Thalassemia is curable
The last century gave birth to numerous unproven and unjustified, moreover, useless and absurd speculative "theories" that spun out of thin air and nonetheless took roots. The "theory" of thalassemia is not an exception.
Only now, after nearly a century, the medical science started waking up from its long hibernation by finally questioning the honesty, justification, and scientism of such "theories", not to mention the tragic consequences that they have casted upon humanity over the course of an entire century.
As the science is being cleansed of all kinds of rubbish, it is about the time to present other authentically scientific theories about the causes of one of the most severe human diseases, especially for children who are deprived of any hope to live to their natural old age.
All information that is presented for scientific assessment in this book is dedicated to patients with thalassemia with the hope that it will serve as a launching point of the new theory that differs from the conventional view and nonetheless possesses the capacity to change the fates of the sick and spark a hope for their recovery and an end to their suffering.
Thalassemia is one of the gravest human diseases, a disease that is spawning a large social problem in many countries of the world. According to official medical statistics, more than 150 million people in more than 60 countries on the globe are carriers of thalassemia’s latent gene. This disease is particularly widespread in Africa, India, Italy, Portugal, Spain, Romania, Arabic countries and Southeast Asia. Based on the generally accepted "theory" of genetic origin of thalassemia, the number of latent gene carriers of this disease constitutes nearly 50% of the population in Saudi Arabia, 40% in some countries of Southeast Asia, 30% in Italy, 15% in Greece, and 10% in Portugal, Thailand, Iran and U.S. According to the World Health Organization, 5% of the total global population has latent genes for thalassemia, which equals 300 million people. Every year, 300 thousand children diseased with thalassemia are born in the world roughly equally distributed between boys and girls.
Thalassemia through the eyes of the "theorists" of current medicine
The widely accepted "theory" of thalassemia grounds on the following key principles:
1. Thalassemia is a genetic disorder.
2. The defect of genes that are allegedly responsible for synthesizing hemoglobin alpha- and beta-protein chains triggers a failure in the synthesis of corresponding proteins resulting in insufficient number of hemoglobin and erythrocytes synthesized in the bone marrow.
3. Alpha- and beta- protein chains deposit in the bone marrow and destroy it, thus triggering bone marrow insufficiency.
4. Increased blood iron levels lead to the development of hemosiderosis.
5. Thalassemia treatment is limited to therapy of its symptoms: regular blood transfusions and removal of excess iron from the body.
This is all we could gather in regards to thalassemia from the current medical database. As it is evident, the information accumulated over the course of almost an entire century leaves no hope for a better future both for the patients with thalassemia and the medical sciences. If we content ourselves with explanations offered by conventional medicine, we shall take a seat, fold our hands and wait for another couple of centuries, in addition to the past 85 years, until genetic sciences finally reaches such level where gene correction will be a reality – then, thalassemia’s turn will come at last!
Therefore, in order to break the deadlock of thalassemia, it would be appropriate to waive the "theory" of its genetic origin that is concealing a wide angle of scientific horizon, and free ourselves from the accepted rules, stereotypes, and entrenched opinions, so that we could at last begin a completely different research. Thousands of patients with thalassemia continue to silently, patiently cope with their difficult, tragic, and doomed survival. With their own bones and skin, each of them acutely senses the degree of discrimination they are subjected to from the medical and social standpoints. Though originating outside of the accepted, inert "theories", the new point of reference will become a ray of light even in the darkness of their daily life, a little hope for a brighter future.
It’s time to prove the invalidity of the generally accepted "theory" that has been confirmed by its long-term ineffectiveness in practice, replacing it with a new, radically different standpoint, a standpoint that can scientifically prove the true origin of thalassemia.
The real face of thalassemia
The very name "thalassemia", meaning "sea-blood" in Greek, suggests the nature of this disease. It hints where we should focus our attention in our search for the causes of this disease, encouraging us to ask the following questions:
1. What kind of secret does the surrounding habitat of the people suffering from thalassemia conceal and why does this disease inflict exclusively people living near the sea shores?
2. Which of the elements that are present in the environment of coastal territories (water, atmospheric pressure, partial pressure of oxygen or hydrogen, moisture, green nature, chlorophyll, sunlight) or perhaps a certain combination of them contributes to the development of thalassemia?
3. Why would the mutation occur solely in the genes of people living by the sea shores, as alleged by the widely accepted "theory" of thalassemia? Whether the gene can possess reason and the option, being guided on the geographical districts, selecting on a choice of people of the given climatic regions?
