Tag Archives: delayed reaction

What Getting Poisoned Looks Like

People think that getting poisoned looks like this:

But in the real world, it looks like this:

People whose cells are being destroyed from the inside out, often look fine.  Looks can be deceiving.

Everyone with an invisible or mysterious illness should ask the question – Were you poisoned?

Something that everyone who suspects that they may have been poisoned should note is that much of the damage, the poisoning, is indirect.  Pharmaceuticals (fluoroquinolones included) and environmental toxins damage mitochondria and, after reaching their tolerance threshold for damage, the mitochondria respond by producing poisonous reactive oxygen species (also known as oxidative stress).  Those reactive oxygen species (peroxynitrite is a particularly toxic one) that result from mitochondrial damage cause multi-symptom chronic illnesses.  It should be noted by people with chronic fatigue / M.E., that mitochondria are the energy centers of our cells and that damage to them can result in debilitating fatigue.  It should be noted by people with fibromyalgia that mitochondrial damage and oxidative stress have been shown to damage nerves and cause body-wide pain.  Autoimmune diseases have also been linked to poisoning, and also to mitochondrial damage.

Mitochondrial damage is tricky in that the tests to show it are woefully new and under-utilized.  Muscle biopsies can show mitochondrial damage, but they’re invasive and not very reliable.  Lactate doublets are a sign of mitochondrial damage, but the research behind them is new and utilization of MRIs to test for lactate doublets are rarely used.

The fact that the tests don’t show anything means that the tests are inadequate (and that they don’t show mitochondrial damage / oxidative stress), not that the problem is “in your head” or that it’s not chemical, or that you haven’t been poisoned.

People who are poisoned are in pain, they are fatigued, they can’t think straight, they are unable to function at the level that they used to.  That should sound familiar to everyone with fibromyalgia, CFS/ME and even autoimmune diseases.  Were you poisoned?  When?  By what?  And by whom?

If doctors looked at the mitochondria, they would see the destruction of the poison.  But they don’t look at mitochondria.  As long as they don’t look at mitochondria, they can tell themselves that their drugs are safe; that they’re not poison.  Ignorance is bliss for the entire medical profession and the FDA.  Too bad their ignorant bliss isn’t reality.

Look around you.  The chronically ill people around you are telling you something.  This is what the poisoning of America looks like.

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Peer Reviewed Sources:

Molecular Nutrition and Food Research, “Medication Induced Mitochondrial Damage and Disease

Toxicological Sciences, “Mitochondria as a Target of Environmental Toxicants

Molecular Interventions, “Mechanisms of Pathogenesis in Drug Hepatoxicity Putting the Stress on Mitochondria

Biochemical Society Transactions, “Mitochondrial Matirix Reactive Oxygen Species Production is Very Sensitive to Mild Uncoupling

Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells

Cleveland Clinic Journal of Medicine, “Mitochondrial cytopathy in adults: What we know so far

Current Pharmaceutical Design, “Nitric Oxide-Derived Oxidants with a Focus on Peroxynitrite: Molecular Targets,Cellular Responses and Therapeutic Implications

Journal of Internal Medicine, “Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise

Biomed Central, “Central role of nitric oxide in the pathogenesis  of rheumatoid arthritis and systemic lupus erythematosus

JAMA Psychiatry, “Mitochondrial Dysfunction as a Neurobiological Subtype of Autism Spectrum Disorder

Expert Opinion on Therapeutic Targets, “The role of mitochondrial dysfunctions due to oxidative and nitrosative stress in the chronic pain or chronic fatigue syndromes and fibromyalgia patients: peripheral and central mechanisms as therapeutic targets?

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