Thalassemia is curable
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 wisdom 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 silent carriers of thalassemia. According to the World Health Organization, 5% of the total global population has latent genes for thalassemia, which equals 300 million people.
Thalassemia, as many other modern human diseases, has a relatively short history. The first report of this disease was published in 1925 by an American pediatrician, Thomas Cooley. He was the first to discover and describe its symptoms.
Consistent with the widely accepted "theory" of thalassemia’s origin that is basically an addendum to the claim that is attributed to Thomas Cooley, the "defect in genes that are supposedly responsible for the synthesis of hemoglobin protein compounds i.e., alpha or beta chains", triggers a disturbance in the synthesis of corresponding proteins in the bone marrow. Unfinished hemoglobin molecules cannot transport oxygen to the tissues or remove СО2 for them, thus, giving rise to thalassemia.
Depending on which chain is damaged, thalassemia is classified as alpha and beta thalassemia. Beta thalassemia is divided up further into three categories: minor or small, intermedia or average, and major or big.
Since according to internalized values, thalassemia is a genetic disease and since genetics and, particularly, genetic engineering, have not yet reached the necessary level of development, a thorough treatment for this disease on the basis of the widely accepted "theory" cannot exist.
Based on the collected set of ideas about the causes and development processes of thalassemia prevalent in the current medicine that lead to the conclusion that there are no etiological solutions, treatment of the ill is confined to symptom therapy alone. To compensate for anemia, doctors resort to regular blood transfusions, which dramatically increase blood iron levels that are already well above normal along with the risk of contracting infectious disease. Daily subcutaneous injections of iron-binding Disferal drug or its oral replacement are then required to withdraw iron from the body.
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 atmospheric pressure. 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.
Long-term residence in climates with strict regime of high atmospheric pressure, oxygen concentration and air humidity triggers a malfunction of the mechanism that regulates the action of substances required for adapting erythrocyte population 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 consistence 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, 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 protein 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 cloudiness and darkening of urea. This process, called hemolysis, is the primary 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.
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, 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.
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. You can find an illustrative example 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 front part and their upper jaw.
New thalassemia treatment
From our point of view, the etiological factor of thalassemia is not concealed in the bone marrow or the genes that are allegedly responsible for the synthesis of α- and β- hemoglobin protein chains or the outer membranes of erythrocytes or 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. When the atmospheric parameters exceed particular limits, including duration limits, they promote a dysfunction 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. 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, echinosis, or hypochromia. Before that, as mentioned above, erythrocytes 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.
In conclusion, I can assure you 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 their hope in the current official medicine that has completely and fully realized and applied its potential over the course of the last 85 years, nonetheless, yielding no improvement for the health status of the patients.
The victory over thalassemia, aside from its scientific value and humane goals, can also serve as matter of any nation’s pride. I do not doubt it for a moment that sooner or later, all these achievements will find their place in the foundation of human science just like any others, but it will be a great pity if the outcomes of my method will not belong to the scientific potential of my homeland, which unfortunately, as history shows, demonstrates no interest not only in the sciences, but even in the fates of its own people.