4. As it is evident, genetic diseases are not limited to a certain time or a specific region. Then, the gene of thalassemia had to impair people all throughout the world, as far back as a thousand years ago, without exceptions or precedence to certain nationalities and regions. After all, why did the gene’s reasoning wake up only after the year 1925 and inflict thalassemia only in people living near the sea shore? Where did it remain up to this time and why is it making an exception for inhabitants of all other regions of the globe?
The true basis of disease’s occurrence
The main function of erythrocytes is transportation of oxygen to all body cells and output of CO2 from the tissues to the lungs. The activity of the human cardiovascular system is organized in such a way that aims to provide all cells of the body with enough oxygen and nutrients to continue their functions. The exact number of blood erythrocytes required at any given time for any given individual in the specific climatic conditions is regulated by the environmental factors that surround the given individual, which are in turn dependent upon the atmospheric pressure and oxygen enrichment of the air. Such adaptation takes into account all nearly constant environmental conditions to synthesize erythrocytes in the exact number required for each cell’s optimal functioning.
Hemoglobin attracts oxygen with iron atoms contained in its molecule, transports them into the tissues where it releases them and further binds to carbon dioxide resulting from this metabolism to carry it out into the lungs. If experimentally to reduce the concentration of oxygen by three times, the blood flow speed and the quantity of erythrocytes would accordingly have to be tripled to ensure normal functioning of the cardiovascular system. If, on the contrary, to triple atmospheric oxygen levels and double atmospheric pressure, to ensure optimal supply of body tissues with products of vital activity, the number of erythrocytes and therefore, the number of hemoglobin molecules would have to be reduced by six times.
Let’s now discuss the two types of environmental change possibilities in detail.
At first, when people move away from areas with high atmospheric pressures and oxygen concentration of the mountainous regions, their body launches immediate compensatory mechanisms in the form of blood pressure and heart rate increase that accelerates the overall blood circulation and therefore, the rate of erythrocytes’ oxygen transportation to various body tissues. However, the human cardiovascular system cannot perform in such a fast mode for long. Therefore, another long-term mechanism activates in parallel resulting in both a proliferation of erythrocytes and an increase of the hemoglobin content in each erythrocyte so that all cells would be provided with sufficient oxygen at a normal pressure and pulse. Three mechanisms are triggered for this purpose:
1. Reduction of erythrolysis intensity. Bone marrow produces a certain number of blood cells based on the average requirement of the body that in turn depends upon the level of physical activity and the state of immunity. Excess cells, especially erythrocytes, are destroyed in the bloodstream. The rate of erythrocyte destruction that has been fixed up for conditions of high oxygen concentration and increased atmospheric pressure drastically slows down or completely stops and the extra cells that were needless in the previous climatic conditions now cease to lyse. In lab experiments, this process manifests in the reduction of bilirubin content in the blood; clinically, this process can be noted by observing the sclera of the people coming from maritime climate to mountainous regions gradually losing yellowness.
2. Increased synthesis of erythrocytes in the bone marrow. In the laboratory, this can be observed in the form of rapid growth of premature reticulocytes entering the bloodstream from the bone marrow, indicating its prompt activation.
3. The number of hemoglobin molecules in each erythrocyte and consequently, the size of erythrocytes increases and their color intensifies, leading to hyperchromia.
Clinical symptoms of this condition in thalassemics manifest more clearly due to ongoing low hemoglobin levels. During the first days of moving to mountainous regions from lowlands, they are prone to shortness of breath, weakness, dizziness, headache, and drowsiness, but after a while, these symptoms wane. Had thalassemia originated from bone marrow insufficiency as experts of current medicine assert, then in the new conditions of mountain climate that are unusual for their body, thalassemics would be immediately subjected to decompensation. Based on the generally accepted "theory", the bone marrow with its "insufficiency" fails to synthesize sufficient numbers of erythrocytes and thus, thalassemics fail to adapt in these conditions at all. Their only escape from this situation would have been a return back home to their native environment. However, numerous studies including those conducted by us prove that in the equal condition of moving to mountainous terrains, the thalassemics bone marrow is capable of synthesizing the additional number of erythrocytes necessary for adaptation to the new environment much faster than in healthy individuals. Laboratory it is expressed by sharp increase in quantity of reticulocyte population, the appearance of hyperchromic erythrocytes, and a reduction in the number of blood microcytes and anisocytes.
Thus, the bone marrow does plays absolutely no etiological role in the occurrence of thalassemia and all far-fetched and naïve observations based on various rumors are merely the end-results of medical science’s hopelessness in resolving the problem of this pathology. Continually elevated reticulocyte levels in thalassemics even while they stay in native lands and familiar climatic conditions further support this conclusion.
