Fruit of the Contemplative Life
Fruit of the contemplative life: => Health, healing and fitness => : Jhanananda February 27, 2017, 06:06:58 PM
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Immune-mediated inflammatory diseases (http://)
An immune-mediated inflammatory disease (IMID) is any of a group of conditions or diseases that lack a definitive etiology, but which are characterized by common inflammatory pathways leading to inflammation, and which may result from, or be triggered by, a dysregulation of the normal immune response. All IMIDs can cause end organ damage, and are associated with increased morbidity and/or mortality.
Inflammation is an important and growing area of biomedical research and health care because inflammation mediates and is the primary driver of many medical disorders and autoimmune diseases, including ankylosing spondylitis, psoriasis, psoriatic arthritis, Behcet's disease, arthritis, inflammatory bowel disease (IBD), and allergy, as well as many cardiovascular, neuromuscular, and infectious diseases. Some current research even suggests that aging is a consequence, in part, of inflammatory processes.
Characterization
IMID is characterized by immune disregulation, and one underlying manifestation of this immune disregulation is the inappropriate activation of inflammatory cytokines, such as IL-12, IL-6 or TNF alpha, whose actions lead to pathological consequences.
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I stumbled across this condition yesterday, and saw that it might just be the description of my medical condition with the inflammatory agent being seasonal allergies, which has led to various organ deterioration, specifically the pancreas, leading to type II diabetes.
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I have come to realize that my decline in health after moving to Prescott, AZ is due to Immune-mediated inflammatory diseases, such as allergies. I have been seeing an allergist for about 9 months, and I have been taking high doses of antihistamines for nearly a year now, with impressive results in improved health, and weight loss of over 50lbs in 1 year.
A resent test showed that I have a total of 2692 Immunoglobulin E (https://en.wikipedia.org/wiki/Immunoglobulin_E). At that time I was tested for 25 common allergens. Among the things that I am allergic to, I am extremely allergic to: cat dander, mountain cedar, American elm, olive tree, cottonwood, Russian thistle, common pigweed, and sheep sorrel.
Immunoglobulin E (IgE) is a type of antibody (or immunoglobulin (Ig) "isotype") that has only been found in mammals. IgE is synthesised by plasma cells. IgE's main function is immunity to parasites such as helminths[2] like Schistosoma mansoni, Trichinella spiralis, and Fasciola hepatica.[3][4][5] IgE is utilized during immune defense against certain protozoan parasites such as Plasmodium falciparum.[6]
IgE also has an essential role in type I hypersensitivity,[7] which manifests in various allergic diseases, such as allergic asthma, most types of sinusitis, allergic rhinitis, food allergies, and specific types of chronic urticaria and atopic dermatitis. IgE also plays a pivotal role in responses to allergens, such as: anaphylactic drugs, bee stings, and antigen preparations used in desensitization immunotherapy.
Variations in the upper limit of normal total serum IgE have been reported: they can range from 150 to 1,000 UI/ml; but the usually accepted upper limit is between 150 and 300 UI/ml.
So, I have 2.5x the upper end of normal total serum IgE, which has led to: type II diabetes (https://en.wikipedia.org/wiki/Diabetes_mellitus_type_2), COPD (https://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease) and coronary heart disease (https://www.nhlbi.nih.gov/health-topics/coronary-heart-disease).
Type I hypersensitivity (https://en.wikipedia.org/wiki/Type_I_hypersensitivity) (or immediate hypersensitivity) is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen.[1] Type I is not to be confused with type II, type III, or type IV hypersensitivities, nor is it to be confused with Type I Diabetes or Type I of any other disease or reaction.
Exposure may be by ingestion, inhalation, injection, or direct contact.
Pathophysiology
In type 1 hypersensitivity, B-cells are stimulated (by CD4+TH2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM. During sensitisation, the IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils.[2] Mast cells and basophils coated by IgE antibodies are "sensitized". Later exposure to the same allergen cross-links the bound IgE on sensitized cells, resulting in anaphylactic degranulation, which is the immediate and explosive release of pharmacologically active pre-formed mediators from storage granules and concurrent synthesis of inflammatory lipid mediators from arachidonic acid;[3] some of these mediators include histamine, leukotriene (LTC4 and LTD4), and prostaglandin, which act on proteins (e.g., G-protein coupled receptors) located on surrounding tissues.[3] The principal effects of these products are vasodilation and smooth-muscle contraction.
Type 1 hypersensitivity can be further classified into immediate and late-phase reactions. The immediate hypersensitivity reaction occurs minutes after exposure and includes release of vasoactive amines and lipid mediators, whereas the late-phase reaction occurs 2–4 hours after exposure and includes the release of cytokines.[4]
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Good to hear, Jeff, that you found the source of those health problems! Hopefully now the doctor can diagnose a way to address them.
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Thanks, Alexander. That is my hope.
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From studying this subject I have come to realize that a number of my symptoms fall into the category of Anaphylaxis.
Anaphylaxis (https://en.wikipedia.org/wiki/Anaphylaxis)
Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death.[4][5] It typically causes more than one of the following: an itchy rash, throat or tongue swelling, shortness of breath, vomiting, lightheadedness, and low blood pressure.[1] These symptoms typically come on over minutes to hours.[1]
Common causes include insect bites and stings, foods, and medications.[1] Other causes include latex exposure and exercise.[1] Additionally cases may occur without an obvious reason.[1] The mechanism involves the release of mediators from certain types of white blood cells triggered by either immunologic or non-immunologic mechanisms.[6] Diagnosis is based on the presenting symptoms and signs after exposure to a potential allergen.[1]
The primary treatment of anaphylaxis is epinephrine injection into a muscle, intravenous fluids, and positioning the person flat.[1][7]
Worldwide, 0.05–2% of the population is estimated to experience anaphylaxis at some point in life.[3] Rates appear to be increasing.[3] It occurs most often in young people and females.[7][8] Of people who go to a hospital with anaphylaxis in the United States about 0.3% die.[9]
Signs and symptoms
Anaphylaxis typically presents many different symptoms over minutes or hours[7][11] with an average onset of 5 to 30 minutes if exposure is intravenous and 2 hours if from eating food.[12] The most common areas affected include: skin (80–90%), respiratory (70%), gastrointestinal (30–45%), heart and vasculature (10–45%), and central nervous system (10–15%)[13] with usually two or more being involved.[3]
Symptoms typically include generalized hives, itchiness, flushing, or swelling (angioedema) of the afflicted tissues.[4] Those with angioedema may describe a burning sensation of the skin rather than itchiness.[12] Swelling of the tongue or throat occurs in up to about 20% of cases.[14] Other features may include a runny nose and swelling of the conjunctiva.[15] The skin may also be blue tinged because of lack of oxygen.[15]
Respiratory
Respiratory symptoms and signs that may be present include shortness of breath, wheezes, or stridor.[4] The wheezing is typically caused by spasms of the bronchial muscles[16] while stridor is related to upper airway obstruction secondary to swelling.[15] Hoarseness, pain with swallowing, or a cough may also occur.[12]
Cardiovascular
Coronary artery spasm may occur with subsequent myocardial infarction, dysrhythmia, or cardiac arrest.[3][13] Those with underlying coronary disease are at greater risk of cardiac effects from anaphylaxis.[16] The coronary spasm is related to the presence of histamine-releasing cells in the heart.[16] While a fast heart rate caused by low blood pressure is more common,[15] a Bezold–Jarisch reflex has been described in 10% of cases where a slow heart rate is associated with low blood pressure.[8] A drop in blood pressure or shock (either distributive or cardiogenic) may cause the feeling of lightheadedness or loss of consciousness.[16] Rarely very low blood pressure may be the only sign of anaphylaxis.[14]
Other
Gastrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomiting.[4] There may be confusion, a loss of bladder control or pelvic pain similar to that of uterine cramps.[4][15] Dilation of blood vessels around the brain may cause headaches.[12] A feeling of anxiety or of "impending doom" has also been described.[3]
Causes
Anaphylaxis can occur in response to almost any foreign substance.[17] Common triggers include venom from insect bites or stings, foods, and medication.[8][18] Foods are the most common trigger in children and young adults while medications and insect bites and stings are more common in older adults.[3] Less common causes include: physical factors, biological agents such as semen, latex, hormonal changes, food additives such as monosodium glutamate and food colors, and topical medications.[15] Physical factors such as exercise (known as exercise-induced anaphylaxis) or temperature (either hot or cold) may also act as triggers through their direct effects on mast cells.[3][19] Events caused by exercise are frequently associated with the ingestion of certain foods.[12] During anesthesia, neuromuscular blocking agents, antibiotics, and latex are the most common causes.[20] The cause remains unknown in 32–50% of cases, referred to as "idiopathic anaphylaxis."[21] Six vaccines (MMR, varicella, influenza, hepatitis B, tetanus, meningococcal) are recognized as a cause for anaphylaxis, and HPV may cause anaphylaxis as well.[22] Physical exercise is an uncommon cause of anaphylaxis;[23] in about a third of such cases there is a co-factor like taking an NSAID or eating a specific food prior to exercising.[24]
