of 3.2 billion "letters". This genetic code is written with only four letters that correspond to the four bases constituting DNA, the cell's genetic material. These letters are the following: A for adenine, T for thymine, G for guanine, and C for cytosine. (This book contains approximately 360,000 letters, meaning that one can write the genetic code of a single cell in 9,700 books of the same length.) Cells duplicate their genetic code before each cell division so that the daughter cells have identical copies of their DNA. Enzymes (proteins) copying the genetic program make a mistake from time to time, inserting an incorrect letter for a given position in the genetic code of the daughter cell. If these errors occur at critical points of the 3.2 billion base pair-long genetic code which plays a key role in controlling cell division, then these cells will behave differently from the surrounding cells and will divide more frequently. This may lead to the group of cells outgrowing its surroundings, the macroscopic manifestation of which is a tumor.
The metabolic approach to cancer states that the underlying cause of cancer is a disruption in the cell's metabolism [2], primarily in the mitochondria, known as the powerhouse of the cell. This hypothesis was postulated by Otto Warburg [3] in the early 1920s, who subsequently received the Nobel Prize in Physiology in 1931 for his work. Adenosine triphosphate (ATP) molecules store the energy found in chemical bonds, resulting from the "burning off" of nutrients, in high-energy (so-called macroergic) bonds. The synthesis of ATP may take place in the presence of oxygen (aerobic metabolism) in mitochondria or without the presence of oxygen (anaerobic metabolism) in the cytoplasm. Terminal oxidation in the mitochondria (Szent-Györgyi-Krebs cycle) produces carbon dioxide and water as final products. Conversely, the complete oxidation of organic compounds does not take place in the cytoplasm. Along with carbon dioxide and water, lactic acid is released in the process, which in turn the cell utilizes for the synthesis of other molecules. Otto Warburg concluded that despite the availability of oxygen for tumor cells to facilitate the complete oxidation of nutrients in the mitochondria, the process takes place instead in the cytoplasm via anaerobic metabolism through glycolysis.
ARGUMENTSSUPPORTINGTHEGENETICTHEORYOFCANCER
Evolution has created accurate repair mechanisms in cells to immediately fix errors resulting from incorrectly copying the genetic code. The sum of the number of errors occurring and the efficiency of the system used for error correction defines the "net" balance of genetic errors. This error-correcting system works with impressive efficiency. Approximately one error occurs when copying every one-thousandth letter in the DNA sequence. As a result of the DNA's repair mechanism, an entire copy of DNA contains less than one error per one million base pairs. In other words, a cell is incapable of repairing only one genetic error out of a thousand. The likelihood of tumor formation, therefore, depends on the frequency of errors occurring in the genetic code, and the accuracy (in percentage) of the cell's repair mechanism. (Note: Just as people are different in many aspects, everyone's repair mechanism is also different.) There are people whose repair mechanisms are very efficient, and there are others whose repair mechanisms work with a greater number of errors. This partly explains why one out of two people with an identical risk factor may fall sick, while the other does not.
Certain chemical substances significantly increase the risk of genetic errors. This explains why people handling carcinogenic, mutagenic, and toxic substances, active or passive smokers or those exposed to strong UV or radioactive radiation are at an increased risk of developing cancer. Is also easy to see that growth in the number of genetic errors increases the chance of something going wrong in the repair mechanism. Flaws in the repair mechanism may initiate a series of changes that can't prevent the cells, once out of control, from rapidly dividing.
In terms of prevention, everything stated above has two important messages: (a) every chemical substance that increases the risk of genetic errors occurring in the body also increases the likelihood of tumor formation; (b) the younger the age the first genetic errors occur, the earlier a cell starts to accumulate genetic errors and mutations that ultimately lead to tumor formation. This explains why smokers, people living in polluted areas, or those working with carcinogenic substances have a higher probability of developing cancer than the general population. As people get older, the chance of developing cancer [4] also increases (see Fig. 2). As more cell divisions take place in the body, the number of genetic errors also grows. Such growth also means that in a specific cell where a few genetic errors affecting the regulation of cell division have already occurred can easily push the cell to a point of no return.
People with a hereditary genetic predisposition to some diseases are also at a higher risk. Nowadays we possess the techniques to fairly accurately detect the genetic predisposition to cancer. For these people, it is extremely important to mitigate the risks and decrease the chance of further genetic errors and keep their bodies in a healthy condition.