Let’s now consider what happens when environmental conditions are reversed?
The number of erythrocytes is much higher in permanent residents of mountainous regions, where atmospheric pressure and oxygen concentrations are lower, than in people living by the sea shores. When they come down to lowlands, especially to lands bordering with the sea, each of their erythrocytes is heavily enriched with oxygen under the influence of high oxygen concentration and high atmospheric pressure characteristic for these places. Given their excess number, erythrocytes supersaturate the tissues and trigger hyperoxia manifested in weakness, drowsiness, shortness of breath and bradycardia. In this case, the body activates a fast mechanism of physiological reactions in the form of reducing blood pressure and pulse rate and thus, reducing blood flow velocity in order to reduce the rate of oxygen transportation to the tissues. Soon, the number of erythrocytes and the hemoglobin content in each erythrocyte is also subjected to reduction by a second, long-term mechanism to prevent the body cells from supersaturating under a normal pulse and pressure. To adapt the blood content for these conditions the following three mechanisms are triggered:
1. The synthesis of erythrocytes in the bone marrow is sharply reduced. In the laboratory, this is manifested in the form of reduced reticulocyte levels. The given process cannot come to zero as the bone marrow is the growth medium for all blood cells, including erythrocytes, and complete cessation of their synthesis as of the synthesis of any other cell, would be possibly only after complete extinction of the bone marrow, which is incompatible with life.
2. The intensity of erythrolysis is increased. A large number of blood erythrocytes are destroyed under the influence of a complex compensatory mechanism, the basis of which we have successfully identified. In the lab, this process manifests as elevated blood bilirubin and clinically, as yellowing of the eye sclera. Due to continuous destruction of excess erythrocytes, residents of areas with high concentrations of oxygen and high atmospheric pressure tend to look paler and have icteric sclera in contrast to inhabitants of mountainous terrains.
Exactly this mechanism of erythrolysis serves as the cause of thalassemia under certain climatic conditions. In exceptional circumstances, the basis of the given mechanism’s regulation goes out of control and under the influence of factors designed for adjusting the numbers of blood cells, erythrocytes in the people’s blood plasma begin to lysis for life, thus leading to the appearance of the disease of thalassemia.
3. The number of hemoglobin molecules in each erythrocyte is reduced. As a consequence, the size of erythrocytes diminishes giving rise to microcytosis and their color fades, triggering hypochromia. These symptoms are sometimes used in contemporary medicine for laboratory diagnosis of thalassemia.
Let us note again that the three above-mentioned mechanisms also occur in physiological conditions in the body of any individual upon a need for adaptation to a new environment.
The mechanism that contributes to the destruction of excessive amounts of erythrocytes in the last example is known to us and as we already mentioned, this is what serves as the main cause of thalassemia. Timely implementation of rapid regulation of the number of erythrocytes is controlled by several chemical substances that must be continually present in the blood serum in small quantities. In emergency situations, including those related to the change of climatic conditions, these substances must immediately enter the bloodstream, triggering a sharp decrease in the concentration of erythrocytes through erythrolysis.
It is important to add that in physiological conditions, the content of the foregoing substances may decrease or increase under the influence of various factors in both cases of the resulted examples, but the synthesis of their average amount in the body is always required for correcting the number of blood cells depending on environmental conditions as well as corresponding to other life circumstances. It is possible to determine, under what altitude, atmospheric pressures and oxygen concentration a particular individual resides according to the intensity of his sclera yellowness.
Hemoglobin is released as a result of erythrolysis. Iron-containing part of the hemoglobin molecule, i.e. the heme part, is separated and poured into the plasma in its free form. As a result, ferritin blood content sharply increases as confirmed by laboratory tests. While circulating in the bloodstream, excess iron accumulates in various organs causing hemosiderosis. Non-iron-containing part of the gem is released into the blood serum in the form of bilirubin pigment, the raised which concentration is defined laboratory. Clinically it manifests as sclera yellowness. The protein part of hemoglobin that consists of α- and β- chains is broken down into its component parts and used by the body in the form of amino acid residues or polypeptide and dipeptide fragments for the synthesis of protein compounds.
