Blog Arasys Perfector - Xanya Sofra Weiss

G. Lally , R. L. M. Faull , H. J. Waldvogel , S. FerrarP, and P. C. Emson; 1997

Calbindin D28 K is a neuronal calcium binding protein which may

act as a buffer of neuronal calcium. Evidence suggests that disturbance of calcium homeostasis is important in neurodegeneration, possibly via changes in calbindin D28K. Immunoreactivity of calbindin D28 N is compared in Alzheimer’s disease and age-matched controls. The size and number of calbindin D28 K positive neurons in Alzheimer’s disease tissue is reduced. There is also shrinkage of the dendritic tree. Continuing work examines the function of calbindin D28 K using transgenic mice. (J Neural Transm 104:1107-1112)

CHRISTINE PETERSON, RATIV RATAN, MICHAEL SHELANSKI, JAMES GOLDMAN; 2006

Several observations indirectly suggest that intracellular calcium regulation may be altered by aging and Alzheimer’s disease. Thus, calcium homeostasis was examined directly in skin fibroblasts from Alzheimer’s patients and compared to cells from normal young and elderly controls. Alterations in both bound and free calcium were noted;

cells from Alzheimer’s donors have higher levels of bound calcium but lower concentrations of free intracellular calcium when compared to cells from young and normal aged donors. These changes in calcium homeostasis may be physiologically significant, since processes that require transient elevations of intracellular free calcium, such as cell spreading, decline in the Alzheimer’s cells. In summary, cultured skin fibroblasts from normal aged and Alzheimer’s patients demonstrate deficits in calcium homeostasis and other metabolic processes when compared to cells from young donors.

C.E. Gagna, H.-R. Kuo, E. Florea, W. Shami, R. Taormina, N. Vaswani, M. Gupta, R.Vijh, and W.C. Lambert; 2001

Apoptosis is the ordered chain of events that lead to cell destruction. Terminal differentiation (denucleation) is the process in which cells lose their nuclei but remain functional. Our group examined cell death in three tissues using two different fixatives and a postfixation procedure, involving young (5 months) and old (2 years) guinea pigs. The data reveal that B-DNA and Z-DNA content decreases, whereas single-stranded (ss-) DNA increases, in older tissues undergoing apoptosis (skin and cornea) and terminal differentiation (ocular lens). We speculate that some of the factors that contribute to the aging process might also be responsible for the enhanced amount of damaged DNA in older tissues undergoing cell death. (J Histochem 49:929–930, 2001)

Atul Tiwari, Vinay Bansal, Anita Chugh & Kasim Mookhtiar; 2006

Hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors represent the most successful class of drugs for the treatment of hypercholesterolaemia and dyslipidaemia implicated in the pathogenesis of coronary heart disease and atherosclerosis. However, the popular profile of statins in terms of efficacy has been maligned by its adverse events. The myotoxicity, ranging from mild myopathy to serious rhabdomyolysis, associated with HMG-CoA reductase inhibitors, during treatment of hypercholesterolaemia is of paramount importance. Rhabdomyolysis is a rare but idiosyncratic muscle wasting disorder of different etiologies. Statinassociated habdomyolysis causes skeletal muscle injury by self-perpetuating events leading to fatal irreversible renal damage through a series of biochemical reactions. Preferential distribution and action of statins in liver could be the key to minimise myotoxicity concerns. Hepato-specific distribution of statins is governed by various factors such as physicochemical properties, pharmacokinetic properties and selective transporter-mediated uptake in liver rather in extrahepatic cells. The interactions of statins with concomitant drugs of different classes merit attention for their safety profile. Although pharmacokinetic as well as pharmacodynamic interactions have been implicated in pathophysiology of statin-induced muscle wasting, the underlying mechanism is not clearly understood. Besides, pharmacokinetic and phramcodynamic factors, statin-associated myotoxcity may also implicate pharmacogenomic factors. The pharmacogenomics characterised by CYP polymorphism and other genetic factors is responsible for inter-individual variations to efficacy and tolerability of statins. The pathophysiological mechanisms may include statininduced differences in cholesterol:phospholipid ratio, isoprenoid levels, small GTP binding proteins and apoptosis. However, the present understanding of pathophysiological mechanisms, does not offer a reliable approach to address the same at preclinical level. Although statin-associated myotoxicity affects compliance, quality of life of patient and discontinuation rate, yet the low incidence of myotoxicty including rhabdomyolysis and less severity of commonly occurring myopathy and myalgia do not raise doubts about the clinical efficacy and tolerability of statins. Medical management of myotoxicity seems to be pivotal for the proper compliance of patients with statin treatment. The appropriate and judicious use of drugs would substantially reduce the likelihood of developing clinically important myopathy.

