Protect Your Family From Toxic Products and Medications
COPPER OVERLOAD ( Cubound ↑↑ ) – THE WESTERN METABOLIC BOMB
” If we are going to discover nature’s form, it is probably imperative to drive as hard as possible at the critical points of mystery.” Henry P. STAPP ( 1989 )
” The EPSICO model ( EPS = Excessive Prolonged Stress ) centered on the ICO = Intracellular Copper Overload = the indisputable Generator of all chronic diseases; connecting the emotional and physiological realms, it could become the biochemical core of the New American Medicine. “
Modern ( conventional ) medicine is very proficient at handling acute care, mainly due to the advanced technology and to the drastically simplified picture of most emergency ( crisis ) situations. However, in the field of chronic disorders, things are very different; despite some local successes, it became clearly that modern medicine experiences serious difficulties when approaching the etiology of chronic diseases. This chronic counter-performance could be explained by ignoring or superficially approaching the essential connection between stress, individual mineral status ( especially the intracellular copper overload – Cu↑) and, correlatively, copper interference toxicity – CIT, a chronic form of mineral toxicity that plays a unique role in the etiology of all chronic diseases – infectious, inflammatory and degenerative.
The main conclusion of this study ( EPSICO model ) is that the true generator of the epidemic of chronic diseases is not the genes, nor the germs, and nor the chronic / silent / hidden inflammation – all these are no more than some important modulators – but the intracellular copper overload – the master metabolic imbalance of the contemporary Western society.
By reading carefully this unusual paper ( refused shortly by a notorious mainstream medical journal ) you’ll understand – as specialists or laymen -some of the ” biggest mysteries ” of the contemporary medicine ( I’ve stubbornly studied them for decades in Brasov and Evanston ). For instance :
– the definitely lack of progress in understanding / preventing / treating of cancer(s) : Copper overload ( neglected by the most cancer experts ) incredibly increases the apoptotic resistance ( biological stability ) of cancerous cells , concomitantly diminishing the vitality of the healthy cells; I think it’s a very… promising starting point for a decisive / generalized application of …chemotherapy, don’t you ?);
– Cu ↑ constitutes the shortest way towards a …firm, inescapable obesity ( via : Cu ↑ → Cr ↓, etc. ); what the numbers say: 66% of Americans are copper dominant / chromium defficient, while 65 % are overweight. A mere coincidence ?
– Dehydration problem can’t be solved simply by drinking 8 ( or more ) water cups / daily because, due to the same copper overload ,the cells are / remain deficient in : choline, sodium, aldosterone ( all being …reputed copper antagonists! );
– Frequent accidents of the first class sportsmen / women are due mainly to a ligamentous laxity , caused by the chronic deficiency of Manganese: Cu ↑ → Mn ↓, correlatively, their poor healing of ( chronic ) wounds being due to : Cu ↑ → Hyaluronic acid ↓ ;
Abbreviations: EPS = excessive, prolonged stress; CIT = copper interference toxicity;
EPS/ICO = excessive, prolonged stress / intracellular copper overload.
MT = metallothionein or stress protein; Cuf ↓= functional copper deficiency, produced by intracellular copper overload ( Cu↔ MT)↑, according to the scheme:
EPS→ Cortisol↑ → MT↑ →(Cu↔MT)↑ → Cuf↓
Attention: All information on this site is for general education purposes only. Because everybody is different , you have to contact your doctor to establish the best treatment / protocol for your specific condition.
1. The most important sources of chronicity
Chronicity is a multifactorial process, the three most important factors being:
1.1 Progressive demineralization of the soil – uncompensated exhaustion of some essential minerals and notorious copper antagonists, such as: chromium ( Cr ), zinc ( Zn ), manganese ( Mn )…
1.2 EPS → Cu↑ → Cr↓, Zn↓, Mn↓
2 out of 3 Americans are copper dominant. The tendency to absorb /retain too much copper is typical for Western societies, currently under a debilitating stress; in normal stress conditions, the copper absorption / retention is about 30 % from the daily intake, while EPS raises this parameter to 80 %.
1.3 Industrial refining of food ( grains / carbohydrates, oils, salt ); for instance, obtaining white flour from whole wheat leads to 92 % loss of the initial content ( already diminished, see 1.1 ) of Cr, Zn, Mn.
