Allergy Treatment Information: Allergy Treatment Information

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Allergy Treatment Information

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Allergies from Wikipedia

Allergy Treatments

From Wikipedia, the free encyclopedia

Allergy

Classification and external resources

Allergy is a disorder of the immune system often also referred to as atopy. Allergic reactions occur to environmental substances known as allergens; these reactions are acquired, predictable and rapid. Strictly, allergy is one of four forms of hypersensitivity and is called type I (or immediate) hypersensitivity. It is characterized by excessive activation of certain white blood cells called mast cells and basophils by a type of antibody known as IgE, resulting in an extreme inflammatory response. Common allergic reactions include eczema, hives, hay fever, asthma, food allergies, and reactions to the venom of stinging insects such as wasps and bees.[1]

Mild allergies like hay fever are highly prevalent in the human population and cause symptoms such as allergic conjunctivitis, itchiness, and runny nose. Allergies can play a major role in conditions such as asthma. In some people, severe allergies to environmental or dietary allergens or to medication may result in life-threatening anaphylactic reactions and potentially death.

A variety of tests now exist to diagnose allergic conditions; these include testing the skin for responses to known allergens or analyzing the blood for the presence and levels of allergen-specific IgE. Treatments for allergies include allergen avoidance, use of antihistamines, steroids or other oral medications, immunotherapy to desensitize the response to allergen, and targeted therapy.

Contents [hide]

1 Classification and history

2 Signs and symptoms

3 Cause

3.1 Genetic basis

3.2 Environmental factors

4 Pathophysiology

4.1 Acute response

4.2 Late-phase response

6.3 Unproven or ineffective treatments

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Classification and history

The concept "allergy" was originally introduced in 1906 by the Viennese pediatrician Clemens von Pirquet, after he noted that some of his patients were hypersensitive to normally innocuous entities such as dust, pollen, or certain foods.[2] Pirquet called this phenomenon "allergy" from the Greek words allos meaning "other" and ergon meaning "work".[3] Historically, all forms of hypersensitivity were classified as allergies, and all were thought to be caused by an improper activation of the immune system. Later, it became clear that several different disease mechanisms were implicated, with the common link to a disordered activation of the immune system. In 1963, a new classification scheme was designed by Philip Gell and Robin Coombs that described four types of hypersensitivity reactions, known as Type I to Type IV hypersensitivity.[4] With this new classification, the word "allergy" was restricted to only type I hypersensitivities (also called immediate hypersensitivity), which are characterized as rapidly developing reactions.

A major breakthrough in understanding the mechanisms of allergy was the discovery of the antibody class labeled immunoglobulin E (IgE) - Kimishige Ishizaka and co-workers were the first to isolate and describe IgE in the 1960s.[5]

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Signs and symptoms

Common symptoms of allergy

Affected organ

Symptom

Nose

swelling of the nasal mucosa (allergic rhinitis)

Sinuses

allergic sinusitis

Eyes

redness and itching of the conjunctiva (allergic conjunctivitis)

Airways

Sneezing, coughing, bronchoconstriction, wheezing and dyspnea, sometimes outright attacks of asthma, in severe cases the airway constricts due to swelling known as angioedema

Ears

feeling of fullness, possibly pain, and impaired hearing due to the lack of eustachian tube drainage.

Skin

rashes, such as eczema and hives (urticaria)

Gastrointestinal tract

abdominal pain, bloating, vomiting, Diarrhea

Many allergens, such as dust or pollen, are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, and itching and redness of the eyes.[6] Inhaled allergens can also lead to asthmatic symptoms, caused by narrowing of the airways (bronchoconstriction) and increased production of mucus in the lungs, shortness of breath (dyspnea), coughing and wheezing.[7]

Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhoea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis.[8] Insect stings, antibiotics, and certain medicines produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system.[9][10][11] Depending of the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered suddenly, or the onset can be delayed. The severity of this type of allergic response often requires injections of epinephrine, sometimes through a device known as the Epi-Pen auto-injector. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a prolonged period of time. [11]

Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema.[12] Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a "wheal and flare" reaction characteristic of hives and angioedema.[13]

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Cause

Risk factors for allergy can be placed in two general categories, namely host and environmental factors. Host factors include heredity, sex, race, and age, with heredity being by far the most significant. There have been recent increases in the incidence of allergic disorders, however, that cannot be explained by genetic factors alone. The four main environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.[14]

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Genetic basis

Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins.[15] Allergic parents are more likely to have allergic children,[16] and their allergies are likely to be more severe than those from non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.[16]

The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.[17] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.[17] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.[18] Overall, boys have a higher risk of developing allergy than girls,[16] although for some diseases, namely asthma in young adults, females are more likely to be affected.[19] Sex differences tend to decrease in adulthood.[16] Ethnicity may play a role in some allergies, however racial factors have been difficult to separate from environmental influences and changes due to migration.[16] Interestingly, it has been suggested that different genetic loci are responsible for asthma, specifically, in people of Caucasian, Hispanic, Asian, and African origins.[20]

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Environmental factors

International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined.[21]

Exposure to allergens, especially in early life, is an important risk factor for allergy. Alterations in exposure to microorganisms is the most plausible explanation, at present, for the increase in atopic allergy.[14] Since children that live in large families or overcrowded households, or attend day care, have a reduced incidence of allergic disease, a relationship has been proposed between exposures to bacteria and viruses during childhood, and protection against the development of allergy, which has been called – the "hygiene hypothesis".[21] Exposure to endotoxin and other components of bacteria may reduce atopic diseases.[22] Endotoxin exposure reduces release of inflammatory cytokines such as TNF-α, IFNγ, interleukin-10, and interleukin-12 from white blood cells (leukocytes) that circulate in the blood.[23] Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.[24]

Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies.[25] Recent research has shown that some common parasites, such as intestinal worms (e.g. hookworms), secrete chemicals into the gut wall (and hence the bloodstream) that suppress the immune system and prevent the body from attacking the parasite.[26] This gives rise to a new slant on the hygiene hypothesis theory — that co-evolution of man and parasites has led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.[27] In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.[28] However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.[21] Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.[29] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.[29] For more information on this topic, see Helminthic therapy.

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Pathophysiology

The pathophysiology of allergic responses can be divided into two phases. The first is an acute response that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.