Food
Many foods can trigger anaphylaxis; this may occur upon the first known ingestion.[8] Common triggering foods vary around the world. In Western cultures, ingestion of or exposure to peanuts, wheat, nuts, certain types of seafood like shellfish, milk, and eggs are the most prevalent causes.[3][13] Sesame is common in the Middle East, while rice and chickpeas are frequently encountered as sources of anaphylaxis in Asia.[3] Severe cases are usually caused by ingesting the allergen,[8] but some people experience a severe reaction upon contact. Children can outgrow their allergies. By age 16, 80% of children with anaphylaxis to milk or eggs and 20% who experience isolated anaphylaxis to peanuts can tolerate these foods.[17]
Medication
Any medication may potentially trigger anaphylaxis. The most common are β-lactam antibiotics (such as penicillin) followed by aspirin and NSAIDs.[13][25] Other antibiotics are implicated less frequently, and the reactions to NSAIDs are agent specific meaning that those who are allergic to one NSAID can typically tolerate a different one.[25] Other relatively common causes include chemotherapy, vaccines, protamine and herbal preparations.[3] Some medications (vancomycin, morphine, x-ray contrast among others) cause anaphylaxis by directly triggering mast cell degranulation.[8]
The frequency of a reaction to an agent partly depends on the frequency of its use and partly on its intrinsic properties.[26] Anaphylaxis to penicillin or cephalosporins occurs only after it binds to proteins inside the body with some agents binding more easily than others.[12] Anaphylaxis to penicillin occurs once in every 2,000 to 10,000 courses of treatment, with death occurring in fewer than one in every 50,000 courses of treatment.[12] Anaphylaxis to aspirin and NSAIDs occurs in about one in every 50,000 persons.[12] If someone has a reaction to penicillins, his or her risk of a reaction to cephalosporins is greater but still less than one in 1,000.[12] The old radiocontrast agents caused reactions in 1% of cases, while the newer lower osmolar agents cause reactions in 0.04% of cases.[26]
Venom
Venom from stinging or biting insects such as Hymenoptera (ants, bees, and wasps) or Triatominae (kissing bugs) may cause anaphylaxis in susceptible people.[7][27][28] Previous systemic reactions, which are anything more than a local reaction around the site of the sting, are a risk factor for future anaphylaxis;[29][30] however, half of fatalities have had no previous systemic reaction.[31]
Risk factors
People with atopic diseases such as asthma, eczema, or allergic rhinitis are at high risk of anaphylaxis from food, latex, and radiocontrast agents but not from injectable medications or stings.[3][8] One study in children found that 60% had a history of previous atopic diseases, and of children who die from anaphylaxis, more than 90% have asthma.[8] Those with mastocytosis or of a higher socioeconomic status are at increased risk.[3][8] The longer the time since the last exposure to the agent in question, the lower the risk.[12]
Pathophysiology
Anaphylaxis is a severe allergic reaction of rapid onset affecting many body systems.[5][6] It is due to the release of inflammatory mediators and cytokines from mast cells and basophils, typically due to an immunologic reaction but sometimes non-immunologic mechanism.[6]
Immunologic
In the immunologic mechanism, immunoglobulin E (IgE) binds to the antigen (the foreign material that provokes the allergic reaction). Antigen-bound IgE then activates FcεRI receptors on mast cells and basophils. This leads to the release of inflammatory mediators such as histamine. These mediators subsequently increase the contraction of bronchial smooth muscles, trigger vasodilation, increase the leakage of fluid from blood vessels, and cause heart muscle depression.[6][12] There is also an immunologic mechanism that does not rely on IgE, but it is not known if this occurs in humans.[6]
Non-immunologic
Non-immunologic mechanisms involve substances that directly cause the degranulation of mast cells and basophils. These include agents such as contrast medium, opioids, temperature (hot or cold), and vibration.[6][19] Sulfites may cause reactions by both immunologic and non-immunologic mechanisms.[32]
Diagnosis
Anaphylaxis is diagnosed on the basis of a person's signs and symptoms.[3] When any one of the following three occurs within minutes or hours of exposure to an allergen there is a high likelihood of anaphylaxis:[3]
Involvement of the skin or mucosal tissue plus either respiratory difficulty or a low blood pressure causing symptoms
Two or more of the following symptoms after a likely contact with an allergen:
a. Involvement of the skin or mucosa
b. Respiratory difficulties
c. Low blood pressure
d. Gastrointestinal symptoms
Low blood pressure after exposure to a known allergen
Skin involvement may include: hives, itchiness or a swollen tongue among others. Respiratory difficulties may include: shortness of breath, stridor, or low oxygen levels among others. Low blood pressure is defined as a greater than 30% decrease from a person's usual blood pressure. In adults a systolic blood pressure of less than 90 mmHg is often used.[3]
During an attack, blood tests for tryptase or histamine (released from mast cells) might be useful in diagnosing anaphylaxis due to insect stings or medications. However these tests are of limited use if the cause is food or if the person has a normal blood pressure,[3] and they are not specific for the diagnosis.[17]
Classification
There are three main classifications of anaphylaxis. Anaphylactic shock is associated with systemic vasodilation that causes low blood pressure which is by definition 30% lower than the person's baseline or below standard values.[14] Biphasic anaphylaxis is the recurrence of symptoms within 1–72 hours with no further exposure to the allergen.[3] Reports of incidence vary, with some studies claiming as many as 20% of cases.[33] The recurrence typically occurs within 8 hours.[8] It is managed in the same manner as anaphylaxis.[7] Pseudoanaphylaxis or anaphylactoid reactions are a type of anaphylaxis that does not involve an allergic reaction but is due to direct mast cell degranulation.[8][34] Non-immune anaphylaxis is the current term used by the World Allergy Organization[34] with some recommending that the old terminology no longer be used.[8]
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This is promising; however, I am not waiting for 10 years of double blind studies before the new drug is cleared. Today I started wearing a respirator all day long to see if it reduces my chronic caugh, so far only a few hours into it, and I seem to be coughing less.
Scientists Think They've Found a Way to Stop Allergic Reactions Before They Happen (http://www.sciencealert.com/discovery-how-antibody-stops-allergies-ige-blocks-reaction-mechanism?utm_source=ScienceAlert+-+Daily+Email+Updates&utm_campaign=43ee4a5320-MAILCHIMP_EMAIL_CAMPAIGN&utm_medium=email&utm_term=0_fe5632fb09-43ee4a5320-365491701)
Researchers have been working to find more effective allergy treatments, and now they've discovered how a particular antibody can stop an allergic reaction from happening altogether.
When the body is exposed to an allergen, the immune system goes into overdrive producing ridiculous amounts of a specific type of antibody called immunoglobulin E (IgE). It's a large, Y-shaped molecule that attaches itself to the immune cells tasked with releasing invader-attacking chemicals.
These compounds - especially histamine - go on to produce the varied and miserable symptoms of an allergy, whether it's a runny nose and eyes, or the more serious anaphylactic reaction that accompanies severe food allergies or insect bites.
Allergy tablets typically target these immune system compounds or their receptors, therefore preventing or at least easing the allergy symptoms. But if we target IgE itself, there's a chance to prevent the allergic reaction from even taking place.
A team led by scientists at Aarhus University in Denmark has now discovered a mechanism through which a particular anti-IgE antibody can make this miracle happen.
This new antibody, called 026 sdab, was first derived from llamas, and is akin to a range of such molecules discovered in camelid species and cartilaginous fishes.
The way 026 sdab works in the human body is by preventing IgE from getting to two specific types of immune receptors - CD23 and FceRI - and thus stopping the allergic reaction before it even starts.
There's already one anti-IgE therapy on the market, called omalizumab - it's approved in over 90 countries for the treatment of stubborn cases of allergic asthma, but isn't always effective.
According to the team, 026 sdab is a much smaller antibody than what's currently available or in development. It's also easier to produce, and is "extremely stable", which means it doesn't have to be injected like omalizumab does.
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Omalizumab (https://en.wikipedia.org/wiki/Omalizumab)
Omalizumab, sold under the trade name Xolair, is a medication originally designed to reduce sensitivity to allergens. It has been used to try to control severe allergic asthma, which does not respond to high doses of corticosteroids. It has been approved for treating people 12 years and older with severe or moderate to severe allergic asthma in more than 90 countries, since its first of such approval in 2002 in Australia. Omalizumab was approved in March 2014 in the European Union and the U.S.A. and in about 10 other countries for treating patients 12 years and above with chronic spontaneous urticaria (CSU) (also referred to as chronic idiopathic urticaria or CIU), which cannot be treated with H1-antihistamines. CSU is not an allergic disease.