2. C I T ( copper interference toxicity ) – a metabolic downward spiral
EPS →(Cu ↔MT)↑ = CIT → Downregulation of antagonists & upregulation of agonists → Hypoadrenalism / Hypothyroidism / Immune System Malfunction → CHRONIC DISEASES ( infectious: Cu↑↓; degenerative: Cu↔MT↑; inflammatory: Cuf↓ )
Intracellular copper overload determines the intracellular, stable depletion of copper antagonists, with serious implications in distortion of mineral and general metabolism:
(Cu↔MT)↑ → Cr↓, Zn↓, Mn↓, S↓( sulfur ), Se↓(selenium ),Vitamin C complex↓, vitamin A ↓, Complex B ↓
Copper overload causes also a stable over- retention ( excess) of its synergists, especially calcium: (Cu↔MT)↑ → Ca↑ ( calcium ), ( Mg↑↓ ). Magnesium , though a copper antagonist, has a special/ better place being a calcium, zinc and chromium agonist. The particular importance of this overlooked chronic toxicity ( CIT ) is that no management of chronic problems ( symptoms, syndromes, diseases ) could be optimal once the intracellular copper overload is present. Only by bringing and maintaining the copper level within the physiological range – accomplished by synergistic procedures – all chronic conditions could be efficiently controlled, from joint laxity and low back pain to diabetes complications, cancers and beyond.
3. Copper Overload = Inefficient Metabolic Regulation
Chromium depletion: ( Cu↔MT)↑ → Cr↓
Chromium depletion constitutes a basic factor of human overweight: 66 % of the Americans are copper dominant / chromium deficient, while 65 % are overweight. Why is the chromium deficiency so massive and so difficult to control in our Western societies ? Here is my answer:
Copper ( Cu ) ↑ → Cr ↓
Sugar ↑ → Cr ↓
Calcium ( Ca ) ↑ → Cr ↓
Potassium ( K )↑ → Cr ↓
Iron ( Fe ) ↑ → Cr ↓
Cr↓ is the major contributor to the so called “ mineral resonances “ which explain why the chronic diseases are sometimes closely related:
Insulin resistance, underactive adrenals: Cr↓
Diabetes: Cr↓, Zn↓, Mg↓, Mn↓
Obesity: Cr↓, Zn↓, Mg↓, Ca↑.
Any regular treatment of these conditions can’t provide optimal and lasting results as long as the ratio Cr↓/ Cu↑ is not normalized.
Zinc depletion: (Cu↔MT)↑ → Zn↓
Sexual dysfunction of the Western population is centered on Zn deficiency. Zinc is still under-evaluated in all Western societies. For instance, people recognize that our soil is low in zinc, our diet is zinc deficient and our life is high in stress ( EPS →( Cu↔MT )↑ → Zn↓ ), however, the same people renovate their houses, replacing the galvanized (zinc) pipes with copper pipes ( leading to about 1.0 mg Cu ↑ /day / person ). It is metabolically counter-indicated to prescribe zinc ( Zn→ MT ↑ → (Cu↔MT)↑ ) to increase the sex drive if EPS / CIT is present since, this way, the estrogenization is amplified ( copper parallels estrogen: Cu↑→ Zn↓ → aromatase↑ → estrogen↑ ). Important to know : taking Zn greatly increases the induced MT, but because copper has a MT affinity much higher than Zinc, the retention of Zn will be drastically diminished and, correlatively , the intracellular copper stores ( and the ratio Cu / Zn ) become higher than beforehand.
Statins or Superoxide dismutase ( SOD )?
Decreasing cholesterol is just a modulator ; more important is to strengthen the antioxidant protection, especially by correcting the usual deficient SOD enzyme , induced according to the diagram:
(Cu↔MT)↑ → Cuf↓, Zn↓ →Cu,Zn SOD↓ → Superoxide Anion↑→ LDL C oxidation
Vitamin C deficiency : ( Cu↔MT)↑ → vitamin C↓ → Silent scurvy
Why are the Western populations prone to gum disease? Statistics show that most Americans reaching 60-65 years, being copper dominant , lost their teeth, despite intensively practicing mechanical procedures such as brushing and flossing. To correct this deficiency , vitamin C complex , meaning ascorbic acid ( as “pure” vitamin C – the old hexuronic acid ) associated with bioflavonoids ( such as rutin and hesperidin ) as metabolic enhancers, seems to be the best option. However, administering vitamin C when CIT is present, doesn’t lead automatically to an increase of the vit.C content in the intra- or extracellular compartments, but , first of all, it contributes to a decrease of toxic deposits of copper (and calcium).This explains why many patients don’t have any normal antioxidant symptoms only after ingesting megadoses ( 5,000 mg vit.C / day or more). Note: under stress ( EPS ), the metabolic requirements of the body for some nutrients ( especially the copper antagonists ) are greatly ( 10 – 100 times ) increased. This should be a very good news for some mega – experts since we can establish as many Pauling ( and, correlatively , ortho- medicines ) as copper antagonists, namely : vitamin C ( sorry, the job is done ), sulfur, chromium, a.s.o.
