Coca-Cola Secret Ingredient 1

The Secret Ingredient in My Beloved Coca-Cola Revealed: "CARMINE"

This substance can be deadly if an allergic reaction occurs. I love Coca-Cola but I think it will be sadly absent from now on from my dinner table. It was discovered by Turkish authorities who did an analysis on it. Read and weep.(((

        Таинственным ингредиентом Соса-Соla оказались червяки. В состав напитка входит еще и таинственный экстрактКомпания Соса-Соla раскрыла секрет производства знаменитого напитка: в его основе - пищевая добавка, добываемая из червяков. Этот факт умалчивался с 1886 года.
        Как оказалось, турецкий фонд Святого Николая подал на Соса-Соla в суд, требуя раскрыть формулу производимого напитка, чтобы узнать, не являются ли ингредиенты, входящие в состав колы, вредными.
        В состав напитка, который можно было увидеть на этикетке, кроме сахара, фосфорной кислоты, кофеина, карамели, двуокиси углерода входит еще и таинственный экстракт. Исследователи установили, что это натуральный краситель кармин или пищевая добавка кошениль, добываемая из кошенильных червяков. В пищевой промышленности этот экстракт также известен как карминовая кислота.
        Кошениль же — это общее название нескольких видов насекомых из разных семейств подотряда кокцид, самки которых используются для получения красной краски — кармина.
        Теперь компания Соса-Соla будет вынуждена обнародовать этот факт. В противном случае путь напитку на турецкий рынок будет закрыт.
http://korrespondent.net/tech/science/720404
http://en.wikipedia.org/wiki/Carmine
http://en.wikipedia.org/wiki/Anaphylactic_shock
        Cochineal Insect, a scale insect traditionally used by Native Americans to make a crimson dye called cochineal. Spanish explorers in the 1550s brought cochineal from Mexico back to Europe. Cochineal became the most widely traded and, next to gold and silver, the most valuable product of the West Indies. Cochineal production was lucrative until the 20th century when synthetic dyes largely replaced cochineal. The cochineal scale that had commercial importance is native to South America. Several other scale insects in the same genus are native to desert areas of the southwestern United States. These scales also were once used to make dye, but to a much lesser extent than the South American cochineal insect.
        The adult female cochineal insect is 2 to 5 mm (0.1 to 0.2 in) long with a distinctly segmented, purplish red or carmine-colored body. Cochineal insects feed on certain prickly pear cacti and are most obvious on the flat pads of the cactus in spring. They occur in colonies covered with a fluffy white wax that they secrete. The cochineal insect's bright reddish body is not visible unless the waxy secretions are scraped away and the scale's outer covering is punctured. Cochineal is produced from the dried, crushed bodies of cochineal scale insects. A carefully tended cactus yields about 20 pounds of scale each year.
        The cochineal industry has an intriguing history. For over 200 years after the insect's discovery, Spain prohibited export of live cochineal insects and prevented foreigners from visiting production areas in the Americas. Many Europeans mistakenly thought the dye was produced from cactus fruit, and Spanish authorities encouraged such misconceptions in order to maintain their cochineal monopoly. The Dutch amateur scientist Antoni van Leeuwenhoek in 1704 used microscopic lenses to analyze dried cochineal. Leeuwenhoek determined that cochineal consisted entirely of female scale insects. Many people found this unbelievable. Wide acceptance that cochineal dye was produced from the cochineal insect did not occur until the late 1700s, when the insects were successfully introduced and established outside of the Americas.
         Cochineal production peaked in the 1870s, when as much as 7 million pounds of dye were produced annually. The development of less expensive, synthetic aniline dyes virtually eliminated cochineal production as well as cultivation of prickly pear cacti for this purpose. A small cochineal industry still exists in the Canary Islands, Peru, and Mexico. Recent findings that some synthetic red dyes may induce cancer has renewed interest in cochineal production. Cochineal-based dye is again becoming popular as a coloring agent, especially in processed foods.
         Scientific classification: The South American cochineal insect is Dactylopius coccus. Cochineal insects belong to the order Homoptera and the scale family, Dactylopiidae. North American dye-producing scales are also in the genus Dactylopius.
