Tag Archives: homeopathy. Hahnemann

IHM Project in the UK 2019/20

I.H.M. International HQ. 14 Shanklin Close, Eastbourne. East Sussex BN23 8EG United Kingdom.
education@instituteforhomoeopathicmedicine.com
https://instituteforhomoeopathicmedicine.wordpress.com

 

In collaboration with our affiliate organisations, colleagues and patients, the I.H.M. has decided to open a dedicated teaching/seminar centre and mobile clinic on the inland waterways of the United Kingdom. We are looking to purchase a 50-60 foot narrowboat and fit it out for teaching and a clinic.

Given the cost of office rental in the UK, this vessel will be considerably cheaper to operate and the savings can be passed on to seminar pricing and patients fees.

The IHM is the producer of the P&W Openrep Synopsis Therapeutic Pocket Book by Boenninghausen computer repertory software and the Book version. tpbpwIt is envisioned that we will conduct one-day seminars on case taking utilising the repertory and show the benefits of the program in the analysis. We prefer to keep the numbers of attendees small so as facilitate personal teaching, so the maximum attendees will be 8-12 persons.

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We will have facilities for refreshments, snacks and lunch if required.

This vessel will be available for rent to non-mainstream medical practices for half-day, full day and 2-day seminars.

Given the present attitude from the government towards alternative medical practices, we see this as a viable project to let the general public have access to professional alternative health care.

We do need some help in making this come to life. We need some financial support to add to our own contributions. We will look to a funding operation and will set a goal of 50K but will go ahead if we can finance more cheaply. We will have to pay for some interior changes, add more 12 volt and mains power to plug in laptops etc. It may require some solar power and a large 3KW inverter. There will, of course, be some thank you rewards for supporters.

We plan on setting the routes geographically. For example London to Bristol. Reading to Birmingham, Birmingham to Liverpool, or Manchester, or Wigan and all points in the zone where groups want to meet. As canals go through cities and are located near rail lines, we can more or less pick convenient locations for mooring and conducting the seminars. We can moor outside restaurants if preferred.

Most of our staff are medically qualified. All have undergone intensive training with the I.H.M. in Hahnemannian homoeopathy. If we get the vessel as we want it, (and ONLY for individuals or 2 persons), we hope to accommodate those attending the IHM 4 day training course for application for the REGISTER. 

Below is a vessel we looked at and let go because it did not quite meet our specifications for having extra people on board.

We will let you know when we open a fund us account. In the meantime please feel free to give us your opinion if this project something you would be interested in using to learn from.

 

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The Institute for Homoeopathic Medicine.

In 1810, Hahnemann presented his groundbreaking new medicine and therapy via the book the Organon of the Medical Art. He presented his method in carefully structured detail. He compiled a database of medical substance proving’s which were listed in the Fragmenta, the Materia Medica Pura and Chronic Diseases. Hahnemann taught his methods to many students and colleagues, but only put his trust in a small number of practitioners, of whom Clemens Maria Franz (Friedrich) Freiherr (Baron) von Bönninghausen was perhaps the most prominent.

Bönninghausen’s projects of reportorial works culminating in the Therapeutic Pocket Book, was approved by Hahnemann as being an accurate representation of the proving’s database and clinical experience. (The T.P.B. actually is an amazing synthetic approach of how Hahnemann’s mind worked in case analysis.)

Although Hahnemann revised the Organon six times before his death and constantly examined possible changes to the methodology, he never made changes to the central prescribing principle of like cures like, without which homoeopathy (the therapy) cannot exist as a separate modality. If the principle of “like cures like”, with its required database of provings, is abandoned, as has been the case with modern approaches and methods, the certainty offered by prescribing to principle is lost, the path obliterated.

At the IHM we look no further than Hahnemann’s circle of trust. We work with Hahnemann’s structure of method and database, Organon and proving’s. We explore the writings of those whom Hahnemann commended, and study and apply the work of Boenninghausen in great depth.

We do not do this slavishly. In order to validate the method, the works and writings of others claiming to be homoeopaths are examined for similarities and differences in approach to the therapy. Sadly, the decline in homoeopathic integrity began with one of its most able practitioners who was politically naïve.