Silent ( asymptomatic ) implications of the copper imbalance:
Silent acidosis : Cu↑ → Ca i ↓, Mg i ↓ ( Me i = mineral in soluble,ionic state );
Silent scurvy: Cu↑→vitamin C ↓;
silent infection: Cu↑↓;
silent inflammation: Cuf↓;
silent degeneration : Cu↑ → XIAP↓( lowering the normal cell apoptotic threshold);
Copper found in our drinking water and food may play a role in the onset of Alzheimer’s disease and other ” silent ” implications ( Courtesy: Medical News Today )
silent estrogenization: Cu↑→Zn↓→ aromatase↑;
silent overweight : Cu ↑ → Cr ↓ ; Cu ↑ → Ca ↑
silent dehydration: Cu↑→ choline↓, sodium↓;
silent hypertension: Cu↑→Cuf↓→Lox activity↓→ arterial fibrosis (collagen deposition)…
silent hypothyroidism : Cu ↑ → Zn ↓, Mn ↓, Se ↓,… ( T4–⁄→ T3 )
silent cancer : Cu ↑→ Zn ↓ → vitamin A ↓ ( abnormal cell differentiation / proliferation );
silent heart failure: Cu↑ → Cu f↓, Zn ↓, Mn ↓→ Cu, Zn SOD ↓; MnSOD ↓ → ( mitochondrial / intracellular hyperoxidative stress )
silent dementia : due to impaired adrenals & liver activity → copper / zinc imbalance leading to over-stimulation of the emotional brain ( di – encephalon)
silent Alzheimer’s : Cu↑ ( due to age, etc. ) → pseudo- chaperone effect of the beta- amyloid proteins → plaque formation
1. It is currently asserted that Alzheimer’s ( and / or dementia ) is incurable. I strongly disagree . I consider that we are actually dealing with a unique ( but very complex! ) problem of copper toxicity ( intra and extra- cellular ,having as modulators some other toxic metals like Fe, Zn, Hg, Cd,…; complex means not just direct hyper-oxidative effect, not just sub/ under or over-methylation ,… but equally – or more exactly especially- copper interference toxicity = CIT , according to our model . A main correlative, aggravating aspect is the deficiency of copper controlling proteins such as MT ( metallothionein ) and CP ( ceruloplasmin ) involving some exhausted ( aged, etc. ) adrenals : EPS → weak adrenals → cortisol ↓ → MT ↓, mainly leading to a lack of sequestration = the main mechanism of controlling copper overload and, implicitly, to the imbalance of a crucial ( emotional ) ratio: copper / zinc, as well as to a lack of preventing – by the drastic different affinities – of the toxic involving of beta-amyloid proteins in pseudo-chaperone effects leading finally to the formation of ” plaque”. What we have to do, in my opinion, is to look for some efficient , synergistic strategies aiming to bring and maintain the intra-cellular copper level and the production of MT / CP within the normal ( highly individualized ! ) physiological range.
Cateva precizari adresate in mod special colegilor din Romania ( ca si nespecialistilor direct interesati ) privind implicarea copper overload in formarea beta – amyloid- plaque, in spatiul extracelular ( vezi Fig. de mai sus ), precum si sugestii pt. preventia / tratamentul AD cu ajutorul unor chelatori metalici specifici . Exista inca nu putini cercetatori – autori care considera contributia -cheie a copper la formarea placii senile ca fiind inacceptabila datorita unor particularitati functionale cum ar fi concentratia insuficienta a ionilor de cupru in compartimentul vizat, afinitatea prea redusa a subsistemelor implicate ( beta amyloid peptides ) fata de acesti ioni, etc. Cea mai concludenta abordare / explicitare a acestor rezerve o ofera articolul publicat de un grup de cercetatori britanici ( Univ. of London ) , condus de C.D.SYME si intitulat “ Copper Binding to the Amyloid – Beta Peptide Associated with Alzheimer ‘s Disease ” ( J.Biol. Chemistry, 2004, vol. 279 / 18, p. 18169 ). Citez un pasaj clarificator:
“There is now direct evidence that copper is bound to Amyloid – Beta ( AB ) peptide in senile plaque of Alzheimer’s disease. Copper is also linked with the neurotoxicity of AB and free radical damage, and Cu2+ chelators represent a possible therapy for Alzheimer’s disease.”