Thus, let’s assume that for any reason, for example, as a result of hypertrophy of the organs that synthesize substances that are responsible for activating timely regulation of blood erythrocyte content or in conditions of high atmospheric pressure and oxygen concentration, the synthesis of these substances goes out of control and its amounts in the body exceed the norm. What happens? On the one hand, this triggers sharp erythrolysis that manifests as hyperbilirubinemia, bilirubinuria and anemia. On the other hand, upon receiving blood content’s signals about erythrocyte deficiency, the bone marrow launches hyperactive erythropoiesis, which can be observed in the laboratory in the form of reticulocytosis. Pressed to make up for missing erythrocyte content, without having time to ripen, these cells enter the bloodstream immaturely, but under the influence of the increased maintenance of aforementioned substances, are immediately destroyed. The bones in which marrow are synthesized erythrocytes, forcedly hypertrophied to compensate for their continuous deficiency. Naturally, all the bones that are involved in the process of hematopoiesis increase in size, but only the outer bones, in the case of thalassemia – bones of the upper jaw, are apparent to the naked eye. This is how the symptom complex of thalassemia is formed.
Summing up the foregoing, contrary to the generally accepted "theories", it is possible to confirm with confidence that neither gene content nor the structures of erythrocyte membrane or the bone marrow are the primary cause of thalassemia.
According to a truly scientific approach, the etiological agent of thalassemia lies in increased synthesis of substances required for the implementation of the second mechanism – long-term regulation of the number of blood elements for adapting human life to various environmental conditions. Areas that happen to be the primarily homelands of thalassemia are characterized by high atmospheric pressure and increased oxygen concentration. Such climate is inherent in coast-sea areas, especially those that are covered by evergreen forests. It is here that the regulatory mechanism that synthesizes the aforementioned substances undergoes sudden disturbances, causing hypertrophy of corresponding organs.
Arguments refuting the generally accepted "theory"
There are many arguments refuting the generally accepted "theory" and hence, confirming the mechanism of thalassemia’s development proposed by us:
1. The "theory" of thalassemia’s genetic origin claims that owing to a defect in the genes that are allegedly responsible for the synthesis of α- and β-hemoglobin protein chains, one of these chains is not synthesized making the hemoglobin molecules defective and thus, triggering anemia.
There is also another opinion that intensive erythrolysis happens in patients with thalassemia due to outer membrane insufficiency. If these claims are valid, then why are erythrocytes obtained from the blood of healthy people subjected to lysis along with autologous erythrocytes within a short period of time post transfusion to patients with thalassemia? There can be no doubt that the hemoglobin content and outer membrane of erythrocytes obtained from the blood donors are absolutely normal, without any kind of genetic and structural defects unless all erythrocytes obtained from donors all around the world for transfusion to thalassemics, accidentally happened to possess defective genes and untenable membranes, owing to what they completely lyse within a week of circulating in the bloodstream of thalassemics. Otherwise, this fact can speak of only one conclusion: the proposed "theory" of thalassemia’s genetic origin and the claims about the insolvency of erythrocyte’s outer membranes fail to withstand any logical criticism.
Perhaps, someone will object and say that not all erythrocytes transfused to thalassemics are young. That’s right and this must also be considered. Therefore, let’s conditionally, in a fair and brotherly manner, divide them out into three categories: suppose that one third of them constitute erythrocytes that were born 120 days ago, the other one third – erythrocytes produced 60 days ago and the last one third – erythrocytes synthesized on the day of transfusion. Thus, at least two thirds of the erythrocytes contained in the transfused blood must circulate in the plasma of patients for an average of 90 days. Then, why is this not occurring so considering that when these same erythrocytes are transfused to a healthy individual, they are found to function until the end of their physiological lifespan? Among other things, proposed opinion contradicts with the very basis of the "theory" of thalassemia’s genetic origin that is based on genetic defect and bone marrow failure in the synthesis of erythrocytes. In the end, it is still unclear, whether erythrocytes are synthesized or not synthesized? If they are not synthesized, then what is it that gets destroyed and by whose outer membrane abnormality? In this case, are we talking about the abnormality of the outer membrane of some non-existing erythrocyte or phantom? But if they are synthesized, then what is the case with bone marrow failure and the defect of various genes. Would someone enlighten the darkness, please?!!
The above argument is one of the strongest arguments against all widely accepted "theories" of thalassemia’s origin, including genetic and aplastic origin.
