Original Article Changes in the isoprenoid pathway with transcendental meditation and Reiki healing practices in seizure disorder R. Kumar A, P. A. Kurup* Department of Neurology, Medical Collage Hospital, Tivandrur, Ker Trvancrum, Kerala, nda ‘A quantal perceptive model of brain function has been pos- tulated by several groups. Reikisike healing practices in sei- zure disorder (ILAE classification ~ II E — generalized sei ‘ures = tonie clonic), involving transfer of lfe force or low level of electromagnetic force (EMF) from the healer to the recipient patient, may act via quantal perceptive mecha: nisms. Increased synthesis of an endogenous membrane Na¥-Ks ATPase inhibitor digoxin and a related tyrosine / tryptophan transport defect has been demonstrated in re fractory seizure disorder (ILAE classification ~ II E ~ gener- ‘alized seizures ~ tonic clonic). Reiki-Ike healing practices in refractory epilepsy results in a reduction in seizure fre- ‘quency. Reikilike healing practices produce membrane stabilization and stimulation of membrane Na+-K+ ATPase ‘activity by quantal perception of low levels of EMF. The con- sequent intracellular hypermagnesemia inhibits HMG CoA reductase activity and digoxin synthesis resulting in the ale teration of the neutral amino acid transport (tryptophan /'ty- rosin) defect. A hypothalamic digoxin-mediated quantal perception model of brain function is proposed. The phe- nomena of biological transmutation and consequent ‘hypermagnesemia occurring in the resultant neuronal quantal state is also discussed. Key Words: Reiki healing practices, Transcendental me- diation, Seizure disorder, Isoprenoid, Na-K’ATPase, Dig- ‘xin, Quantal perception. Introduction _Aquuantal perception model for br funetion and conssious- al groups of workers. 7 is hypothesized to finetion as a quantum eomput rain Reiki- like healing practices involving transfer of life foree or low level of EMF from the healer to the patient have been in use in patients with seizure disorders. The Reikilike treatment ess has be oporsedl bye 3, India: and “Department of Biochemistry, University of Kerala, practices, if effective, are hypothesized to act via quantal per red hy nor ial sensory perceptive mechanisms, The present study was ception singe the EMF is too weak to be trans! conducted to asses the ef y of such treatment protocols is, The seize frequeney’ was used as the ‘end point to assess the effieney of the treatment, P reports have demonstrated! an endoxenous membrane Na’ K¢ ATPase inhibition-related biochemical easeade in primary generalized epilepsy cated! levels of an hypothalam ne Na*-IC" ATPase inhibitor digoxin hav {Lin epilepsy. Tt was considered pertinent to study rine Na*-K° ATPa n seizure patients unde tices. The resnlts ar hypothalamic digoxin-mediated quantal pereep brain fi ogenos me been report the changes isthe mem ule ing Reiki-like treatment prac diseassed in this paper and a ive model of Material and Methods Fifteen patients with refractory seizure disorder (ILAE HE ized seiares = tonie eloni tients.with persistent seizmres, on or more antiepileptic drass in full dosage, and total eompliance over a period of 3 years) were chosen for the study: They were chosen randomly from those attending the epilepsy clinic of the Department of Neu rologg, Medical College Hospital, Trivandrum. ‘They were in the age gronp of 20-30 ye 7 of them were f sification gener ) (pe +. Bight of the patients were ales, Patients with systemic diseases like hypertension, diabetes wells, eardine, renal and hepatic ves were excluded from the stndy. Thriee a week they ike healing hand therapy, where the healer reditates, rwaches at his life forwe or low level of EMP by the toueh of his hand to th underwent Reikt snee-like state and transfe patient, They also underwent daily one hour of transeenden: tal meditation, They were clinically assessed with seizure fr nl parameters were com queney counts at the end of 8 months of therapy. The pre post-therapy biochemical and ¢ Kuru Gov Sadan, TC. 4/1525, Noth of Cit House, Kats Road, Kowdar PO, Tvandrum-695008, Kerala, Ina. E-ml:kygnair@eatyam tin Neurology ina Api-une 2008 Vol St isu 2 mKumar AR, etal: A mecel for quantal perception pared inthe refra epilepsy gromp. An equal number of fage and sex matched I the