Here we go, some conventional medicine relevance; IgA deficiency is real and according to wikipedia (this is just a quick skim) it can affect 1 in 333:

http://en.wikipedia.org/wiki/Selective_imm...in_A_deficiency

Holy shit. Where is all the news on this?

I'm going to quote her latest post, there's some relevant information for every theorist here:

Here is more information from the book aoeFood Allergies and Food Intolerances.a I have mainly picked out sentences or paragraphs here and there that might apply to us. PLEASE NOTE: the term aoefood intolerancea here is a broader concept than sensitivity to lectins. Lectins are one cause of food intolerance, but the book makes the point that there are other potential causes as well.

 

Chapter 2: aoeIt seems that some item found in some foods, stimulates the immune system to respond more aggressively. One group of natural substances that might do this are the lectins. These are protein molecules, found in many foods, which are not usually allergens themselves, but which bind to human cells. They cling to cells in the gut, and they may be able to pass through the gut wall into the blood stream, thus reaching every part of the body. Some lectins are known to affect the immune response, and a few promote the formation of IgE at the expense of other antibodies. Many foods that commonly feature in food allergy, such as peanuts, are particularly rich in lectins.a

 

Chapter 5: aoeThe purpose of inflammation, in the healthy individual, is to fight off infection. The body assumes that the antibodies have attached themselves to an invading bacterium or virus and sends in the troops (other white cells). Obviously, the body needs to have control systems that tell it NOT to react when the antibodies are bound to something innocuous a such as a food protein that happens to have wandered into the blood through the gut wall. That is the function of the IgA antibodies. Because they do not activate the complement system, they can quietly mop up non-harmful food proteins for disposal without setting off a damaging episode of inflammation. For this system to work, the body must somehow distinguish food from other sorts of antigen. And it must make sure that IgA arather than IgG, another more inflammatory type of antibody - is manufactured for the food molecules. a. It seems that the system for producing IgA (rather than IgG) to react to food molecules breaks down in some people. When this occurs, the immune complexes circulating in the blood after a meal will be potentially inflammatory.a

 

Chapter 7: aoeIn food intolerance, it is almost always commonly eaten foods that are the source of the problem. In the United States, this means wheat, milk, and corn, which are usually consumed several times a day.a

 

aoeAny food can produce intolerance, but some foods are more likely to be a problem than other. Oranges, for example, are regularly identified as culprit foods, whereas apples are incriminated much less frequently. Similarly, wheat appears to be a more potent cause of intolerance than other cereals. a. In the general pattern of food intolerance, patients begin with a sensitivity to milk, wheat, corn, eggs, or some commonly eaten food. As time goes by new sensitivities appear along with new symptoms, and the patientsa health deteriorates. In those who have had food intolerance for many years, a large number of foods may be at fault. Such people tend to be quite severely affected by their symptoms. aoe

 

aoeFood intolerance generally produces a slower response to a food than an allergy. The symptoms may appear several hours after the food is eaten, or the following day, or even 48 hours later. There may be no obvious link between eating the food and having the symptoms.a

 

Chapter 12: aoeThere is evidence that people with food intolerance have leakier gut walls than healthy individuals a so they let more undigested (or incompletely digested) food molecules through. This has major health implications.a

 

aoeInflammation, produced by an immune attack, can make the gut wall leakier. One source of inflammation is a gut infection. Alternatively, foods themselves might provoke inflammation of the gut wall if there is a localized allergic response to them.a

 

aoeThere is a third way in which the gut wall might be made leakier. We all produce a special type of antibody called secretory IgA, which pours out into the gut, where it binds to certain food molecules, locking them into large complexes that are more difficult to pass through the gut wall. There is some evidence that people with food intolerances have less secretory IgA than healthy people. a. If more food molecules get through the gut wall, more immune complexes will form in the blood.a

 

aoeThere is one other way in which the immune system might be involved in food intolerance. All immune cells use small messenger molecules to communicate with each other. a One important messenger molecule is interferon, whose main job is to combat viral infections. a. It may be that the immune system has overreacted to a viral infection and is continuing to produce excessive amounts of interferon (which keeps inflammation going). aoe

 

aoeViruses themselves might also play a part in food intolerance; it is known that they can alter our immune responses in subtle ways. Some people date their food intolerance to a bout of influenza or other viral infection. Viruses in the gut could alter the structure of the gut wall, simply by binding to its cells a they might even do this without causing any noticeable signs of infection.a