Omalizumab is a recombinant DNA-derived humanized IgG1k monoclonal antibody that specifically binds to free human immunoglobulin E (IgE) in the blood and interstitial fluid and to membrane-bound form of IgE (mIgE) on the surface of mIgE-expressing B lymphocytes.[1] Unlike an ordinary anti-IgE antibody, it does not bind to IgE that is already bound by the high affinity IgE receptor (FcεRI) on the surface of mast cells, basophils, and antigen-presenting dendritic cells.[2]
IgE is commonly involved in type I hypersensitivity, which manifests in the most common allergic diseases. It has been estimated that as high as 20 to 40% of the populations who live a western lifestyle in economically advanced countries are affected by allergy and seek medical help.[3] In the U.S., 8% of adults and 10% of children have asthma.[4] Allergy occurs more frequently in individuals with higher serum IgE levels, though some allergic individuals have very low serum IgE, and some people with very high IgE have no allergic problems.[2]
Allergic asthma
Omalizumab received approval by the U.S. Food and Drug Administration (FDA) in 2003 for treating patients 12 years and older with moderate to severe allergic asthma.[5] It has also received approval in many other countries for treating patients 12 years and older with severe, persistent allergic asthma. Omalizumab was approved by the European Union in 2009 for treating patients 6 to 12 years old with severe, persistent allergic asthma. Thus, its primary use is for patients mostly with severe, persistent allergic asthma, uncontrollable with oral or injectable corticosteroids.[6] Those patients have already failed step I to step IV treatments and are in step V of treatment. Such a treatment scheme is consistent with the widely adopted guidelines for the management and prevention of asthma, issued by Global Initiative of Asthma (GINA), which was a medical guidelines organization launched in 1993 in collaboration with the National Heart, Lung, and Blood Institute, National Institutes of Health, USA, and the World Health Organization.[7] The efficacy is more evident among severe asthmatics than among those with moderately severe disease. The response rates among treated severe "allergic" asthma patients are 60-80% or higher, probably depending on the patient screening procedures used by the various clinical groups of different specialties. In real-life clinical practice of 142 and 195 patients in Italy and Germany, respectively, 77 to 79% of patients or physicians gave a response of “excellent or good” for GETE (global evaluation of treatment effectiveness) scale after being treated with omalizumab for four months.[8][9] Because 20 to 30% of adult asthma cases are not related to allergy,[9] a reliable way to identify treatable patients has been a subject of considerable research interest.[10][11] The primary benefits for the responding patients are reduced numbers of exacerbations, improved lung function, reduced numbers of emergency visits to the doctors, reduced days of hospitalization, and increased quality of life measurements.[8][9] The other major benefit is that most responding patients can reduce or spare entirely the use of corticosteroids, which cause multiple serious side effects, when used at high doses for extended periods.[12]
Due to the requirement for long-term administration and hence the high cost of an omalizumab treatment regimen, and to the concern over long-term safety, treatment is not yet very common, especially in developing countries where medical funds are relatively scarce. Another barrier to wide use is its injectable dosage form, which requires the patient to visit a physician's office or clinic every 2 to 4 weeks during treatment. In August 2010, the National Institute for Clinical Excellence (NICE) in the United Kingdom ruled that omalizumab should not be prescribed on the National Health Service (NHS) to children under 12, causing widespread condemnation from asthma charities.[13] NICE concluded that the high costs of the compound, over £250 per vial, did not represent a sufficiently high increase in quality of life. However, on March 7, 2013, NICE issued “final draft guidance” about the allowance of omalizumab. It recommended the drug as an option for treating severe, persistent allergic asthma in adults, adolescents and children following additional analyses and submission of a patient access scheme (PAS) by Novartis, the manufacturer.[14] Some immunologists have also suggested that because IgE may be a natural defense against parasitic diseases, treatment should not be recommended when living in environments where the presence of parasites is common.
Chronic spontaneous urticaria
Xolair was approved in March 2014 in the European Union and the U.S.A. and in about 10 other countries for treating patients 12 years and above with chronic spontaneous urticaria (also called chronic idiopathic urticaria), which cannot be treated with elevated doses of H1-antihistamines.
Chronic urticaria affect about 0.5 to 1% of the world population and among those patients, two thirds have CSU, and among them, about half cannot be adequately treated even with high doses (4 times regular doses) of H1-antihistamines.[15][16] Since CSU is not an allergic disease and does not obviously involve IgE, how omalizumab effectively treats CSU is currently a hotly pursued research subject. The serum concentrations of IgE in CSU patients are generally much lower than those in patients with allergic asthma.
Adverse effects
The main adverse effect is anaphylaxis (a life-threatening systemic allergic reaction), with a rate of occurrence of 1 to 2 patients per 1,000.[6][17] Like other protein and antibody drugs, omalizumab also causes anaphylaxis, although at a relatively low frequency among antibody drugs. The allergic reaction is probably not due to the binding characteristics of the antibody drug, but to the protein nature of the antibody[citation needed]. The patients who use omalizumab are generally highly allergic. Thus, even though the drug is administered with the purpose to suppress allergy (including anaphylactic reactions), it does not work immediately after injection.
It also increases the risk of strokes and heart disease by a small amount.[18]
IgE may play an important role in the immune system's recognition of cancer cells.[19] Therefore, indiscriminate blocking of IgE-receptor interaction with omalizumab may have unforeseen risks. The data pooled in 2003 from the earlier phase I to phase III clinical trials showed a numeric imbalance in malignancies arising in omalizumab recipients (0.5%) compared with control subjects (0.2%).[6] To clarify this imbalance, a more recent study was performed based on pooled analysis using much more comprehensive data from 67 phase I to IV clinical trials. The prespecified primary analysis assessed the incidence of primary malignancy in 32 randomized, double-blind, placebo-controlled (RDBPC) trials. In this analysis, there were 11,459 unique patients in all clinical trials (7,789 received omalizumab). The primary analysis identified malignancies in 25 patients (RDBPC trials): 14 in 4,254 omalizumab-treated patients and 11 in 3,178 placebo-treated patients. Incidence rates per 1,000 patient-years of observation time for omalizumab- and placebo-treated patients were 4.14 (95% CI, 2.26-6.94) and 4.45 (95% CI, 2.22-7.94), respectively; the corresponding rate ratio was 0.93 (95% CI, 0.39-2.27). Primary malignancies were of varying histologic type and occurred in a number of different organ systems; no cluster of histologies was identified. The study thus concluded that in this pooled analysis no association was observed between omalizumab treatment and risk of malignancy in RDBPC trials; the rate ratio was below unity. The data suggest that a causal relationship between omalizumab therapy and malignancy is unlikely.[20]
Concerns were raised earlier about possible induction of eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), a rare form of systemic vasculitis associated with asthma, in patients receiving the drug.[21] A retrospective review, which identified and analyzed cases of Churg-Strauss syndrome using the Novartis Argus global drug safety database for omalizumab in asthma patients, has indicated that Churg-Strauss syndrome may develop in patients who have an underlying eosinophilic disorder that is unmasked by the withdrawal of corticosteroids, which is common among patients receiving this treatment.[22]
20 to 40% of the populations who live a western lifestyle in economically advanced countries are affected by allergy
The above seems significant, and suggests industrial pollution as a cause.
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To understand how allergies work, and how to prevent an allergic reaction, we need to understand: Pollen (https://en.wikipedia.org/wiki/Pollen)and spores (https://en.wikipedia.org/wiki/Spore), and Terpene (https://en.wikipedia.org/wiki/Terpene).
Pollen (https://en.wikipedia.org/wiki/Pollen)
The smallest pollen grain, that of the forget-me-not (Myosotis spp.),[which?] is around 6 µm (0.006 mm) in diameter.[citation needed] Wind-borne pollen grains can be as large as about 90–100 µm.[2]
Allergy to pollen
Nasal allergy to pollen is called pollinosis, and allergy specifically to grass pollen is called hay fever. Generally, pollens that cause allergies are those of anemophilous plants (pollen is dispersed by air currents.) Such plants produce large quantities of lightweight pollen (because wind dispersal is random and the likelihood of one pollen grain landing on another flower is small), which can be carried for great distances and are easily inhaled, bringing it into contact with the sensitive nasal passages.
In the US, people often mistakenly blame the conspicuous goldenrod flower for allergies. Since this plant is entomophilous (its pollen is dispersed by animals), its heavy, sticky pollen does not become independently airborne. Most late summer and fall pollen allergies are probably caused by ragweed, a widespread anemophilous plant.[13]
Arizona was once regarded as a haven for people with pollen allergies, although several ragweed species grow in the desert. However, as suburbs grew and people began establishing irrigated lawns and gardens, more irritating species of ragweed gained a foothold and Arizona lost its claim of freedom from hay fever.
Anemophilous spring blooming plants such as oak, birch, hickory, pecan, and early summer grasses may also induce pollen allergies. Most cultivated plants with showy flowers are entomophilous and do not cause pollen allergies.
The number of people in the United States affected by hay fever is between 20 and 40 million,[14] and such allergy has proven to be the most frequent allergic response in the nation. There are certain evidential suggestions pointing out hay fever and similar allergies to be of hereditary origin. Individuals who suffer from eczema or are asthmatic tend to be more susceptible to developing long-term hay fever.[15]
In Denmark, decades of rising temperatures cause pollen to appear earlier and in greater numbers, as well as introduction of new species such as ragweed.[16]
The most efficient way to handle a pollen allergy is by preventing contact with the material. Individuals carrying the ailment may at first believe that they have a simple summer cold, but hay fever becomes more evident when the apparent cold does not disappear. The confirmation of hay fever can be obtained after examination by a general physician.[17]
Treatment
Main article: Allergic rhinitis § treatment
Antihistamines are effective at treating mild cases of pollinosis, this type of non-prescribed drugs includes loratadine, cetirizine and chlorpheniramine. They do not prevent the discharge of histamine, but it has been proven that they do prevent a part of the chain reaction activated by this biogenic amine, which considerably lowers hay fever symptoms.
Decongestants can be administered in different ways such as tablets and nasal sprays.
Allergy immunotherapy (AIT) treatment involves administering doses of allergens to accustom the body to pollen, thereby inducing specific long-term tolerance.[18] Allergy immunotherapy can be administered orally (as sublingual tablets or sublingual drops), or by injections under the skin (subcutaneous). Discovered by Leonard Noon and John Freeman in 1911, allergy immunotherapy represents the only causative treatment for respiratory allergies.
spores (https://en.wikipedia.org/wiki/Spore)
In biology, a spore is a unit of sexual or asexual reproduction that may be adapted for dispersal and for survival, often for extended periods of time, in unfavourable conditions. Spores form part of the life cycles of many plants, algae, fungi and protozoa.[1] Bacterial spores are not part of a sexual cycle but are resistant structures used for survival under unfavourable conditions.