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Acute response

Degranulation process in allergy.1 - antigen; 2 - IgE antibody; 3 - FcεRI receptor; 4 - preformed mediators (histamine, proteases, chemokines, heparine); 5 - granules; 6 - mast cell; 7 - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)

In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a T_H2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These T_H2 cells interact with other lymphocytes called B cells, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FcεRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage are sensitized to the allergen.[14]

If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.[14]

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Late-phase response

After the chemical mediators of the acute response subside, late phase responses can often occur. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages to the initial site. The reaction is usually seen 2-24 hours after the original reaction.[30] Cytokines from mast cells may also play a role in the persistence of long-term effects. Late phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of T_H2 cells.[31]

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Diagnosis

An allergy testing machine being operated in the diagnostic immunology lab at Lackland Air Force Base

Before a diagnosis of allergic disease can be confirmed, the other possible causes of the presenting symptoms should be carefully considered.[32] Vasomotor rhinitis, for example, is one of many maladies that shares symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis.[33] Once a diagnosis of asthma, rhinitis, anaphylaxis, or other allergic disease has been made, there are several methods for discovering the causative agent of that allergy.

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Skin testing

Skin Testing

For assessing the presence of allergen-specific IgE antibodies, allergy skin testing is preferred over blood allergy tests because it is more sensitive and specific, simpler to use, and less expensive.[34] Skin testing is also known as "puncture testing" and "prick testing" due to the series of tiny puncture or pricks made into the patient's skin. Small amounts of suspected allergens and/or their extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to sites on the skin marked with pen or dye (the ink/dye should be carefully selected, lest it cause an allergic response itself). A small plastic or metal device is used to puncture or prick the skin. Sometimes, the allergens are injected "intradermally" into the patient's skin, with a needle and syringe. Common areas for testing include the inside forearm and the back. If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from slight reddening of the skin to a full-blown hive (called "wheal and flare") in more sensitive patients. Interpretation of the results of the skin prick test is normally done by allergists on a scale of severity, with +/- meaning borderline reactivity, and 4+ being a large reaction. Increasingly, allergists are measuring and recording the diameter of the wheal and flare reaction. Interpretation by well-trained allergists is often guided by relevant literature.[35] Some patients may believe they have determined their own allergic sensitivity from observation, but a skin test has been shown to be much better than patient observation to detect allergy.[36]

If a serious life threatening anaphylactic reaction has brought a patient in for evaluation, some allergists will prefer an initial blood test prior to performing the skin prick test. Skin tests may not be an option if the patient has widespread skin disease or has not avoided antihistamines for several days.

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Blood testing

Various blood allergy testing methods are also available for detecting allergy to specific substances. This kind of testing measures a "total IgE level" - an estimate of IgE contained within the patient's serum. This can be determined through the use of radiometric and colormetric immunoassays. Radiometric assays include the radioallergosorbent test (RAST) test method, which uses IgE-binding (anti-IgE) antibodies labeled with radioactive isotopes for quantifying the levels of IgE antibody in the blood.[34] Other newer methods use colorimetric or fluorometric technology in the place of radioactive isotopes. Some "screening" test methods are intended to provide qualitative test results, giving a "yes" or "no" answer in patients with suspected allergic sensitization. One such method has a sensitivity of about 70.8% and a positive predictive value of 72.6% according to a large study.[37]

A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens.[38] Statistical methods, such as ROC curves, predictive value calculations, and likelihood ratios have been used to examine the relationship of various testing methods to each other. These methods have shown that patients with a high total IgE have a high probability of allergic sensitization, but further investigation with specific allergy tests for a carefully chosen allergens is often warranted.

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Treatment

This article or section deals primarily with the United States and does not represent a worldwide view of the subject.

Please improve this article or discuss the issue on the talk page.

There have been enormous improvements in the medical treatments used to treat allergic conditions. With respect to anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin diseases, advances have included the identification of food proteins to which IgE binding is associated with severe reactions and development of low-allergen foods, improvements in skin prick test predictions; evaluation of the atopy patch test; in wasp sting outcomes predictions and a rapidly disintegrating epinephrine tablet, and anti-IL-5 for eosinophilic diseases.[39]

Traditionally treatment and management of allergies involved simply avoiding the allergen in question or otherwise reducing exposure. For instance, people with cat allergies were encouraged to avoid them. While avoidance may help to reduce symptoms and avoid life-threatening anaphylaxis, it is difficult to achieve for those with pollen or similar air-borne allergies. Strict avoidance still has a role in management though, and is often used in managing food allergies.

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Pharmacotherapy

Several antagonistic drugs are used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes. These include antihistamines, cortisone, dexamethasone, hydrocortisone, epinephrine (adrenaline), theophylline and cromolyn sodium. Anti-leukotrienes, such as Montelukast (Singulair) or Zafirlukast (Accolate), are FDA approved for treatment of allergic diseases.[citation needed] Anti-cholinergics, decongestants, mast cell stabilizers, and other compounds thought to impair eosinophil chemotaxis, are also commonly used. These drugs help to alleviate the symptoms of allergy, and are imperative in the recovery of acute anaphylaxis, but play little role in chronic treatment of allergic disorders.

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Immunotherapy

Desensitization or hyposensitization is a treatment in which the patient is gradually vaccinated with progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity altogether. It relies on the progressive skewing of IgG antibody production, to block excessive IgE production seen in atopys. In a sense, the person builds up immunity to increasing amounts of the allergen in question. Studies have demonstrated the long-term efficacy and the preventive effect of immunotherapy in reducing the development of new allergy.[40] Meta-analyses have also confirmed efficacy of the treatment in allergic rhinitis in children and in asthma.[citation needed] A review by the Mayo Clinic in Rochester confirmed the safety and efficacy of allergen immunotherapy for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insect based on numerous well-designed scientific studies.[41] Additionally, national and international guidelines confirm the clinical efficacy of injection immunotherapy in rhinitis and asthma, as well as the safety, provided that recommendations are followed.[42]

A second form of immunotherapy involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free and B-cell associated IgE; signalling their destruction. They do not bind to IgE already bound to the Fc receptor on basophils and mast cells, as this would stimulate the allergic inflammatory response. The first agent of this class is Omalizumab. While this form of immunotherapy is very effective in treating several types of atopy, it should not be used in treating the majority of people with food allergies.[citation needed]

A third type, Sublingual immunotherapy, is an orally-administered therapy which takes advantage of oral immune tolerance to non-pathogenic antigens such as foods and resident bacteria. This therapy currently accounts for 40 percent of allergy treatment in Europe.[citation needed] In the United States, sublingual immunotherapy is gaining support among traditional allergists and is endorsed by doctors who treat allergy.[citation needed]