Studiul colegilor londonezi face cateva trimiteri semnificative (inclusiv referitoare la dizolvarea placii toxice de catre chelatori bine alesi ) dintre care eu recomand in special cele 3 references ( nr, 14;24; 25 ) semnate de ATWOOD C.S., CHERNY R.A. , DONG J. , and coll. Un paper mai recent ( 2012 ) , scotand in evidenta , de asemenea rolul chelatorilor metalici este semnat de gruparea condusa de GENG J. ( J.Med. Chem, 55 / 21 , pp 9146-55 ).
In opinia mea – bazata atat pe cercetarile proprii cat si pe concluziile altor specialisti, cel mai specific chelator pt. Cu2+ este resveratrol-ul , care poate fi utilizat atat in preventie cat si in tratamentul AD. Intrucat acest ” trifenol ” natural ( denumire sistematica : 3,5,4′-trihydroxystilbene ) este ” ridicol de ieftin “, el neputand fi ” imitat ” ( sintetizat ) in laborator ( si daca totusi ar fi , pacientii naturisti au la dispozitie o sursa pe cat de accesibila pe atat de…delicioasa =the red wine / vinul rosu ). Fraza anterioara explica faptul ca resveratrol-ul nu este promovat de catre medicina si farmacologia conventionala al caror obiectiv major il constituie nu optimizarea starii de sanatate ( health / wellness ) a populatiei ci realizarea unui profit maxim, repet : MAXIM. Prezint in continuare cateva dintre performantele general-protective ( in perspectiva deopotriva profilactica si curativa ) ale resveratrol-ului, conform jurnalului “Natural Health News Report” issue # 120 :
” Resveratrol protects you from Head to Toe”:
– Healthy heart, arteries ( promoting normal cholesterol levels and healthy homocysteine concentration );
– fortifies your immunity by fighting free radicals;
– prevents oxidation of fatty foods ( for cardiovascular boost );
– protects brain and memory ( brain = more than 90 % fat ! );
– maintains healthy veins , circulation and blood pressure ( red wine acting as a vasodilator );
– keeps skin looking young, tight , fresh…
I like to underline that my optimistic conclusion is based on some remarkable accomplishments due to a series of dedicated researchers such as: Anne Louise GITTLEMAN, Paul C. ECK, Lisa MILLER, James L. WILSON, Carl PFEIFFER ( d. in 1988 ), William J.WALSH, Emily MULLIN, Veronika A.SZALAI, Rashid DEANE, Yadong HUANG , Zhijian SU and coll. The relevant discovery of my conceptual friends from Northwestern University – Evanston ( Javeria HASMI and A.V. APKARIAN’s team ) = the ” distant ” link between chronic back pain associated with marked changes in brain activity is not at all omitted / overlooked by me , rather it is embedded in general stress symbol “EPS”.
2. Don’t confuse the stress induced functional copper deficiency ( Cuf↓ ) – the major form of copper deficiency for the Western societies – and the copper nutritional deficiency, a rare, unlikely phenomenon.
Cuf↓ is defined as low availability of copper for intra – and extracellular activity ( enzyme activation, etc.), despite of high copper stores in the body ( tissues, cells ).
For instance, lysyl oxidase inactivation due to copper deficiency, leads to diminished cross-linking collagen and elastin and, consequently, to connective tissue defects ( Steinmann et al, 1993 ). The two forms of copper deficiency (stress and malnutrition induced ) should be corrected by two radically different procedures: activation of intracellular copper overload versus normal copper supplementing.To prescribe copper supplements in the case of stress induced deficiency constitutes a “ toxic supplementation”, unfortunately frequently practiced with many Holocaust survivors.