Terpene (https://en.wikipedia.org/wiki/Terpene)
Terpenes (/ˈtɜːrpiːn/) are a large and diverse class of organic compounds, produced by a variety of plants, particularly conifers,[1] and by some insects such as termites or swallowtail butterflies, which emit terpenes from their osmeteria. They often have a strong odor and may protect the plants that produce them by deterring herbivores and by attracting predators and parasites of herbivores.[2][3] The difference between terpenes and terpenoids is that terpenes are hydrocarbons, whereas terpenoids contain additional functional groups.
They are the major components of resin, and of turpentine produced from resin. The name "terpene" is derived from the word "turpentine". In addition to their roles as end-products in many organisms, terpenes are also major biosynthetic building blocks within nearly every living creature. Steroids, for example, are derivatives of the triterpene squalene.
Terpene Toxicity (https://emedicine.medscape.com/article/818675-overview)
Background
Terpenes are natural products derived from plants that have medicinal properties and biological activity. Terpenes may be found in cleaning products, rubefacients, aromatherapy, and various topical preparations. Terpenes may exist as hydrocarbons or have oxygen-containing compounds such as ketone or aldehyde groups (terpenoids).
Pathophysiology
Terpenes are local irritants and, thus, are capable of causing GI signs and symptoms. CNS manifestations may range from an altered mental status to seizures to coma. Aspiration is a particular concern and can result in fatalities and long-term complications.
Absorption begins in the oral cavity and is rapid as evidenced by the early onset of toxicity in significant ingestions. Terpenes are metabolized through cytochrome P450 and are excreted as conjugated metabolites by the kidney.
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I have had an allergy caused lung infection for several weeks now. To deal with air-borne allergies it seems to me that just wearing a respirator would eliminate the allergen, so that anti-histamines may not be needed. Last week I purchased a respirator with a p95 filter on it. My health has improved since.
I chose the P95 filter because it is meant to filter out both particles, as well as hydrocarbons, such as terpenes.
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Are you able to enter jhana despite your illness?
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Yes.
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I developed a lung infection in mid January. My allergist has sent me in for a lot of tests. He tested me for TB, it was negative. He tested me for Valley Fever, it too was negative. However, he found I tested positive Aspergillosis.
Definition of Aspergillosis
Aspergillosis (https://www.cdc.gov/fungal/diseases/aspergillosis/index.html)is an infection caused by Aspergillus, a common mold (a type of fungus) that lives indoors and outdoors. Most people breathe in Aspergillus spores every day without getting sick. However, people with weakened immune systems or lung diseases are at a higher risk of developing health problems due to Aspergillus. The types of health problems caused by Aspergillus include allergic reactions, lung infections, and infections in other organs. There are different types of aspergillosis. Some types are mild, but some of them are very serious.
Types of aspergillosis
Allergic bronchopulmonary aspergillosis (ABPA): Aspergillus causes inflammation in the lungs and allergy symptoms such as coughing and wheezing, but doesn’t cause an infection.2
Allergic Aspergillus sinusitis: Aspergillus causes inflammation in the sinuses and symptoms of a sinus infection (drainage, stuffiness, headache) but doesn’t cause an infection.3
Aspergilloma: also called a “fungus ball.” As the name suggests, it is a ball of Aspergillus that grows in the lungs or sinuses, but usually does not spread to other parts of the body.4
Chronic pulmonary aspergillosis: a long-term (3 months or more) condition in which Aspergillus can cause cavities in the lungs. One or more fungal balls (aspergillomas) may also be present in the lungs.5
Invasive aspergillosis: a serious infection that usually affects people who have weakened immune systems, such as people who have had an organ transplant or a stem cell transplant. Invasive aspergillosis most commonly affects the lungs, but it can also spread to other parts of the body.
Cutaneous (skin) aspergillosis: Aspergillus enters the body through a break in the skin (for example, after surgery or a burn wound) and causes infection, usually in people who have weakened immune systems. Cutaneous aspergillosis can also occur if invasive aspergillosis spreads to the skin from somewhere else in the body, such as the lungs.6
Symptoms of Aspergillosis
The different types of aspergillosis can cause different symptoms.1
The symptoms of allergic bronchopulmonary aspergillosis (ABPA) are similar to asthma symptoms, including:
Wheezing
Shortness of breath
Cough
Fever (in rare cases)
Symptoms of allergic Aspergillus sinusitis2 include:
Stuffiness
Runny nose
Headache
Reduced ability to smell
Symptoms of an aspergilloma (“fungus ball”)3 include:
Cough
Coughing up blood
Shortness of breath
Symptoms of chronic pulmonary aspergillosis4,5 include:
Weight loss
Cough
Coughing up blood
Fatigue
Shortness of breath
Invasive aspergillosis1 usually occurs in people who are already sick from other medical conditions, so it can be difficult to know which symptoms are related to an Aspergillus infection. However, the symptoms of invasive aspergillosis in the lungs include:
Fever
Chest pain
Cough
Coughing up blood
Shortness of breath
Other symptoms can develop if the infection spreads from the lungs to other parts of the body.
Sources of Aspergillosis
Aspergillus lives in the environment
Aspergillus, the mold (a type of fungus) that causes aspergillosis, is very common both indoors and outdoors, so most people breathe in fungal spores every day. It’s probably impossible to completely avoid breathing in some Aspergillus spores. For people with healthy immune systems, breathing in Aspergillus isn’t harmful. However, for people who have weakened immune systems, breathing in Aspergillus spores can cause an infection in the lungs or sinuses which can spread to other parts of the body.
I’m worried that the mold in my home is Aspergillus. Should someone test the mold to find out what it is?
No. Generally, it’s not necessary to identify the species of mold growing in a home, and CDC doesn’t recommend routine sampling for molds. For more information about indoor mold, including cleanup and remediation recommendations, please visit CDC’s Basic Facts about Mold web page.
Types of Aspergillus
There are approximately 180 species of Aspergillus, but fewer than 40 of them are known to cause infections in humans. Aspergillus fumigatus is the most common cause of human Aspergillus infections. Other common species include A. flavus, A. terreus, and A. niger.
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A year and a half ago I found a dead tree with a large colony of oyster mushrooms growing on it. I have studied foraging behavior through foraging. I took up foraging for wild edible mushrooms about 12 years ago, when I lived in the Inyo National Forest. So, I looked up the mushroom in my Audubon Mushroom guide, and confirmed that it was in deed oyster mushroom. So, I extracted as much usable oyster mushroom. It was rainy season here, so I thinly sliced the mushrooms, and put them into cloth bags, and hung them from hooks inside my van. Within days I had a massive lung infection. A friend here had been looking into commercially growing mushrooms, so when he heard that I had been drying oyster mushrooms in my van, and saw that I had a lung infection, then he told me about "mushroom worker's lung."
Hypersensitivity pneumonitis (https://en.wikipedia.org/wiki/Hypersensitivity_pneumonitis)
Hypersensitivity pneumonitis (HP; also called allergic alveolitis or extrinsic allergic alveolitis, EAA) is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts. Sufferers are commonly exposed to the dust by their occupation or hobbies.
Signs and symptoms
Hypersensitivity pneumonitis (HP) is categorized as acute, subacute, and chronic based on the duration of the illness.[1]
Acute
In the acute form of HP, symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.[2]
Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.[2]
On chest radiographs, a diffuse micronodular interstitial pattern (at times with ground-glass density in the lower and middle lung zones) may be observed. Findings are normal in approximately 10% of patients." In high-resolution CT scans, ground-glass opacities or diffusely increased radiodensities are present. Pulmonary function tests show reduced diffusion capacity of lungs for carbon monoxide (DLCO). Many patients have hypoxemia at rest, and all patients desaturate with exercise.[2] Extrinsic allergic alveolitis may eventually lead to Interstitial lung disease.[3]
Subacute
Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones.[2] Findings may be present in patients who have experienced repeated acute attacks.
The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.[2]
Chronic
In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.[2]
On chest radiographs, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans.[2]
Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) associated with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.[2]
In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise.
Pathophysiology
Hypersensitivity pneumonitis involves inhalation of an antigen. This leads to an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity can both occur depending on the cause.[4]
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Last Friday I moved the ice-chest out of my van and discovered a large mat of fungi growing under it, which suggests the source of the fungi that is killing me, is in my van. It is probably Aspergillus. And, I bet it is common in Prescott.
Last Friday I moved the ice-chest out of my van and discovered a large mat of fungi growing under it, which suggests the source of the fungi that is killing me, is in my van. It is probably Aspergillus. And, I bet it is common in Prescott.
My new host here, has offered a trailer for me to move into. I plan to do so today, to reduce further exposure to Aspergillus.
Also, two toes on my right foot have been in extreme pain for the last 24 hours. During my morning shower today I found one swollen and the other white. They may have to be amputated soon, but I am going to try soaking them in hot water and salt, and massaging them regularly to see if I can rehab them. It is the consequence of diabetic neuropathy.Peripheral neuropathy
Peripheral neuropathy (https://en.wikipedia.org/wiki/Peripheral_neuropathy)
Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include systemic diseases (such as diabetes or leprosy), hyperglycemia-induced glycation,[1][2][3] vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including metronidazole and the fluoroquinolone class of antibiotics (Ciprofloxacin, Levaquin, Avelox etc.), traumatic injury, including ischemia, radiation therapy, excessive alcohol consumption, immune system disease, Coeliac disease, or viral infection. It can also be genetic (present from birth) or idiopathic (no known cause).[4][5][6] In conventional medical usage, the word neuropathy (neuro-, "nervous system" and -pathy, "disease of")[7] without modifier usually means peripheral neuropathy.