On the political level, Carroll Dunham was a peacemaker. It was said of him that he had no enemies. His liberal and generous mind made it easier for him to accept compromise. Unfortunately, compromise on the search for the truth leads to error. In 1870 he made a notable presentation before the American Institute of Homœopathy (AIH) called ‘Freedom of Medical Opinion and Action: a Vital Necessity and a Great Responsibility’. He believed, contrary to his predecessors, that liberty of opinion and practice should prevail within the AIH. He said that he was sure that “perfect liberty will sooner bring knowledge of the truth and that purity of practice which we all desire.” His speech provided license to the pseudo-homoeopaths to practice as they wanted and be still identified as homoeopaths. Subsequent to his address knowledge of homoeopathy was removed in 1874 as a requirement for membership in the AIH. Dunham died in 1877 and did not witness the disastrous effect his noble but naïve vision eventually had on the course of homoeopathy in the U.S.A. as most of our institutions disappeared after its members had adopted practices at variance with the teachings of Hahnemann.

(Our Noble and Beloved Carroll Dunham by Dr André Saine, D.C., N.D., F.C.A.H.)

We work with great care and certainty because we value our integrity as homoeopathic practitioners, and we owe it to our patients to treat based on a tried and true principle, to avoid speculation, theorizing, and invented systems whether based on sensation, the periodic table, kabala, shamanism, kingdoms, families and the like.

Hahnemann’s homoeopathy is the modality which achieved tremendous successes in the cholera epidemic of the early 1830s, leading to its acceptance in medical faculties in Europe at the time as a discipline for study. The original works are filled with discussions and cases demonstrating the efficiency of the method across the spectrum of diseases afflicting mankind.

Today homoeopathy is either being outlawed or relegated to treatment of the most minor problems. Its vast ability as a medical modality is being lost. Poor training, poor understanding of the medical science behind its development and a search for novelty in case analysis all have contributed to its demise as a valid therapy and is thought of as an intuitive healing method rather than the effective treatment it really is.

The IHM puts all its efforts into teaching from original materials, working with practitioners to achieve greater certainty and effectiveness in prescribing through a full understanding of the central principle of homoeopathy and the best ways to apply it in homoeopathic practice.

We do not wish to add more novel ideas to the world of homoeopathy. We do see it as part of our professional duty, to keep the standards high and teach the real methodology to all who desire to practice proper medicine in the prescribed manner. We lay no claim to being ‘better’ prescribers. We do however concede that our results based on the instructions of Hahnemann give better resolution to medical problems than other interpretive methods of prescribing. There is great latitude in applying the therapy, however, deviating from its central core or adding a false overlay of psychological analysis and emphasizing or interpreting physical symptoms as delusional states are not the answer.

Hahnemanns concept of illness.

Hahnemann’s concept of Illness. We need to look at this and see if or where our thinking deviates from it.

Hahnemann believed that the signs and symptoms of a case of illness represented an attempt by the body to heal itself. According to this view, the signs and symptoms do not represent the illness, but rather the reaction of the person to his illness. The illness and the reaction to illness are separate.

At first glance, this would appear to be at odds with the latter part of Aphorism 6.  “…………All these perceptible signs represent the disease in its whole extent, that is, together they form the true and only conceivable portrait of the disease.”

a little thought will clarify the apparent differences. Hahnemann is emphasising that the signs and symptoms exhibited by the patient are the true reactive process of the body which represent the individual disease per se, and not the named disease.

Therefore Hahnemann reasoned that physician should administer that medicine to the patient (which produced in the healthy signs and symptoms similar to those of the patient). In this manner, the natural attempt of the body to heal itself would be re-inforced, rather than neutralised or interfered with. Hahnemann called this treatment of illness with medicines produced in the healthy, symptoms similar to those of the ill.

Homoeopathy (Homois: Similar; Pathos: suffering).

If an ill person receives no treatment, he either dies, remains chronically ill or recovers. If he recovers, his pattern of recovery is like that of all sick persons and separate from his particular disease. As people become ill, old symptoms of previous illness often reappear. The symptoms move from non-vital organs, like the nose and throat, to more vital organs, like the kidneys and lungs. Then there is a period of crisis. Following this crisis, one by one and in reverse order of their appearance, the symptoms move from vital to less vital organs until the patient is well again. This natural response is called autotherapy.

