UNFOLDING THE MYSTERIES OF GENETIC SCIENCES IN INCURABLE DISEASES LIKE CORONARY ARTERY DISEASES, CANCER, & RAREST OF THE RARE DISEASES LIKE MOYAMOYA, SLE, TAKAYASU ETC.

Misconceptions in cardio-vascular ScienceS

        Recent years, it has been observed that  nearly 33% people suffer from coronary artery disease and only 3% suffer from cancer. Coronary artery disease (CAD) becomes a major killer disease. Clinicians and researchers are blaming the modern life style to be a major contribution to this disease. My observations have suggested that this cannot be an absolute  contributory factor as we have treated the patients with CAD from various geographical area where modern civilization has not yet touched, but less in number. Therefore, superficially, it is confusing scenario whether modernization or modern civilization is absolutely needed to be blamed. The reversal of life style does not appear to reduce the coronary artery disease. My research findings during last several years suggest that something else is a contributory factor or cause of CAD.

I have started cardiac surgery after completion of my four years general surgical training and during that period, I have completed my primary FRCS from Royal College of Surgeons and physicians , Glasgow. I was allowed to  work in the department of cardiac surgery from 13th July, 1978 in Royal Victoria Hospital, Northern Ireland, UK. Eversince, continued open heart surgery in several hospitals in west, before I settled in Glasgow, UK. Probably, it is not out of proportion to mention that I am the only heart surgeon, who has carried out more than 500 large animal experimentation to bring revolution in cardio-vascular sciences as I found treatment of dreaded cardio-vascular disease  is wrong more than 80% if not 100% and some of the investigations are inconclusive and unnnecessary. Since 1978, I had dealt with several hundred thousands of heart patients and amongst those, I have no comment to make about the characteristic of the patient having congenital heart disease and acquired valvular disease. But I regret to make comment on patients suffering from coronary artery disease. My close and careful observations and experience on patients with CAD have suggested that modern civilization and change of life style, which are blamed by clinicians and scientists in recent years have very small and insignificant role to play .

An individual with corruption and crookedness always suffer from CAD, which plays a major role. However, 0.2% patients are with honest characteristic also suffer from CAD. Therefore, in conclusion, 99.8% people with this chracteristic are mostly sufferer from CAD. Almost 0.2% sufferers of CAD are influenced by change of life style and modern civilization.

Genetic involvement:-

DNA is not found to be invoved in CAD. m-RNA expressed diseased genes are to be blamed for this dreaded disease. This genes are influenced by the characteristic of the person with extreme crookedness or corruption.

Our laboratory work has reached to the stage, that where without knowing the  individual, by analysing the morphology of the gene, identification can be made of the individual and can predict about his Coronary artery disease..

Incidence of CAD is found to be more in western countries and probably, it was not much exaggerated to say that residents of US are worst sufferers. However, CAD was relatively found to be uncommon in eastern India, but  in recent years, India has nearly reached to the level of US in terms of CAD.

             Recent survey (Not done by us) report has suggested that approx.70millions people are suffering from CAD in India with acceleration of 10% every year, out of which 5 million die prematurely every year. 50%  of this 70 million within the age group belongs to 40-65years and 80% of the CAD patients, are suffering from more than three vessel disease. 86% of these patients are not isolated with CAD, but with combination of diabetes mellitus and hypertension, ypothyroidism. We found that hypothyroidism is most commonly associated with CAD, diabetes, hypertension and kidney disorder. I do not consider Electrocardiogram (ECG) a diagnostic tool of heart disease. It is a tool to give suspicion to proceed for further investigation. A doctor can clinically diagnose when a patient complains of heart disease, doctor should walk with the patient either inside the building or outside the building provided doctor has no CAD and if the patient is breathless or  allow the doctor to investigate further.

           Tread mill test (TMT) is meaningless investigation for patients with CAD. TMT does not indicate anything at subcellular level and in fact, problems of CAD  always begin at subcellular level and ends at intraluminal pathology. This concept has not been grown in clinicians’ mind. It  is done on plane surface with 100% oxygen breathing air which is not a ideal situation for analysis of CAD. In our Institute, we made ECG and TMT totally obsolete.

          Ventricular performance is best observed during the test, we carried out in our Institute. We allow the patient to climb the hill of 700ft height. Two things happened in this test::-1. The patient’s heart has to pump more as he goes up and air becomes thin with loss of Oxygen, where as heart requires more Oxygen to work. If the ventricles are unable to work at this condition, patient will have breathlessness and chest pain or both and he will abandon the test. He cannot proceed with test. We found that  actual ventricular performance cannot be monitored by TMT.

          Colour Doppler echocardiography is done to observe the movement of the ventricle in the resting stage, whatever the results in terms of ejection fraction, the clinicians predicts and tells the patient the condition of the heart. This test is totally useless and resulted ejection fraction does not produce the actual performance of the ventricle as the test is carried out at resting position. It must be done while ventricles are working under stress. We obtain the actual ventricular performance while patient is climbing the height at low oxygen level by using a portable colour doppler echocardiography and we found what is usually reported by the cardiologists in term of ventricular performance at resting and what we get during performing exercise, in terms of ejection fraction in reality is hell and heaven difference. Therefore, I conclude, ventricular performance  in terms of ejection fraction  reports after doing colour doppler echocardiography studies is illusive.