Neuropathy affecting just one nerve is called "mononeuropathy" and neuropathy involving nerves in roughly the same areas on both sides of the body is called "symmetrical polyneuropathy" or simply "polyneuropathy". When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called "mononeuritis multiplex", "multifocal mononeuropathy", or "multiple mononeuropathy".[4][5][6]
Peripheral neuropathy may be chronic (a long-term condition where symptoms begin subtly and progress slowly) or acute (sudden onset, rapid progress, and slow resolution). Acute neuropathies demand urgent diagnosis. Motor nerves (that control muscles), sensory nerves, or autonomic nerves (that control automatic functions such as heart rate, body temperature, and breathing) may be affected. More than one type of nerve may be affected at the same time. Peripheral neuropathies may be classified according to the type of nerve predominantly involved, or by the underlying cause.[4][5][6]
Neuropathy may cause painful cramps, fasciculations (fine muscle twitching), muscle loss, bone degeneration, and changes in the skin, hair, and nails. Additionally, motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or skin allodynia (severe pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally.[4][5][6]
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I feel so bad reading the status of your health. I m not sure but cant deep meditation give some not yet known remedy for the issues u r having with ur health, the diabetes? I wish u speedy recovery from all the pain without having to amputate any Toes!!
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Thank-you, Naman, for expressing your kind thoughts for my recovery. Yesterday I moved out of the van and into a trailer that a friend offered to me to stay in. My health has improved considerably. So, I am sure that the van was a disease vector for me.
In my experience deep meditation can be a very powerful tool for healing work. I regularly use it on myself; and I have used it for decades for the treating of others. Another use that deep meditation offers is insight. I have used insight to work through the causes of my ill-health. I am confident that when I can move from Prescott, AZ, then my health will improve.
The current plan is, once the deuce and a half is finished being brought up to road-worthy performance, then I plan to purchase a cab-over camper for it, and install solar panels on it, and travel about the sw USA.
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That sounds great, have you thought of washing out the van with betadine or alcohol?
I'm pretty interested in how deep meditation can be used for treating others as well.
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Thank-you, Naman, for expressing your kind thoughts for my recovery. Yesterday I moved out of the van and into a trailer that a friend offered to me to stay in. My health has improved considerably. So, I am sure that the van was a disease vector for me.
In my experience deep meditation can be a very powerful tool for healing work. I regularly use it on myself; and I have used it for decades for the treating of others. Another use that deep meditation offers is insight. I have used insight to work through the causes of my ill-health. I am confident that when I can move from Prescott, AZ, then my health will improve.
The current plan is, once the deuce and a half is finished being brought up to road-worthy performance, then I plan to purchase a cab-over camper for it, and install solar panels on it, and travel about the sw USA.
Thats great to hear that ur health is improved.
Im sure that meditation is also helping to improve ur body.
Whats the destination ? Anywhere specific are you aiming to go or will u keep moving around the location?
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Thank-you, bodhimind and Naman, for posting your comments and concern. The van is toast, so I do not plant to do anything with it, except to bake it out at about 120F to kill any molds or bugs in it. I plan only to remove useful things out of it, then call the junkyard, and have them tow it away.
It is reasonable that regular access to deep meditation, as I have had for 45 years, may be good for one's health; nonetheless, my health problems seem to be an inherited autoimmune disorder; and associated with airborne allergens, so my current solution is to wear a respirator during the day, and sleep with a HEPA filter near my bed. I am also now wearing swimmer's goggles to protect my eyes from airborne allergens. These three measures, in addition to evacuating the van, seem to have improved my health.
The plan is to hit the road as soon as I can get my deuce and a half running, and a camper on it, then I plan to travel until I find a place where I have fewer allergies. In the past, it has required moving with the seasons. So, I might just go back to that.
Yes, deep meditation can be used for healing self, and others. We can discuss that under another topic thread.
This resent article supports my findings.
Type 2 Diabetes Was Misdiagnosed All Along, It Could Actually Be Several Diseases (https://www.sciencealert.com/type-2-diabetes-could-be-many-diseases-not-one)
What if diabetes wasn't just one condition with two types, but a whole bunch of diseases under the same label?
That's the conclusion of new research, and it could revolutionise the way we detect and treat diabetes in the future.
Analysing past studies covering a total of 14,775 type 1 and type 2 adult-onset diabetes patients across Sweden and Finland, scientists have found five different and distinct disease profiles, including three severe and two mild forms of the condition.
The more precise we can be about different categories of diabetes, the better we can understand and treat it, according to the team of researchers from Scandinavia
It might even give doctors an earlier window of opportunity for preventing the onset of diabetes.
"Evidence suggests that early treatment for diabetes is crucial to prevent life-shortening complications," says senior researcher Leif Groop, from the Lund University Diabetes Centre (LUDC) in Sweden.
"More accurately diagnosing diabetes could give us valuable insights into how it will develop over time, allowing us to predict and treat complications before they develop."
Six different measurements were used across four separate studies: age at diagnosis, body mass index (BMI), long-term glycaemic (blood sugar) control, the function of insulin-producing cells in the pancreas, insulin resistance, and the presence of specific autoantibodies linked to autoimmune diabetes (http://diabetes.diabetesjournals.org/content/54/suppl_2/S68).
Instead of splitting diabetes simply into type 1 and type 2, the researchers came up with five different disease profiles - one autoimmune type of diabetes and four other distinct subtypes. All five types were found to be genetically distinct, with no shared mutations.
This is enough to suggest we're looking at five distinct diseases that all affect the same body system, rather than the same disease at different stages of progression, say the researchers.
So how did they differ? One of the three more serious forms was a group of people with severe insulin resistance and a significantly higher risk of kidney disease. Another more mild type was seen mostly in elderly people.
You can see how those distinctions could improve the way we tackle diabetes – by identifying the types of patients involved and the complications they're at risk from, doctors could work out more personalised courses of treatment.
Indeed, the researchers found that many in the study weren't being given the right treatment for the particular characteristics of the diabetes they had.
With diabetes now the fastest-growing disease on the planet, more options for dealing with it can't come soon enough. More than 420 million people are now thought to have diabetes worldwide.
Between 75-85 percent of people with diabetes have the more common type 2, where the body can't produce enough insulin to cope with levels of insulin resistance.
The researchers do note some limitations though: there's no evidence yet that these five types of diabetes have different causes, and the sample only included Scandinavian patients, so a wider study is going to be required to investigate this further.
"Existing treatment guidelines are limited by the fact they respond to poor metabolic control when it has developed, but do not have the means to predict which patients will need intensified treatment," says Groop.
"This study moves us towards a more clinically useful diagnosis, and represents an important step towards precision medicine in diabetes."
The research has been published in The Lancet Diabetes & Endocrinology.
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The original article on Autoimmune diabetes was published in Lancet:
Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables (http://www.thelancet.com/journals/landia/article/PIIS2213-8587(18)30051-2/fulltext?elsca1=tlpr)
Summary
Background
Diabetes is presently classified into two main forms, type 1 and type 2 diabetes, but type 2 diabetes in particular is highly heterogeneous. A refined classification could provide a powerful tool to individualise treatment regimens and identify individuals with increased risk of complications at diagnosis.
Methods
We did data-driven cluster analysis (k-means and hierarchical clustering) in patients with newly diagnosed diabetes (n=8980) from the Swedish All New Diabetics in Scania cohort. Clusters were based on six variables (glutamate decarboxylase antibodies, age at diagnosis, BMI, HbA1c, and homoeostatic model assessment 2 estimates of β-cell function and insulin resistance), and were related to prospective data from patient records on development of complications and prescription of medication. Replication was done in three independent cohorts: the Scania Diabetes Registry (n=1466), All New Diabetics in Uppsala (n=844), and Diabetes Registry Vaasa (n=3485). Cox regression and logistic regression were used to compare time to medication, time to reaching the treatment goal, and risk of diabetic complications and genetic associations.
Findings
We identified five replicable clusters of patients with diabetes, which had significantly different patient characteristics and risk of diabetic complications. In particular, individuals in cluster 3 (most resistant to insulin) had significantly higher risk of diabetic kidney disease than individuals in clusters 4 and 5, but had been prescribed similar diabetes treatment. Cluster 2 (insulin deficient) had the highest risk of retinopathy. In support of the clustering, genetic associations in the clusters differed from those seen in traditional type 2 diabetes.
Interpretation
We stratified patients into five subgroups with differing disease progression and risk of diabetic complications. This new substratification might eventually help to tailor and target early treatment to patients who would benefit most, thereby representing a first step towards precision medicine in diabetes.
Funding
Swedish Research Council, European Research Council, Vinnova, Academy of Finland, Novo Nordisk Foundation, Scania University Hospital, Sigrid Juselius Foundation, Innovative Medicines Initiative 2 Joint Undertaking, Vasa Hospital district, Jakobstadsnejden Heart Foundation, Folkhälsan Research Foundation, Ollqvist Foundation, and Swedish Foundation for Strategic Research.
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Last week the local newspaper ran an article on the Prescott, AZ local allergy problem (https://www.dcourier.com/news/2018/apr/14/why-allergies-prescott-are-so-bad/). It claims that Prescott, AZ has the worst seasonal allergies of any city in the USA. I believe it.
It has been a month since I was last in the hospital, and I am 2.5 weeks into full recovery, just from using HEPA filters in my trailer, and when I leave the trailer, then I now wear a full-face respirator. It is all helping. From disastrous experiments I have found that I can get away with a few minutes without the respirator, but an hour will result, during peak allergy season, in a health crisis.