2. If we mix the blood plasma of thalassemics with blood obtained from a healthy individual in the laboratory, erythrocytes of the health person will be destroyed. This proves that the mystery of thalassemia lies in the blood serum of patients with thalassemia and that it manifests as hemolytic anemia. At that, erythrolysis is solely triggered by increased synthesis of substances that are responsible for regulating the number of blood cells. These very substances trigger lysis of a healthy individual’s erythrocytes in the given in vitro experiment and in vivo, in the case of patients with thalassemia. Genes, erythrocyte membrane, and bone marrow play absolutely no role in the etiology and pathogenesis of thalassemia. None of the listed "defects" that are attributed to thalassemics in the given experiment in vitro did not accept participation and was not transferred to blood erythrocytes of the healthy individual, and basically could not be transmitted in any way.
3. If to mix isolated erythrocytes from a thalassemic patient with the blood of a healthy individual, no pathological changes and signs of erythrolysis that are accompanied with increased bilirubin in his blood occur, neither in vitro nor in vivo experiments. Most importantly, these erythrocytes even retain their natural lifespan in the blood serum of healthy person because it is a physiological environment of their support, an environment in which they should not and cannot be subjected to breakdown. The blood serum of patients with thalassemia is a damaging environment for all erythrocytes, including those of a healthy individual. Thus, erythrocytes of thalassemics are no different from erythrocytes of healthy people. They are synthesized in the bone marrow in the exact same way and they enter the bloodstream as completely normal cells, yet they are forced to lyse here under the influence of previously mentioned factors. The only distinguishing feature of this process in thalassemics is that their erythrocytes, pressed to make up for the continuously missing erythrocyte content, fail to mature due to intensive synthesis in the bone marrow and mostly enter the blood in the form of reticulocytes.
This given experience completely proves that no defect in thalassemics’ genes, hemoglobin, erythrocytes and the bone marrow exists in fact.
4. Administration of drugs that neutralize substances promoting the destruction of erythrocytes completely stops the process of erythrolysis in the blood of thalassemics. The given experiment, performed solely by us, proves once again the validity of our new explanation of the causes of this disease and refutes all other views that are long since outdates. This is the principle that lies at the heart of our proposed new method of treating thalassemia.
Summarizing all aforesaid, it is possible confidently to assure that not only is thalassemia not a genetic disease caused by defective synthesis of hemoglobin protein chains or erythrocytes membrane insufficiency, but it cannot be a bone marrow disease as well for the following reasons:
1. The bone marrow has never been considered and still is not considered as a reasonable being possessing the capacity of selectively synthesizing blood cells. From a biological perspective, the bone marrow is the growth environment of all blood cells, be it erythrocytes or leukocytes. According to books on hematology, stem cells or more specifically, one of their branches that synthesizes erythrocytes, are also the precursors of thrombocytes and leukocytes such as granulocytes, basophils, neutrophils, eosinophils, and monocytes. Thus, the synthesis of all blood cells, without an exception, occurs unconsciously and naturally. Therefore, a failure of the bone marrow that subjects all blood cells to equal conditions cannot affect only one type of cell, triggering selective inhibition of erythrocyte synthesis without influencing the production of other cells. Such proposition has no logic, unless we allow the laws of sociology to guide our understanding of bone marrow and by deliberately endowing all blood cells with reasoning, grant each cell with the right to exercise its freedom of opinion and choice pursuant to the principles of democracy.
In reality, contrary to the views of the visionaries of the contemporary medicine, thalassemics’ bone marrow possesses a hyperactive ability owing to a continuous shortage of erythrocytes due to their lysis in the bloodstream. It is precisely for the purpose of compensating for missing cells content that the bone marrow was induced to continually synthesize a larger quantity of erythrocytes. This is the main reason of bone hypertrophy in the patients with thalassemia.
However, as it was already mentioned, the bone marrow cannot induce intensified production of solely one type of blood cells. Pursuant to the principle of feedback, given a continuous erythrocyte deficiency, the synthesis of other blood cells is also intensified. This is confirmed by the fact that patients with thalassemia are subjected to an associated pathology in the form of splenomegaly. Excess numbers of other blood cells, especially in the case of leukocytes, accumulate in the spleen as in a storage reservoir, thus triggering its enlargement. In this case, as in similar instances, the contemporary medicine finds suitable only one, but nevertheless, specific and radical "effective" treatment: since an organ enlarged, let’s remove it to have no more problems. This is yet another fight with the consequences of a disease rather than its cause. As a result of this nonsense, leukocytes have nowhere to go after spleen removal, triggering oversaturation of the cardiovascular system which promotes the formation of white thrombi and enhances the risk of heart attacks, strokes, and thromboembolism that often lead to lethal consequences for patients impaired with splenectomy. Following the iron-hard and most importantly "logical" principles of the conventional medicine, we are perplexed by one last question: how come other organs hypertrophied by thalassemia, including heart, liver and upper jaw are still not subjected to extirpation after all?
