Dr. Jose Mackliff
Behind the development of BEAM was the immense love and scientific curiosity that one doctor had for his schizophrenia patients in a schizophrenic ward of a psychiatric hospital in Guayaquil, Ecuador. He was passionate about understanding the metabolism behind schizophrenia and to find a cure for the terrible disease schizophrenia. He watched his patients daily for 13 years, never improving and only growing more apathetic, stressed by additional chronic diseases with each year.
Dr. Joseph Mackliff’s was head of the San Jose ward of Lorenzo Ponce Psychiatric Hospital in Guayaquil, Ecuador. He could have felt disheartened by treating patients with schizophrenia; but instead he felt stimulated by the various metabolic and autonomic questions that arose about the disease. Mackliff’s research grew over 30 years culminating with the first BEAM surgery done on a human in 2006.
The BEAM surgery is a response to the constant discomfort felt by a psychiatrist when his patients who should be cured or their symptoms or alleviated at least, continue to express the same disease every day and the symptoms cannot be removed with a medicine that relieves their condition only mildly.
Scientific investigation is a methodical and patient effort where careful notes are taken, results documented and evaluated from each study done. This is commendable under ideal circumstances, but Dr. Mackliff’s studies were entirely self-funded and most of his work was done by himself, and later with his colleague Dr. Sanchez, when surgeries began to be done first on dogs and later on patients.
The first question about the metabolism of schizophrenia occurred to him while visiting Mont Sinai Medical Center in Miami where research employing PET and dioxiglucosa 18 fluoride was used to determine the cerebral consumption of glucose and oxygen in normal patients. He was surprised that glucose and oxygen were not consumed proportionately throughout the brain, but were consumed more in the visual cortex and gray matter.
Stimulated by this knowledge, he wondered what would happen in schizophrenics who maintain a metabolic disorder of gluco–regulation, if he increased the blood glucose levels with hypertonic glucose 30% and thereby produced a temporary hyperglycemia, indirectly promoting cerebral circulation and nutrition of neurons.
This research took a different turn when Mackliff sought an answer to the big question, why schizophrenics are improved with hypertonic glucose? This study provided him with sufficient information to conclude that hyperglycemia was caused by more than 8 hours of inhibiting the release of gluco-regulation hormones including adrenaline. This factor deserved critical attention. And from this moment a value judgment came:
“To resolve (Hypothalamus-Pituitary-Thyroid-Adrenal (HPTA) axis fatigue) is a scientific priority closely related to schizophrenia treatment.”
This scientific finding was based on a scientific truth proclaimed by several researchers such as Hosking, Dide Girard, Korenyi and Lowenstein, Tomard and Newman, Von Meduna, Subramanian etc. They concluded: “In schizophrenia there is a pituitary failure.” which causes a post prandial hypoglycemia, and a HPTA axis fatigue. This fact constituted for Mackliff the main stimulus for further research.
The meritorious work of Arvid Carlsson, Nobel Prize winner 2000, captivated Mackliff, especially with regard to dopamine and schizophrenia, and dopamine and Parkinson which allowed him to work with cell interaction and cytology from the molecular point of view
Considering that the adrenal medulla produces 100% epinephrine, 20% norepinephrine and a small amount of dopamine, Mackliff determined that it should be possible to eliminate adrenaline and reduce the overload of the hypothalamic, pituitary, thyroid, adrenal axis.
Removing epinephrine surgically was a challenge as well as a risk. He did not begin directly on humans and made this intervention in previously drug-induced psychosis in dogs treated with amphetamine. The only way of supporting the HPA axis was by eliminating the source of epinephrine (adrenal medulla), without altering the function of the adrenal cortex.