HEPA filter (https://en.wikipedia.org/wiki/HEPA)
High efficiency particulate air (HEPA),[1][2] originally called high-efficiency particulate absorber but also sometimes called high-efficiency particulate arresting or high-efficiency particulate arrestance, is a type of air filter. Filters meeting the HEPA standard have many applications, including use in medical facilities, automobiles, aircraft and homes. The filter must satisfy certain standards of efficiency such as those set by the United States Department of Energy (DOE).
To qualify as HEPA by industry standards, an air filter must remove (from the air that passes through) 99.97% of particles that have a size greater-than-or-equal-to 0.3 µm.[3] Although the ASME industry standard is not published by any government, it is recognized as an authoritative standard by many governments.
HEPA was commercialized in the 1950s, and the original term became a registered trademark and later a generic term for highly efficient filters.[4]
What they do
HEPA filters are composed of a mat of randomly arranged fibres.[5] The fibres are typically composed of fiberglass and possess diameters between 0.5 and 2.0 micrometers. Key factors affecting its functions are fibre diameter, filter thickness, and face velocity. The air space between HEPA filter fibres is typically much greater than 0.3 μm. The common assumption that a HEPA filter acts like a sieve where particles smaller than the largest opening can pass through is incorrect and impractical. Unlike membrane filters at this pore size, where particles as wide as the largest opening or distance between fibres can not pass in between them at all, HEPA filters are designed to target much smaller pollutants and particles. These particles are trapped (they stick to a fibre) through a combination of the following three mechanisms:
Interception
where particles following a line of flow in the air stream come within one radius of a fibre and adhere to it.
Impaction
where larger particles are unable to avoid fibres by following the curving contours of the air stream and are forced to embed in one of them directly; this effect increases with diminishing fibre separation and higher air flow velocity.
Diffusion
an enhancing mechanism that is a result of the collision with gas molecules by the smallest particles, especially those below 0.1 µm in diameter, which are thereby impeded and delayed in their path through the filter; this behaviour is similar to Brownian motion and raises the probability that a particle will be stopped by either of the two mechanisms above; this mechanism becomes dominant at lower air flow velocities.
Diffusion predominates below the 0.1 μm diameter particle size. Impaction and interception predominate above 0.4 μm. [6] In between, near the most penetrating particle size (MPPS) 0.21 μm, both diffusion and interception are comparatively inefficient.[7] Because this is the weakest point in the filter's performance, the HEPA specifications use the retention of particles near this size (0.3 μm) to classify the filter.[6] However it is possible for particles smaller than the MPPS to not have filtering efficiency greater than that of the MPPS. This is due to the fact that these particles can act as nucleation sites for mostly condensation and form particles near the MPPS.[7]
Lastly, it is important to note that HEPA filters are designed to arrest very fine particles effectively, but they do not filter out gasses and odor molecules. Circumstances requiring filtration of volatile organic compounds, chemical vapors, cigarette, pet, and/or flatulence odors call for the use of an activated carbon (charcoal) or other type of filter instead of or in addition to a HEPA filter.[8]
Specifications
HEPA filters, as defined by the United States Department of Energy (DOE) standard adopted by most American industries, remove at least 99.97% of airborne particles 0.3 micrometers (µm) in diameter. The filter's minimal resistance to airflow, or pressure drop, is usually specified around 300 pascals (0.044 psi) at its nominal volumetric flow rate.
The specification usually used in the European Union is the European Norm EN 1822:2009. It defines several classes of HEPA filters by their retention at the given most penetrating particle size (MPPS):
Today, a HEPA filter rating is applicable to any highly efficient air filter that can attain the same filter efficiency performance standards as a minimum and is equivalent to the more recent National Institute for Occupational Safety and Health N100 rating for respirator filters. The United States Department of Energy (DOE) has specific requirements for HEPA filters in DOE regulated applications. In addition, companies have begun using a marketing term known as "True HEPA" to give consumers assurance that their air filters are indeed certified to meet the HEPA standard.[9]
Products that claim to be "HEPA-type", "HEPA-like", "HEPA-style" or "99% HEPA" do not satisfy these requirements and may not have been tested in independent laboratories. Some of these sub-par quality filters may come reasonably close to HEPA filtration, while others will fall significantly short, making them truly inferior.[10]
Biomedical applications
HEPA filters are critical in the prevention of the spread of airborne bacterial and viral organisms and, therefore, infection. Typically, medical-use HEPA filtration systems also incorporate high-energy ultra-violet light units to kill off the live bacteria and viruses trapped by the filter media. Some of the best-rated HEPA units have an efficiency rating of 99.995%, which assures a very high level of protection against airborne disease transmission.
3M Cartridges & Filters for Worker Health & Safety (https://www.3m.com/3M/en_US/company-us/all-3m-products/~/All-3M-Products/Safety/Worker-Health-Safety/Personal-Protective-Equipment/Reusable-Respirators/Cartridges-Filters/?N=5002385+8709322+8711017+8711405+8720539+8720550+8720746+3294857497&rt=r3)
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Its been long since i visited GWV. How is your health Jhanananda?
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Thank-you, Naman, for expressing your concern for my health. It took me about 8 years to work through my health problems, which turned out to be off-scale allergies to local pollens, molds, and terpines. It turned out all I had to do was sleep every night with purified air from a HEPA filter. My health has improved immensely. Even arthritic joint pain is way down.
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Good to hear you're hanging in there and feeling better. What a struggle life is sometimes, but a chance to use our enginuity and learn. Jhanananda, what do you think of the keto diet?
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Thanks, DDawson. The ketogenic diet really did nothing for my diabetes, and other health issues. I finally got all of my vitals normalized, even my blood sugar, by getting my allergies under control. At first it took 3x normal dose of antihistamines to do so; but it lead to kidney disease. Then I switched to filtering the air I breath when my body sleeps with a HEPA filter. At that point I stopped taking antihistamines.
Along the way I started losing 5lbs (2KG) per month. At first losing the extra weight that I had gained after moving to Prescott, AZ was nice. However, when I got to 160lb (80KG) I felt like I was wasting away. So, I started adding carbohydrates to my diet. When I got to about 50g of carbohydrates per meal my weight increased to 165lbs, and it has now stabilized.
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Such a hard painful work it is sometimes to find the cause of physical ailment which no other is able to identify or have a cure for.
Im so glad that u finally were able to pin point the cause and work it all out for good.
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Thanks, Naman, yes, it took me 8 years to realize that both the medical model and the natural health model of healing are deeply flawed. I plan to write a book on my findings, to help others.
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It wud be really great if u will sum it up all for the rest of the humanity to learn from.
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Thanks, I am working on it.
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This is what my life has been for 19 years Snowflake, Arizona: where the residents are allergic to life (https://youtu.be/sMzEmvv48pE)
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Wow this is happening to others as well.
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Yes, Naman, MCS suffers are a very small part of the population. We often times are driven mad with the condition, which few doctors understand.
Multiple chemical sensitivity (https://en.wikipedia.org/wiki/Multiple_chemical_sensitivity) (MCS), also known as idiopathic environmental intolerances (IEI), is a complex chronic condition symptoms characterized by non-specific symptoms that the affected person attributes to encountering small amounts of common substances, such as perfume. The etiology, diagnosis and treatment of MCS are controversial and still debated among researchers, but a 2018 review concluded that a hyperactive limbic system and autonomic nervous system were confirmed features of the condition.[1] A 2018 systematic review concluded that the evidence suggests that organic abnormalities in sensory processing pathways and the limbic system combined with some specific, uncommon personality traits (such as heightened attentional bias) best explains this condition.[2]
Commonly attributed substances for MCS symptoms include scented products, pesticides, plastics, synthetic fabrics, smoke, petroleum products, and paint fumes.[3]
MCS symptoms are typically vague and non-specific. They may include fatigue, headaches, nausea, and dizziness. Although the symptoms of MCS themselves are real, and can be disabling, MCS is not recognized as a separate, discrete disease by the World Health Organization, American Medical Association, or by several other professional medical organizations.
Signs and symptoms
Symptoms range in severity from mild to disabling.
Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.[3]
A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic, anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth and eyes, and an overactive bladder.[3][8][9][10]
Causes
There is no clear consensus for the cause or causes of the symptoms of MCS. A 2007 National Institute of Environmental Health Sciences paper defined MCS as a "chronic, recurring disease caused by a person's inability to tolerate an environmental chemical or class of foreign chemicals".[11] A 2018 systematic review concluded that the evidence suggests that abnormalities in sensory processing pathways combined with peculiar personality traits best explains this condition.[2]
In addition to extreme sensitivity to low concentrations of certain chemicals, several hypotheses have been proposed. The distinction between physiological and psychological causes is often difficult to test,[6] and it is particularly challenging for MCS because many substances used to test for sensitivity have a strong odor. Odor cues make double blind studies of MCS patients difficult, as scents can provoke a psychosomatic response or recall expectations and prior beliefs.[6]
Chemical triggers
Many chemicals have been reported to trigger MCS symptoms.[12] Substances with strong scents are the most commonly reported triggers. These include a variety of cleaning agents, pesticides, perfumes, vehicle exhaust, the products used in barber shops and beauty salons, new carpeting, new furniture, chlorine and fluoride in drinking water, fresh ink, and less commonly wood smoke and secondhand tobacco smoke.[13][14] Food items reported as triggers include tartrazine (a.k.a. FD&C Yellow #5 or E102), and other azo dyes[15] (in the absence of an allergy), caffeine, and monosodium glutamate.[16]
Immune
One proposed hypothesis for the cause of multiple chemical sensitivity is immune system dysfunction after being sensitized by a chemical exposure.