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Unproven or ineffective treatments

An experimental treatment, enzyme potentiated desensitization (EPD), has been tried for decades but is not generally accepted as effective.[43] EPD uses dilutions of allergen and an enzyme, beta-glucuronidase, to which T-regulatory lymphocytes are supposed to respond by favouring desensitization, or down-regulation, rather than sensitization. EPD has also been tried for the treatment of autoimmune diseases but again is not FDA approved or of proven effectiveness.[43]

In alternative medicine, a number of allergy treatments are described by its practitioners, particularly naturopathic, herbal medicine, homeopathy, traditional Chinese medicine and kinesiology. Systematic literature searches conducted by the Mayo Clinic through 2006, involving hundreds of articles studying multiple conditions, including asthma and upper respiratory tract infection showed no effectiveness of any alternative treatments, and no difference compared with placebo. The authors concluded that, based on rigorous clinical trials of all types of homeopathy for childhood and adolescence ailments, there is no convincing evidence that supports the use of alternative treatments.[44]

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Epidemiology

Many diseases related to inflammation such as type 1 diabetes, rheumatoid arthritis and allergic diseases—hay fever and asthma—have increased in the Western world over the past 2-3 decades.[45] Rapid increases in allergic asthma and other atopic disorders in industrialized nations probably began in the 1960s and 1970s, with further increases occurring during the 1980s and 1990s,[46] although some suggest that a steady rise in sensitization has been occurring since the 1920s.[47] The incidence of atopy in developing countries has generally remained much lower.[46]

Allergic conditions: Statistics and Epidemiology

Allergy type

United States

United Kingdom[48]

Allergic rhinitis

35.9 million[49] (about 11% of the population[50])

3.3 million (about 5.5% of the population[51])

Asthma

10 million suffer from allergic asthma (about 3% of the population). The prevalence of asthma increased 75% from 1980-1994. Asthma prevalence is 39% higher in African Americans than in Anglo Saxons.[52]

5.7 million (about 9.4%). In six and seven year olds asthma increased from 18.4% to 20.9% over five years, during the same time the rate decreased from 31% to 24.7% in 13 to 14 year olds.

Atopic eczema

About 9% of the population. Between 1960 and 1990 prevalence has increased from 3% to 10% in children.[53]

5.8 million (about 1% severe).

Anaphylaxis

At least 40 deaths per year due to insect venom. About 400 deaths due to penicillin anaphylaxis. About 220 cases of anaphylaxis and 3 deaths per year are due to latex allergy.[54] An estimated 150 people die annually from anaphylaxis due to food allergy.[55]

Between 1999 and 2006, 48 deaths occurred in people ranging from five months to 85 years old.

Insect venom

Around 15% of adults have mild, localized allergic reactions. Systemic reactions occur in 3% of adults and less than 1% of children. [56]

Unknown

Drug allergies

Anaphylactic reactions to penicillin cause 400 deaths.

Unknown

Food allergies

2-4% of children and 1-2% of adults. Peanut and/or tree nut (e.g. walnut, almond and cashew) allergy affects about three million Americans, or 1.1% of the population.[55]

5-7% of infants and 1-2% of adults. A 117.3% increase in peanut allergies was observed from 2001 to 2005, an estimated 25,700 people in England are affected.

Multiple allergies

(Asthma, eczema and allergic rhinitis together)

2.3 million (about 3.7%), prevalence has increased by 48.9% between 2001 and 2005.

Although genetic factors fundamentally govern susceptibility to atopic disease, increases in atopy have occurred within too short a time frame to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes.[46] Several hypotheses have been identified to explain this increased prevalence; increased exposure to perennial allergens due to housing changes and increasing time spent indoors, and changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise.[45] The hygiene hypothesis maintains[57] that high living standards and hygienic conditions exposes children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from T_H1 type responses, leading to unrestrained T_H2 responses that allow for an increase in allergy.[58][59]

Changes in rates and types of infection alone however, have been unable to explain the observed increase in allergic disease, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. Evidence has shown that exposure to food and fecal-oral pathogens, such as hepatitis A, Toxoplasma gondii, and Helicobacter pylori (which also tend to be more prevalent in developing countries), can reduce the overall risk of atopy by more than 60%,[60] and an increased prevalence of parasitic infections has been associated with a decreased prevalence of asthma.[61] It is speculated that these infections exert their effect by critically altering T_H1/T_H2 regulation.[62] Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.[62]

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Medical specialty

In the United States physicians who hold certification by the American Board of Allergy and Immunology (ABAI) have successfully completed an accredited educational program and an evaluation process, including a secure, proctored examination to demonstrate the knowledge, skills, and experience to the provision of patient care in allergy and immunology.[63] An allergist-immunologist is a physician specially trained to manage and treat asthma and the other allergic diseases. Becoming an allergist-immunologist requires completion of at least nine years of training. After completing medical school and graduating with a medical degree, a physician will then undergo three years of training in internal medicine (to become an internist) or pediatrics (to become a pediatrician). Once physicians have finished training in one of these specialties, they must pass the exam of either the American Board of Pediatrics (ABP) or the American Board of Internal Medicine (ABIM). Internists or pediatricians who wish to focus on the sub-specialty of allergy-immunology then complete at least an additional two years of study, called a fellowship, in an allergy-immunology training program. Allergist-immunologists who are listed as ABAI-certified have successfully passed the certifying examination of the American Board of Allergy and Immunology (ABAI), following their fellowship.[64]

In the United Kingdom, allergy is a subspecialty of general medicine or pediatrics. After obtaining postgraduate exams (MRCP or MRCPCH respectively) a doctor works as several years as a specialist registrar before qualifying for the General Medical Council specialist register. Allergy services may also be delivered by immunologists. A 2003 Royal College of Physicians report presented a case for improvement of what were felt to be inadequate allergy services in the UK.[65] In 2006, the House of Lords convened a subcommittee that reported in 2007. It concluded likewise that allergy services were insufficient to deal with what the Lords referred to as an "allergy epidemic" and its social cost; it made several other recommendations.[66]

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See also

▪ Allergic inflammation

▪ Allergen

▪ Hypersensitivity

▪ Hypoallergenic

▪ Multiple chemical sensitivity (MCS)

▪ Urticaria

▪ Immunoglobulin

▪ IgE

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References

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30. ^ Grimbaldeston MA, Metz M, Yu M, Tsai M, Galli SJ (2006). "Effector and potential immunoregulatory roles of mast cells in IgE-associated acquired immune responses". Curr. Opin. Immunol. 18 (6): 751–60. doi:10.1016/j.coi.2006.09.011. PMID 17011762.