Manganese depletion (connective tissue degeneration): (Cu↔MT)↑→ Mn↓
Human manganese deficiency is still underevaluated though it is involved in some major metabolic disorders such as: ligamentous laxity, poor healing of ( chronic ) wounds, improper thyroid function, etc. Before deciding for cortisone shots or for surgery ( knee, wrist, discectomy,..) – these interventions of last resort being able to amplify the local degeneration- the world class sportsmen / women need to assimilate a simple metabolic truth: it is high intracellular copper level ( that is the exceptional emotional overload, often unprofessionally compensated ) that contributes to a stable but reversible Mn deficiency and, correlatively, to inactivation of glycosyl transferase enzyme, that determine the most connective tissues defects. The same about CIT and poor healing of chronic wounds:
(Cu↔MT)↑ → Mn↓, ( Mg↓ ) → Hyaluronic acid↓.
4. Degeneration – a non-inflammatory issue. The Degenerator
Degeneration constitutes one of the most interesting problems of the contemporary, post-genomic medical science. Unfortunately, its specific approach is still slowed down because of the facile temptation to consider degeneration an annex of the inflammation ( Andre Weil, MD: ” Chronic inflammation just may be the root of all degenerative diseases “ ). Here are some of the most important methodological shortcomings that keep the degeneration category conceptually underdeveloped:
1. subevaluation of the stress role in starting and promoting degeneration – stress is often considered just a modulator, and with no genuine generator, an artificial and painful deterministic play follows between symptoms / effects: inflammation is the cause of degeneration ; infection is the cause of inflammation, etc …I called this comfortable swimming into the sea of effects / symptoms – the downstream syndrome of the contemporary medical research ( the idea of inactivating the caspase machinery to promote a regular apoptosis – while the upstream generator ( Cu↔MT)↑ remains untouched – is just one of the last, high tech examples).
2. the regular use of anti-inflammatory strategies / medications in situations that are totally or predominantly degenerative ( apoptotic degeneration );
3. the conceptual confusion between degeneration and degradation ( this way masking the fact that primary degenerative events take place not in ECM – extracellular matrix- but intracellularly ) : “ collagen and /or ECM degeneration” ( the correct term – degradation ) also, “ cartilage degradation “ ( the correct term – degeneration );
4. ignoring , confusing or underevaluating the MT’s ( metallothionein ) role in the normal and pathologic metabolism. Don’t confuse the acute copper toxicity ( due to mineral saturated MT ) and chronic copper toxicity ( CIT ) involving copper undersaturated MT.
Centered on cellular damage – the primary event in any degeneration – here is my working definition of degeneration:
inefficient regulation of cell activity during post-injury healing and / or tissue turnover (development, disease state, aging ), resulting in a reduced tissue organization / cellularity ( excessive apoptosis ) and subsequently matrix degradation.
Special merits for differentiation between degenerative and inflammatory, go to some researchers from the tendinopathy field ( PUDDU G. et al.) who, since 1976, proposed to use the term ‘ tendinosis ” instead the incorrect term “ tendinitis “, every time the tendon degeneration is implied, without some clinical or histological signs of inflammation. Using our model, the two chronic conditions can be efficiently distinguished as follows:
tendinosis ( degeneration ) : (Cu↔MT)↑, Ca↑, Vitamin C↓
tendinitis / tendonitis ( inflammation ) : Cuf↓, Ca↓, vitamin C↑
A similar distinction ( though not separation ! ) between arthrosis / arthritis has been elaborated by this author (2006, unpublished work ).
Some reputed authors ( Johns Hopkins Univ., 2006 ) stated that presently is no cure for arthritis ; methodologically, this statement is already history since whether the main cause of arthropathy is the hidden copper imbalance, each of the traditionally admitted causes such as infection ( Cu↑↓), inflammation ( Cu↓ ) and…even joint’s laxity ( Cu↑→ Mn↓ = degeneration ), could be controlled by bringing / maintaining copper within the physiological range.
Recent studies showed that there is an established connection between the stress ( emotional ) level, degeneration and apoptosis, Ap ( programmed cell death ). It could be concluded that there are two main types of degeneration: apoptotic ( with zero or minimal inflammation) and necrotic ( with relative high inflammation), having a gradual transition between the two types. The EPSICO model develops these new alignments, suggesting a series of fruitful molecular approaches based on the following main etiologic equation of degeneration:
EPS→ (Cu↔MT)↑→Cuf↓, Zn↓, Mn↓, vit C↓→Mt !→ Ap↑→ Tissue Degeneration
In the above sequence Mt! represents the mitochondria as a sensor of perturbation of cellular homeostasis by the CIT.