Under homoeopathic treatment, an identical response usually follows, rather than the abrupt disappearance of symptoms or the introduction of new symptoms which often follows other types of therapy. Homoeopathy, from its inception, has been based on an inclusive, descriptive attitude towards the patient AND the medicine. The response of the patient is equally inclusive in relation to the natural course his illness would have taken without treatment.

 

 

The real source of Gout

This is the missing chapter from, “Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health”, by Gary Taubes on Gout.

Disclaimer as requested by Gary:This chapter is in draft form and has not gone through the same fact-checking as the rest of Taubes’ published work, even though there are 32 citations (some incomplete). I wanted to show the writing process at its mid-point. The only deletions I’ve make are “TK”, which–for unknown reasons–is traditional shorthand in publishing for indicating that something is “to come”.

I have bolded several sections for those who would like a 2-3-minute skim of content highlights before digesting the entire piece, which is 7 pages long.

Enter Gary Taubes: –

Gout and the condition known technically as hyperuricemia, or elevated levels of uric acid, are the most recent examples of this kind of institutional neglect of the potential health effects of fructose, and how pervasive it can be.

Gout itself is an interesting example because it is a disease that has gone out of fashion in the last century and yet the latest reports suggest it is not only as prevalent as ever, but becoming more so. Recent surveys suggest that nearly 6 percent of all American men in their fifties suffer from gout, and over ten percent in their seventies. The proportion of women afflicted is considerably less at younger ages but still rises over 3 percent by age 60.(1) Moreover, the prevalence of gout seems to have doubled over the last quarter century, coincident (perhaps not coincidentally) with the reported increase in obesity, and it may have increased five- or even six-fold since the 1950s, although a large portion of that increase may be due to the aging of the population.(2)

Until the late 17th century, when the spread of gout reached almost epidemic proportions in Britain, the disease afflicted almost exclusively the nobility, the rich and the educated, and so those who could afford to indulge an excessive appetite for food and alcohol. This made gout the original example of a disease linked to diet and over-consumption, and so, in effect, the original disease of civilization.

But once gout became easily treatable, in the early 1960s, with the discovery of the drug allopuranol, clinical investigators and researchers began to lose interest. And the pathology of gout has been understood since the British physician Alfred Garrod, in the mid-19th century, identified uric acid as the causative agent; the idea being that uric acid accumulates in the circulation to the point that it falls out of solution, as a chemist would put it, and so crystallizes into needle-sharp urate crystals. These crystals then lodge in the soft tissues and in the joints of the extremities – classically, the big toe — and cause inflammation, swelling and an excruciating pain that was described memorably by the 18th century bon vivant Sydney Smith as like walking on one’s eyeballs.(3) Because uric acid itself is a breakdown product of protein compounds known as purines – the building blocks of amino acids – and because purines are at their highest concentration in meat, it has been assumed for the past 130-odd years that the primary dietary means of elevating uric acid levels in the blood, and so causing first hyperuricemia and then gout, is an excess of meat consumption.

The actual evidence, however, has always been less-than-compelling: Just as low cholesterol diets have only a trivial effect on serum cholesterol levels, for instance, and low-salt diets have a clinically insignificant effect on blood pressure, low-purine diets have a negligible effect on uric acid levels. A nearly vegetarian diet, for instance, is likely to drop serum uric acid levels by 10 to 15% percent compared to a typical American diet, but that’s rarely sufficient to return high uric acid levels to normality, and there is little evidence that such diets reliably reduce the incidence of gouty attacks in those afflicted.(4) Thus, purine-free diets are no longer prescribed for the treatment of gout, as the gout specialist Irving Fox noted in 1984, “because of their ineffectiveness” and their “minor influence” on uric acid levels.(5) Moreover, the incident of gout in vegetarians, or mostly vegetarians, has always been significant and “much higher than is generally assumed.” (One mid-century estimate, for instance, put the incidence of gout in India among “largely vegetarians and teetotalers” at 7%.)(6) Finally, there’s the repeated observation that eating more protein increases the excretion of uric acid from the kidney and, by doing so, decreases the level of uric acid in the blood.(7) This implies that the meat-gout hypothesis is at best debatable; the high protein content of meats should be beneficial, even if the purines are not.