31. ^ Holt PG, Sly PD (2007). "Th2 cytokines in the asthma late-phase response". Lancet 370 (9596): 1396–8. doi:10.1016/S0140-6736(07)61587-6. PMID 17950849.

32. ^ Allergic and Environmental Asthma at eMedicine - Includes discussion of differentials

33. ^ Wheeler PW, Wheeler SF (2005). "Vasomotor rhinitis". American family physician 72 (6): 1057–62. PMID 16190503.

34. ^ a b Ten RM, Klein JS, Frigas E (1995). "Allergy skin testing". Mayo Clin. Proc. 70 (8): 783–4. PMID 7630219.

35. ^ Verstege A, Mehl A, Rolinck-Werninghaus C, et al (2005). "The predictive value of the skin prick test weal size for the outcome of oral food challenges". Clin. Exp. Allergy 35 (9): 1220–6. doi:10.1111/j.1365-2222.2005.2324.x. PMID 16164451.

36. ^ Li JT, Andrist D, Bamlet WR, Wolter TD (2000). "Accuracy of patient prediction of allergy skin test results". Ann. Allergy Asthma Immunol. 85 (5): 382–4. PMID 11101180.

37. ^ Vidal C, Gude F, Boquete O, et al (2005). "Evaluation of the phadiatop test in the diagnosis of allergic sensitization in a general adult population". Journal of investigational allergology & clinical immunology 15 (2): 124–30. PMID 16047713.

38. ^ Kerkhof M, Dubois AE, Postma DS, Schouten JP, de Monchy JG (2003). "Role and interpretation of total serum IgE measurements in the diagnosis of allergic airway disease in adults". Allergy 58 (9): 905–11. doi:10.1034/j.1398-9995.2003.00230.x. PMID 12911420.

39. ^ Sicherer SH, Leung DY (2007). "Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects". J. Allergy Clin. Immunol. 119 (6): 1462-9. doi:10.1016/j.jaci.2007.02.013. PMID 17412401.

40. ^ Ross RN, Nelson HS, Finegold I (2000). "Effectiveness of specific immunotherapy in the treatment of allergic rhinitis: an analysis of randomized, prospective, single- or double-blind, placebo-controlled studies". Clinical therapeutics 22 (3): 342–50. doi:10.1016/S0149-2918(00)80038-7. PMID 10963288.

41. ^ Rank MA, Li JT (Sep 2007). "Allergen immunotherapy". Mayo Clin. Proc. 82 (9): 1119–23. PMID 17803880.

42. ^ Passalacqua G, Durham SR (2007). "Allergic rhinitis and its impact on asthma update: allergen immunotherapy". J. Allergy Clin. Immunol. 119 (4): 881–91. doi:10.1016/j.jaci.2007.01.045. PMID 17418661.

43. ^ a b Terr AI (2004). "Unproven and controversial forms of immunotherapy". Clinical allergy and immunology 18: 703–10. PMID 15042943.

44. ^ Altunç U, Pittler MH, Ernst E (2007). "Homeopathy for childhood and adolescence ailments: systematic review of randomized clinical trials". Mayo Clin. Proc. 82 (1): 69–75. PMID 17285788.

45. ^ a b Platts-Mills TA, Erwin E, Heymann P, Woodfolk J (2005). "Is the hygiene hypothesis still a viable explanation for the increased prevalence of asthma?". Allergy 60 Suppl 79: 25–31. doi:10.1111/j.1398-9995.2005.00854.x. PMID 15842230.

46. ^ a b c Bloomfield SF, Stanwell-Smith R, Crevel RW, Pickup J (2006). "Too clean, or not too clean: the hygiene hypothesis and home hygiene". Clin. Exp. Allergy 36 (4): 402–25. doi:10.1111/j.1365-2222.2006.02463.x. PMID 16630145.

47. ^ Isolauri E, Huurre A, Salminen S, Impivaara O (2004). "The allergy epidemic extends beyond the past few decades". Clin. Exp. Allergy 34 (7): 1007–10. doi:10.1111/j.1365-2222.2004.01999.x. PMID 15248842.

48. ^ Chapter 4: The Extent and Burden of Allergy in the United Kingdom. House of Lords - Science and Technology - Sixth Report (24 July 2007). Retrieved on 2007-12-03.

49. ^ AAAAI - rhinitis, sinusitis, hay fever, stuffy nose, watery eyes, sinus infection. Retrieved on 2007-12-03.

50. ^ Based on an estimated population of 303 million in 2007 U.S. POPClock. U.S. Census Bureau.

51. ^ Based on an estimated population of 60.6 million UK population grows to 60.6 million

52. ^ AAAAI - asthma, allergy, allergies, prevention of allergies and asthma, treatment for allergies and asthma. Retrieved on 2007-12-03.

53. ^ AAAAI - skin condition, itchy skin, bumps, red irritated skin, allergic reaction, treating skin condition. Retrieved on 2007-12-03.

54. ^ AAAAI - anaphylaxis, cause of anaphylaxis, prevention, allergist, anaphylaxis statistics. Retrieved on 2007-12-03.

55. ^ a b AAAAI - food allergy, food reactions, anaphylaxis, food allergy prevention. Retrieved on 2007-12-03.

56. ^ AAAAI - stinging insect, allergic reaction to bug bite, treatment for insect bite. Retrieved on 2007-12-03.

57. ^ Strachan DP (1989). "Hay fever, hygiene, and household size". BMJ 299 (6710): 1259–60. PMID 2513902. Full text at PMC: 1838109

58. ^ Yazdanbakhsh M, Kremsner PG, van Ree R (2002). "Allergy, parasites, and the hygiene hypothesis". Science 296 (5567): 490–4. doi:10.1126/science.296.5567.490. PMID 11964470.

59. ^ Renz H, Blümer N, Virna S, Sel S, Garn H (2006). "The immunological basis of the hygiene hypothesis". Chem Immunol Allergy 91: 30–48. doi:10.1159/000090228. PMID 16354947.