 

aoeDigestive enzymes are mostly found in the gut, where they break food down into smaller molecules. One group of these are the detoxification enzymes, which are charged with destroying or disarming all the toxins that get into our bodies. Other toxins are produced by the bacteria living in our gut. To add to this natural load, there are a variety of synthetic substances that have to be detoxified, including alcohol and nicotine, medicinal drugs, food additives, and pesticide residues in food. Most of the bodyas detoxification enzymes are found in the liver. a. In some people certain enzymes are either in short supply or fail to work properly because their structure is abnormala.. People with food intolerance are much more likely to be deficient in some digestive enzymes than healthy people are.a

 

Chapter 13: aoeSince commonly eaten foods are the most frequent offenders in food intolerance, varying the diet is recommended. In particular, avoid eating milk and wheat too often a try to restrict these foods to just one meal a day. Avoid eating large quantities of the other high-risk foods, notably eggs, orange juice, and peanuts. a.. Avoid anything that increases the permeability of the gut wall: excess alcohol, highly spiced food, and raw pineapple or papaya. Certain drugs also make the gut leakier, notably aspirin and other similar drugs (non-steroidal anti-inflammatory drugs). You should take these only if you really need them.a

 

aoeOne thing that is thought to trigger food intolerance is a heavy exposure to toxic chemicals. Avoid insecticides, fungicides, and pesticides used on crops, and keep household chemicals to a minimum. Treating the early stages of food intolerance is a great deal easier than trying to tackle entrenched symptoms and multiple sensitivities. The longer you leave it, the more difficult it may be.a

 

The remainder of the book goes into great detail about how to do a proper elimination diet, and how to go about eating after the diet is completed. I found this book generally interesting, but it didnat have much more to say that would clearly relate to our p.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1904854/

IgA deficiency (IgA-D) has been associated with the HLA region, in particular with the North European haplotype HLA-A1, -B8, -DR3, but the exact location of the susceptibility gene(s) is unknown. Some reports suggest that a susceptibility gene is encoded in the class II region, while others implicate the class III region. We exploited differences between the common Sardinian and North European HLA-DR3 haplotypes to help localize the IgA-D susceptibility gene(s). With the knowledge that approximately 13% of HLA-DR3 homozygous individuals of North European origin are IgA-D, we examined 43 HLA-DR3 homozygous Sardinians to find that all had normal serum IgA, IgG and IgM levels. A detailed analysis of their MHC haplotypes indicated a common Sardinian HLA-DR3 haplotype TAP1A, TAP2A, HLA-DQB1*0201, -DQA1*0501, -DRB1*0301, LH1-(Z + 2), D3A-(Z + 2), C4B-0, C4A-L, G11-15, Bf-0.4, C2-a, HSP70-7A5, 9N3-(Z + 10), 82I-(Z a 2), TNFI-9, 62-(Z a 20), HLA-B18, -Cw5, -A30 which diverges from the common North European HLA-DR3 haplotype telomeric to the HLA-DR region. In parallel studies of five Sardinians with IgA-D, two of the 10 HLA haplotypes (20%) contained HLA-DR3, a frequency similar to that observed in the background population. One of these was the HLA-DR3- B8 North European haplotype, which occurs rarely in Sardinia. Our data favour the hypothesis that a class III region allele, present on the common North European but not on the Sardinian HLA-DR3 haplotype, confers susceptibility to IgA-D.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1904854/

QUOTE

IgA deficiency (IgA-D) has been associated with the HLA region, in particular with the North European haplotype HLA-A1, -B8, -DR3, but the exact location of the susceptibility gene(s) is unknown. Some reports suggest that a susceptibility gene is encoded in the class II region, while others implicate the class III region. We exploited differences between the common Sardinian and North European HLA-DR3 haplotypes to help localize the IgA-D susceptibility gene(s). With the knowledge that approximately 13% of HLA-DR3 homozygous individuals of North European origin are IgA-D, we examined 43 HLA-DR3 homozygous Sardinians to find that all had normal serum IgA, IgG and IgM levels. A detailed analysis of their MHC haplotypes indicated a common Sardinian HLA-DR3 haplotype TAP1A, TAP2A, HLA-DQB1*0201, -DQA1*0501, -DRB1*0301, LH1-(Z + 2), D3A-(Z + 2), C4B-0, C4A-L, G11-15, Bf-0.4, C2-a, HSP70-7A5, 9N3-(Z + 10), 82I-(Z a 2), TNFI-9, 62-(Z a 20), HLA-B18, -Cw5, -A30 which diverges from the common North European HLA-DR3 haplotype telomeric to the HLA-DR region. In parallel studies of five Sardinians with IgA-D, two of the 10 HLA haplotypes (20%) contained HLA-DR3, a frequency similar to that observed in the background population. One of these was the HLA-DR3- B8 North European haplotype, which occurs rarely in Sardinia. Our data favour the hypothesis that a class III region allele, present on the common North European but not on the Sardinian HLA-DR3 haplotype, confers susceptibility to IgA-D.

Check EpiCor to boost IgA.