The alternative hypothesis is suggested by the association between gout and the entire spectrum of diseases of civilization, and between hyperuricemia and the metabolic abnormalities of Syndrome X. In the past century, gout has manifested all of the now-familiar patterns, chronologically and geographically, of diseases of civilization, and so those diseases associated with western diets. European physicians in World War I, for instance, reported a reduced incidence of gout in countries undergoing food shortages.(8) In primitive populations eating traditional diets, gout was virtually unknown or at least went virtually unreported (with the conspicuous exception of Albert Schweitzer who says he saw it with surprising frequency.) The earliest documented cases reported in Asia and Africa were in the late 1940s.(9) And even in the 1960s, hospital records from Kenya and Uganda suggested an incidence of gout lower than one in a thousand among the native Africans. Nonetheless, by the late 1970s, uric acid levels in Africa were increasing with westernization and urbanization,(10) while the incidence of both hyperuricemia and gout among South Pacific islanders was reportedly sky-rocketing. By 1975, the New Zealand rheumatologist B.S. Rose, a colleague of Ian Prior’s, was describing the native populations of the South Pacific as “one large gouty family.”(11)

Gout has also been linked to obesity since the Hippocratic era, and this association is the origin of the assumption that high-living and excessive appetites are the cause. Gouty men have long been reported to suffer higher rates of atherosclerosis and hypertension, while stroke and coronary heart disease are common causes of death.(12) Diabetes is also commonly associated with gout. In 1951, Menard Gertler, working with Paul Dudley White’s Coronary Research Project at Harvard, reported that serum uric acid levels rose with weight, and that men who suffered heart attacks were four times as likely to be hyperuricemic as healthy controls.(13) This led to a series of studies in the 1960s, as clinical investigators first linked hyperuricemia to glucose intolerance and high triglycerides, and then later to high insulin levels and insulin resistance.(14) By the 1990s, Gerald Reaven, among others, was reporting that insulin resistance and hyperinsulinemia raised uric acid levels, apparently by decreasing uric acid excretion by the kidney, just as they raised blood pressure by decreasing sodium excretion. “It appears that modulation of serum uric concentration by insulin resistance is exerted at the level of the kidney,” Reaven wrote, “the more insulin-resistant an individual, the higher the serum uric acid concentration.” (15)

These observations would suggest that anything that raised insulin levels would in turn raise uric acid levels and might cause gout, which would implicate any high carbohydrate diet with sufficient calories. But this neglects the unique contribution of fructose. The evidence arguing for sugar or fructose as the primary cause of gout is two-fold. First, the distribution of gout in western populations has paralleled the availability of sugar for centuries, and not all refined carbohydrates in this case. It was in the mid-17th century, that gout went from being exclusively a disease of the rich and the nobility to spread downward and outward through British society, reaching near epidemic proportions by the 18th century. Historians refer to this as the “gout wave,”(16) and it coincides precisely with the birth and explosive growth of the British sugar industry(17) and the transformation of sugar, in the words of the anthropologist Sydney Mintz, from “a luxury of kings into the kingly luxury of commoners.”(18) British per capita sugar consumption in the 17th century was remarkably low by modern standards, a few pounds per capita per year at the turn of the century, but the change in consumption over the next century and a half was unprecedented: between 1650 and 1800, following the British acquisition of Barbados, Jamaica and other “sugar islands”, total sugar consumption in England and Wales increased 20- to 25-fold.(19)

The second piece of evidence is much less circumstantial: simply put, fructose increases serum levels of uric acid. The “striking increase” in uric acid levels with an infusion of fructose was first reported in the Lancet in the late 1960s by clinicians from Helsinki, Finland, who referred to it as fructose-induced hyperuricemia.(20) This was followed by a series of studies through the late 1980s confirming the existence of the effect and reporting on the variety of mechanisms by which it came about. Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid. Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it.(21) Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism.(22)

These mechanistic explanations of how fructose raises uric acid levels were then supported by a genetic connection between fructose metabolism and gout itself. Gout often runs in families, so much so that those clinicians studying gout have always assumed the disease has a strong hereditary component. In 1990, Edwin Seegmiller, one of the few veteran gout researchers in the U.S., and the British geneticist George Radda, who would go onto become director of the Medical Research Counsel, reported that the explanation for this familial association seemed to be a very specific defect in the genes that regulate fructose metabolism. Thus, individuals who inherit this defect will have trouble metabolizing fructose and so will be born with a predisposition to gout. This suggested the possibility, Seegmiller and Radda concluded, that this defect in fructose metabolism was “a fairly common cause of gout.”(23)