60. ^ Matricardi PM, Rosmini F, Riondino S, et al (2000). "Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma: epidemiological study". BMJ 320 (7232): 412–7. doi:10.1136/bmj.320.7232.412. PMID 10669445. Full text at PMC: 27285

61. ^ Masters S, Barrett-Connor E (1985). "Parasites and asthma--predictive or protective?". Epidemiol Rev 7: 49–58. PMID 4054238.

62. ^ a b Sheikh A, Strachan DP (2004). "The hygiene theory: fact or fiction?". Curr Opin Otolaryngol Head Neck Surg 12 (3): 232–6. PMID 15167035.

63. ^ ABAI: American Board of Allergy and Immunology. Retrieved on 2007-08-05.

64. ^ AAAAI - What is an Allergist?. Retrieved on 2007-08-05.

65. ^ Royal College of Physicians (2003). Allergy: the unmet need. London, UK: Royal College of Physicians. ISBN 1-86016-183-9. PDF version PDF (1.03 MiB)

66. ^ House of Lords - Science and Technology Committee (2007). Allergy - HL 166-I, 6th Report of Session 2006-07 - Volume 1: Report. London, UK: TSO (The Stationery Office). ISBN 0104011491.

[edit]

Good SEO

I found this article on SEO in Nashville. Good info!

Choosing a reputable SEO in Nashville, Tennessee can be daunting, considering that there is so little knowledge available on what to look for. Companies paying for advertisements in the Nashville Scene, Citysearch or the Tennessean are trying to attach their name to the credibility of those established organizations, but it does help you choose a top ranked or top rated SEO Firm. So we here at Nashville SEO Info are going to give you the four key scams to watch out for, when searching for an SEO Firm as good as ours:

SEO WANNA-BE’S

Search engine optimization is one of those unknown fields that has no established standards. Anyone can say they are an SEO or can do SEO work, but that does not mean they have the talent, time or tools to produce any results. There are also programs that claim to help search engine ranking. They do not work either. Period.

An easy way to spot an unknowledgeable SEO or a web designer who poses as an SEO is to ask them if they optimized your site when they designed it. They will answer, "Oh yeah, I optimized it."

That is equivalent to saying, "Oh yeah, I've been worked out." Working out and SEO are never one time events. They are always on-going projects.

SEO SUBMISSION SCAMS

A lot of companies will also call people and tell them that they will submit their sites to 2000 directories, which will build their search engine ranking. It is a form of link campaigning--albeit lopsided and one-dimensional. The problem with these "auto-submissions" is that the directories to which they are submitting have safe-guards in place to reject these kinds of mass submissions. Now, here is the scam: the company has technically done what they promised they would do, SUBMIT your site, even though 99% of those submissions will be rejected and thus be of no use to building a client’s search engine ranking.

SEO KEYWORD SCAMS

Another prevalent scam in the industry is for SEOs to try to gull you into letting them pick the phrases to dominate. For instance, say you are real estate agent and your website is: www.MollyLynnMorganRealEstate.com

A scam SEO will come to you and say, "We can get you a #1 ranking for ‘Molly Lynn Morgan Real Estate." They can probably do that for you. Unfortunately, none of your potential clients are going to Google and typing in that phrase.

More sophisticated SEOs will come to you and tell you, "I will try to get you the ranking 'Real Estate in Middle Tennessee.'" That sounds like a wonderful phrase to dominate, but their data has told them that no legitimate SEOs are going after that phrase; because, again, while it might sound good, very few people are actually typing that in. People are actually most often using either 'Nashville Real Estate' or 'Nashville Tennessee Real Estate.'

What a legitimate SEO will do (like we do here at Nashville SEO Info) is to show you the actual data. We will show you the exact numbers of how many people per month are searching for the product or services you offer and what exact keyphrases they are typing in. We won’t go after any of the silly phrases above. We will show you the data AND LET YOU CHOOSE!

BLACK HAT SEO

There are short cuts that can be used to quickly build a ranking. These shortcuts involve “spammy” techniques that are referred to as Black Hat SEO. One of these techniques includes overloading a website with keywords. This works temporarily, but once the Google algorithm figures out what the site is doing, they will banish the site to what is referred to as “Google hell.” This simply means that the site is marked to never be allowed to have a good ranking in the system.

SEOs will sometimes do this because it is the easier than doing the work the honest way. In the long run, the hard, honest way is more effective and far more safe, but it does take longer. A few years ago BMW of Germany hired an SEO firm. This SEO firm applied some black hat techniques and Google found out. BMW of Germany was banished to Google hell and the auto giant spent the next few years and millions of dollars wooing Google to allow them back in to the system. Google finally agreed, but unless you have millions of dollars and the power of a automotive giant, you have to be careful who you allow to do SEO work on your behalf.

We at Nashville SEO Info know where the line is and we stay miles away from it. This puts us in a position where we end up having to do more work to achieve our results, but it ensures that once we attain high rankings for our clients, they will never have to worry about Google one day deleting their site!

e c p

taken from www.biblestudyauthor.com

INTRODUCTION

This article is an introductory look at the persecution of the early church. The Jewish social setting and subsequent persecution of the Christians by the Jews will be looked at first, followed by the Roman social setting and persecution of the Christians by the Romans.

PERSECUTION OF CHRISTIANS BY JEWS - IN JERUSALEM

SOCIAL SETTING

Jewish Scholars point to the rejection of the Torah as the basis of the conflict between Christians and Jews, while many Christian scholars have pointed to the rejection of the Messiah as the basis of the conflict.1 A closer look at the complex social setting of Jerusalem during the first century will reveal a much more complex set of events.

Judaism of the first century was composed of eight very different groups of Jews. In the same way that it would be a gross misrepresentation to lump Mormons, Muslims and Atheists in the same category, so it would be likewise inaccurate to lump Jews of this time period into one category, simply based on their national or ethnic identity. Here is a brief overview of the various groups, focusing on the political aspects of their identity, since politics were at a fever pitch in this complex and struggling nation:

Sadducees: This was a group of wealthy Jews who controlled the Temple, which enabled them to continuously generate the financial resources to remain in power. While not completely embracing their Roman occupiers, they sided with the Romans to help themselves remain in power over the temple.

Am Ha- 'aretz: The people of the land. These were the segment of the common peasant population, which paid little attention to the observance of the Torah and seemed to shun the study of the Torah.2 This group would have included any Jews who proclaimed atheism and by and large held little political power.

Scribes: Literally translated as one who can write. These were the scholars of their day.