The entity ( Cu↔MT)↑→Cuf ↓,Zn↓,Mn↓,( Se↓,Cr↓), vit.C↓, essential in any degeneration, has been designated by me as Degenerator. For instance , the copper overload determines the activation of caspase machinery ( “ silent degeneration ”) :
Cu↑→ XIAP↓→ ( caspase machinery )↑→ lowering the normal cell apoptotic threshold ( XIAP designates a certain X- protein from the IAPs group of inhibitors of Ap).
Also, Cu↑ plays a major role in the carcinogenesis and cell cycle dysregulation,via TP53 mutants. The TP53 or p53 ( proteine ) is tumor suppressive ( pro-apoptotic ) in Zinc-wild state, but becomes anti-apoptotic in mutant states mainly generated by ( Cu↔MT)↑, this way contributing to the apoptotic resistance of the cancerous cells ( don’t confuse the two opposite contribution of the copper overload to apoptosis : while the normal cells are “debilitated ” the cancerous cells are protected ). Important to know : beyond this anti-apoptotic contribution , intracellular copper overload induces cells transformation ( carcinogenesis ) through: a. intense , uncompensated oxidative stress ( Cu ↑ →Zn ↓ ,Cuf ↓ → Cu,Zn SOD ↓ ) and b. Cu ↑ → Zn ↓, vitamin A ↓ ( abnormal differentiation and proliferation ).
5. Instead of conclusions: some methodological challenges
One could wonder how it was possible that for an almost a century since it was established the nutritional essentiality of copper ( 1920 ), the modern researchers to ignore the role of the intracellular copper overload as a generator of the chronic diseases, respectively to ignore the non-Cartesian , emotional root ( nature ) of all chronic disorders. The main explanation of this extremely critical overlook is given by not taking in consideration or by underevaluation of the 3 following essential connections:
a. The stress ( EPS ) / Metallothionein. Without this primary link, the EPS could not to surpass the status of a subsidiary / modulator factor.
b.The Metallothionein / Copper = the biounavailability riddle (see § 5.2 ),
c. Excessive copper→ deficient ( functional ) copper. The main copper deficiency proved to be not a nutritional one but a weird deficiency induced by the copper overload ( Cu↔MT )↑→ Cu f ↓.
Finally, there are presented some relevant details concerning these connections.
5.1 Stress / MT – the missing link in the classical theory of stress
“ The stress from any source generates copper imbalance ” – this phrase full of metabolic signification ( bridging the emotional and physiological realms ) has remained for a longtime at the margin of the modern medical research, as a purely descriptive statement, rebel to any trial of causal approach. The chances of transposing this into a coherent and quantifiable biochemical mechanism have considerable increased with the discovery of MT as a unique chelator for some electrophile agents, especially the metal ions such as Cu+, Cu2+, Cd2+, Zn2+. Fundamental progress in connecting the stress ( as primary emotional factor ) and the epidemic of chronic illnesses has been achieved in two distinct / inseparable stages:
5.1.1. The knowledge of the structural-functional characteristics of MT ( 1985 – 2005 ).
Mammalian studies showed that MT can bind 7 divalent metal ions :
Cu, Cd, Zn ( or, alternatively, 12 monovalent copper ions ) per protein molecule in TWO DISTINCT DOMAINS ( clusters ): the alpha cluster or the carbon terminal domain ( including 11 cysteine residues) and the Beta cluster or the nitrogen terminal domain ( containing 9 cysteine residues ). It is remarkable that the chelation promoted by the two domains is done SEQUENTIALLY- the fixation of the cations on the Beta domain happens only after the alpha domain has been saturated with electrophile agents.This fact – due to the net difference of affinity attributed to the two domains – allows an efficient delimitation between the stable sequestration of toxic heavy metals ( Cd2+ , Cu↑ ) on the alpha domain and the homeostatic regulation of the essential metals ( Cuf, Zn ) essentially distributed on the Beta domain.