2. The primary cause of increased blood levels of unconjugated bilirubin is erythrolysis.
Logically thinking, bone marrow insufficiency, and consequently, reduced erythrocyte synthesis cannot serve as the basis substances of high unconjugated bilirubin levels.
For a reasonable person absence of eggs, by itself means also absence of its yolk. By the same principle, absence of erythrocytes cannot mean bilirubin presence in any way and in addition in considerable quantities. For a vast erythrocyte breakdown excreting bilirubin to have place, erythrocytes must be produced by the bone marrow in the first place (according to the principle that "to sell something unnecessary, at first it is necessary to buy something unnecessary, but we have no money"). If there was a bone marrow failure as claimed by the "great" scientists, then where are erythrocytes coming from, not to mention unconjugated bilirubin excreted in the process of their lysis that exceeds erythrocytes by a thousandfold, considering that it can have no other source? This contradiction, while disregarded by representatives of the conventional "theory" for thalassemia, is one of the key principles distinguishing hemolytic anemia from aplastic anemia, caused by a bone marrow insufficiency indeed. High levels of unconjugated blood bilirubin and blood iron are only typical for hemolytic anemia and, conversely, completely uncharacteristic for aplastic anemia. If thalassemia was an aplastic anemia (meaning, anemia caused by bone marrow failure), what could explain the surplus numbers of bilirubin and iron in the plasma of the ill and, besides, in quantities that are much greater than those observed in healthy people? This condition provides for only one possible conclusion: the actual number of blood erythrocytes, whose lysis is the main source of appearance of blood iron and bilirubin, along with hemoglobin concentration, is proportionately higher in the blood serum of thalassemics than in healthy people. Another variant dose not place to be. And the third, too.
If we agree that bilirubin blood levels are normal in healthy individuals with hemoglobin levels in the range of 120–160 g/l, then it is illogical to assume that in thalassemics, they will be considerably higher while blood level of erythrocytes synthesized by the bone marrow and consequently, hemoglobin concentration stay at levels substantially lower than in healthy individuals. Judging by the views accepted by contemporary medicine, thalassemia comes with virtually terminated bone marrow synthesis of erythrocytes while blood bilirubin level, which is, in fact, a product of erythrolysis, is hundreds or thousands times higher in thalassemics than in healthy individuals. The real picture of hemoglobin of such patients truly coincides with laboratory test results; however, in reality, their actual erythrocyte content is substantially higher than in healthy individuals. So high levels of unconjugated bilirubin found in the blood serum of thalassemics are precisely the result of the mass erythrolysis occurring. This fact in any way does not correspond to representations of wide accepted "theory" of occurrence of thalassemia.
3. Essentially, from the standpoint of scientific medicine, a bone marrow insufficiency can be interpreted by two variants:
а) either there is a decrease in the volume of the bone marrow itself, which constitutes the growth environment for all blood cells. Such case must be accompanied by the atrophy of bones involved in erythropoiesis and all know that people with thalassemia suffer from the exact opposite condition as it is clearly visible by their facial bones.
b) Or the marrow insufficiency consists in its decreased blood circulation leading to oppression of its synthesizing capability.
It is not difficult to guess that in both cases, the synthesis of not just erythrocytes, but all blood cells will be affected. As a result, the number of blood cells synthesized by the bone marrow that will enter the bloodstream will be very low, meaning that cell destruction in the blood plasma and high blood bilirubin levels would be completely out of question. When the number of erythrocytes entering the bloodstream is low, the body activates a variety of mechanisms to protect them. Then, whence such high blood ferritin and unconjugated bilirubin levels in patients with thalassemia given that the only source of their excretion in such large numbers can be the destruction of a large number of erythrocytes? Nevertheless, according to representatives of contemporary medicine, due to failure of the bone marrow, the number of red blood cells entering the bloodstream is very low. As it is clearly evident, there is not a single claim of the conventional "theory" for thalassemia that would be free of inner contradictions.
4. The deformation of the bones, including facial bones, in patients with thalassemia occurs in compensation, for purposes of increasing bone marrow volume to provide for additional, continually missing erythrocyte content. This bone marrow mechanism occurs in response to increased erythrolysis taking place in the plasma of thalassemics. In other words, it undergoes a compensatory enlargement only when blood cells are destroyed in the bloodstream. This is a natural bodily compensatory reaction to the lysis of erythrocytes. Possibly, the bone marrow response reaction is triggered by increased blood levels of erythrocytic bilirubin or iron from the heme group of hemoglobin in the serum. In fact, this is the argument that completely negates the view that thalassemics suffer from bone marrow insufficiency. For acknowledgement of this fact there is no necessity for any statements made by a silly brain, in the guise of a clever kind. To extract corresponding conclusions, it is enough to look at the faces of thalassemics.