Essences: A sect which separated themselves from the cities, observing extreme purity and piety in the deserts, awaiting a sure eschaton to come in their generation, which would remove the foreign invaders from Judah and establish a new order.

Zealots and Sicarii: The Sicarii were the terrorists of their day. They would hide small knives under their garments and in the midst of busy crowds stab specific offenders. Politically they served to stir up sentiments of war against those they opposed.3

Hellenized Jews: An ever-growing population of Jews who were embracing the new order of Hellenism to the exclusion of Judaism. The reasons for this transformation were numerous, chief of which were financial and political gains that came with embracing and trading in Hellenized areas.

Pharisees: The people who were most focused on Torah worship and observing with rigid detail not only the laws of the Torah, but also the laws created to build a fence around the Torah. This group of people felt great pressure from multiple directions. They had the Sadducees controlling the temple, the Hellenized world enticing Jews to view Judaism as the old way, Hellenism as the wave of the future and the Roman government oppressing them. They were holding on to a belief that seemed to be fading away in this complex and changing world.

Going back to the initial arguments of why the Jews persecuted the Christians, Jewish scholars who point to the lack of Torah worship as the basis for the conflict discount the fact that many groups in this world were not observing the Torah, with little to no persecution being directed at them. Paul was said to have observed the Torah worship when in the company of Jews, but he still faced persecution.4 In addition, records found in the Dead Sea Scrolls speak of an anti-ritualistic sentiment within the Jewish population. Christian scholars who point to the rejection of the Messiah as the basis of the conflict fail to recognize than the Essences and other obscure sects used messiah language and some even claimed to be a messiah, yet there is no record of directed persecutions among those groups. To better understand what could have caused the persecution of the Christians within Jerusalem, the record of Christian activity in Acts must be observed.

In the first seven chapters of Acts, during the Apostles' witness to Jerusalem, the Apostles were found in the temple preaching. Those in attendance of such sermons would have been the Sadducees and Pharisees. The message of a new kingdom reserved only for those who professed Christ would have angered the Sadducees by threatening their power hold on the temple. As much as they would have desired freedom from foreign invaders their link with the Romans helped to keep them in power and thus the Christian message was an affront to their capital. Likewise, the same message would have been even more distasteful to the Pharisees. It would have struck the same already raw nerve of the invading Hellenism in that Christianity, like Hellenism, demoted the very symbols of their ethic solidarity of purity, food laws, Sabbath and circumcision. Judaism was once again being portrayed as obsolete by yet another new philosophy in the new, enlightened world.

It was not merely the message of the Christians that resulted in persecution, but the combination of the wrong message to the wrong people at the wrong time. Had the Christians been preaching their message to groups such as the Hellenized Jews or the Am Ha- 'aretz they would have probably been met with either acceptance or at worst disinterest. However, their choice of groups and venues ignited a powder keg that was already set to explode. Josephus observed this great hatred and unrest poised to strike back at the Hellenistic and Roman threats. In his autobiography he talks about his effort to defuse an impending revolt:

I perceived that innovations had already begun, and that there were a great many very much elevated in hopes of a revolt from the Romans. ... [I] Persuaded them to change their minds...and this I said with vehement exhortation, because I foresaw that the end of such a war would be most unfortunate to us. But I could not persuade them; for the madness of desperate men was quite too hard for me.5

Needless to say, "loving your enemies" was not met with the greatest enthusiasm.

So the motivation for the persecution of the Jews in Jerusalem changes, based on which group is being addressed. The Sadducees were fighting to maintain the established order, the Pharisees were fighting against the degeneration of the Torah worship and many others were poised to invoke a revolution against the Roman invaders. There was no one reason for the persecution, but rather a complex web of cause and effect relationships.

RESULTING PERSECUTION

In the eyes of the Roman government Christianity, which at this time had no official title, was seen as merely another religious segment within Judaism. With so many sects within the Jewish community, it is easy to see how Romans viewed Christians as merely one more peculiarity in a nation of peculiar people and religious beliefs. So the Jews had very little recourse in turning to the Romans to persecute Christians. This resulted in the trial and stoning of Stephen without help from the Roman authorities.6 While it was unusual for Jews to execute capital punishment under the Roman governance, it was not unheard of. In John's account of the trial before Pilot, Pilot tells the Jews to judge him themselves. They respond that it is not lawful for them to put anyone to death.7 However, in the context of them demanding Jesus be put to death, the comment by Pilot seems to suggest they were known for doing just such a thing, on occasion.

Before the stoning of Stephen, the Christians were living in Jerusalem, worshiping and praying in the temple daily. After the beginning of the Christian persecution in Jerusalem, they were forced out and subsequently began to travel to other cities, spreading the gospel to the Diaspora Jews first and the Gentiles second. It must also be noted here that the persecution of Christians by the Jews was not a unified effort. It was largely the Pharisees and the Sadducees who pressed for the persecutions.

PERSECUTION OF CHRISTIANS BY JEWS - IN THE ROMAN WORLD

SOCIAL SETTING

Unlike the Jews of Jerusalem who viewed the Romans solely in terms of an enemy occupation, the Jews of the Diaspora had learned to co-exist with the Romans in a tense truce, having lived in many of the Roman cities for generations. The Roman Pagans had accepted the Jewish people as a reality and each group had their own butchers and did their own separate sacrifices for their meats to be sold in the marketplace. The Jews in the Roman Diaspora had also attained a measure of wealth and influence in the Roman world.8

RESULTING PERSECUTION

When Paul would arrive at a new city he would first go to the synagogue and preach to the Diaspora Jews. The Jews who rejected his message were often the ones who would go to the Roman authorities to incite them against Paul. This union of Roman and Jewish persecution of Christians is seen in Acts 14. In that story, the Jews go to the Roman authorities to seek Roman action, subsequently resulting in the punishment of stoning, which was the Jewish form of capital punishment.9

Jews who rejected the message of Paul, desired both to disassociate themselves and to prejudice authorities, portraying Christians as dangerous revolutionaries. It was a mass-conversion in Antioch when Christians first received a nickname differentiating themselves from their Jewish counterparts.10 This differentiation opened a new era of persecution from a Roman world that gave no such religious immunities to Christians, as it had for the Jews.