pre-therapy refractory epilepsy group. The eontroly were thy subjects served as controls for chosen randomly from the general population of Trivandrum city. They wer patie and renal diseases. They apy for any disease. All patients and controls were on the same dietary rgimen which gave adequate amounts of trace elements, especially magnesium, throughout the coarse of the study. The following biochemical start of the therapy fre from systemie diseases like hypert ‘were not on any drug the parameters were assessed at the und at 3 months — plasma HMG CoA reductase, seram mn maynesium and RBC membrane Na*-K* ATPase activity. The serum levels of tyrosine, dopamine, adrenaline, tryptophan, serotonin and quinolinie aciel were also assessed. Fasting blood was taken from eae of the pa for various estimations. RBCs were separated within 1 hour of the collection of the blood for the estimation of brane Na*-K* ATPase, Serum was used for the estimation of HIMG CoA red ity: Plasma /serum was used for the estimation of the other parameters. All hiocherieals use in this stady were obtained from M/s Sigma Chemieals, USA. ‘The activity of HMG CoA reductase of the plasma was dete ad using the method of Rao and Ramakrishnan, by deter- ‘mining the ratio of HMG CoA to mevalonate.” For the deter- Imination of the Na*-K* ATPase activity of the erythrocyte membrane, the procedure deseribeal hy Wallach and Kamat was used, Digoxin in the plasma was determined by the HPLC procedure described by Arun et al? Magnesium in the plasma was estimated by atomie absorption spectrophotometry* Tryp- tophan was estimated by the method of Bloxam ancl Wi and tyrosine by the method of Wong et al! Serot estimated by the method of Curzon et al and eatecholamines by the method of Well-Malherbe et al’* Quinolinie acid eo tent of plasma was estimated by HPLC (C18 column micro BondaparkTM 4.6 x 150 mm), solvent system 0,01 M acetate butter (pET 3.0) and methanol (6:4), low rate 1,0 mV/mninnte and deteetion-UV 50 nm. Statistical analysis was done by the Students t’ test with modified degwe of freedom, Results activity of HMG CoA rwduetase and the mn of serum digoxin wore increased and RBC mem: brane Na*-K* ATPase activity and serum magnesia reduced. Post-therapy the activity of HMG CoA reduet the concentration of digoxin were reduced and RBC mem- brane Na*-K* ATPase activity and serum magnesium were yereased (Tube 1) Prectherapy’ th concentrat ‘The concentration of 1m tryptophan, quinolinie a eased in the plasina while that of tyrosine dopamine and noradrenaline was decreased in the pre-therapy group. Post-therapy the concentration of serum tryptophan, ‘quinolinie acid and serotonin was reduced in the plasma while that of tyrosine, dopamine and noradrenaline was ink (Tible 2), ‘The post-therapy seize frequency showed a significant eervase (Table Discussion ‘The results showed that plasma FIMG CoA reduetas tiv- ity and serum digoxin wore increased in seizure disorder (ILAE ication — ILE — generalized seizutes — toni elonie) Provions studies in this laboratory have de poration of 14¢ into digoxin in a rat brain indi that acetyl Cod is the precursor for digoxin bivsynt The elevated HMG Coa reductase activity correlates well with wated digoxin Jevels and redueid RBC membrane Na*-K? ATPase activity: The inerease in endogenous digoxin, a po: tent inhibitor of membrane Na*-K* ATPase, can deetease this, enzyme activity." ‘The inhibition of Na*-K* ATPase by di Table 1: Concentration of serum digoxin, magnesium and RBC membrane Na’-K* ATPase activity in refractory primary generalized epilepsy Groups HMG CoA reductase Digoxin ngidt Na-K: ATPase Magnesium mga Roductase ratio of ‘/p/mg protein) HMG CoA! mevalonate 4 Control 1.4520.12 12,8041.09 5.0440.201 2.403024 2 Epilepsy prohorapy 0. 884+0.075" 23.0561.76" 1.4840.139° 2.0840.117 3. Epilepsy post therapy _1.12+0.12" 44,041.07" 4.0240.132" 2.564022" {Mean of the values from 15 samples + SD. “plese than 0.07; Group 2 has Doan Compared with group 1, Group @ has been compared with group 2 ‘Table 2: Tyrosine and Tryptophan catabolic patterns in refractory primary generalized epilepsy Groups Tyrptophan (mg/dl) Tyrosine (mg/dl) SHT (ug/al) op (ng/d!) _Norepi (ng/al) QA (ngiat) 4.Contro! 1.4140.08 1:1440.08 209819 12894067 45.1812.95 _9370.60421.07 2.