Carmine
         Carminic acidCarmine (IPA: /?k??m?n, ?k?rma?n, -mi?n/), also called Crimson Lake, Cochineal, Natural Red 4, C.I. 75470, or E120, is a pigment of a bright red color obtained from the carminic acid produced by some scale insects, such as the cochineal and the Polish cochineal, and is used as a general term for a particularly deep red color. Carmine is used in the manufacture of artificial flowers, paints, rouge, yogurt, cosmetics, food additives, and crimson ink.

Production
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       Carmine may be prepared from cochineal, by boiling dried insects in water to extract the carminic acid and then treating the clear solution with alum, cream of tartar, stannous chloride, or potassium hydrogen oxalate; the coloring and animal matters present in the liquid are thus precipitated. Other methods are in use in which egg white, fish glue, or gelatine are sometimes added before the precipitation.
        The quality of carmine is affected by the temperature and the degree of illumination during its preparation, sunlight being requisite for the production of a brilliant hue. It also differs according to the amount of alumina present in it. It is sometimes adulterated with cinnabar, starch and other materials; from these the carmine can be separated by dissolving it in ammonia. Good carmine should crumble readily between the fingers when dry.
        Carmine lake is a pigment obtained by adding freshly precipitated alumina to decoction of cochineal.
      Carmine can be used as a staining agent in microbiology, as a Best's carmine to stain glycogen, mucicarmine to stain acidic mucopolysaccharides, and carmalum to stain cell nuclei. In these applications, it is applied together with a mordant, usually an Al(III) salt.
Allergy
         Carmine is used as a food dye in many different products such as juices, ice cream, yogurt, and candy, and as a dye in cosmetic products such as eyeshadow and lipstick. Although principally a red dye, it is found in many foods that are shades of red, pink, and purple. As a food dye it has been known to cause severe allergic reactions and anaphylactic shock in some people.[1] [2]
         Food products containing carmine-based food dye may prove to be a concern for people who are allergic to carmine, or people who choose not consume any or certain animals, such as vegetarians, vegans, and followers of religions with dietary law (e.g. kashrut in Judaism and halaal in Islam).
Regulations for use in foodstuffs
        In the United States, carmine is approved as dye for foodstuffs. In January 2009, FDA passed a new regulation requiring carmine and cochineal to be listed by name on the label. This regulation is effective January 5, 2011.
        In January 2006, the FDA evaluated a proposal[3] that would require food products containing carmine to list it by name on the ingredient label. It was also announced[citation needed] that the FDA will separately review the ingredient labels of prescription drugs which contain colorings derived from carmine. A request from the Center for Science in the Public Interest (article titled: "FDA Urged to Improve Labeling of or Ban Carmine Food Coloring" [1])[citation needed] to require ingredient labels to explicitly state that carmine may cause severe allergic reactions and anaphylactic shock and that is derived from insects was declined by the FDA. Food industries were aggressively opposed to the idea of writing "insect based" on the label and they finally agreed to simply putting "carmine"[citation needed].
       Although concerns over hazards from allergic reactions have been asserted,[citation needed] the United States Food and Drug Administration agency (FDA) has not banned the use of carmine and states it found no evidence of a "significant hazard" to the general population.[2]
Anaphylaxis
From Wikipedia, the free encyclopedia, (Redirected from Anaphylactic shock), Anaphylaxis, Classification and external resources, ICD-10 T78.2, Diseases DB 29153, Medicine med/128, MeSH D000707
        Anaphylaxis is an acute systemic (multi-system) and severe Type I Hypersensitivity allergic reaction in humans and other mammals. The term comes from the Greek words ??? ana (against) and ??????? phylaxis (protection).[1] Minute amounts of allergens may cause a life-threatening anaphylactic reaction. Anaphylaxis may occur after ingestion, skin contact, injection of an allergen or, in some cases, inhalation.