As these observations appeared in the literature, the relevant investigators were reasonably clear about the implications: “since serum-uric-acid levels are critical in individuals with gout, fructose might deserve consideration in their diet,” noted the Helsinki clinicians in The Lancet in 1967, and so the chronic consequences of high-fructose diets on healthy individuals required further evaluation.(24) Gouty patients should avoid high-fructose or high-sucrose diets, explained Irving Fox in 1984, because “fructose can accelerate rates of uric acid synthesis as well as lead to increased triglyceride production.”(25) Although none of these investigators seemed willing to define what precisely constituted a high-fructose or a high-sucrose diet. Was it 50 pounds of sugar a year? 100 pounds? 150 pounds? 300 pounds? And would high-fructose diets induce gout in healthy individuals or would they only exacerbate the problem in those already afflicted? In 1993, the British biochemist Peter Mayes published an article on fructose metabolism in the American Journal of Clinical Nutrition that is now considered the seminal article in the field. (This was in the special issue of the AJCN dedicated to the health effects of fructose.) Mayes reviewed the literature and concluded that high-fructose diets in healthy individuals were indeed likely to cause hyperuricemia, and he implied that gout could be a result, as well, but the studies to address that possibility had simply never been done. “It is clear,” Mayes concluded, “that systematic investigations in humans are needed to ascertain the precise amounts, both of fructose consumption and of its concentration in the blood, at which deleterious effects such as hyperlipidemia and hyperuricemia occur.”(26) Add to this Reaven’s research reporting that high insulin levels and insulin resistance will increase uric acid levels, and it suggests, as Mayes had remarked about triglycerides, that sugar (sucrose) and high fructose corn syrup would constitute the worst of all carbohydrates when it comes to uric acid and gout. The fructose would increase uric acid production and decrease uric acid excretion, while the glucose, though its effect on insulin, would also decrease uric acid excretion. Thus, it would be reasonable to assume or at least to speculate that sugar is a likely cause of gout, and that the patterns of sugar consumption explain the appearance and distribution of the disease.

Maybe so, but this hypothesis has never been seriously considered. Those investigators interested in gout have focused almost exclusively on alcohol and meat consumption, in part because these have historical precedents and because the implication that gouty individuals and particularly obese gouty individuals shy away from meat and alcohol fit in well with the dietary prescriptions of the 1970s onward.

More than anything, however, this sugar/fructose hypothesis was ignored, once again, because of bad timing. With the discovery and clinical application of allopurinol in the 1960s, those clinical investigators whose laboratories were devoted to studying the mechanisms of gout and purine metabolism – James Wyngaarden’s, for instance, at Duke and Edwin Seegmiller’s at NIH – began focusing their efforts either on working out the nuances of allopurinol therapy, or to applying the new techniques of molecular biology to the genetics of gout and rare disorders of hyperuricemia or purine metabolism. Nutritional studies were simply not considered worthy of their time, if for no other reason than that allopuranol allowed gout suffers to eat or drink whatever they wanted. “We didn’t care so much whether some particular food might do something,” says William Kelley, who is a co-author with Wyngaarden of the 1976 textbook, Gout and Hyperuricemia and who started his career in Seegmiller’s lab at NIH. “We could take care of the disease.”(27)

This exodus, however, coincided with the emergence of research on fructose-induced hyperuricemia. By the 1980s, when the ability of fructose and sucrose consumption to raise uric acid levels in human subjects was demonstrated repeatedly, the era of basic research on gout had come to an end. The major players had left the field and NIH funding on the subject had dwindled to a trickle. Wyngaarden published his last research paper in 1977 and spent the years 1982 to 1989 as director of the National Institutes of Health. Kelley published his last papers on the genetics of gout in 1989, when he became dean of medicine at the University of Pennsylvania. Irving Fox, who did much of the basic research on fructose- and alcohol-induced hyperuricemia in Kelley’s lab, went to work in the biotechnology industry in the early 1990s. Only Edwin Seegmiller remained interested in the etiology of gout, and Seegmiller says that when he applied to the NIH for funding to study the relationship between fructose and gout, after elucidating the genetic connection with Radda in 1990, his grant proposals were rejected on the basis that he was too old and, as an emeritus professor, technically retired.(28) “In the 1950s and 1960s, we had the greatest clinical scientists in the world working on this disease,” says Kelley. “By the 1980s and 1990s, there was no one left.”

