The Roman philosophy of Janus states that to figure out what is in front of us now it helps to look back. How did we discover allergies and how can that change our view of allergies now?
Clemens von Pirquet and Bela Schick in the 1890s noticed a serum sickness with 10% of their dipertheria antitoxin vaccines. Since the reaction was not serum dose dependent they concluded that it must be a difference in the immune system. Clemens coined the term "allergy" in order to explain the new concept that one's own immune system can cause sickness.
What was not answered back then and remains unanswered now is why do some people develop allergies? What was different about the immune system in the 10%? What causes the immune system to malfunction? A genetic flaw?
For years without genetic evidence for this belief it has been said that allergies must be genetic because of the observed clustering and inheriting of allergies in families. Reality is that a person can go through most of their life allergy free then suddenly develop a severe one. If allergies were only genetically based, a genetic flaw, allergies couldn't spontaneously develop later in life. An infection on the other hand could easily be shared between family members or caught out in the environment.
When an infection occurs the immune system marks as much foreign infection material as it can with antibodies. Then memory B cells circulate with these infection crime scene antibodies for future identification. Perhaps the 10% who had the serum sickness reaction had seen the material before?
In 1913 Charles Richet received the Nobel prize for recognizing that the most severe allergic reactions, he coined "anaphylaxis", were due to a second exposure. Ten to twelve days after dogs were given a first octopus toxin exposure if a second toxin exposure was given to the dogs they had severe and sometimes fatal reactions.
Looking at the known plant based allergies: trees, grass, poison ivy, daisies, and lilies which a person could see daily and all of which are not considered toxic it does not make sense to apply the second exposure notion of Richet unless you add pathogenic infections. why? because the immune system needs a reason to be making antibodies and memories.
Let us take this even one step further: why this allergen? With all the substances we are exposed to why does an allergen get selected? Perhaps the allergen is something the infection doesn't like.
Allergy Hypothesis: An allergen has an antimicrobial effect against an infection within us.
Imagine a spirochete infection like lyme disease or h.pylori. Often the infected person has no idea they are infected. Spirochetes can be killed by a compound found in poison oak and poison ivy. Now imagine that a person infected with spirochetes is exposed to poison ivy. Instead of a typical reaction of rash and itchiness the person has a severe reaction boarding on anaphylactic.
Now, imagine a person infected with T.gondii or T.cruzii. These parasites can be killed with the venom of bees. Now imagine the possibility that people with anaphylactic bee allergies are the people with these T.gondii or T.cruzii infections. This would not be the people working with bees who are constantly stung thus becoming allergic rather people who are allergic because of the T.gondii parasite.
Which brings us to the notorious peanut allergy which is strongly associated with eczema. The peanut protein itself is not an antimicrobial but the aflatoxin so commonly contaminating peanut butter is. Aflatoxin has been found to be antimicrobial against the antibiotic sensitive strains of staph and e.coli. The more susceptible to traditional antibiotics the more susceptible to aflatoxin the bacteria is. (http://www.ncbi.nlm.nih.gov/pubmed/3091837)
The association of staph and eczema has been sketchy. Staph has, but not always, been isolated from skin scrapings. The anaphylactic peanut allergy is a bit convoluted but it could be that peanut is seen with aflatoxin by the immune system and it is guilt by association. The peanut is not harming the infection the aflatoxin is but our immune system remembers everything there. The aflatoxin acts as an antimicrobial against staph which fits our allergy hypothesis. Do antibodies to aflatoxin exist in children with peanut anaphylaxis?
Clemens von Pirquet and Bela Schick in the 1890s noticed a serum sickness with 10% of their dipertheria antitoxin vaccines. Since the reaction was not serum dose dependent they concluded that it must be a difference in the immune system. Clemens coined the term "allergy" in order to explain the new concept that one's own immune system can cause sickness.
What was not answered back then and remains unanswered now is why do some people develop allergies? What was different about the immune system in the 10%? What causes the immune system to malfunction? A genetic flaw?
For years without genetic evidence for this belief it has been said that allergies must be genetic because of the observed clustering and inheriting of allergies in families. Reality is that a person can go through most of their life allergy free then suddenly develop a severe one. If allergies were only genetically based, a genetic flaw, allergies couldn't spontaneously develop later in life. An infection on the other hand could easily be shared between family members or caught out in the environment.
When an infection occurs the immune system marks as much foreign infection material as it can with antibodies. Then memory B cells circulate with these infection crime scene antibodies for future identification. Perhaps the 10% who had the serum sickness reaction had seen the material before?
In 1913 Charles Richet received the Nobel prize for recognizing that the most severe allergic reactions, he coined "anaphylaxis", were due to a second exposure. Ten to twelve days after dogs were given a first octopus toxin exposure if a second toxin exposure was given to the dogs they had severe and sometimes fatal reactions.
Looking at the known plant based allergies: trees, grass, poison ivy, daisies, and lilies which a person could see daily and all of which are not considered toxic it does not make sense to apply the second exposure notion of Richet unless you add pathogenic infections. why? because the immune system needs a reason to be making antibodies and memories.
Let us take this even one step further: why this allergen? With all the substances we are exposed to why does an allergen get selected? Perhaps the allergen is something the infection doesn't like.
Allergy Hypothesis: An allergen has an antimicrobial effect against an infection within us.
Imagine a spirochete infection like lyme disease or h.pylori. Often the infected person has no idea they are infected. Spirochetes can be killed by a compound found in poison oak and poison ivy. Now imagine that a person infected with spirochetes is exposed to poison ivy. Instead of a typical reaction of rash and itchiness the person has a severe reaction boarding on anaphylactic.
Now, imagine a person infected with T.gondii or T.cruzii. These parasites can be killed with the venom of bees. Now imagine the possibility that people with anaphylactic bee allergies are the people with these T.gondii or T.cruzii infections. This would not be the people working with bees who are constantly stung thus becoming allergic rather people who are allergic because of the T.gondii parasite.
Which brings us to the notorious peanut allergy which is strongly associated with eczema. The peanut protein itself is not an antimicrobial but the aflatoxin so commonly contaminating peanut butter is. Aflatoxin has been found to be antimicrobial against the antibiotic sensitive strains of staph and e.coli. The more susceptible to traditional antibiotics the more susceptible to aflatoxin the bacteria is. (http://www.ncbi.nlm.nih.gov/pubmed/3091837)
The association of staph and eczema has been sketchy. Staph has, but not always, been isolated from skin scrapings. The anaphylactic peanut allergy is a bit convoluted but it could be that peanut is seen with aflatoxin by the immune system and it is guilt by association. The peanut is not harming the infection the aflatoxin is but our immune system remembers everything there. The aflatoxin acts as an antimicrobial against staph which fits our allergy hypothesis. Do antibodies to aflatoxin exist in children with peanut anaphylaxis?
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