5.1.2. The second stage (2002 – 2006 ) dedicated to the verification of the hypothesis according to which the synthesis of the MT could be easily induced IN VIVO by glucocorticoid hormones, especially cortisol:
EPS → Cortisol ↑ → MT ↑
5.2 The Copper Biounavailability Riddle – a new mineral ratio concept
The right solution of the copper biounavailability problem was late by several decades due to the preference given by the medical establishment to some plausible ( but false ) current analytical clichés such as: a. the copper deficiency is a very unlikely phenomenon, even in the case of a suboptimal nutrition and b. the copper overload cannot exist but in some exceptional cases ( mutations, accidents ). In this context, the copper biounavailability was sometimes looked at as… a simple biochemical curiosity or, at othertimes, it was considered as a sleeper phenomenon associated with dehydration. In reality, we deal with a new understanding of the mineral ratio concept, when the excess of one mineral ( intracellular Cu↑) determines the deficiency of the same mineral found in a different metabolic state ( Cu functional, intra- and extracellular). Note – in passing- that in mammals, the copper deficiency leads to the iron deficiency as Fe2+ , the only soluble, assimilable form : ( Cu ↔MT )↑ and / or Mo↑→ Cuf ↓ ( → Fe2+ ↓ ). This detail should be suggestive for Bovine Spongiform Encephalopathy ( Mad Cow disease ) research, and for its human counterpart ( Creutzfeld – Jakob disease ), both based on a deep imbalanced mineral metabolism ( Cu , Fe, Zn ); Mo = Molibdenum.
The copper biounavailability conceived as sequestration, is based on the large difference of affinity of the coordinative bonds generated by the two domains (clusters ) of MT: relatively recent studies, due especially to the group led by the Swiss professor KAGI G. H. ( presently retired ) , showed that the Cadmium binding sites generated by the alpha domain of MT are 30 times more stable than those generated by the Beta domain. Transposing this result into the copper biochemistry ( important to know: the affinity of Copper to MT is even higher than that of the Cadmium ! ) one can conclude that copper from system becomes biounavailable, being preferentially fixed on the MT alpha domain ( sequestration ). Considering that excessive ionic ( free, soluble ) copper is much more dangerous than the functional copper deficiency, it results that the copper biounavailability represents a particularly valuable adaptive acquisition into the field of the oxidative metabolism, the evolution solving this vital problem through the so called chaperone effect of the MT. It can be stated that the only efficient answer of the living systems to the copper overload is the induction of MT ( MT ↑). This way a nonlinear risk was transformed by the evolution into a linear / chronic one, involving a transition from a potential hyperoxidative, acute toxicity to a chronic copper interference toxicity ( CIT ).Note: MT becomes copper active only in special ( overload ) situations, the normal , physiological copper works without any MT involvment.
The well established inseparability between the intracellular excess and the induced deficiency of functional copper leads to the general conclusion that not the separation between degeneration, infection and inflammation represents the right methodological solution since all these conditions ( symptoms ) suppose the intracellular copper imbalance. A better strategy – perhaps the only one – consists in bringing and maintaining the intracellular copper level within the normal, physiological range.
ANEXA: Rolul iodului in prevenirea / tratamentul bolilor
Deficienta de iod
Se apreciaza ca aproape 3/4 ( mai exact: 72 % ) din populatia globului este afectata in grade diferite de deficienta de iod. Iodul – un element esential a devenit deficient datorita schimbarilor in sens unic intervenite in conditiile vietii moderne. Iata cateva dintre acestea:
1. Scaderea consumului specific de sare ( rafinata, sare iodata , sare de mare ) vizat fiind controlul hipertensiunii arteriale;
2. diminuarea progresiva a gradului de mineralizare a solului , ca urmare a unei agriculturi intensive , irationale , cu o compensare ( fertilizare ) partiala, defectuoasa, introducand sistematic , impreuna cu fosfatii si fluorura de sodiu ( 1-5 % ), anionul fluorura fiind fixat preferential de numeroase vegetale , inclusiv sau mai ales – ceaiul verde ;
3. prezenta excesiva a antagonistilor metabolici ai iodului ( fluor, brom, anion clorhidric ) in apa de baut / sucuri , pasta de dinti, medicamente, etc.