Meanwhile, the medical journals would occasionally run articles on the clinical management of the gout, but these would concentrate almost exclusively on drug therapy. Discussions of diet would be short, perhaps a few sentences, and confused about the science. On those occasions when the authors would suggest that gouty individuals might benefit from low-purine diets, they would invariably include “sugars” and “sweets” as among the recommended foods with low-purine contents.(29) In a few cases – a 1996 article in the New England Journal of Medicine, for instance (30)– the articles would also note that fructose consumption would raise uric acid levels, suggesting only that the authors had been unaware of the role of fructose in “sugars” and “sweets.” Even when the New England Journal published a report from Walter Willett and his Harvard colleagues in March 2004, this same kind of nutritional illiteracy manifested itself. Willett’s article had reported that men with gout seemed to eat more meat than healthy men. But Willett, who by this time was arguably the nation’s most influential nutritional epidemiologist, later explained that they had never considered sugar consumption in their analysis because neither he nor his collaborators had been aware of the hyperuricemic effect of fructose. Willett’s co-author, Gary Curhan, a nephrologist and gout specialist with a doctorate in epidemiology, said he might have once known that fructose raised uric acid levels, but it had slipped his mind. “My memory is not what it used to be,” he said. He also acknowledged, in any case, that he never knew sucrose was half fructose.

The addenda to this fructose-induced hyperuricemia story may be even more important. When the New England Journal of Medicine published Willett’s gout study, it ran an editorial to accompany it written by the University of Florida nephrologist Richard Johnson. Over the past decade, Johnson’s research has supported the hypothesis that elevating the uric acid concentration in the circulation also damages the blood vessels leading into the kidneys in such a way as to raise blood pressure directly, and so suggests that fructose consumption will raise blood pressure.

This is another potentially harmful effect of fructose that post-dates the official reports exonerating sugar in the diet. And it is yet another mechanism by which sugar and high fructose corn syrup could be a particularly unhealthy combination. The glucose in these sugars would raise insulin levels, which in turn would raise blood pressure by inhibiting the kidney’s secretion of sodium and by stimulating the sympathetic nervous system, as we discussed in an earlier chapter, and the fructose would do it independently by raising uric acid levels and so damaging the kidney directly. If this were the case, which has never been tested, it would potentially explain the common association of gout and hypertension and even of diabetes and hypertension.(31) Johnson is only now looking into this possibility, however. Unlike Willett and his colleagues, Johnson had long been aware of the ability of fructose to raise uric acid levels, and so was studying that phenomenon in his laboratory. But it was only in the summer of 2004, he explained, three months after his NEJM editorial was published, that he realized that sucrose was half fructose and that his research of the past years was even relevant to sugar.(32)

A decade later, Thomas Benedek described the epidemiology of gout in The Cambridge World History of Human Disease this way: “Worldwide the severity and prevalence of gout have changed paradoxically since the 1940s. In the highly developed countries, as a result of the advent of effective prophylactic drug therapy, the disease is now rarely disabling. Elsewhere, however, it has become more prevalent, predominantly as a result of `improved diets.’”

###

Footnotes and endnotes:

The economist and historian Ralph Davis estimates that the supply of sugar from the Caribbean into Britain rose from three or four thousand tons a year in the late fifteenth century to over two hundred thousand tons by the 1770s, or an increase of over fifty-fold. (davis r, the rise of the atlantic economies, cornell university press, 1973, p. 251, 255)

1 Kramer hm, curhan g, the association between gotu and nephrolithiasis: the national health and nutrition examination survey III. 1988-1994. Am J Kidney Dis 2002;40:37-42

2 Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE. Epidemiology of gout: is the incidence rising? J Rheumatol. 2002 Nov;29(11):2403-6.

2Interview with choi, sept 16, 2004

2Lawrence RC, Helmick CG, Arnett FC, Deyo RA, Felson DT, Giannini EH, Heyse SP, Hirsch R, Hochberg MC, Hunder GG, Liang MH, Pillemer SR, Steen VD, Wolfe F. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States.

