Why not a cure for Schizophrenia?

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Dr. Joseph Hildalgo Mackliff, discoverer of B.E.A.M procedure

Why is it so hard to believe that through pure dedication and excellent scientific knowledge, credentials and experience, a doctor could find a way to improve the symptoms and the cause of the disease schizophrenia itself?

There was no million dollar funding from pharmaceutical companies funding his research and defining the parameters of the research; there was only a doctor, an intent motivated by compassion and interest and his relationship with God.

Dr. Jose Mackliff said, “It is only with the help of God and my desire to ease the suffering of my patients that allowed B.E.A.M to be discovered.

As a psychiatrist I can say that these comparisons with the way the patients were after surgery, never occurred before with other patients treated in the hospital setting. The changes that can be observed after B.E.A.M are the cause for great happiness for the patient, the doctor and the family on the road to recovery.”

History of Dr. Mackliff’s Research

When I started my research with the study of the curves of blood glucose before, during and after meals in chronic schizophrenic patients, I clearly saw that the rates of glucose fell markedly after meals, and lowered the glucose levels by the insulin action that apparently did not cause the release of hormones of gluco-regulation.

By finding that blood glucose levels dropped only with meals and without a regulatory response, it was possible to establish what would happen with hormones against regulation after causing hyperglycemia using a liter of hypertonic glucose 30% (300 g) of glucose intravenously in one hour. The result was that blood sugar levels rose and the insulin response strengthened. This was followed by two or three hours of hypoglycemia. We noted that schizophrenic patients improved their symptoms the next day after administration of 300 g glucose to 30% to 90 drops per minute. This result encouraged me to increase blood glucose levels more which elevated blood glucose levels to 700 and 800g of glucose, thereby improving schizophrenic symptoms.

While higher hyperglycemia improved mental illness by decreasing positive and negative symptoms, with sustained hyperglycemia, the output of insulin was stimulated and at the end of the administration was forcefully released, causing hypoglycemia for two or three hours that was as low as 40 to 35 mg/dl. All this was a normal hormonal reaction which corresponded to an immediate and powerful output of insulin, after raising blood glucose in non-diabetic schizophrenic patients.

This caused a constant question in my research. Why does the hyperglycemia improve the patients? If they have constant post prandial hypoglycemia while they are seriously deluded seemed logical; but it did not seem scientific that hyperglycemia should improve the patients.

Gluco-regulation is the notorious delay of epinephrine, glucagon and cortisol release (axis fatigue) which causes a Hypothalamus Thyroid Adrenal (HTA) axis failure that must be resolved. When we were sure how to solve HTA axis fatigue, we implemented a solution that offered many possibilities for improving the alteration of HTA Axis and diseases associated with it.

Research Notes:

If the HTA Axis delays the timely release of the three hormones of gluco-regulation (glucagon-cortisol-epinephrine), the axis fatigue could be resolved by eliminating one of them. For anatomical, physiological, and biochemical reasons, we decided that the hormone epinephrine or adrenaline could be eliminated and not affect the body.

This simple thought had a powerful biochemical basis without needing technical tests. It created a surgical discovery which focused on the destruction of the medullary tissue of the adrenal glands. Then we could do endocrinological and biochemical research on the damaging action of stress and its inhibitory and destructive effect of nor-adrenaline on AC (adenylate cyclase). This knowledge came from the contribution of specialists in biochemistry from the University of New Jersey (Bennun H. , 2012).

Then the surgical interventions in previously drug induced psychosis in dogs with amphetamines, and later in humans diagnosed with schizophrenia were done with spectacular results in schizophrenia and Parkinson’s, allowing us unequivocally to conclude that at the brain level, the hypothalamus managed brain dopamine regulation and other neurotransmitters.

Several investigators had described the failure of the axis (hypothalamic-thyroid-adrenal) in schizophrenia (1960-2000), but they had not resolved it. We knew this after performing the investigation and strengthening the theory.

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