Objective: Statins (3-hydroxymethylglutaryl-coenzyme A reductase inhibitor) are widely used to treat hypercholesterolemia. They are generally well tolerated, but myotoxic effects have been reported and the corresponding mechanisms are still a matter of debate. The aim of the present study was to determine whether impairment of calcium homeostasis and/or mitochondrial impairment could account for the adverse effects of statins in skeletal muscle.

Methods: Eleven patients with increased creatine kinase levels and myalgias after statin treatment were evaluated using in vitro contracture tests (IVCTs), histology, and 31P magnetic resonance spectroscopy (31P-MRS).

Results: IVCT results were abnormal in 7 of the 9 patients, indicating an impaired calcium homeostasis. The 31P-MRS investigation disclosed no anomaly at rest, and the aerobic function assessed during the postexercise recovery period was normal. On the contrary, the pH recovery kinetics was significantly slowed down as indicated by a reduced proton efflux, which could be ultimately linked to a failure of calcium homeostasis. Overall, our observations indicate a normal mitochondrial function and raise the possibility that statins may unmask a latent pathology involving an impairment of calcium homeostasis such as malignant hyperthermia (MH).

Conclusion:

In case of susceptibility to MH, statins treatment must be administered with caution, and signs of adverse effects should be checked.

STUART A. LIFTON

Our laboratory has a long-standing interest in the relationship of neuronal viability and outgrowth to intracellular Ca2+ levels (reviewed in ref. 1). Glutamate, or a related excitatory amino acid (EAA), is the major excitatory neurotransmitter that controls the level of intracellular neuronal Ca”Our laboratory has a long-standing interest in the relationship of neuronal viability and outgrowth to intracellular Ca2+ levels (reviewed in ref. 1). Glutamate, or a related excitatory amino acid (EAA), is the major excitatory neurotransmitter that controls the level of intracellular neuronal Ca2+([Ca2+]i). Escalating concentrations of glutamate have been measured in vivo following focal stroke and head injury (reviewed in refs. 2 and 3). As a result, there is a rapid rise in [Ca2+]i CaZtli may not account by itself for the ensuing neuronal injury, several laboratories have now reported that prevention of the increase in [Ca2+]i Jlie ads to amelioration of anticipated neuronal cell death (reviewed in refs. 2 and 3). Excessive intracellular Ca2+ is thought to contribute to the triggering of a series of potentially neurotoxic events leading to cellular necrosis orperhaps apoptosis. Many mechanisms are involved in intracellular calcium homeostasis, and this subject is beyond the scope of this article (but see the review in ref. 4).Here we will consider only two modes of Caz+ entry into neurons during these pathological processes. These two routes of entry of Ca2+o ccur via ion channels that are permeable to Ca2+ and can be summarized as follows: (1) Glutamate or related EAAs trigger voltage-dependent calcium channels by depolarizing the cell membrane; a major voltage-dependent calcium channel subtype that is chronically activated by prolonged depolarizations is the L-type calcium channel (reviewed in ref. 5). (2) Glutamate or related EAAs activate ligand-gated ion channels directly; a predominant glutamate receptor-operated channel that is permeable to Ca2+ under these conditions is the Nmethyl-D-aspartate (NMDA) subtype, but other non-NMDA types may also contribute (reviewed in refs. 2 and 6). We have shown that activation of these channel types can control neuronal plasticity during normal development, but our laboratory and many others have shown that in excessive amounts this stimulation can lead to neuronal death, for example, after a stroke (reviewed in ref. 1). Similar mechanisms may obtain in various neurodegenerative conditions. In fact, although not involved in the primary pathophysiology of a neurologic disorder, this mechanism may represent a final common pathway of neuronal injury. Most importantly, this pathway makes the disease process amenable to pharmacotherapy. This line of reasoning led us to think that this mechanism might be involved in acquired immunodeficiency syndrome (AIDS)-related neuronal injury.

