Collateral Damage
ADRs, ME/CFS, GWVs, Infections, MCS, metabollic syndromes and other "Syndromes"
It is no coincidence that many suffering ADRs are labeled as suffering from ME/CFS.
The mechanism leading to long term illness, stemming from ADRs, vaccines and the aforementioned, triggers glycation, inflammation, oxidative stress, producing too much Nitric Oxide and other free radicals, leading to degeneration over a long period of time, spanning between ten to twenty years.
Dis-Ease state manifests over a period of time, affecting the individual with a myriad of symptoms. Symptoms vary, but the mechanism is the same - TOXICITY. The mechanism begins with oxidization of endothelial cells leading to apoptosis (programmed cell death).
The general consensus amongst progressive medical doctors and scientists is that TOXICITY or nutritional imbalances are main causes of degenerative diseases.
It has already been established that medication causes damage to the mitochondria, leading to progressive degeneration manifesting as diabetes, and other auto-immune illnesses, metabolic syndromes, (http://aac.asm.org/cgi/reprint/AAC.00729-05v1.pdf and http://www.ceri.com/mito.htm) such as depleting L-Carnitine http://www.ncbi.nlm.nih.gov/sites/entrez and http://ods.od.nih.gov/factsheets/carnitine.asp, antibiotics weakening the immune system, activating viruses such as EBV and HHV-6. L-Carnitine deficiency is very difficult to diagnose, can lead to dangerous arrythmia and heart failure!
Furthermore, the principle that drugs only benefit a small percentage of the population as in this article: http://jcp.sagepub.com/cgi/content/abstr....ourcetype=HWCIT and hundreds more published articles, taking medicines is not only redundant, but will cause more harm.
Antibioitics can activate EBV & HHV6: http://tinyurl.com/yetmly3 and C.Difficile: http://tinyurl.com/ykqauw4
Likewise, antimicrobials are no longer effective, mutating pathogens, whilst weakening the immune system whilst causing even more damage to the digestive tract, which is 80% responsible for a healthy immune system!
Reading about oxidative stress, Nitric Oxide Cycle, Free Radicals, Inflammation over a period of two years, leads to the conclusion that preventing escalation of symptoms from ADRs is crucial to maintain good health.
Lastly, it is irrelevant if ME/CFS was triggered by an infection, which could have been triggered by the effects of antibiotics, or toxicity form vaccines, or medications. It will lead to oxidization and inflammation.
See articles below:
Treatment of myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS), a multisystem disease, should target the pathophysiological aberrations (inflammatory and oxidative and nitrosative stress pathways), not the psychosocial "barriers" for a new equilibrium.
Maes M, Twisk FN.
Patient Educ Couns. 2010 Mar 17. [Epub ahead of print]
Maes Clinics, Belgium.
Maes Clinics, Belgium.
In a recent article published by B. van Houdenhove and P. Luyten it is claimed that cognitive behavioral therapy and graded exercise therapy (CBT/GET) are evidence based and are the most adequate treatments to control symptoms and improve quality of life of patients with myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS). However, these authors do not disclose that their own treatments at the Belgian CFS Reference Centers with CBT/GET have proven to have no clinical effects. The Belgian minister declared in the parliament that CBT/GET at those centers are no curative therapies. Even more, measured by objective standards the CBT/GET approach has shown to be counterproductive. van Houdenhove and Luyten neglect or deny all scientific findings on the pathophysiology and possible medical treatments of ME/CFS. However, there is now a consensus that inflammatory and oxidative and nitrosative (IO&NS) pathways underpin the pathophysiology of ME/CFS in humans and in animal models as well. Human and animal data show that treatments which target IO&NS pathways are useful in treating ME/CFS. van Houdenhove and Luyten also propose that the time has come to shift treatment research in CFS from efficacy studies to effectiveness studies in 'real life'. In our opinion, future research should use a high throughput screening, made possible by the translational approach, in order to further examine the IO&NS pathways in detail; further delineate novel drug-targets in the IO&NS pathways and develop new drugs to treat this complex and serious medical disorder.
Medication-induced mitochondrial damage and disease.
Neustadt J, Pieczenik SR.
Montana Integrative Medicine, Bozeman, MT 59718, USA. drneustadt@gmail.com
Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis.
Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others.
While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies.
This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
In conclusion, staying from medication and finding the key to restoring health post ADRs is crucial. Doctors who risk their careers to expose this genocide should be taken seriously!!
Toxic Injury
According to toxicologists, varied and multiple toxicity symptoms will manifest from identical mechanism that is oxidization of endothelial cells.
Worth noting, the medical establishment is very quick at making judgments concerning toxicology of herbal remedies, but reluctant, even defiant about known adverse drug reactions (ADRS) and side effects ...
To recapitulate concerning the toxicology of Lariam/Mefloquine or other meds:
In general, pharmacologist accept that approximately, only 10% of meds are effective. Genetic variations, polymorphisms, biochemistry, ethnicity, weight, age, gender, body temperature, weather, etc ... all contribute to pharmacodynamics and pharmacokinetics. To date, it has not been possible to manufacture meds tailored for individuals precisely, because, there are so much that we don't know happening at cellular level.
The question here is why some don't react, rather, than, why we reacted? After all, Lariam/Mefloquine is toxic, as are fluoroquinolones and most meds.
The general consensus is that drug metabolism is unpredictable. http://tinyurl.com/yc6empe
DRUG METABOLISM/TRANSPORT
Nuclear Receptors and the Regulation of Drug-Metabolizing Enzymes and Drug Transporters: Implications for Interindividual Variability in Response to Drugs
From the Division of Clinical Pharmacology, Department of Medicine (Dr Urquhart, Dr Tirona, Dr Kim), and the Department of Physiology & Pharmacology (Dr Tirona), University of Western Ontario, London, Ontario, Canada.
Division of Clinical Pharmacology, London Health Sciences Centre-University Hospital, Room ALL-152, 339 Windermere Road, London, Ontario N6A 5A5, Canada.
Erratic or unpredictable response to drugs remains a challenge of modern drug therapy. An important determinant of such interindividual differences in drug response is variability in the expression of drug-metabolizing enzymes and/or transporters at sites of absorption and/or tissue distribution. Variable drug-metabolizing enzyme and transporter expression can result in unpredictable exposure and tissue distribution of drugs and may manifest as adverse effects or therapeutic failure. In the past decade, important new insights have been made relating to the regulatory mechanisms governing the expression of drug-metabolizing enzymes and transporters by ligand-activated nuclear receptors. Specifically, there is compelling evidence to demonstrate that PXR, CAR, FXR, LXR, VDR, HNF4alpha, and AhR form a battery of nuclear receptors that regulate the expression of many important drug-metabolizing enzyme and transporters. In this review, the authors focus on clinically important drug-metabolizing enzymes such as CYP3A4, CYP2B6, CYP2C9, CYP2C19, UGT1A1, SULT2A1, and glutathione S-transferases and their regulation by nuclear receptors. They also review the nuclear receptor-mediated regulation of drug transporters such as MDR1, MRP2, MRP4, BSEP, BCRP, NTCP, OATP1B3, and OATP1A2. Finally, they outline how the drug development process has been affected by the current understanding of the involvement of nuclear receptors in the regulation of drug disposition genes.
No comments:
Post a Comment