Figure 2A graph of the number of those deceased as a result of cancer by age. The plot shows a surge in the death rate starting from age forty. In the population of people in their fifties, approximately thirty out of one million people die every year, whereas the same number is 400 for people in their eighties. (Source: [4] p. 1193)
ARGUMENTSSUPPORTINGTHEMETABOLICTHEORYOFCANCER
The genetic approach states that the formation of cancer is caused by amassing many genetic errors. However, a contrary view states that the formation of clear cell renal cell carcinoma, a type of kidney cancer, for instance, is due to the mutation of one single gene in the mitochondrion, the gene encoding the enzyme fumarase hydratase [5]. Losing this genetic function also means that the TCA cycle (or Szent-Györgyi-Krebs cycle) of the mitochondria stops working. The cell is then unable to produce metabolic water which reduces the amount of deuterium. Research in which mitochondria have been transferred from tumor cells to healthy cells has demonstrated the key role of mitochondria. Once the mitochondria from the tumor cells were transferred to healthy cells, the latter also exhibited a tumor phenotype [2]. Contrary to expectations, when the nuclei of tumor cells were transferred to the cytoplasm of healthy cells, the cells remained healthy. Why do these cells not exhibit the characteristics of tumor cells even if their genetic material contains the mutations of tumor cells? The key role of metabolism is also suggested by epidemiological data showing significant variation in the incidence of certain cancers depending on the geographical region, lifestyle, and diet of the examined population group.
The secondary role of genetic errors is evidenced by the fact that the existence of genetic errors alone is not a sufficient condition for tumor formation. Genetic errors can be detected in many individuals, yet those people do not develop cancer. A good example is when in identical twins, one of the twins develops cancer and the other twin does not, despite their entirely identical genetic makeup.
I could go on and on, citing both supporting and opposing arguments [6] in favor and against each of these approaches, but it is difficult to come up with a final answer that reconciles the proponents of both ideas. I hope that the scientific evidence presented in this book and a new, submolecular approach to cancer resolves the apparent dispute between the two theories and show that both approaches are right in their own way.
WHATISTHEFOREFRONTNOWINTHETREATMENTOFCANCER, ANDWHEREISITHEADED?
Different views may be made about the current situation in the treatment of cancer. These views depend on the professional background and considerations of those who voice them. The most important thing to make clear is that it is not justified to deal with cancer as if it were an incurable disease. Medical science has seen massive developments in the past few decades, making it possible for a significant proportion of patients with specific tumor types, such as testicular cancer or childhood leukemia, to be cured effectively with the proper treatment regimen. Even if a patient is not cured completely, a considerable breakthrough is that now it is possible to "tame" a chronic disease into becoming just an acute disease and to extend a patient's life while simultaneously maintaining his quality of life.
To provide a figure of how efficient modern therapies are, 9.6 million [7] cancer-related deaths were reported worldwide in 2018, with 33,000 in Hungary alone, even though the majority of patients received proper oncological treatment.
Given statistical data and trends, the question arises whether modern oncology is efficient. If we cannot face, accept and deal with the fact that further developing the current methods do not lead us to a real solution, then we cannot change the current situation. Embellishing and exaggerating partial results disregards today's available tools, instead of capitalizing on them. We need every new insight, every new area of development, and every new method that transcends the current treatment approaches and strategies. Using deuterium depletion is one such treatment strategy. To this day, nearly a hundred scientific papers have been published on the research and clinical results about deuterium depletion. This growing body of evidence supports the crucial role of naturally occurring deuterium in the regulation of biological processes.
In my book Defeating Cancer!, published in 1999, I quoted a few paragraphs of Tim Beardsley's editorial article from 1994 [8], reflecting on how President Nixon's war on cancer and the National Cancer Act of 1971 did not bring enough progress. That article's message is still relevant today. It quoted Dr. Peter Greenwald of the National Cancer Institute as being optimistic about how gene therapy, immunotherapy, and modifying the activity of specific genes would step up to the challenge. Reading this article from twenty-five years ago today, in 2020, it's apparent that no real breakthrough has been made in this time. While the therapies envisioned in the article have become available in the past twenty-five years, nevertheless we are not any closer to solving the real problem. Because today, cancer still beats us. In specific cases, new therapies have increased the life expectancy of the patients. However, this does not change the fact that every year, nine million people die of tumors (not to mention the sharp increase of treatment costs), and this number is expected to exceed thirteen million by 2030, according to the World Health Organization.
Massive databases are available on the incidence and survival rate of cancer, organized by tumor type, gender, and geographical distribution, etc. It is generally considered valid that 40 to 60% of detected new cases worldwide die of the disease (numbers vary across countries). On a global scale, 14 million new cases are detected, and 8.8 million people succumb to cancer. Detailed data sets are available, showing the number of new cases per year (morbidity) and the number of deaths per year (mortality). See Table 1 for these figures in
Table 1New cancer cases (morbidity) and cancer-related deaths (mortality) in men and women in the United States in 2018, displaying the efficiency of therapies.