5. The main hemoglobin function consists of transporting oxygen to the tissue and withdrawing СО2 to the lungs. This process is conducted by the iron-containing heme groups of the hemoglobin molecule. If we infer that the disturbance occurs in this function, then it should only relate to the heme part and it can have no relation to the globin, whatsoever. In such case, either the assertion that the heme molecules conduct the transportation of oxygen and the output of СО2 from the tissues is incorrect or the "theory" of the defect of the protein part of hemoglobin is untrue. The fact that this function is performed by the heme group is unquestionable; therefore, a destruction of the synthesis of the protein group should have no effect on hemoglobin physiological mission. Hence, the validity of such "theory" is the only subject for questioning. On the other hand, if the synthesis of α- and β-chains would have been impeded indeed, then how would the heme molecule bind to the oxygen molecule if there was nothing to affix it to the hemoglobin molecule in the first place? If hemoglobin had no protein component, its iron-containing heme groups would not be present as well. In such a case, whence would the excess iron population come from and what would explain the elevated bilirubin levels in the blood plasma of thalassemics?
Summarizing our explanation of thalassemia’s origin
Any chemical reactions and in this case, the reactions between oxygen and iron atoms, is boosted in conditions of higher atmospheric pressure. Molecules of oxygen and hydrogen bind, transforming into water, precisely under pressure which is rendered by atmosphere on the surface of globe. In thalassemics, the chemical bonding between oxygen and iron is so strong that one erythrocyte can repeatedly migrate from the lungs to the tissues and vice versa without losing oxygen. Such an exclusive event triggers a breakdown in the mechanism that regulates the size of erythrocyte population in response to environmental conditions.
As the result of long-term residence in climates with strict regime of raised atmospheric pressure, high oxygen concentration and air humidity, occurs a malfunction of the mechanism that regulates the action of substances required for adapting erythrocytes quantities to these climatic conditions. Subsequently, these substances start synthesizing in excessive amounts, causing massive erythrolysis.
In other words, the blood plasma of patients with thalassemia has a special compound, in which blood cells and particularly erythrocytes, whose population outnumbers all other blood cells, are impeded from circulation in the bloodstream to perform their physiological purpose. Under the influence of aforementioned substances, as already has been mentioned, erythrocytes are destroyed and the hemoglobin contained in them is released into the blood serum in its free form, eventually separating into two parts: the globin and the heme. Globin portion splits down to amino acids and polypeptides that the body will use for the synthesis of autologous proteins. The heme molecule loses its iron and its remaining part circulates in the blood in the form of bilirubin, causing yellow coloration of thalassemics’ sclera as well as turbidity and darkening of urea. This process, called hemolysis, is the primary principle of differential diagnosis of hemolytic anemia and the only true mechanism of the onset of thalassemia. In the meantime, the bone marrow synthesizes completely healthy and full-fledged erythrocytes that are destroyed only after their entry into the bloodstream. In physiological conditions, i.e. in their supporting environment, which is the blood of a healthy individual, these cells can live and function for 120 days.
The signal about massive erythrolysis in the form of somatic tissues’ hypoxia goes from the plasma to the bone marrow, which, as a form of compensatory reaction, activates synthesis of all blood cells, including erythrocytes. However, since erythrocyte destruction in the blood outpaces their synthesis in the bone marrow iteratively, the bone marrow fails to develop these cells to full maturity and forcedly releases them into the bloodstream in the form of reticulocytes, which are smaller and have less hemoglobin content and hence, less color. The reticulocytosis observed in the blood of all thalassemics proves that their bone marrow is perfectly functioning. This is common knowledge amongst all hematologists. Even in healthy people following loss of blood and especially in women after menstruation, the bone marrow activates and supplies the bloodstream with a larger number of reticulocytes. In hematology, an increase in the population of reticulocytes is a major sign of hyperactivity and healthy bone marrow functioning.