            As I have said repetitively in the past that CAD is not a localised isolated disease, it is a generalised systemic disease involving entire arterial system. We have routinely carried out forward flow studies through carotid, subclavian, descending aorta, renal and femoral arteries which allows us to find out the extent of CAD and ventricular performance and predict whether the patient is going to have a stroke in normotensive or hypertensive conditions. Patient is relatively safer if having calcified atheromatic lesions comparatively soft non-calcified lesions. To engineer  the m-RNA expressed disease genes with Baruah molecules, it makes no difference whether patient has done coronary artery angiography or not. We get the exact idea of patient’s coronary arteries atheromatic occlusive lesions by performing patient’s forward flow studies of carotids using colour doppler and prepare the patient for treatment of coronary artery disesase by Baruah molecules. In reality for genetical engineering for m-RNA expressed diseased genes, Coronary  artery angiography is a useless investigation. It does not tell us what is happening at subcellular level. That is why bypass surgery is totally failed to improve the ejection power of myocardium as it cannot supply oxygen at subcellular level where intracellular calcium occupies the space.  Thereby, ATP is synthesized inadequately, leading to loss of energy at subcellular level and ejection power as a whole  and at the end, ventricles are ceased to function prematurally.

Biochemistry:-

                  When patient comes to the clinician with chest pain and discomfort, he normally analysed the lipids and accordingly treatment is given. Patients and clinicians get scared of high content of lipids if there is any and prescribes lipid reducing drugs and controlled the diet containing fat. My research findings have a strong point to suggest that high lipids in blood cannot cause the cessation of the function of the ventricles, it is the Baruah syndrome, which causes the cessation of cellular function. The clinicians should concentrate on electrolytic imbalance rather lipid imbalance. Baruah syndrome occurs in every patient with CAD, with execessive accumulation of Calcium at mitochondrial level and functional dysfunction of Sodium Pump. These lead to two things:-

          1.Mitochondria are generators where oxygen is used as fuel to generate the energy called ATP, which is utilised by every cell to function normally. When mitochondrial lumen is filled with Calcium, then energy is generated inadequately, thereby, normal cellular function cannot be continued for too long. This situation occurs when the ratio of lipids at membranous level viz. cholesterol and phospholipids which allows eflux and influx of Calcium across the membrane of mitochondria and endoplasmic reticulum, get disturbed, which allows influx of Calcium but does not allow to come out. Simultaneously, functional dysfunction of sodium pump causing electrolytic imbalance, leading to ventricular arrhythmia like bradycardia, tachycardia and supra-ventricular ectopics depending upon the severity of the sodium pump. Unless this dysfunctional sodium pump is corrected and excessive accumulation of mitochondrial Calcium is removed,  the abnormality of the myocardium is not possible to correct by anti-arrhythmic synthetic drugs. This scenario has never been understood by the clinicians and probably will not and I predict damage to the heart patient will be continued with this misunderstanding and misconcept.  However, even clinicians understand this concept, they do not have tools to correct it. Therefore, all patients of CAD die prematurely and the gap between biological and real age becomes more and more.

            Every patient of coronary artery disease looks more aged compared to his /her real age. It is primarily due to low oxygen supply at subcellular level and inadequate ATP synthesis. This situation also occurs in hypertensive patients. Therefore, hypertensive patients, angiotensin blocking synthetic agents which are normally used in hypertension have miserably failed to cure hypertension permanently. It can only suppress high blood pressure temporarily and damage of the organs due to hypertension continues. Hypertension is becoming a major global problem affects almost every person on this planet and till today no body has found the cure. The concept of hypertension is basically wrong. It is like CAD problem caused by errors in m-RNA expressed genes which becomes diseased, causes disturbance in  the metabolic pathways. This condition can be cured by reversing the disturbed metabolic pathways by changing the m-RNA expressed diseased genes. To do that, clinicians or scientists must have tools. I have carefully and closely observed that till now, no one has any tool to reverse the metabolic pathways and to cure hypertension permanently. I have understood the basic mechanism of this biological derangement of metabolic pathways and its correction by using Baruah  biology molecules isolated from edible medicinal plants which engineered these diseased genes.

Beta blockers-

Role of Beta blockers on hypertension:- Hypertension is usually treated by beta blockers and diuretics. Beta blockers are used to stop the function of angiotensin whereas cause of hypertension is somewhere and treatment is given somewhere. This works on systolic pressure only, and it decreases the pulse pressure by reducing the systolic pressure, which is detrimental to the heart . On the other hand, it increases diastolic phase, thereby, reducing the heart rate, leading to inadequate cardiac output because of reducing stroke volume.As the diastolic pressure is increasing, pulmonary venous flow is decreasing, and as a result, there by, increasing pulmonary congestion and patient becomes breathless. As time goes by, the congestion increases, so is the breathlessness and in this condition, life cannot sustained too long.