There's a morbidity/mortality (the ratio of detected cases and deaths) column added to the American Cancer Society's chart. This column shows how efficient the current treatment for a specific cancer type is. This ratio is above 5 for breast, prostate, endometrial, and lip-oral cavity cancers. For cervical and bladder cancer, it is above 3. In women, the ratio is above 2 for three tumor types (colorectal cancer, stomach cancer, and leukemia). In men, the ratio is below 2 for colorectal cancer. The ratio is below 2 for all other tumor types (lung, ovarian, esophageal, and liver cancer), meaning that half of these patients die within a year. Tumor types for which the ratio is 5 or above respond well to treatment. A complete remission is possible, and the disease is curable when detected early on. Only a few tumor types belong to this group. For most cancers, the ratio is between 1 and 3. For lung cancer, the ratio is 1.45 in men and 1.59 in women, meaning that almost all patients diagnosed with lung cancer live hardly more than one year after the diagnosis. This figure is especially appalling, as lung cancer is one of the most common cancers.
In the past few decades, genomic research has been a trendsetter in the development of anti-cancer drugs. The development aims to detect and analyze genetic errors, with the ultimate goal of finding a tailor-made solution to cure cancer. While in recent years, new anti-cancer drugs have improved cancer death statistics and the life expectancy of the patients, no substantial breakthrough has been made. Developing these drugs has been and still is enormously expensive. Manufacturers incorporate these costs in the price of therapies. The monthly cost of an anti-cancer drug per patient is somewhere between $3,000 and $6,000. A disturbing fact is that while the cost of drugs and treatments multiply, minimal to no improvement is reported on efficiency.
Despite all our efforts, we are still facing the same challenge: can we make a substantial breakthrough in treating cancer?
CHAPTER TWO A Paradigm Shift in Biology
THECONCEPTOFMOLECULARANDSUBMOLECULARBIOLOGY
The areas of science concerning biological processes have their foundations on primarily the molecular view. In recent decades, chemistry and molecular biology research has revealed the biochemical and genetic processes in cells, explored biochemical pathways, and discovered the chemical reactions responsible for the integrity and basic functions of a cell. Research has also shown how biomolecules are formed and broken down and has mapped the structure of many proteins. In the modern era of drug development, researchers for decades have tested thousands of molecules to see which ones exhibit a positive physiological effect in a specific area of indication and whether the known biochemical processes can explain their mode of action. In modern-day oncology, it was the result of such tests that the effectiveness of a number of drugs against tumors was verified, and the drug was registered. Even despite the partial results, it is clear that there still isn't an effective cure for cancer. Identifying the first oncogene was an initial breakthrough. Molecular genetics research has enabled targeted drug development. However, this approach still worked on the molecular level, targeting the protein encoded by a specific gene. It has been generally accepted that with the new approach, a real and palpable breakthrough is within reach and is only a few years ahead. We have identified hundreds of genes associated with cancer formation, and there are hundreds of currently ongoing clinical research projects, yet we are still waiting for a truly effective cure.
The important question to ask - and we should have asked this question decades ago - is whether the regulation and harmonizing of the rapid and complex biochemical, genetic, and cell physiology processes can take place on a molecular level. Albert Szent-Györgyi was ahead of his time, as he asked the same question more than forty years ago [10, 11]. His thinking was that large protein molecules (usually these are the main targets of drug development) cannot fulfill this role of regulating the rapid, complex processes that take place in cells. Szent-Györgyi reasoned that if two molecules are composed of identical atoms, with one of them having one electron more or less, then these molecules differ on a submolecular level, and this fact may be crucial with respect to the regulation of cellular processes. He stated that this subatomic particle (the electron) is able to fulfill the role of regulation due to its small weight and mobility. Electrons are capable of regulating and synchronizing molecular processes. If their free movement is disrupted, it can lead to cancer.
After watching Szent-Györgyi's famous television interview in the 1970s, I continued thinking about submolecular regulation. I formulated the idea that perhaps it's not the negatively charged electrons, but the positively charged hydrogen ions that have a key role in regulating cell division and thus the formation of cancer. I held this idea with such certainty that from then on, I reviewed and reflected on all scientific knowledge based on it. Four years later, as a student of biology at the József Attila University at Szeged, Hungary (today's University of Szeged), I was preparing for my exam in physical chemistry. When learning about enthalpy, entropy, and pH, all of a sudden, I realized that deuterium, a naturally occurring heavy isotope of hydrogen and the other isotope of hydrogen together may fulfill a key role in the functioning of genes and enzymes, and in regulating cell division [12]. Following a career detour in the field of molecular biology, earning a doctoral degree, and completing two scholarships abroad, I waited altogether ten more years to finally begin to conduct experiments to prove the existence of a submolecular regulatory system (SMRS).