        Anaphylactic shock, the most severe type of anaphylaxis, occurs when an allergic response triggers a quick release from mast cells of large quantities of immunological mediators (histamines, prostaglandins, leukotrienes) leading to systemic vasodilation (associated with a sudden drop in blood pressure) and edema of bronchial mucosa (resulting in bronchoconstriction and difficulty breathing). Anaphylactic shock can lead to death in a matter of minutes if left untreated.
        An estimated 1.24% to 16.8% of the population of the United States is considered "at risk" for having an anaphylactic reaction if they are exposed to one or more allergens, especially penicillin and insect stings. Most of these people successfully avoid their allergens and will never experience anaphylaxis. Of those people who actually experience anaphylaxis, up to 1% may die as a result.[3] Anaphylaxis results in approximately 18 deaths per year in the U.S. (compared to 2.4 million deaths from all causes each year in the U.S.[4]). The most common presentation includes sudden cardiovascular collapse (88% of reported cases of severe anaphylaxis).
        Researchers typically distinguish between "true anaphylaxis" and "pseudo-anaphylaxis" or an "anaphylactoid reaction." The symptoms, treatment, and risk of death are identical, but "true" anaphylaxis is always caused directly by degranulation of mast cells or basophils that is mediated by immunoglobulin E (IgE), and pseudo-anaphylaxis occurs due to all other causes.[5] The distinction is primarily made by those studying mechanisms of allergic reactions.
Causes
         Anaphylaxis is a severe, whole-body allergic reaction. After an initial exposure ("sensitizing dose") to a substance like bee sting toxin, the person's immune system becomes sensitized to that allergen. On a subsequent exposure ("shocking dose"), an allergic reaction occurs. This reaction is sudden, severe, and involves the whole body.
        Hives and angioedema (hives on the lips, eyelids, throat, and/or tongue) often occur. Angioedema may be severe enough to block the airway. Prolonged anaphylaxis can cause heart arrhythmias.
        Some drugs (polymyxin, morphine, x-ray dye, and others) may cause an "anaphylactoid" reaction (anaphylactic-like reaction) on the first exposure.[6] This is usually due to a toxic reaction, rather than the immune system mechanism that occurs with "true" anaphylaxis. The symptoms, risk for complications without treatment, and treatment are the same, however, for both types of reactions. Some vaccinations are also known to cause "anaphylactoid" reactions.[7] Antitoxins and antivenins may cause similar reactions.
        Anaphylaxis can occur in response to any allergen. Common causes include insect bites/stings, food allergies (peanuts and tree nuts are the most common, though not the only), and drug allergies. Pollens and other inhaled allergens rarely cause anaphylaxis. In opthamology, the dye fluorescein used in some eye exams is a well known trigger. Some people have an anaphylactic reaction with no identifiable cause (idiopathic).
Symptoms
Symptoms of anaphylaxis are related to the action of Immunoglobulin E (IgE) and other anaphylatoxins, which act to release histamine and other mediator substances from mast cells (degranulation). In addition to other effects, histamine induces vasodilation of arterioles and constriction of bronchioles in the lungs, also known as bronchospasm (constriction of the airways).
        Tissues in different parts of the body release histamine and other substances. This causes constriction of the airways, resulting in wheezing, difficulty breathing, and gastrointestinal symptoms such as abdominal pain, cramps, vomiting, and diarrhea. Histamine causes the blood vessels to dilate (which lowers blood pressure) and fluid to leak from the bloodstream into the tissues (which lowers the blood volume). These effects result in shock. Fluid can leak into the alveoli (air sacs) of the lungs, causing pulmonary edema.
Symptoms can include the following: polyuria, respiratory distress, hypotension (low blood pressure), encephalitis, fainting, unconsciousness,   urticaria (hives), flushed appearance, angioedema (swelling of the lips, face, neck and throat): this can be life threatening, tears (due to angioedema and stress), vomiting, itching, diarrhea, abdominal pain, and anxiety
        The time between ingestion of the allergen and anaphylaxis symptoms can vary for some patients depending on the amount of allergen consumed and their reaction time. Symptoms can appear immediately, or can be delayed by half an hour to several hours after ingestion.[8] However, symptoms of anaphylaxis usually appear very quickly once they do begin.
