21/07/2018
I made this post a decade ago, when my daughter started getting sick, when she self weaned.
Breastfeeding Immunity
I have posted on a couple of threads that my daughter, Morgan aka Zilla has been very sick and that we are working on a theory that she was using my immune system up until this past November. I've been doing research to back my theory, one which was initially blown off by the doctors at the hospital. Now it appears that I am onto something. I got an email from Morgan's ped this morning, responding to the information I sent her a couple of days ago about IgA immunity and breastfeeding. This morning she said that she didn't think I was crazy {poor thing she really has no idea that I'm nuts} and she thanked me for helping her to 'think outside the box'. Which the Immunologist in the hospital was simply unable to do and he has now been fired. He was ignorant enough to tell me that a 'baby only gets antibody benefits for the first six months of nursing.'
So if you are interested in how antibodies work with breastfeeding, this thread might interest you. I was told flat out by the Immunologist at the hospital that there was no need to redo the Igame {IgG, IgA, IgM, IgE} test that was done in December, because those numbers never change. Ummmm....what if they do in a child that was breastfed for 3 years? He wasn't even willing to consider the possibility. I demanded that the test be done after he left our room. We are waiting on the results from the Mayo Clinic now, and if I'm right then he is OMG so wrong and I will be doing all sorts of happy dances cuz we can fix or at least treat an IgA problem.
I know this information is hard to understand, it's hard for me to figure out too.
http://pw1.netcom.com/~nbwc/breastfeeding.html
Breastfeeding Stimulated the Infant Immune System
By Lars A. Hanson
Mammals breastfeed their offspring to provide optimal nutrition and protection against infection. Human interference with this natural process is not new. Ashurbanipal, who was king of Assyria in the 7th century B.C., was artificially fed with cow's milk. The Sushruta Samhita, a collection of Indian writings from 2200 to 2400 years old, prescribed that various herb extracts, honey, and clarified butter should be given to the newborn before breastfeeding was started. The practice of prelacteal feeding is still widely employed on the Indian subcontinent, bringing a high risk of neonatal infection because these materials are often heavily contaminated.
The Greek physician Soranus, writing in the 2ndcentury A.D., taught that nothing should be given to a newborn for the first two days and then animal milk for the next three weeks, during which time the mother's milk was regarded as unsuitable. Delaying the start of breastfeeding was common during the Middle Ages in some parts of Europe, for example Norway. Newborns were instead given foodstuffs such as sour cream, porridge, and butter, which were considered the best foods available but which sadly increased the risk of infection. In England between 1680 and 1840, there was a 75% decline in the rate of neonatal mortality, which is believed to have been related to a return to immediate breastfeeding.
Sweden has useful statistics for a long time back, and it has been possible to determine that in the 19th century, mothers were not breastfeeding at all in certain areas of the county. During the summer months, mothers living on farms participated in the farm work and left their infants at home in a cot above which was hung a cow's horn filled with fresh milk or buttermilk. The baby sucked through a small hole in a piece of goatskin wrapped around the tip of the horn. These horns easily became dirty and infected, and there are reports from 19th century district doctors that the smell of cow horn feeding could be recognized when the home was entered. The result was a striking increase in neonatal deaths from "digestive diseases" (diarrhea) in these farming regions during the summer, which might be taken as the first "controlled" study of the protective effect of breastfeeding.
Most Human Milk Antibody is Secretory IgA
When antibodies were first found in human milk, at about the turn of the century, they were considered to be of the same structure as those found in blood. However, antibodies were not found in the blood of breastfed infants, whereas antibodies were found in the blood of piglets and calves after they had been fed with the early milk, or colostrum. In these animals, the milk antibodies are of the IgG1 isotype and move straight from the gut lumen into the circulation, where they make up the y-globulin fraction, which is totally lacking in newborn calves and piglets.
Human infants are born with a substantial y-globulin fraction, consisting of IgG that has been actively transferred from the mother via the placenta. Human milk antibodies are a special isotype called secretory IgA, which functions on mucosal membranes and not in the blood. Secretory IgA is an unusaually stable tetravalent antibody that binds microbes and other antigenic materials to prevent them from reaching mucosal membranes, where they might cause infections or other harm such as depositing toxins on intestinal epithelial receptors. This simple protective mechanism is important in host defense, because an absolute majority of human infections begin at mucosal surfaces.
Secretory IgA comprises 70 to 80% of all human antibodies. Major sites of secretory IgA production are mucosal membranes and exocrine glands emptying onto mucosal surfaces, and a major part of the immune system of the gut is active in secretory IgA production. The importance of this is emphasized by the fact that two thirds of the whole immune system is located in the gut. The amount of immunologically active tissue in the gut may be appreciated if it is realized that the immune system and the nervous system are about the same size.
The next remarkable fact is that the secretory I~ in milk, although produced locally in the mammary, glands, results from antigen exposure in the gut. Antigenic material in the gut lumen is selectively taken up by Peyer's patches in the gut wall. These are aggregates of T and B lymphocytes and antigen presenting cells, such as dendritic cells, covered by a specialized epithelium, the M cells, with the capacity to sample antigenic material from the gut lumen.