ROMAN PERSECUTION OF CHRISTIANS

SOCIAL SETTING

It was not long before Christians became a recognizable and particularly detested segment of the Roman world. By 64 AD they were already so set that Nero was able to use them as a likely scapegoat in his Smokey the Bear campaign, which will be discussed in the next section.11

The problem with converted Christians is the way in which they broke from the social norms that were vastly important in the Roman world. From arranged marriages to well prepared dinner banquets for select guests, political positioning of families was key to survival in this world. However, when friends or political acquaintances converted to Christianity they would withdraw almost entirely from the political structure. They refused to partake in the festivals and games, rejecting the gods, which they felt kept their nation strong for so long. They rejected the divinity of the Emperor--a sin that the gods would not allow go unpunished for long. They even refused to partake in joyous sexual ritual prostitution and lively drinking bouts. In addition, some of the Christians refused the meat from the markets, because it was routine for the cuts to be part of the sacrificial system. And most personal, they refused invitations to dine with other long time friends and families. These kill-joys were shunning their former political alliances and beginning to make enemies out of one time allies and friends.12

The difficulty for Christians only compounded as the tensions leading to the persecutions grew. For Jewish Christians the temptation to fall back to their safe Jewish roots in which they were raised also held the lure of being able to once again claim Jewish religious legal immunity. Gentile Christians had no natural link to this religion with its' roots in Judaism and no political power to protect or aid them or their families. The fact that the Christian church was able to survive was nothing short of a miracle.13

RESULTING PERSECUTIONS

The ten persecutions of the Christians spanning from 64 AD to 313 AD was ascribed by the fourth century Christian church as the ten horns of the beast in Revelation and by the ten plagues seen in Egypt.15 The persecutions, each with varying motives and reasons, all share the same peculiar markings in that while the persecutions were historically verifiable, no recorded laws have survived that specify reasons for the persecutions. As the persecutions evolved from one generation to the next, the subsequent generation seemed to use the past persecutions as edict enough for continuing or reigniting them. For example, in response to Pliny on how to deal with and prosecute Christians, Emperor Trajan writes, "No general rule can be laid out in fixed terms." However, he does say unequivocally, "Certain accusations published anonymously should not be entertained on any charge. For they both set a very bad precedence and are alien to the spirit of our age." Pliny was content in sentencing Christians to death for simply being too stubborn in their holding to Christianity in the face of certain death.16

Stemming from the second persecution under Domitian, the charge of refusing to worship the Imperial Cult seemed to be the first and great charge against the Christians. Some have argued that atheism was the charge against Christians; however, atheism in and of itself was not a crime in the Roman Empire. If, though, Christianity was held to with such stubbornness that one refused to pay alms to the Imperial Cult, then the subject was in violation of law. However, the worship of the Imperial Cult was not an issue until the reign of Domitian who, unlike his predecessors, forced the people to address him as their "Lord and their God" during his lifetime, and not after--when Caesars ascended to the level of a god. Domitian even had coins made bearing his likeness that read "father of the gods."17

THE TEN PERSECUTIONS

1. Persecution under Nero 67 AD -- Nero burned a great portion of Rome in a fire that lasted nine days. When word got out that Nero started the fire an uproar forced him to find a scapegoat and so he blamed Christians. During this first great persecution of the Christians Nero started a trend that lasted throughout all ten of the persecutions in that he devised new and increasingly gruesome punishments, including sewing animal skins to Christians and releasing wild dogs to eat them alive. He also put shirts dipped in wax on some of the Christians and then lit them on fire, using them to illuminate his gardens for his invited guests. His acts were so heinous that even the Romans felt sorrow toward the Christians. Paul and Peter died in this first round of persecution.18

2. Persecution under Domitian 81 AD -- Known for cruelty, he killed his brother and many senators, some due to his hatred of them and others to simply confiscate their lands. He also ordered the death of the entire lineage of David. His persecution of Christians stemmed from their refusal to worship him as a god, something most emperors up to this point refused to accept. Among those killed during this persecution was Simeon, the Bishop of Jerusalem. He tried to boil John alive, but when he miraculously survived he was banished to Patmos. Timothy was beaten by a crowd of people on their way to celebrate a pagan feast. He was beaten so badly that he died from his wounds two days later. During the persecution, if any famine pestilence or earthquake happened, the blame was laid on the Christians.19

3. Persecution under Trajan 108 AD -- Much the same continued regarding Imperial Cult worship during Trajan's reign. Ignatius was the most famous of the martyrs of this persecution.20

4. Persecution under Marcus Aurelius Antonius 162 AD -- So brutal were the means by which these martyrs were persecuted that it is said the Pagan onlookers would shutter with horror at the sights and some became converts at, "A faith which inspired such fortitude." Polycarp and Justin Martyr were given crowns of martyrdom during this persecution.21

5. Persecution commencing with Severus 192 AD -- The age of Tertullian, who said that if the Christians removed themselves from Rome at this time, it would have suffered a great depopulation. In a reversal of the source of the persecutions a Christian healed Emperor Severus of a sickness, but the multitudes demanded the execution of Christians and the reapplication of the defunct Imperial Cult laws to apply to Christians. Many who suffered martyrdom under this persecution fell during games at the amphitheaters. Leonidus, father of Origen was beheaded during this persecution.22

6. Persecution under Maximus 235 AD -- In Cappadocia the president Seremianus did all he could to exterminate the Christians from that province. During this time Christians were martyred without trial and their bodies were cast into pits as many as 50 or 60 at a time.23

7. Persecution under Decius 249 AD -- There were two causes of this persecution. First, Decius hated his predecessor Philip, who was deemed a Christian and second he was jealous of the rampant growth of Christianity, causing the heathen temples to decrease in attendance. By this time many schisms in the Church body had formed and the persecution was met by a divided Church. Fabian, Bishop of Rome was entrusted by Philip to care for his treasure. When Decius seized it and found less than he expected he had Fabian decapitated--the first martyrdom of this persecution. Many soon followed with yet another new set of imaginative deaths to befall those refusing to renounce Christ. Of note, Origen, like his father before him, was sentenced to death. He was thrown in prison where his feet were pierced and his legs were stretched for several days. He was threatened by fire and tortured with long, slow pains such as these for days upon days. However, before any death could befall him, Emperor Decius died and his successor Gallus engaged in a war with the Goths, leaving the Christians with a respite. Origen, having been given a release, retired to his home and died of natural causes five years later. During the reign of Gallus a plague broke out in the empire. So Gallus ordered sacrifices be made by all in the empire. When Christians refused the magistrates had many of them put to death.24