Colloids are held in suspension via a very slight negative electrical charge on the surface of each particle. Like charges repel each other. This charge is called zeta potential. Blood is a colloidal solution, and all blood cells have a slight negative charge.

Zeta potential is a measure of the electrical force that exists between atoms, molecules, particles, and cells ina fluid. Zeta potential’s strength determines the amount of material (nutrients, wastes) that fluids such as your blood and lymph can carry. Increasing the electrical force in the solution allows the fluid to dissolve and hold more material. In this way, more nutrients can be carried throughout your body and accumulated deposits of waste can be removed. When the zeta potential is too low, blood begins to coagulate. This is a condition known as intravascular coagulation. Blood becomes a sludge that is increasingly difficult for the heart to pump, and decreasingly effective at performing the usual functions of blood. “Blood sludge” is widespread in the population (more than half the population will die from heart problems). Intravascular coagulation is clearly visible in the blood vessels of the eye when viewed under relatively low level (60x) magnification. Blood is in constant motion at constant temperature and the pH of blood is fixed at 7.35 to 7.4, but its concentration of electrolytes is not fixed, and the electrolytes directly affect the zeta potential. “So long as the Zeta Potential (ZP) of the system remains constant, the fluidity (viscosity) of the system will also remain constant. But if the ZP of the system is progressively lowered by the introduction of cationic electrolytes or polyelectrolytes, then the stability of the system will undergo progressive changes — from simple agglomeration to fluid gel formation — and finally to a rigid gel.”- Thomas M. Riddick.

One lab found that best results in reducing intravascular coagulation were obtained by drinking 8 glasses per day of water with a mix of potassium citrate and potassium bicarbonate added sufficient to raise the pH of the water to 8.0 to 8.4. The minerals MUST be taken with the water in order to be effective, because intravascular coagulation is also related to insufficient water intake. Potassium works better than sodium to reduce intravascular coagulation, in fact too much sodium in the diet is part of the problem. The lab recommends that everyone replace table salt with a mixture of 60% potassium chloride and 40% sodium chloride to better reflect the potassium/sodium balance found in foods. Forty to fifty percent of the people examined by this lab had significant blood coagulation. To increase your zeta potential you must avoid aluminum. Aluminum is used in water treatment plants to cause materials to settle out of solution. It does this by reducing the zeta potential. In your body aluminum does the same thing, causing coagulation of your blood, and deposits and plaques in your arteries, brain and throughout your body. Aluminum is found in municipally treated water, cooking utensils, vaccinations, non-clumping salt and baking powder, antiperspirants, antacids, drugs (read the label carefully), soft drinks and other canned goods where the plastic liner has cracked during sealing, and in other unexpected places. Consumption of alcohol produces intravascular coagulation. Editor’s note: Alcohol also hardens the brain.The brain is a jelly, like raw egg white. To study the brain under a microscope, scientists must harden it and then they can slice it, stain it and view the slices. To harden the brain they use alcohol. As we saw in the quote from Thomas M. Riddick above, a rigid gel results from loss of zeta potential. Physicians use EDTA chelation therapy to increase zeta potential and remove toxic heavy metals from the body. The increased zeta potential allows toxic deposits in the body to re-enter solution so that they can be removed by the kidneys, liver, and in the sweat, etc. A study in Switzerland found that people who had chelation therapy to remove lead from their body also had less cancer in later years.

Xanya Sofra-Weiss, Ph.D & and Stephen Holt, MD, PhD, DSc, LLD(Hon.) DNM, ChB, FRCP (C), MRCP (UK), FACP, FACG, FACN, FACAM, KSJ, Distinguished Professor of Medicine (Emerite)