Diagnosis
No characteristically unique signs, laboratory test abnormalities, tissue pathology, or course of illness have been identified, and it remains unclear whether symptoms are physiologically or psychologically generated.[32][33]
International Classification of Diseases
The International Statistical Classification of Diseases and Related Health Problems (ICD), maintained by the World Health Organization, does not recognize multiple chemical sensitivity or environmental sensitivity as a valid diagnosis.[4] The American Medical Association does not recognize MCS as an organic disease because of the lack of scientific evidence supporting a cause-and-effect relationship between very low level exposure and the symptoms of MCS. The American Academy of Allergy, Asthma, and Immunology, the California Medical Association, the American College of Physicians, and the International Society of Regulatory Toxicology and Pharmacology also do not recognize MCS.[5][12][34] The US Occupational Safety and Health Administration (OSHA) indicates that MCS is highly controversial and that there is insufficient scientific evidence to explain the relationship between the suggested causes of MCS and its symptoms. OSHA recommends evaluation by a physician knowledgeable of the symptoms presented.[35]
Other
In response to a WHO call for papers at the 5th Paris Appeal Congress of Environmental Idiopathic Intolerance conference that took place in Belgium on 18 May 2015, a report that was generally supportive quoted a number of international practitioners.[36] This was provisionally accepted by the Spanish health ministry, and later found proven by a judge in the case of a plumber in the Province of Castellón.[37]
MCS is a diagnosis of exclusion, and the first step in diagnosing a potential MCS sufferer is to identify and treat all other conditions which are present and which often explain the reported symptoms. For example, depression, allergy, thyroid disorders, orthostatic syndromes, lupus, hypercalcemia, and anxiety need to be carefully evaluated and, if present, properly treated. The "gold standard" procedure for identifying a person who has MCS is to test response to the random introduction of chemicals the patient has self-identified as relevant. This may be done in a carefully designed challenge booth to eliminate the possibility of contaminants in the room. Chemicals and controls, sometimes called prompts, are introduced in a random method, usually scent-masked. The test subject does not know when a prompt is being given. Objective and subjective responses are measured. Objective measures, such as the galvanic skin response,[38] indicate psychological arousal, such as fear, anxiety, or anger. Subjective responses include patient self-reports. A diagnosis of MCS can only be justified when the subject cannot consciously distinguish between chemicals and controls, and when responses are consistently present with exposure to chemicals and consistently absent when prompted by a control.
A 1999 consensus statement recommends that MCS be diagnosed according to six standardized criteria:[4][39]
Symptoms are reproducible with repeated (chemical) exposures
The condition has persisted for a significant period of time
Low levels of exposure (lower than previously or commonly tolerated) result in manifestations of the syndrome (i.e. increased sensitivity)
The symptoms improve or resolve completely when the triggering chemicals are removed
Responses often occur to multiple chemically unrelated substances
Symptoms involve multiple-organ symptoms (runny nose, itchy eyes, headache, scratchy throat, ear ache, scalp pain, mental confusion or sleepiness, palpitations of the heart, upset stomach, nausea, diarrhea, abdominal cramping and aching joints).
Treatment
It has been suggested that a multidisciplinary approach be taken to treating this condition that takes into account peculiar personality traits often seen in affected individuals and physiological abnormalities in sensorary pathways and the limbic system.[2]
In various studies, about one half of the patients who seek medical treatment for symptoms of MCS meet the criteria for depressive and anxiety disorders.[17] Because many people eliminate whole categories of food in an effort to reduce symptoms, a complete review of the patient's diet may be needed to avoid nutritional deficiencies.[40]
Epidemiology
Epidemiological data from three states put the prevalence of chemical sensitivity in 1999 at 16% to 33% of the general population, 2% to 6% of whom have already been diagnosed with MCS.[41] Women complain of MCS significantly more often than men, and most patients are 30 to 50 years old at time of diagnosis.
History
MCS was first proposed as a distinct disease by Theron G. Randolph in 1950. In 1965, Randolph founded the Society for Clinical Ecology as an organization to promote his ideas about symptoms reported by his patients. As a consequence, clinical ecology emerged as a non-recognized medical specialty.[46] In 1984, the Society for Clinical Ecology changed its name to American Academy of Environmental Medicine (AAEM). In the 1990s, an association was noted with chronic fatigue syndrome, fibromyalgia, and Gulf War syndrome.[41]
In 1994, the AMA, American Lung Association, US EPA and US Consumer Product Safety Commission published a booklet on indoor air pollution that discusses MCS, among other issues. The booklet further states that a pathogenesis of MCS has not been definitively proven, and that symptoms that have been self-diagnosed by a patient as related to MCS could actually be related to allergies or have a psychological basis, and recommends that physicians should counsel patients seeking relief from their symptoms that they may benefit from consultation with specialists in these fields.[47]
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Thankyou for the quoted information.
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My goal in this post is to make public recent findings before death. As many of you know I came down with a severe lung infection almost 2 years. At that time I garnered the diagnosis of Chronic Obstructive Pulmonary Disease (COPD), even though I was not a smoker. I also received a referral to several other doctors, so I acquired 5 more. Lots of tests later, I could see that none of them expected me to live much longer.
I recall at the moment of "infection" I had left my van, which I lived in at the time, and was parked at the curb in a commercial neighborhood, to do something, I cannot recall. However, I do recall seeing the neighborhood was full of smoke from one or more smoldering hearth fires, and I could tell from the offensive smell of the smoke at least one of those hearths was burning elm-wood, which is a local wood, considered trash, because it produce such an offensive smelling smoke.
That night I coughed none stop until I called a friend that morning to transport me to the ER. They conducted an x-ray which revealed several sights of damage. Days later blood tests were conducted by my allergist who had concluded that I most probably had acquired a fungal infection. He prescribed an anti-fungal medication to be taken 1 does per day for 7 days. The box said it was a medication used to treat anthrax." I looked up the medication on Google, and found that it could lead to kidney disease.
After the medication cycle I did have some recovery, but I was still very ill. A friend invited me to move into a vacant travel trailer in her yard, and provided me with a power cord. I moved right over to her yard. I also asked a friend to take me to Walmart where I purchased a HEPA filter, because it seemed reasonable to filter out the allergens in the air that I would breath. I found as long as I remained within 2 feet of the HEPA filter 24/7, with all of the windows and doors closed, then I had continual recovery, which took 2 months. After that I had 2 relapses, the last of which the ER doctor found I had kidney failure.
So, 2 years into slow, but sure recovery I can conclude that the HEPA filter has done more for improving my health than anything I have done in my life that has been dedicated to optimum health for 45 years. However, I have been back in the ER with respiratory, and/or autoimmune issues two more times that year since recovery; and 4 times now this year.
A few days ago I began to feel very ill, even though I had been in my HEPA filtered environment with a new HEPA filter for about 18 hours. Not understanding why I felt so bad I drove to the ER. They found all my vitals relatively normal, but marginal; however my blood sugar was 2 times over normal, but I felt profoundly ill. I have had a blood sugar at 200 or higher without feeling as bad as I did that day. After 4 hours I had sufficient recovery to be released. I drove to the Salvation Army where I picked up some surplus donated perishables, and drove back to the park.
At the park I started to feel severely ill again. During my 4 hour stay in the ER I pondered my current ill health, and why the HEPA filter did not seem to work that day. I also had observed that there was a control burn in the nearby forest, and there was cloud cover with an approaching storm. I reasoned that there must have been elevated levels of organic vapor in the air that was being held in by the cloud cover, which a HEPA filter is not going to remove. I also recalled that one of my DIY air purifiers had activated charcoal, which I had added to see if it would improved my health. Since I built it last March I had found that DIY air purifier made me feel healthier, and had recovery faster, than just a HEPA filter only.
However, feeling bad after only a 1/2 hour from the ER, I checked my blood oxygen concentration with a pulse oximeter. I found my blood oxygen concentration was at 50%. I was experiencing a dark halo around my vision suggesting unconsciousness was coming soon. So, I struggled to get my current model air purifier running, and put on the respirator mask. I found my blood oxygen concentration rose to 98% (my normal) within minutes. I remained resting with the air purifier running until I had full recovery. It took only an hour. I now use it 24/7.
Sadly, the medical equipment industry does not offer any air-filtration equipment for people with COPD; and none of my medical doctors, and ER doctors, seem to understand my auto-immune problems.
Conclusions: The original lung infection from 2 years ago was most probably caused by a severe allergic reaction to air-borne combustion byproducts, among other things. HEPA filtration of air is insufficient to remove all of those byproducts of the combustion of wood to maintain my health, but it is a partial solution, Adding activated charcoal to my air-processing system appears to be a complete solution. We will see if I have full recovery. I feel much better now, and am now designing modifications to the 3 air-purifying systems that I use to include activated charcoal.
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Hello Jeff,
I hope you are feeling better after going through all this! Are you on Medicare? Do they give you adequate care? The only other thing I can think of is perhaps relocating, to another state, or even to another country with socialized medicine, where perhaps you could escape the pollutants and get better treatment. Do you think you might fare better in CA, OR, or CO?
While I am not hastening the arrival of death just as you are, I for one ultimately look forward to it. Perhaps recompense will finally come then, leaving the difficult adversities of this experience behind at last. :)
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Hello Jeff,
I hope you are feeling better after going through all this! Are you on Medicare? Do they give you adequate care? The only other thing I can think of is perhaps relocating, to another state, or even to another country with socialized medicine, where perhaps you could escape the pollutants and get better treatment. Do you think you might fare better in CA, OR, or CO?