           One of the side effect of Beta blocker is atherogenicity and it causes intra- luminal arterial occlusion. It never cures the hypertension, but causes the premature failure of the myocardium, loses the ejection power and death due to pulmonary congestion. On the other hand, heart is becoming voluminous due to hypertrophy and reducing intra-luminal volume. In conclusion, beta blockers which are used conventionally for hypertension of any trade name is very dangerous. There are frequent incidence of stroke even after patients are on beta blockers called anti-hypertensive drugs. This stroke is not due to hypertension, but due to embolization of intra-luminal  atheromatic plaques of carotid arteries which started prior to occurance of hypertension.

Remedy for hypertension- 

Angiotensin blocking synthetic agents are used to cure hypertension, but have miserably failed. It can only suppress hypertension temporarily and damage of the organs due to hypertension continues. Hypertension is becoming a major global problem affects almost every person on this planet and till today nobody had found the cure. The concept of hypertension is basically wrong. It is like Coronary artery disease caused by errors in m-RNA expressed genes which becomes diseased, disturbed the metabolic pathways. This condition can be cured by reversing the disturbed metabolic pathways by changing the m-RNA expressed diseased genes. To do that, clinicians or scientists must have tools. I have carefully and closely observed that till now, no one has have any tool to reverse the metabolic pathways and to cure hypertension permanently. I have understood the basic mechanism of the biological derangement of metabolic pathways and its correction by using Baruah biological molecules which engineered these diseased genes. Baruah biological molecules isolated from edible medicinal plants are used as the tools to engineer the diseased genes, which are m-RNA expressed and gives permanent cure..

DIABETES MELLITUS-

It is a metabolic disorder known  to be incurable. It causes unimaginable and uncountable complications, keeps the patient unwell till premature death. Many drugs including human and porcine insulin are used without any success and recently, use of stem cell therapy has also not been successful. Transplant of porcine beta cells is one of the option in theory, but has not been come into practice so far. Type I and Type II diabetes are described for the purpose of treatment and to observe its progress.  However, the results become illusive as the actual cause of diabetes mellitus is not yet found. Our research work has suggested that m-RNA expressed diseased genes are involved, which can be engineered to cure this disease permanently. Baruah biological molecules isolated from edible medicinal plants are used successfully as tools to engineer this diseased genes and achieving permanent cure.  Over 800 patients are treated whose diseased genes are engineered and none of our patients have come back with recurrence. We identified the following variable abnormalities with our patients;-

              One group of patient is having insufficient synthesis of active insulin.    It is due to damage of beta cells at subcellular level due to low oxygen followed by partial occlusion of pancreatic arteries due to deposits of intracellular calcium.

    Second group of patients have sufficient or more than sufficient inactive insulin. Third group has sufficient active insulin, but inactive receptors. Type I and type II diabetes described here have not given any importance in our case as the treatment of both are same in case of genetical engineering.Both the cases are cured, once Baruah biological molecules have engineered the genes responsible for diabetes mellitus which are expressed under m-RNA.

   Thyroid dysfunction- It is an endocrine gland listed in book, but it should be included in cardio-vascular science as it plays a major role on cardio-vascular system. Thyroid dysfunction either hypo- or hyper (under or overactive) is known since many years. In both the conditions, cardio-vascular system is affected badly. In hypothyroidism, fluid retention is a common factor to be noted with hypertension. The clinician is treating this with thyroxine supplement for life.

        Hyperthyroidism-This is as bad as hypothyroidism. It directly acts on cardio-vascular and digestive system. Complete cure is yet to be found. Heart beat increases due to hyperthyroidism leading to cardiac dysfunction.

Both conditons are regulated by Central nervous system.While we are treating coronary artery patients with kidney failure by genetical engineering, we always find hypothyroidim is associated.  We found that damage of thyroid gland causing hypothyroidism is due to deposition of intracellular calcium like coronary arteries and m-RNA expressed diseased genes are responsible for this condition. Thyroid dysfunction is permanently cured when Baruah biological molecules are used to engineer the m-RNA expressed diseased genes. It was not thought in the past that thyroid dysfunction is a genetical problem.

       Polycystic kidneys- It is a genetical disorder due to mistake in DNA. As the DNA is involved, cyst can occur in any organ like liver, pancreas, heart and brain. We have experience in treating patients with polycystic kidneys involving liver, thyroid, brain and heart.  Hypertension is inherent complications of polycystic kidneys. We have reached to the stage where this condition is successfully treated with decoding of DNA by using Baruah biological molecules and stops further progress of damage permanently.  

(Part of the above literature is taken from an article “Misconception in cardio-vascular sciences” with prior permission from author Dr.D.R.Baruah, FRCSGlas. published in International Journal of Evolutions & Revolutions in Cardio-vascular sciences- vol II, September,2007 issue).

 

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