8. Persecution under Valerian 257 AD -- This emperor likewise invented new and distasteful ways of persecuting Christians. Most interesting, however, was the turn of events that marked the end of this, one of the greatest persecutions of the church. Sapor, the King of Persia, captured Valerian and literally used him as a footstool when he mounted his horses. After subjecting him to be a slave in his kingdom for eight years the Persian king then had Valerian's eyes put out. Still seeking more gruesome ways to torment him, he had Valerian flayed alive and then rubbed with salt until he died.25

9. Persecution under Aurelian 274 AD -- The reign of Aurelian, though not this persecution, was short-lived as his own servants put him to death. However, the following emperors who replaced him (and subsequently were likewise met with quick ends) continued the persecution.26

10. Persecution under Diocletian 303 AD -- Commonly called the Era of martyrs. Christians were increasing and becoming wealthy. On February 23, 303 Diocletian set forth his work to extinguish Christianity in one day. Watching on from on high the churches were raided, razed to the ground, and the documents burned. Not satisfied with just this, he purposely burned a portion of the city so that he could blame the Christians and further his cause. Countless Christians were martyred in an endless number of ways. The entire city of Phrygia, known for all of its inhabitants being Christian, was burned to the ground with all the people of the city dying in the fire. The torture and martyrdom was so severe that several pagan governors accused the Imperial Court with impropriety. Because of this, some Christians escaped death, but not before having their ears cut off, right eyes poked out, noses slit, limbs dislocated with such severity that they were rendered useless, and finally branded with red-hot irons.27

One final item of note: The persecution of the Christians was not a continuing event in the Roman Empire. With some expected exceptions, the time in between these distinct persecutions was rather peaceful for the Church. With each new emperor however, they were met with new uncertainties.

CONCLUSION

In conclusion, the reasons for the various persecutions of the Christians were as varied and complex as the world in which the early church lived. It is a mistake to oversimplify the issue in an effort to categorize it. As has been documented, Christians suffered persecution from both Jews and Gentiles. The reasons for the persecutions varied with each group, as well as from within each group. There is much speculation as to the motives and reasons behind the persecutions. However, there are very few surviving documents, legal or otherwise, which express the grounds for such persecutions, other than the fact that they were simply, "Christians."

WORKS CITED

Fox, John. Fox' Book of Martyrs. New York, NY: Holt, Rinehart and Winston, 1962.

Hare, Douglas R. A. The Theme of Jewish persecution of the Christians in the Gospel According to St. Matthew. Cambridge: Cambridge University Press, 1967.

Josephus, Flavius. The Works of Flavius Josephus, Translated by William Whiston. Philadelphia, PA: Henry T. Coates & CO.

Roetzel, Calvin. The World That Shaped the New Testament. London: Westminster John Knox Press, 2002.

Whittaker, Molly. Jews & Christians: Graeco-Roman Views. Cambridge: Cambridge University Press, 1984.

Workman, Herbert. Persecution in the Early Church. London: The Epworth Press, 1923.

APPENDIX

Christian and Pagan Primary Sources Speaking of the Persecution

This information is taken largely from Molly Whittaker's Jews and Christians: Graeco-Roman Views. See the Works Cited Page for more details. This is not intended as an exhaustive list.

New Testament:

Mark 15:39

Matthew 27:54

Luke 23:47

Acts 11:19-26

Acts 13:42-50

Acts 14:1-6

Acts 14:18-20

Acts 16:13-40

Acts 17:1-9

Acts 17:10-14

Acts 17:17-21

Acts 17:32-33

Acts 18:12-18

Acts 19:23ff

Acts 19:40

Acts 22:25-9

Acts 23:26-33

Acts 24:22-7

Romans 13:1-6

I Peter 4:12-16

Hebrews 10:32-4

Revelation 2:13ff

Early Christian Sources:

Ignatius Letter to Romans 5.1

Martydom of Polycarp 1-19

Justin martyr Apology 2.9-20

Acts of Justin

Letter of the Gallican Church

Octavius 8.3-5

Octavius 9.1-6

Octavius 10.1-4

Octavius 31.1-2

Acts of the Scillitan Martyrs

Origen Celsum 1.9

Origen Celsum 1.28

Origen Celsum 2.55

Origen Celsum 3.12

Origen Celsum 3.55

Origen Celsum 5.14

Origen Celsum 7.9

Origen Celsum 8.24

Origen Celsum 8.67-9

Origen Celsum 1.28

Galen Reference 6 (Pg. 15)

Epictetus 4.7.6

Lucian On the Death of Peregrinus 333-8; 341

Alexander the False Prophet 232.25; 244.38-245

Tertullian Apology 50

Pagan Sources:

Tacitus Ann. 13.32.3-5

Tacitus Ann. 15.44.2-8

Life of Nero 16

Pliny Letter 10.96.1-10

Pliny Letter 10.97

FOOTNOTES

1. Douglas R. A. Hare, The Theme of Jewish persecution of the Christians in the Gospel According to St. Matthew (Cambridge: Cambridge University Press, 1967), 2.

2. Calvin J. Roetzel, The World That Shaped the New Testament, (London: Westminster John Knox Press, 2002), 59f.

3. Ibid, 57ff.

4. Hare, 6f.

5. Flavius Josephus, The Works of Flavius Josephus, trans. William Whiston (Philadelphia, PA: Henry T. Coates & CO.), 3.

6. Molly Whittaker, Jews & Christians: Graeco-Roman Views, (Cambridge: Cambridge University Press, 1984), 133.

7. John 18:31

8. Whittaker, 133

9. Whittaker also notes similar incidents in 13:42-50, 17:1-9, 10-14, (Whittaker, 133).

10. Acts 11:19-26

11. Whittaker, 134.

12. Ibid, 133f.

13. Ibid, 133.

14. Revelations 17:3, 6.

15. Herbert B. Workman, Persecution in the Early Church, (London: The Epworth Press, 1923), 9.

16. Wittaker, 134.

17. Roetzel, 113f.

18. John Fox, Fox' Book of Martyrs, (New York, NY: Holt, Rinehart and Winston, 1962), 5f.

19. Ibid, 6f.

20. Ibid, 7f.

21. Ibid, 8ff.

22. Ibid, 12f.

23. Ibid, 14.

24. Ibid, 14ff.

25. Ibid, 18ff.

26. Ibid, 22ff.

27. Ibid, 24ff.

Thursday, April 17, 2008