Thank-you, Alexander, for posting your concern for my welfare. Actually I have been on AHCCCS for the 20 years that I have dropped out of society in pursuit of truth. AHCCCS has actually provided me, as a poor person, with excellent medical health. In fact in the last 2 years of severe health issues I have surely cost US American socialized medicine great deal of money.
By the way, my last trip to the ER, which was last week, the EKG tech who did an EKG on me, said,"Did you know that Prescott often has the highest pollen levels in the nation."
I heard that 3 years ago from their respiratory therapist when she was giving me a breathing treatment. I have to thank her, especially, and him as well, for being the only health professionals in Prescott, AZ, who told me that. To date, none of my physicians told me that, which alerts me to the fact that the AMA might not be doing any of us a favor.
Since then I have been paying a great deal of attention to air quality in Prescott, AZ. I have found that they were right, Prescott has phenomenal levels of pollen during the warmer part of the year, but not during the winter, when I have my worst respiratory problems.
I also found out that during the sunny half of the year Prescott often has extremely high levels of ozone (O3), making Denver, which is famous for its extremely high levels of ozone, a wise place for the people with respiratory problems in Prescott, AZ, worth considering moving to. For your information, ozone (O3) is a well documented respiratory irritant, which should make us all question why most air purifiers offer ozone.
With further investigations into my health problems, and having studied the local fungi for edibles, and I have found a larger variety of fungi in Prescott, AZ, than anywhere in the western states that I have been in since starting my study of edible fungi, I have had to conclude that fungal spores have to be part of the air-borne allergens that cause the levels of respiratory problems in Prescott, AZ. However, sadly, air quality monitoring station generally do no measure levels of fungal spores in the air we all breath. But spores are more a problem in the fall, and before the first frost.
However, during the darker half of the year my respiratory problems have been clearly linked for me now to air-borne organic by-products of the combustion of wood, from people in Prescott, AZ heating their homes with wood, plus the national forest here conducting control burns every fall.
I moved here 10 years ago to get away from industrial pollution while I waited for the next archaeology project I could work on. I have found massive allergies here, which have been caused by pure mountain air.
I did find traveling to treat my allergies worked. I have done it since the mid 70s. It worked very well until I arrived here in Prescott. Along the way I have spent large amounts of time in California, Colorado, and Arizona. I also traveled around the world as an adolescent. I have never found a place where I do not experience allergies. I simply come from the conjunction of two families with allergies, so genetically I got a double LL for allergies.
Realizing that Prescott is the worst place that I have found on this planet for my autoimmune system I did not just leave here, I decided that I would use Prescott, AZ as my perfect storm to develop a system whereby I can treat my allergies allowing me to live anywhere. I am now prepared to leave Prescott, AZ, because I know have a much better idea of the allergens that cause me problems; however, I am still developing a suit of respiratory equipment, which is progressing well, but will need a perfect allergen storm to be tested in.
While looking for places to move, I have seriously considered moving to Cuba, which has excellent social medicine, and is only 50 south of Florida. I have also found a valley in Columbia which as ideal looking weather, which is worth investigating. I have also seriously considered moving to Iceland, because I like their politics better than any country that I have investigated. It seems to me that the people of Iceland are simply more intelligent than most other nations.
While I have traveled through Oregon several times, and I have spent weeks there, I have not spent enough time there to know whether it would be better or worse for me, but with a robust suite of respiratory equipment I am getting to the point that I can start traveling again, and I plan to spend more time in Oregon to see how well my health is there, if I live that long.
While I am not hastening the arrival of death just as you are, I for one ultimately look forward to it. Perhaps recompense will finally come then, leaving the difficult adversities of this experience behind at last. :)
Well, I too do not hasten death, but having traveled out of body for decades, then I know what death is all about, so I do not fear death, but look forward to it. I am definitely done with life in a body, and thus do not expect to return again to biology.
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As this record shows, two years ago I became very ill with a lung infection. At that time it seemed reasonable to me to purify the air I breath. In two months I moved from my death bed to mobility. My health continues to improve directly proportional to how much, and how well, I purify the air I breath. I have come to realize that both HEPA filtration, and activated charcoal are necessary for continued, and improve, health.
Forty five years ago I made a radical change in my lifestyle. At that time I took up a contemplative life, which as you know has been most fruitful. At that time it seemed reasonable to take up a lifestyle that was also based upon optimum health. The concept of optimum health that I embraced was based upon pure food, pure water and pure air, which seemed reasonable to me. I have spent 45 years honing that concept based upon observed health.
Having had a lifetime of respiratory health issues I moved to a mountain community, where the air is pure. Unfortunately, my health took a steep nose dive after moving here. I have found that I am severely allergic to pure mountain air; and filtering the air I breath has produced the most radical improvement in my health in the 45 years of the pursuit of optimum health.
Six months before I moved here I had a full physical. At that time the doctor told me, "Mr. Brooks you have the cardiovascular system of an athlete, and all of your organs are functioning at optimum."
Six months later I moved to Prescott, AZ, a mountain community with no mining or heavy industrial activity, and no highway. After arriving here I was in and out of the ER about every 2 months. After six months here I went to a doctor for a full physical.
He said, "Mr. Brooks, you are full-on diabetic with a blood sugar 2.5 times over normal. You also have high blood pressure."
The only change in my life was the move to a mountain community with pure, fresh, air. After two years on purified air, my health has improved. My blood pressure is normal most of the time, and my blood sugar is almost normal most of the time. The improvement in my health is definitely directly proportional to how much of the air I breath is purified, and how well it is purified.
Last week I was back in the ER. I have only been in the ER 4 times this year, which is a radical improvement. Up until last weekend I had been depending primarily upon HEPA filtration of the air I breath. Before driving myself to the ER, because I observed severe malaise arising, I had been in HEPA filtered air for 18 hours. In the ER there my malaise did not exhibited respiratory involvement, nor high blood pressure.
I now realize that, while HEPA has definitely solved part of my health problem; however, not all of it. During my recovery in the ER I realized that HEPA filtration is not a complete solution for my health. I reasoned that activated charcoal would also have to be added to my air purification system.
Thirty minutes after I was released from the ER, I developed severe lack of oxygen concentration in my blood. I parked my van, and moved into my living compartment, and powered up an experimental air purifier that I had been developing for 9 months It included activate charcoal. Once I was breathing through the powered respirator that I developed, which included activated charcoal, my blood oxygen level rose from 50% (severely bad) to 98% (athletic level).
It has become clear I need to breath purified air for health; and pure mountain air is not pure enough. US American health has been in decline since the 50s. Is it possible that the over-all health of US Americans, and everyone else in the world, would be significantly better if more people breathed purified air? I believe that it is reasonable enough that every one who is interested in optimum health should also breath as much purified air as they can accommodate in their lifestyle.
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Hello Jeff,
Still hoping you are feeling well. I would offer you help but you are on the other side of North America! Perhaps your children can help? I am just concerned with all the ER visits!
Have you shared your idea on the effects of the air with your GP? What were his thoughts on it?
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I have both an allergist and a pulminologist, as well as a GP. I have mentioned it to all of them, asked them if the equipment is available, which they said it is not, and they humor me. The increase in activated charcoal, which I baked out myself, is still working great.
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The single best thing I ever did for my health has been to filter the air that I breath.
A woman collapsed and died after being exposed to bushfire smoke as she got off a plane in Australia. (https://www.mirror.co.uk/news/world-news/breaking-woman-dies-after-collapsing-21200009)
Installing air filters in classrooms has surprisingly large educational benefits (https://www.vox.com/2020/1/8/21051869/indoor-air-pollution-student-achievement?ncid=newsltushpmgnewworld)
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Why cardiologists should be interested in air pollution (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1767973/)
Abstract
Despite major improvements in air quality resulting from increasingly stringent legislation, there remains a strong association between daily mortality and current levels of air pollution. Growing epidemiological evidence suggests that many, perhaps the majority, of these deaths are caused by cardiovascular disease.
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Here is an interesting article on Why Does Inflammation Seem to Underlie All Sickness? (https://bioreports.net/why-does-inflammation-seem-to-underlie-all-sickness/). The article provides some history on medical researchers finding inflammation tends to underlie most diseases. We have seen this hypothesis before. I am convinced that it is air-pollution that is the cause of chronic inflammation, which leads to disease.
Since the industrial revolution coal has been burned to fuel it as a primary fuel source, and coal is toxic. However, we have the collapse of many civilizations throughout history. I think it is reasonable to consider that you put too many people into a relatively small space, like a city, and combine that with burning wood, and eventually, the air pollution is going to start killing the inhabitants.
Here is a research report from 2012, The inflammation theory of disease (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492709/)
The second link also says gee inflammation seems to be behind lots of diseases, so maybe it is a gene that can be turned off.
Another interesting research paper that examines the psychiatric and neurological side of chronic inflammation. From inflammation to sickness and depression: when the immune system subjugates the brain (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919277/)
Another article examines how exercise reduces inflammation. They found about a third of the benefit of regular exercise is attributable to reduced inflammation
: Raw and Red-Hot Could inflammation be the cause of myriad chronic conditions? (https://www.harvardmagazine.com/2019/05/inflammation-disease-diet)
Another article links inflammation all sickness and depression, Why Does Inflammation Seem to Underlie All Sickness? (https://www.lewrockwell.com/2019/11/no_author/why-does-inflammation-seem-to-underlie-all-sickness/)
Another article attempts to define inflammation: Inflammation, Explained: What It Is and How It Affects Your Health (https://nutritiouslife.com/eat-empowered/inflammation-definition-health-impact/)