Diagnosis
        Apart from its clinical features, blood tests for tryptase (released from mast cells) might be useful in diagnosing anaphylaxis.[9]
        In some cases, it is unclear from the patient interview what triggered the anaphylaxis. In this setting, skin allergy testing (with or without patch testing) or RAST blood tests can sometimes identify the cause.
Treatment Emergency treatment
        Anaphylaxis is a life-threatening medical emergency because of rapid constriction of the airway, often within minutes of onset, which can lead to respiratory failure and respiratory arrest. Brain and organ damage rapidly occurs if the patient cannot breathe. Due to the severe nature of the emergency, patients experiencing or about to experience anaphylaxis require the help of advanced medical personnel. First aid measures for anaphylaxis include rescue breathing (part of CPR). Rescue breathing may be hindered by the constricted airways, but if the patient stops breathing on his or her own, it is the only way to get oxygen to him or her until professional help is available.
        The primary treatment for anaphylaxis is administration of epinephrine (adrenaline). Epinephrine prevents worsening of the airway constriction, stimulates the heart to continue beating, and may be life-saving. Epinephrine acts on Beta-2 adrenergic receptors in the lung as a powerful bronchodilator (i.e. it opens the airways), relieving allergic or histamine-induced acute asthmatic attack or anaphylaxis. If the patient has previously been diagnosed with anaphylaxis, he or she may be carrying an EpiPen or Twinject for immediate administration of epinephrine. However, use of an EpiPen or similar device only provides temporary and limited relief of symptoms.
        Tachycardia (rapid heartbeat) results from stimulation of Beta-1 adrenergic receptors of the heart increasing contractility (positive inotropic effect) and frequency (chronotropic effect) and thus cardiac output.[10] Repetitive administration of epinephrine can cause tachycardia and occasionally ventricular tachycardia with heart rates potentially reaching 240 beats per minute, which itself can be fatal. Extra doses of epinephrine can sometimes cause cardiac arrest. This is why some protocols advise intramuscular injection of only 0.3–0.5mL of a 1:1,000 dilution.
        Some patients with severe allergies routinely carry preloaded syringes containing epinephrine, diphenhydramine (Benadryl), and dexamethasone (Decadron) whenever they go to an unknown or uncontrolled environment.
Clinical care
Paramedic treatment in the field includes administration of epinephrine IM; antihistamines IM (such as chlorphenamine or diphenhydramine); steroids, such as hydrocortisone or dexamethasone; IV Fluid administration and in severe cases, pressor agents (which cause the heart to increase its contraction strength) such as dopamine for hypotension, administration of oxygen, and intubation during transport to advanced medical care.
        In severe situations with profuse laryngeal edema (swelling of the airway), cricothyrotomy or tracheotomy may be required to maintain oxygenation. In these procedures, an incision is made through the anterior portion of the neck, over the cricoid membrane, and an endotracheal tube is inserted to allow mechanical ventilation of the patient.
        The clinical treatment of anaphylaxis by a doctor and in the hospital setting aims to treat the cellular hypersensitivity reaction as well as the symptoms. Antihistamine drugs such as diphenhydramine or chlorphenamine (which inhibit the effects of histamine at histamine receptors) are continued but are usually not sufficient in anaphylaxis, and high doses of intravenous corticosteroids such as dexamethasone or hydrocortisone are often required. Hypotension is treated with intravenous fluids and sometimes vasopressor drugs. For bronchospasm, bronchodilator drugs (e.g. salbutamol, known as Albuterol in the United States) are used. In severe cases, immediate treatment with epinephrine can be lifesaving. Supportive care with mechanical ventilation may be required.
         It is also possible to undergo a second reaction prior to medical attention or using an Epipen. It is suggested to seek one to two days of medical care.
        The possibility of biphasic reactions (recurrence of anaphylaxis) requires that patients be monitored for four hours after being transported to medical care for anaphylaxis.[10]
         Many anaphylactic patients will be sent home or released after the initial reaction is declared over. Yet, rebound reactions are almost always bound to happen. Most people with anaphylaxis have a rebound a few hours after the initial reaction, yet there are cases where a rebound would occur after as much time as a week.