€pilepsy 1,960.09" 08834005 SO.5+46" 594053" 34181117 549.3441 21° 3.Epllepsy posttherapy 1.124007" 4.1140.08" 25817" 11.88,0.66" _44.1541.12" __390.62420.07° ‘Moon of he valves rom $8 samples + SD, ~ poss than 001; Group 2 has been compared wih Group 1, Group & has boon compared wih group 2, § HT Serotonin; DOP ~ Dopane; Norepl~ Norepnephing, GA ~ Quinoli ald 22 Neurology Inda Apri-June 2003 Vol St Ise 2“Table 3: Seizure frequency in refractory primary generalized ‘eplepsy pre and post-thorapy izure Frequency 2 Pretherapy — Post-therapy 1. Male 21 42 per month 2 per month 2. Malo 32 10/month—3/ month 3. Male 35 8/ month 3 month 4. Male 26: 42/ month 3/month 5. Male 28 9/ month 1 / month 5 Male 19 8/month ——1/ month 7 month 47 moni 8 12/month 2 / month 15/menth —3/month 42/ month 3/ month $1/month —3/ month $1/ month 4/ month 8/ month = 2/ month 14, Female 30 9/month ——_0/ month 48. Female 22 @/month 2 month werage seizure frequency 9 / month __2/ month Fess tan 0.0%, Group 2 was compared wih group 1 isin is known to cause an inerease im and a restnetion ular maumne' reported previously in the literature.” Seru finund to be reduced in seizure disorder (ILAE classit TL E — generalized seizures — toni ). Membrane Na K® ATPase inhibition ean produce dete nal depolarization shift tracellular caleiu n. This has been ive neuronal nd paroxy brane repobarizatc rvsalting in epileptagenesis." "There is an inerease in tryptophan and its reduction in tyrosine and its eatabolites in the patient's se- ‘rum, ‘This could be due to the fact that dgosin can regulate nent sansport system with preferential pro: motion of tryptophan transport aver tyrosine." ‘The deer in membrane Na*-K* ATPase activity in seizure disorder dL. ion ~ IL E ~ generalized svizures lonie) could also be dne to the faet that the hyperpolarizing snd nor dboites and classifi tonic nourotransmaittors (dopsan snaline) anv reduced and the depolar neurvactive compounds (serotonin. zal ‘quinoline neil) are inereased."* Quinolinie acid and serotonin being NMDA (N-Methy! D-Aspartate) agonist ea ute to NMDA eseitotoxicity reported in epilepsy. In the pres- m block on the NMDA otasicity. plasma membrane ghitamate transporter (on the surface of the glial cell and presynaptic neuron) is coupled to a Na* gra- dient whieh is disrupted by the inhibition of memb a K* ATPase, resulting in decreased clearance of glutamate by presynaptic and glial uptake at the end of sion." By these mechanisms, inhibition of neuronal Na'-K? ATPase can promote glu cewitotoxieity eontesbutin contrib: ce of hypomagnesemia, the magne receptor is removed leadin waptie transmis yen atorgie transtuission and leptogenesis ‘A quantal pereeption model of brain finetion has bee tulated by several groaps of workers." A low level of EMF er is. probably tr from the psferred to th tient hy quantal perception, The pereeived e recipient pa antal Neurology India Api-June 2008 Vol St Issue 2 Kumar AR, eta: A model for quantal perception ‘or subliminal perception could be the quanta of matter-de- pendent electric and maynetie fields, ‘The brain funetions as a quantum computer with the quantum compnter memory ele ments consisting, rerfervnee of superconducting, quantum deviees-the SQUIDS—which ean exist as superposition of macroscopic states." Bose condensation, the basis of super concluctivityis achievable at rom temperature in the Froblieh model in biological systems, Th and polar sphingolipids of the neuronal membran ss and ‘molecules dicleetrie protei nucleosomes which are a combination of basie histo nucleic acid, and cytoplasmic magnetite molecules are excel- lent electric dipole oscillators which exist under a steep ne ronal membrane voltage gradient. ‘The individual oscillators are energized with a eons ‘outside, hy dg nit sour of pumping enersy from in binding to membrane Na*-K* ATPase and produce & paroxysmal depolarization shift in the neuro snbrane. This prevents the dipole oseil tling into thermal equilibrium with the eytoplasm and inte stitial fluid whieh is always kept at constant temperature.! lators from ever set= are direct eo cortes ‘This results in a neuronal quantal state. The nections hetween the hypothalannas and the eereb and digoxin ma cortical ynapses. Bose condensed stat finetion as a modulator of the