IM Ion Bio-Resonance was engineered to treat sports injury and muscle atrophy, as well as promote lipolysis and muscle hypertrophy. A clinical study with individuals presenting abnormally clumped RBCs was completed in February 2009 (Weiss et al, 2009) indicated that this technology rapidly and efficiently leads to normalized erythrocytes’ separation at the microscopic level. Red Blood Cells’ (RBCs) separation is crucial for the timely transport of hormones, antibodies, oxygen and nutrients to the cells and waste products to the kidneys. Therefore, RBCs separation plays a key role biological processes involving cellular cleansing, nourishment oxygenation, endocrine and immune functioning. This technology that was initially based on research associated with the Pacemaker is now coming full circle by offering benefits that can be potentially used in Medicine to reduce the incidence or progression of cardiac disorders resulting from erythrocyte aggregation. Enhanced oxygen transport may enhance ATP production in the mitochondria which can be also increased by the electron transport chain probing the proton motive force spin the ATPase module clockwise, the key mechanism producing ATP The dynamic, multi-sine, analogue waveform of the device (IM) used in the study was originally tested at the cellular level by Dr. Donald Gilbert (1992), a molecular biologist, and was electronically composed by the Co-Inventor of the first Pacemaker (2008) to resonate the motor nerve’s signal of strenuous exercise normally emitted by the brain. Due to its resonance with the biological signal, IM’s signal spreads throughout the CNS ultimately triggering endogenous hormonal secretion such as Growth Hormone (GF), Thyroxine (T4) and Triiodothyronine (T3) for lipolysis and Insulin Growth Factor (IGF-1) for muscle hypertrophy. Power detox is an additional benefit induced by the effortless and painless isometric and isotonic muscle contractions. Enhanced endogenous hormonal secretion and optimum hormonal transport to sites of action can significantly contribute to anti-aging Medicine specializing in Hormone Therapy. Overall, aging is intricately connected to insufficient biological microelectricity represented by: a) impaired calcium homeostasis affecting ion channels; b) mitochondrial impairment leading to energy shortage; c) oxidative stress, as a result of free radicals which are stable molecules missing one of their electrons; d) calcium homeostasis. By virtue of being in sync with neuronal inputs, IM bio-resonant signal can spread into the CNS to enhance oxygen transport and ATP production in the mitochondria, via the electron transport chain. It can donate electrons to the electron seeking free radicals hence turning them into stable molecules to reduce oxidative damage. Reduced oxidative stress may re-establish calcium homeostasis, a process crucial to stabilization of ion channels that has also been directly connected with aging (Squil et al, 2008). The electron influx can be used by DNA to deflect oxidative damage from itself thus safeguarding against a number of diseases and ensuring adequate protein synthesis thus enhancing cellular intelligence, as proteins represent the intelligence of the cell. The major antioxidant functions provided by electrons can be amplified by the use of REDOX balanced antioxidant nutrients. The synergistic value of REDOX balanced antioxidant administration with combined ion magnum therapy is a novel approach to counter oxidative stress which is the principal and most tenable theory behind premature aging. Cellular function can be enhanced by elimination of toxins from the body and convenient therapeutic approaches include the use of natural chelating agents and herbal or botanical combinations that assist in body cleansing. Optimum cellular structure involves the maintenance of cell membrane phospholipids, which are supported by supplementation with omega 3 fatty acids, in current circumstances where there is a relative or absolute deficiency of these essential fatty acids in many western diets. Ion magnum therapy has become popular among sports medicine professionals and it is highly valued in medical spas that offer treatments to individuals with excessive visceral fat. While the mechanism of adipose tissue reduction with electricity remains poorly understood, there is an additive benefit of using natural compounds that may enhance the oxidation of fat and act against insulin resistance, e.g. fucoxanthin, green tea polyphenols, EPA and chlorogenic acid. Recent research has identified the value of fucoxanthins, which are ubiquitous in brown algae (seaweed). The anti-aging benefits of seaweed have been “touted” for years and highlighted in recent scientific studies. Japanese researchers have shown in studies1 that the fucoxanthin components of Undaria spp. (Wakame seaweed) may cause up to a 10% weight loss in experimental animals by direct effects on shrinking abdominal fat stores. Fucoxanthin appears to stimulate proteins (Uncoupling protein-1) that cause the oxidation of fat and its conversion to energy or heat (thermogenesis). Uncoupling protein-1 (UCP-1) appears to be present in white adipose tissue (belly fat) and it acts on mitochondria in a direct manner that promotes the oxidation of free fatty acids thereby reducing fat tissue stores. The preponderance of white fat in abdominal fat stores leads to the inference that this upregulating activity of UCP-1 may be valuable in reducing the size of a “pot belly.” Pot bellies are a hallmark physical sign of insulin resistance and Syndrome X. In summary, there are several exciting and novel approaches with the use of nutraceuticals to enhance the biological effects of IM bio-resonance that can be used in a number of medical and anti-agin settings.

