A series of succeeding questions for the informed reader –
1. Why do some people who have “bad nerves” seem to manifest as epidemiological and neuropsychological case studies as people with both a) initially poorly functioning HPA axis b) genetic susceptibility to disruption in their HPA axis? How much of a part do damaged detoxification organs, electrolyte imbalance caused by malabsorbtion and toxaemia, chronic stress events, and immune related issues such as Chronic-Fatigue-Syndrome play a part in precipitating HPA-axis dysfunction? How much of a role does HPA-axis function play in the prognosis of environmental illness? How much of an impact do life experiences and early trauma have in the development of these conditions? Is our food really making us sick or are we so sick and depressed we cannot tolerate a normal diet to begin with? Can meditation, CBT, and EFT attenuate central sensitization and sympathetic dominance? Can controlling the mind prevent the cascade of worsening health conditions in a modern age of toxemia?
2. What are the underlying pathologies of a poorly functioning endorphin system, neuroendocrine response, HPA axis, hippocampal, hypothalamic, and amygdyla in mediating psychic awareness, learning, and empathy as governed by the mesocortical limbic reward system? What kind of physical brain abnormalities could cause cognitive dysfunction and emotional dysfunction, and would they be the result of a poorly functioning HPA axis or the cause, and would they physically (without psychological affect) attenuate/potentiate environmental diseases? Is it the change in the HPA axis that 'releases' the higher functions and healthier cognitive behavior (meaning we are much more controlled by our environmental stimuli), or is it a peripheral brain action (meaning we have built in pre -determined behavior) that antagonises abnormal stress responses or excessive desensitization to stimuli? How might the HPA axis and CNS be further related? Is their poor inter-hemispheric communication of the brain or excitotoxicity? Immune and rheumatological pathologies that could alter limbic function, musculoskelatal, and neuroendocrine function? How might dysautonomia and evolutionary adaptations to chronic infection be involved in this neuralgia?
3. What underlying metabolic disorder is present? Its causes? What are the roles of TSH, T3, T4, and ACTH, CRH, AVP, ADR, FH, LSH, IGF-1, HGH, GnRH, Testosterone, Androgen, Pregnenolone, Progesterone in synthesizing or stimulating the release of catecholamine, especially dopamine, adrenaline, dynorphin, enkephalin; the role of immunoglobulin, t-lymphocytes, beta cells, natural killer cells, Th1 and Th2 immune responses, and leukocytes in neurotransmitter synthesis; What is the relation of general metabolism of neurotransmitters and the pathology of defective inhibitory systems in the limbic areas; How might these same neurotransmitters and hormones play a role in causing dysautonomia, neuralgia, and peripheral neurological conditions? Why do adrenergic alpha and beta receptor function play a role as the most critical physiological subject, outside of mitochondrial physiology, when studied in neuropsychological, rheumatological, immunological, and endocrino-metabolic disorders? Does dysfunctional gluconeogenesis, cellular metabolism, and glycolysis involved in metabolic diseases such as obesity, insulin resistance, autoimmunity triggered insulin deficiency, autoimmune triggered adrenal and/or thyroid deficiency, and other autoimmune conditions point to genotoxin, neurotoxin, teratogen, and endocrine disruptor exposure;
4. Could the kidney, liver, gaul bladder, or pancreas involved along with the lymphatic system be acting sluggishly, resulting in poor detoxification caused by toxic metabolites, malabsorption, stones, acidity, parasites, infection, and sequestered heavy metals? How would this effect cell levels of anti-oxidants, ATP synthesize, mitochondrial function, co-factors and enzymes, Krebs cycle, and cellular metabolism? How might nutrition elucidate an imbalance in aerobic vs. anaerobic metabolism at the cellular level? Could the metabolic acidosis incurred by sluggish detoxification organs and chronic malnutrition negatively affect neurotransmitter metabolism, synaptic meta-plasticity, and energy supply to the brain? Does targeted nutrition and allergy elimination only treat the symptom? What is more important to curing root pathology- targeted anti-pathogenic therapy or diet and immune balancing? Can endocrine disruptors, metals, teratogens, carcinogens, neurotoxins, and genotoxic compounds truly be removed from the body? Could dysautonomia, autoimmunity, chronic infection, pollution exposure, and genetic mutation be combining to create the perfect storm of debilitating conditions?
But essentially, these conditions are a neuroendocrinological, metabolic(circulatory disease), psychological, and gastrointestinal disorder, possibly mediated by immune responses consisting of chronic infection and autoimmunity, co-morbidly diagnosed with pathological GI tract, displaying IBS like symptoms characterized by central sensitization, inflammatory, and immunological responses BUT perpetuated by neuroendocrine dysfunction. It is also further thought that the CAUSE of the systemic disorders could be a combination of opportunistic infections, xenotoxins and endocrine disruptors, e.g. mercury, pesticides, fertilizers.
1) It starts off as a stress response mediated by the locus ceruleus-norepinephrine and CRH mechanisms of the endocrine system.
2) Next, three steps of inflammatory modes are identifiable:
a) Endogenous reactions of the body characterized by central sensitization and hormone, neurotransmitter, and CNS mediated dysfunction. Nociceptive pain is not controlled due to sympathetic dominance.
b) Enterochromaffin, immunocytes, cytokine, lymphocyte, and mast cell proliferation occur throughout the submucosa and mucosa, and potentially other organs. This contributes to the above, but is caused by xenotoxics, endocrine disruptors, and allergy causing peptides from food. These do physical and chemical damage to the nerve cells.
c) Another gut-brain imbalance, characterized by improper pain mediation and serotonin balance, possibly mediated by raphe nuclei, the paraventricular nucleus of the hypothalamus, suprachiasmatic nucleus, and locus ceruleus, resulting in cholinergic dysfunction of the ascending and descending neuron fibers of the circular muscles of gut.
How dangerous are these sources of disease?
How do they interact with the human body in a way which is detrimental to long term health?
How is the ligation and policy within the current establishment structured to indemnify the pharmaceutical companies, seed companies, fertilizer companies, bio-tech companies, commodity distributors such as Archer Daniel midland/Walmart/Cargill, and centralized meat processing companies such as Tyson/Pilgrim pride?
What are the epidemiological correlations between autism, diabetes, pulmonary obstruction, arteriosclerosis, heart disease, high blood pressure, high triglycerides, high cholesterol, cancers, chrons disease, inflammatory bowel disease, irritable bowl syndrome, attention deficit disorder, depression, psychosis, pathological behavior, and other chronic diseases- in relation to the current establishment of cooperating industries and their policy decisions and the resulting organizational culture and disease management approach which is created in the medical community because of those policies?
What type of business deals have been engineered between this spectrum of related industries?
How do these agreements influence legislation, the broader economy, and patient care?