To validate my hypothesis, I only needed to ask one simple question: "Does naturally occurring deuterium play a role in regulating physiological processes?" The easiest way to provide an answer to the question is to examine whether a lower than natural deuterium concentration (deuterium depletion) changing the deuterium/hydrogen ratio affects physiological processes in the cells and living organisms.
Results of our research conducted in the past thirty years [12, 13, 14, 15, 16, 17, 18, 19, 20, 21], [22, 23] and independent research results [24, 25, 26, 27, 28, 29, 30] confirmed that deuterium depletion changes a number of cellular processes in different biological systems. Observations indicate that cells sense a change in the concentration of deuterium, and these changes induce and influence several processes in the cells and other organisms.
Results hint at the existence of a submolecular regulatory system, evolved during the billions of years since the appearance of life. This system uses the deuterium/hydrogen ratio to regulate fundamental genetic, biochemical, and physiological processes.
DEUTERIUM
Hydrogen has three naturally occurring variants (isotopes): 1H (hydrogen, H), 2H (deuterium, D), and 3H (tritium, T). Deuterium is a stable, non-radioactive isotope of hydrogen, having a proton and a neutron (of the same weight) in its nucleus (see Fig. 3). (The nucleus of tritium contains two neutrons alongside a single proton. This makes the nucleus unstable and causes this isotope of hydrogen to be radioactive.) It has been known for decades that as a result of the weight difference between H and D, molecules containing deuterium behave differently in chemical reactions. For instance, if a chemical bond contains deuterium instead of hydrogen, it takes six to ten times more time to split the bond during a chemical reaction [31, 32, 33]. The first attempt to produce heavy water (D2O) was also based on this observation. During the electrolysis of water (as a result of an electric current, hydrogen and oxygen molecules are released from the water in a chemical reaction), the dissociation speed of H2O exceeds that of D2O by several times. In the remaining water, the concentration of heavy water steadily increases. Substituting hydrogen for deuterium somewhere else in the molecule, and not in the chemical bond that is about to split, substantially slows down chemical reactions. This so-called kinetic isotope effect offers a rare insight into how chemical reactions work, and why substituting hydrogen for deuterium is a widely used method in chemical research.
Figure 3Hydrogen, the simplest chemical element, consists of a positively charged proton and a negatively charged electron. (Its atomic weight is 1). A deuterium's nucleus is made up of a proton and a neutrally charged neutron of equal weight. This fact causes a 100% weight difference between the two stable isotopes of hydrogen. In terms of the D/H isotopes, a glass of water contains three types of water molecules: light water (H2O), semi-heavy water (HDO), and heavy water (D2O). In deuterium-depleted water, the number of deuterium-containing molecules is smaller, therefore the D/H ratio substantially shifts towards hydrogen.
DEUTERIUMINNATURE
On our planet, the deuterium content of living organisms is primarily determined by the deuterium content of evaporating ocean water, which after atmospheric circulation returns to the surface of the Earth in the form of precipitation such as rain and snow.
When evaluating deuterium measurements in precipitation at hundreds of points on Earth [34], we can conclude that the deuterium content of precipitation decreases from the Equator to the North Pole and the South Pole, from the oceans to the inland, and decreases with higher altitude above sea level. The difference in vapor pressure between H2O and D2O (also HDO) explains this observation. (As a matter of fact, the so-called fractional distillation process used in some nuclear reactors to produce heavy water is also based on this difference.)
The measurement unit ppm (parts per million) is used to determine the deuterium content of deuterium-depleted water (DDW). The number of ppm units shows how many deuterium (D) atoms there are out of one million hydrogen atoms (H). It also shows how many heavy water molecules (D2O) there are out of one million water molecules (H2O). (Note: In surface waters, deuterium is usually not present in the form of D2O, but as HDO.)
In the temperate climate zone, the deuterium content of surface waters is 143-150 ppm (that is to say, out of one million hydrogen atoms, there are 143-150 deuterium atoms) with minimal fluctuation. Contrarily, around the Equator, the deuterium content of surface waters is 155 ppm, and 135-140 ppm in inland Northern Canada (see Fig. 4).
Figure 4While the deuterium concentration of precipitation samples from different parts of the Earth varies, the reason for this is due to the different physical properties of H2O, HDO, and D2O. In the equatorial regions, the deuterium content of water evaporating from the oceans is approximately identical to the deuterium concentration of ocean water (154-155 ppm). However, as clouds move to the north or the south and release their water content in the form of rain and snow, HDO and D2