Ca urmare a acestei deficiente , functia esentiala a iodului de a produce hormoni tiroidieni ( tiroxina / T4 si triiodotironina / T3 ) a devenit suboptima, blocarea graduala a activitatii tiroidei, in deosebi de catre fluor si brom , contribuind in mod direct direct la numeroase dezordini cronice, de la dureri de cap / migrene, hemoroizi, diabet, obezitate si pana la cancere ( san , ovarian , prostata,…). Concomitent si corelativ, s-au impus atentiei unele noi functii vitale ale iodului, cum ar fi detoxifierea tesuturilor , lupta anti-cancer , reenergizarea , s.a. care plaseaza iodul in centrul asa-numitei pleiotropic revolution , reliefand specificul multifunctional al acestui element de baza . Situarea iodului alaturi de alti nutrienti multifunctionali cum sunt : IP- 6 ( inositol hexa fosfat ), resveratrol , vitamina D3 ( cholecalciferol ), vitamina K ( menachinona sau vit. K2 ), a atras atentia totodata asupra necesitatii actualizarii recomandarilor uzuale pentru consumul zilnic ( vechi de cateva decenii: RDA, RDI, etc. ), elaborate pe baze unilaterale , monofunctionale cum ar fi combaterea hipotiroidismului, a gusei ( goiter ), sau retardarii mintale extreme.
Dozele optime de iod , raportate la organismul uman ca intreg
In urma cu un deceniu , recomandarile uzuale pentru ingestia de iod considerata normala la nivel de adulti de ambele sexe ( in USA si Europa de Vest ) erau cuprinse intre 150 – 300 micrograme/ zi ( respectiv 0,15 – 0,30 mg ) si vizau exclusiv functionarea normala a glandei tiroide. Raportate la optimizarea starii de functionalitate a intregului organism aceste cifre erau absolut insuficiente ,dar la acea data , lucru destul de curios , nu existau cercetari consacrate nemijlocit noii situatii , statuata deja, la modul general , de revolutia pleiotropica. Abia in 2002 si urm., grupul de cercetatori condus de Dr. G.E. Abraham (medic ) a publicat o serie de articole de referinta ( in deosebi in ” The Original Internist ” ), articole care au servit drept baza pentru elaborarea unor protocoale noi, integrative, de competente largite , incluzand abordarile preventiv – terapeutice ale cancerului la san. Doua au fost punctele de plecare ale Grupului Abraham : 1.utilizarea cu succes a solutiei LUGOL standardizate ( testata deja pe o durata de peste 150 ani ) : 2 picaturi din aceasta solutie continand 12,5 mg iod / iodura . 2. Studiile demografice avand in centru consumul diurn de iod al femeilor din Japonia contemporana ( prezentand riscuri minime pentru cancerul la san, uterin si ovarian ): 13,80 mg iod elementar total. Intrucat administrarea de iod / iodura in solutie prezinta anumite inconveniente ( dozare nu tocmai acurata, gust metalic, neplacut, cauzand totodata iritatie gastrica ), solutia adoptata de Abraham et comp. a fost pastilarea : noul produs ( marca inregistrata sub numele IODORAL ) se prezinta sub forma unei tablete precis cuantificate , continand 5 mg iod neutru si 7,5 mg iodura sub forma sarii de iodura de potasiu. Consumul minim sugerat de Dr. Abraham s-a situat f. aproape de cifra japoneza , fiind o tableta sau 12,50 mg iod / iodura pe zi ( limita maxima fiind de 4 tablete / zi , respectiv 50 mg iod / iodura ), doza optima si durata fiind strict individuale , stabilite de medic. Dupa cativa ani de utilizare a acestor indicatii cu pacientii mei, pot atesta ca cifrele mentionate corespund noii situatii, permitand un control eficient atat al functionalitati tiroidiene cat si al celei extra-tiroidiene ( aflata dincolo de problematica traditionala T3 / T4 ), cu un minim de efecte secundare , negative. Pentru informatii suplimentare, ca si pentru comenzile de Iodoral , recomandarea mea este sa se contacteze direct firma producatoare OPTIMOX- Torrance , California ( www.optimox.com ).
Efecte secundare potentiale ale utilizarii IODORAL
Ingerarea de Iodoral , intre limitele stabilite , nu este lipsita de anumite simptome neplacute ( minime ), dintre care merita a fi subliniate :
– dureri de cap in zona sinus frontal;
– salivare excesiva si stranut persistent ;
– leziuni ale pielii de tip acnee , in anumite zone ale corpului.
Daca unii pacienti ( 2-3 % ) au astfel de simptome , recomandarea este intreruperea imediata a tratamentului si contactarea medicului care supervizeaza administrarea Iodoral , in vederea unei reconsiderari .
Cei interesati in comandarea unei carti accesibile , foarte apreciata aici in America , scrisa cu nerv, de catre unul dintre membrii Grupului Abraham – Dr. David Brownstein , MD , intitulata ” IODINE : Why You Need It, Why You Can’t Live Without It” pot folosi adresa : drbrownstein.com