Once a B cell response to a luminal antigen is initiated, the cells begin to produce IgA dimers and J or joining chains. The committed B lymphocytes leave the Peyer's patches and migrate to various mucosal membranes and exocrine glands, including the mammary glands. There the B lymphocytes produce the dimeric IgA antibodies with J chains that make the antibodies capable of binding to the extramural portions of receptors on the basal surfaces of epithelial cells in the in mammary glands. These receptors are called poly-Ig receptors or the secretory component.
After binding, the antibodies are transported through the glandular epithelium to the epithelial surface, where they are secreted into milk. They have carried with them the secretory component, so that the complete secretory IgA molecule of milk and other exocrine secretions is a stable complex of the IgA dimer, J chain, and secretory component.
The secretory IgA produced by the mammary glands and appearing in the mother's milk is directed against all the bacteria, viruses, fungi, and other antigenic substances to which the mother has been recently exposed. I~ production starts when lactogenic hormones initiate lactation, making the mammary glands a target for migrating B cells from the Peyer's patches. At that time, it seems that memory lymphocytes are also directed into the mammary glands, so that milk may also contain secretory IgA directed against microbes to which the mother has been exposed earlier in life.
A breastfed infant receives a high dose of secretor, IgA in milk. Whereas a 65-kg mother may produce some 2.5 gm of IgA daily for her own use, a breastfed infant weighing only a few kilograms may receive 0.5 to 1 gm per day.
Milk Is Protective in Other Ways
In addition to secretory IgA, milk contains numerous other factors of likely significance for the defense of the infant. The protective capacity of secretory IgA against numerous bacteria has been proven, but other factors can only be assumed to be effective. Human milk contains small amounts of IgM and IgO, some of which have been found to be directed against various E. coli antigens, but they are of unknown clinical significance.
Lactoferrin is the major protein in mature milk; in colostrum, the major protein is secretory IgA. Lactoferrin is anti-inflammatory, turning off production of the inflammatory cytokines IL-1, IL-6and TNF- . These cytokines might be expected to be produced after colonization of the newborn gut by Gram-negative bacteria, so the action of lactoferrin might be one explanation why breastfed infants lose significantly less weight than non-breastfed infants during the first week of life.
Although human milk contains only small amounts of anti-inflammatory substances such as components of complement and of the fibrinolytic, kallikrein, and coagulation systems, milk has numerous anti-inflammatory effects. Lactoferrin contains a peptide, lactoferricin, which is bactericidal against E. coli, Klebsiella, Pseudomonas, Proteus, Yersinia, Staphylococcus, Listeria, and other bacterial species, and lactoferrin also kills viruses, fungi, and certain tumor cells.
Another antimicrobial substance in human milk is lysozyme, which attacks the cell walls of Gram-positive bacteria, but its biological role is still unclear. Preliminary data from my laboratory suggest that human milk may also contain antisecretory factors, a group of peptides discovered in the pig and shown to stop diarrhea. Moreover, human milk contains a number of growth factors and cytokines that may contribute to the maturation of the intestine and the immune system.
The large oligosaccharide fraction of human milk may be of sp~ (jal significance because it includes analogs to receptors for microbes on epithelial cells. The binding of microbes to such receptors is the first step in most infections that are initiated at mucosal membranes. Scandinavian workers, including my group, have shown that milk oligosaccharides prevent binding of cholera toxin to its receptor as well as binditig of pneumococci and Haemophilus influenzae to pharyngeal epithelium. Fucose-containing carbohydrate moieties of human milk K-casein have recently been shown to prevent adherence of Helicobacter pylon to human gastric mucosa.
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Infants Are Protected Against Infection During Lactation
There are many studies on the possible protective capacity of human milk. However, several of them were planned and executed before modern epidemiology had developed, and others show problems with the many confounding factors that can confuse the issue, such as differences in socioeconomic conditions and educational levels, the degree of microbial exposure, the definition of breastfeeding as exclusive or partial, and the role of extra water given to breastfed infants in hot climates.
By now there are a number of quite reliable studies that permit conclusions to be drawn. In developing countries, the effects are often dramatic. In fact, breastfeeding has become a public health issue with consequences even at the population level because of its demonstrated reduction in infant mortality as well as its contraceptive effect. The World Health Organization has indicated that increasing breastfeeding by 40% would reduce respiratory deaths by 50% and diarrhea deaths by 66% worldwide in children less than 18 months of age.
The most striking effects are seen against diarrhea. The risk of dying of diarrhea is 25 times higher for a non-breastfed infant than for an exclusively breastfed infant in a poor area. In Pakistan, partial breastfeeding reduced the risk of neonatal septicemia 18-fold. The mortality in neonatal septicemia in Pakistan is about 60%, and this disease together with diarrhea make up the two most common
LARS A. HANSON is Professor and Head of the Department of Clinical Immunology at the University of Goteborg, from which he obtained M.D. and Ph.D. degrees in 1961. Dr. Hanson has published more than 500 papers in pediatrics, immunology, and bacteriology.
SCIENCE & MEDICINE
NOVEMBER/DECEMBER 1997
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