Roger M. Macklis; 1993

Although the biological effects of low-frequency electromagnetic radiation have been studied since the time of Paracelsus, there is still no consensus on whether these effects are physiologically significant. The recent discovery of deposits of magnetite within the human brain as well as recent, highly publicized tort litigation charging adverse effects after exposure to magnetic fields has rekindled the debate. New data suggest that electromagnetic radiation generated from power lines may lead to physiologic effects with potentially dangerous results. Whether these effects are important enough to produce major epidemiologic consequences remains to be established. The assumption of quackery that has attended this subject since the time of Mesmer’s original “animal magnetism” investigations continues to hamper efforts to compile a reliable data base on the health effects of electromagnetic fields. In January 1992, lawyers for a 21-year-old Connecticut woman who had a malignant brain tumor filed the first widely recognized and authoritatively researched U.S. lawsuit charging that the tumor was the direct result of the patient’s protracted exposure to the electromagnetic field (EMF) generated in a nearby power line. This case and other similar tort cases are being based in part on new suggestive evidence for adverse EMF bioeffects. Well-known investigators in the field have recently published position papers on both sides of the EMF bioeffects problem. Both sides apparently agree that the debate has been hampered by the lack of a biochemical transduction mechanism capable of explaining how low-energy magnetic fields interact with human tissue. If confirmed, the recent discovery by Kirschvink and colleagues of substantial deposits of elemental magnetite in human brain tissue may finally provide a mechanistic framework within which to analyze the epidemiologic and toxicologic data concerning EMF bioeffects. However, the sensational media coverage accorded the neural magnetite discovery and the instant skepticism and partisan hostility engendered by the magnetite announcement reflect the fact that the EMF bioeffects problem continues to be surrounded by an aura of pseudoscience, quackery, and disrepute. This article traces the history of biomagnetism and magnetic healing, concentrating on the charlatanism and quackery that have plagued the field for centuries and that may now be limiting legitimate scientific investigation by placing the field off-limits to respectable medical investigators.

Hiroshi Shimoda, Emi Seki, and Michio Aitani; 2006

An epidemiological study conducted in Italy indicated that coffee has the greatest antioxidant capacity among the commonly consumed beverages. Green coffee bean is rich in chlorogenic acid and its related compounds. The effect of green coffee bean extract (GCBE) on fat accumulation and body weight in mice was assessed with the objective of investigating the effect of GCBE on mild obesity.
Methods: Male ddy mice were fed a standard diet containing GCBE and its principal constituents, namely, caffeine and chlorogenic acid, for 14 days. Further, hepatic triglyceride (TG) level was also investigated after consecutive administration (13 days) of GCBE and its constituents. To examine the effect of GCBE and its constituents on fat absorption, serum TG changes were evaluated in olive oil-loaded mice. In addition, to investigate the effect on hepatic TG metabolism, carnitine palmitoyltransferase (CPT) activity in mice was evaluated after consecutive ingestion (6 days) of GCBE and its constituents (caffeine, chlorogenic acid, neochlorogenic acid and feruloylquinic acid mixture) Results: It was found that 0.5% and 1% GCBE reduced visceral fat content and body weight. Caffeine and chlorogenic acid showed a tendency to reduce visceral fat and body weight. Oral administration of GCBE (100 and 200 mg/kg· day) for 13 days showed a tendency to reduce hepatic TG in mice. In the same model, chlorogenic acid (60 mg/kg· day) reduced hepatic TG level. In mice loaded with olive oil (5 mL/kg), GCBE (200 and 400 mg/kg) and caffeine (20 and 40 mg/kg) reduced serum TG level. GCBE (1%), neochlorogenic acid (0.028% and 0.055%) and feruloylquinic acid mixture (0.081%) significantly enhanced hepatic CPT activity in mice. However, neither caffeine nor chlorogenic acid alone was found to enhance CPT activity.
Conclusion: These results suggest that GCBE is possibly effective against weight gain and fat accumulation by inhibition of fat absorption and activation of fat metabolism in the liver. Caffeine was found to be a suppressor of fat absorption, while chlorogenic acid was found to be partially involved in the suppressive effect of GCBE that resulted in the reduction of hepatic TG level. Phenolic compounds such as neochlorogenic acid and feruloylquinic acid mixture, except chlorogenic acid, can enhance hepatic CPT activity.