Meeting with Professor Ebringer
29/30 July, 2000, San Antonio, Texas.
Summary by John—Calif [my comments are in brackets]
Background
Professor Alan Ebringer B.Sc, MD, FRCP, FRACP, FRCPath, is the Professor of Immunology at Kings College, London, U. K., and has published nearly sixty papers, most related to Ankylosing Spondylitis, often exploring the role of Klebsiella pneumoniae in this condition and others. His pioneering work has led to the most successful therapies for AS, as applied in his clinical practice as Honorary Consultant Rheumatologist at University College School of Medicine, Middlesex Hospital, London, U.K. Promising treatments for Multiple Sclerosis, Rheumatoid Arthritis, Lupus (SLE), and elimination of BSE ("Mad Cow disease"), are certain other benefits of the autoimmune research he has been directly involved with. His recent visit to San Antonio was very kindly sponsored by George McCaffery.
The Cause of AS
All Ankylosing Spondylitis family diseases (AS, iritis, IBS/IBD, UC, and Reiter’s Syndrome), including those B27 negative, should be renamed "Klebsiella Reactive Arthritis." In almost thirty years and over 600 AS patients treated at the Middlesex London AS Clinic, each and every one of them have been attributed to the activity of the Klebsiella bacterium. There have, to date, been no exceptions identified. [As many as 50% of B27negs. have actually retested positive, and several other MHCs have been linked to AS; B39/40, B7, and H8.] [I was able to confirm, through a very reliable source, that some of the studies contrary to the Klebsiella and AS connection, have been driven by—as I first suspected—the ever-present funding need; self-preservation above the needs of the suffering.]
Molecular Mimicry
This was proven as the mechanism for heart damage due to rheumatic fever by Zabriske, working in the US: The Streptococcus bacterium has a sequence that resembles heart tissue, and the antibody produced by our immune systems against this pathogen attacks it—and heart cells, too. ["Autoimmune"]
Could any other rheumatic conditions work exactly the same way? AS does to the Klebsiella bacterium, and RA does to the Proteus bacterium, and MS probably does to the Acinetobacter bacterium (as does kuru, BSE, and CJD). These have each been verified in Professor Ebringer’s research laboratories.
The older, and still widely-held theory to explain AS is called "The Receptor Theory," and it requires more steps: An (as-yet) unidentified agent must co-mingle with the B27 cell and then trigger immune attack. In over twenty years, no such agent has been found, and the theory has at least one more step than molecular mimicry [This almost certainly means that Occam’s Razor will cut it to shreds.]. [Another theory, not discussed, was proposed by Dr. Thomas Brown, a research associate of Dr. Albert Sabin: The mycoplasm agent theory. Fortunately, whether this theory is accurate or not, the treatments do work because antibiotics are employed. The Road Back Foundation promotes this approach.]
The Successful Treatment of AS
In nearly 20 years experience with over 600 patients, the low-starch (London AS Diet) diet has been of significant, meaningful, and measurable benefit. There have been no cases of negative health consequence from the slightly increased protein, sugar, and fat levels, and decreased starch intake. The combination of salazopyrin (sulfasalazine; must be enteric-coated, ie. Azulfidine—EN; 0.5—>2g tid), and the London AS Diet, has resulted in a dramatic decrease of symptoms in the majority of patients. Some individuals have been able to remain in remission using dietary restrictions alone. Anecdote: Those who do not respond well to the diet seem to not be able to stay on it [they are ratted on by their relatives, also patients at Dr. Ebringer’s clinic.]. Those able to remain on the programme long-term, are able to completely halt the progression of AS.
The presence of starches (especially the "four major poisons:" Bread, potatoes, cakes, and pasta) causes the number of Klebsiella pneumoniae bacteria to multiply, and it also allows them to produce a thicker outer wall. [This could possibly be hampering their early elimination by the primary immune system, and might make them less susceptible to certain antibiotics, too.]
Pre-AS
Early detection of AS is critical in avoiding damage, and criteria have been proposed to identify those likely to have this condition: A positive test for HLA B27, plus five out of these six conditions; 1-backache in lumbar area, 2-leg pains that resemble sciatica, 3-these pains move from side to side, 4-pains in the morning to the extent that the subject must "roll" out of bed, 5-morning stiffness, 6-this morning stiffness can be relieved by exercise. [Perhaps a blood-relative with AS, IBS/IBD, UC, Crohn’s, Reiter’s Syndrome, or iritis, or even a history of respiratory illnesses might also add to the case for a Pre-AS classification.] [The nonsense about not testing children for HLA B27 should be well out of our collective thoughts, for A) Not everyone with B27 gets AS, so insurance companies need not worry—or even be informed, and B) with this knowledge, it may be possible to avoid getting the condition altogether, by reducing starches and staying well away from aspirin and other NSAIDs.] Anecdote: A fighter pilot had backache and tested positive for HLA B27, and was nearly dropped from the service for an initial diagnosis of AS. He did not have it, but did have a backache and is B27+.