hypothalamo- produced by digos mediated dielectric protein moleenlar pumped phonon syste ‘ould be nsed to store information which might be encoded all within the lowest collective frequency mede-by appropri: ately adjusting the amplitudes of and phase rations between the dipole oscillators. The external world sensory impressions exist in the cortical dipole oseillators as probabilstie multiple superimposed patterns—the U phase of quantum mechanics. ‘The part of the incoming quantal data maps of th world bnilt by quantal pereeption in logical seq ollary to the pre-existing cortieal external world maps built by ‘conscious perception is chosen. Hypothalamo-corti tions modulated by digusin acting on the neuronal metnbs help to magnify the chosen map to 1 graviton criteria, ‘This model of quantal perception gives a mechanism for extrase sory or subliminal perception. Reiki-like healing practices ean transmit nr level of body MIF from the healer to the recipient al perveptive sn. Post-therapy, there was an inerease in RBC mem- bra KK* ATPase activity and serum magnesium reduction in HMG CoA rede thesis. Also, the level of tyrosine and its hyperpolarizing y qua rmieeha da se activity and digoxin sym catabolites was increased while that of tryptophan and its ‘depolarizing eatabolites was decreased, A low level of EMF can stabilize the neuronal membrane and increase neuronal ne Na*-K* ATPase activity: The stimulation of the membrane Na’-K* ATPase is known to eanse ade cecease in intracellular ealeium and an intracelhu Jar magnesium.” Magnesium excess is known to inhibit HM¢ CoA reductase activity.” This leads to redueed digoxin syn- thesis. Reduced levels of digaxin ean stimulate membrane Na PyKumar AR, eta: A model for quantal perception K+ ATPase activity further and increase intraneuronal mag: n to a greater extent. This starts off a easeade whieh membrane Na-K ATPase further and stabilizes saronall membrane, ‘The stinuulation of membrane Na K* ATPase ean promote neuronal membrane repolarization ‘and inhibit the generation of a parosysial depolarization shift and epileptogenesis. Digoxin is known to promote tryptophan transport over tyrosine.” Low levels of digoxin ean lead to:an Jevels and a deerease in seram tryp- rease in the levels of hyperpolatiz tophan. This leads to an in ws tyrosine eatabolites and a deerease in the levels of depo larizing tryptophan catabolites, which inhibits epileptoge ‘The inerwased levels of noradrenaline und dopamine have an antiepileptic aetion."" The inerease in serum magnesium also equate ghitamatergie transmission snd inib- is. The magnesium blocs ou the NMDA receptor is strengthened.” ‘The increase in serum magnesium in the post-therapy group ‘could also be due to the phenomenon of biological trans sum magnesium levels are inervased, suggesting an we in the total body magnesium rather than functional replacement of ealeium with magne W by several groups of workers. trie protein molecular tation has been postal Hypothalamic digoxin induced dis iped phonon system produces a quantal state within the neuron and in the cell membrane. In this quantal sta logical transmutation ean happen leading to 2 serum magnesium levels despite only adequate intake, ‘The effect of Reikislike treatment practices and transeen: ental meditation on seizure count and freq ss related to metubrane well us eal path AT e stimulation provides evidence regains quantal pereep= tion and brain funetion. It also provide lation of metabolic processes by quantally per els of EMF induced changes in nenronal trans phenomena of psychonetromlecular, biologie ‘mental low level of EMF mediated regulation of metabolic processes needs further study, widenee on the regu: eived,Jow lee nission, The Announcement References {Gonna Te Compo hae ATP eoent. Are Neat &. Rao AV Raksha 8, Keintion of FEM Cd rita mei. Cin Wal DP Kana VB. Mia age Nits 1 AmB Msi TA. Hesifeaton {enter dina ns by 1A al PLA te Bee Harp 10515. 1. Pre ¥Ed peel tli she ein: Now Yn Jn Wie Hann of (aia Neorg: RhieAnt 1%, Tak A, Raat 8, Taken X, Abs ele Wegener ttl aden Se ‘Accepted on 11.02.2002. ‘The journal office will be sending galley proofs to authors two to four weeks prior to final printing, All page proofs are returnable within 48 hours. 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