One of the criteria for the diagnosis of thalassemia in conventional medicine is the presence of three features of erythrocytes: microcytosis, hypochromia, and poikilocytosis. In hematology, these three distinctive erythrocyte properties are used for differentiating the diagnosis of posthemorrhagic anemia from all other kinds of anemia. Yet, the microcytosis and the hypochromia along with the poikilocytosis can be found in all people who have lost blood for various reasons, for example, in women after intense menstruation. In this case, can really form a thalassemia diagnosis solely on the basis of these three characteristics? It turns out you can. In current medicine, the identification of microcytosis, hypochromia, and echinosis is enough to diagnose someone with thalassemia!!! Perhaps, all women of the planet regularly fall ill with thalassemia on a monthly basis?!
As the volume of standard bone marrow in patients with thalassemia fail to meet the requirements of their body’s physiology, all of their bones containing bone marrow for the synthesis of cells, hypertrophy in compensation. A bright illustrative example of the given process well to observe by taking a look at the faces of thalassemics, which are subjected to deformation as a result of growth of their cranial bones, especially their upper jaw. Yet, in the current medicine, no one seeks an explanation of this nor will they ever be interested in finding it until Desferal dealers are satisfied with their successful business, a business built on deaths of innocent children suffering from thalassemia.
New method of thalassemia treatment
Proceeding from all aforesaid, the etiological factor of thalassemia is concealed neither in the bone marrow nor in the genes that are allegedly responsible for the synthesis of α- and β- hemoglobin protein chains neither in the outer membranes of erythrocytes nor in the hemoglobin molecules themselves. The main pathological process that leads to the development of thalassemia is the lysis of completely healthy erythrocytes that enter the bloodstream from the bone marrow, due to excessive amounts of substances intended for regulating the number of blood cells present in the blood plasma, in this particular case, in response to climatic conditions of the environment. In the condition, when the atmospheric parameters exceed particular limits, including duration limits, occurs a failure in the mechanism that controls the synthesis of the given substances. Their excessive excretion into the bloodstream activates a massive erythrolysis that brings about the full spectrum of symptoms characteristic for thalassemia. By neutralizing these substances in the patient’s organism, we completely stop the process of erythrocyte destruction in the blood and within a short time and without any blood transfusions that were formerly simply inevitable, the number of erythrocytes easily comes back to the norm. Considering the hyperactive functioning of their bone marrow due to previously induced hypertrophy, thalassemics’ erythrocyte population easily multiplies, often exceeding their physiological norm. Following logic thinking, until the bone marrow along with its specific features acquired in previous conditions adapts to the level of functioning required in the new situation, there will be excess blood content now that would have to be regularly excluded from the patient’s circulatory system. Exonerated of the need to urgently replenish erythrocytes subjected to constantly lysis in the bloodstream, reticulocytes will now have the time to mature in the bone marrow and enter the plasma as full-fledged, healthy cells that acquire a normal size, shape and hemoglobin content, i.e. without any symptoms of microcytosis, poikilocytosis, or hypochromia. Before that, as mentioned above, reticulocytes rushed out of the bone marrow to compensate for the continuous erythrocyte deficiency in the bloodstream, simply running short of time to mature, which is exactly why they possessed the characteristics of young cells.
As a result of all stated, it is possible to declare with firm confidence that thalassemia is completely curable. However, unfortunately, I had no chances of realizing and confirming my theoretical developments in practice because there are no thalassemics in the country of my residence and therefore, no opportunity for conducting trial treatments.
I did, however, complete the bulk of the research in this field. No more scientific and experimental studies are needed. The mystery of thalassemia is finally unraveled. It only remains to practically confirm the effectiveness of my new treatment based on completely different views on the etiology of this disease. This means that we are facing the most important part of the whole process – saving the lives of millions of people who have lost any hope in the current official medicine, as already over the past 85 years entirely and fully it could realize and apply all its possible potential, on which it just was capable, but except replenishment of the pharmaceutical swindlers’ pockets, any improvement in the patients’ health status has not brought.
The victory over thalassemia, in addition to its scientific value and humane goals, can become also a subject of any nation’s pride. I do not doubt for a moment that sooner or later these achievements, just like any others will find their place in the foundation of human science, but it will be a great pity if the outcomes of given method will not belong to the scientific potential of my own homeland, where unfortunately, as history shows, not only the science, but also the people themselves are not needed to anybody.
Finally, since skeptics find it convenient to brand any new scientific discovery as "folk medicine" to refute it without going to further troubles, we want to emphasize that new theory and the treatment method derived from it have no relation to traditional medicine in any of its forms whatsoever and while they are significantly different from the treatment methods adapted in the current medicine, and are implemented solely within the scope of modern medicamentous medicine and all drugs administered are on the pharmacological market for over 40 years and are registered with heath ministries of virtually all countries around the world.