Sub-clinical AS
Although nearly 2% of peoples with European ancestry have AS, most are not being treated and are unaware that their symptoms warrant attention. [This is not necessarily a bad thing, since doctors do not have any idea how to treat AS, and their NSAIDs and immunosuppressives will make the condition worse!]. Up to 20% of people with the HLA B27 MHC experience some level of discomfort attributable to AS/pre-AS. [These people are at-risk from over-the-counter drugs and the high consumption of starches.]
HLA B27—General Distribution by Latitude
A) Eskimos have the highest percentage, with some groups at 50% occurrence: 90% of their diet is meat; almost no starch.
B) Nordic peoples have a high incidence with 12-14%: Historically (and especially pre-) very little starches consumed; salted fish and fresh vegetables.
C) Germanic (includes Anglo-Saxon and Norman) peoples have moderate populations at 8%: Low-to-medium historic consumption of starches (especially high after introduction of the potato).
D) Mediterranean (includes Spanish) and Aryan (N. India) populations have about 4% B27s: Medium-to-high consumption of starches.
E) Tropical Africa, Polynesian, S. Indian, and oriental populations have very low incidence of B27, often less than 1%: Highest consumption of starches.
The numbers of persons expressing symptoms of AS are increasing in northern populations, due to greater availability of refined starches. It is possible that, over past aeons, HLA B27 genotypes were eliminated due to starchy diets causing AS in individuals early enough to make them unfit for procreation, and unable to transmit their genetics to future generations. [This miserable disease is one of the best arguments for eugenics that I can imagine; we have the technology…]
Men and Women
Get AS, but there seems to be a greater incidence in men (4:1). This may be due to two factors: 1- Women, especially at the age of AS onset, typically are figure conscious to the extent of excluding much starch from their diets, and have better control, opting for less-convenient, non-starchy foods. 2- The structure of the lymph ducts in the mesentery differs to the extent that they are longer in women, to accommodate expansion of the womb. This extra length means later onset, and often less severe symptoms. Women respond better to the starch-restrictions in the diet because they probably follow it much more closely than do men. [being closer to the kitchen may have something to do with this. Nearly every snack food is starchy, and they are the most convenient choices. Although both men and women may work at stressful jobs, the frenetic style of ‘eat and run’ that most men have is not conducive to a starch-reduced or starch-free diet. Women seem to also better understand that food, long-term, can be medicine—bad or good.]
Exercise
Swimming is best, but walking is very good. High-impact aerobics or serious running are not encouraged. Stretching and pre-conditioning are also very important. Surprising muscle (determined via biopsy) changes occur in nearly every condition of AS, from cellular derangement to extreme atrophy.
Hemoglobin versus ESR
Erythrocyte Sedimentation Rates are indicative of inflammation, and a majority of AS patients exhibit elevated (>15mm/hr) rates. As this ‘sed rate’ increases, the hemoglobin level decreases; they are inversely proportional. [This should be obvious, since the "E" in ESR is the red blood cell; as they are attacked and eliminated, their numbers go down. This probably contributes to the universal tiredness experienced by sufferers. The result is that even less oxygen becomes available to persons who do not inhale very well in the first place.]
[Coulda…Woulda…Shoulda
(If I had only known then, what I know now): Professor Ebringer is no stranger to Texas, for he presented some of his findings at an AS conference in Dallas, away back in 1985; it was the introduction of the London AS Diet in the control of AS. I sure wish that any one of my rheumatologists had attended—and then passed the information on to me, if only as a friendly ‘see how this works for you.’ The connection between Klebsiella and AS was proposed by Ebringer in Paris, 1976. He had published, in many common circulating professional journals, at least twenty-four technical papers by the time of the Dallas conference, many on the subject of how Klebsiella is directly related to AS. In the ensuing fifteen years, he has gained substantial clinical experience, and even more supportive empirical data. Ignorant of this, physicians in the US continue to incorrectly treat AS and most of the major other autoimmune conditions. This is a national disgrace and there is no excuse for it. As patients suffering from a potentially crippling disease, we have had to manage our own treatments because of the continued and protracted ignorance of physicians who should have taken the time to know better.]