2Arthritis Rheum. 1998 May;41(5):778-99.

3 gout, the patrician disease, p. 3

4

5 hydrick and fox, p. 748-749.

6 Duncan’s diseases of metabolism, p. 632.

7 Hydrick cr and fox ih, nutrition and gout, in present knowledge in nutrition, fifth edition, the nutrition foundation, Washington dc, 1984, p. 743

8 duncans diseases of metabolism, p. 638

9 Traut ef, rheumatic diseases, diagnosis and treatment, the C.V. Mosby Company, St. Louis, 1952 p. 303.

9benedek, in Cambridge history of diseases

9Trowel hc, a case of gout in a ruanda African, the east African medical journal, oct. 1947, p. 346-348

10 Beighton p et al, 1977, rheumatic disorders in th south African negro, part IV. Gout and hyperuricemia. South Af Med J. 51(26):969-72

11 Gout in the Maoris, B.S. Rose, Seminars in Arthritis and Rheumatism. Vol. 5, no. 2, (November) 1975, pg. 121-145.

12 duncan’s diseases of metabolism, 1947, p. 631

13 gertler mm, et al, erum uric acid in relation to age and physique in health andin coronary ehart disease, Ann Intern Med. 1951 Jun;34(6):1421-31. Reiser S, Uric Acid and Lactic Acid, in REISER S AND HALLFRISCH J, METABOLIC EFFECTS OF FRUCTOSE, crc press, boca raton fl, 1987 p. 113-134

13

14 duncan’s diseases of metabolism, p. 631

14 reaven gm, The Kidney: An Unwilling Accomplice in Syndrome X, Am J Kid Dis, Vol. 30, n0 6, December, 1997: pp. 928-931.

15 Facchini F et al, Relationship Between Resistance to Insulin-Mediated Glucose Uptake, Urinary Uric Acid Clearance, and Plasma Uric Acid Concentration, JAMA, December 4, 1991, vol. 266, no. 21, 3008-3011

16 Wyngaarden and Kelley p. ix

17 mintz

18 Sydney Mintz, Sweetness and Power, The Place of Sugar in Modern History, penguin books, ny 1985 p. 96.

19 mintz p. 64, 66

20 perheentupa j raivio k, fructose-induced hyperuricaemia, lancet, September 9, 1967, p.528531

21 emmerson bt, getting rid of gout

22 mayes pa, metabolism of fructose, ajcn, 1993

22hydrick c fox i, nutrition and gout, in modern reviews of nutrition

23 Seegmiller JE, Dixon RM, Kemp GJ, Angus PW, McAlindon TE, Dieppe P, Rajagopalan B, Radda GK. Fructose-induced aberration of metabolism in familial gout identified by 31P magnetic resonance spectroscopy.

23Proc Natl Acad Sci U S A. 1990 Nov;87(21):8326-30

24 peerheentupa ibid

25 hydrick and fox, p. 748-749.

26 Mayes pa, metabolism of fructose, ajcn 1993

27 Kelley interview

28 seegmiller interview

29 See for instance, fam ag, gout, diet and the insulin resistance syndrome, j. rheum. 2002;29, 1350-55

30 Emmerson BT. The management of gout.

30N Engl J Med. 1996 Feb 15;334(7):445-51

31 get citation from Richard Johnson articles on uric acid and hypertension.

32 Johnson interview, june 3, 2004

End of an era as NHS cancels funding for homeopathy in Bristol U.K.

Funding for homeopathy on the NHS in Bristol is to end after health bosses agreed to drop homeopathy remedies from the list of options available for patients.The Portland Centre for Integrative Medicine was the last in England to offer publicly-funded homeopathy.

But Bristol Clinical Commissioning Group (CCG) has approved changes that mean patients will now only be able to access homeopathy for free in “exceptional circumstances”.

In a statement, the Portland Centre said it was extremely sorry that the service was ending as it supported a much-needed model of wellness.

“Over the 70 years of playing a part within the NHS, medical homeopathy has helped thousands of people across Bristol and the region. The Portland Centre has about 1,500 registered patients who access NHS medical homeopathy. As ever this change in service provision most impacts those who might not know about or who can’t afford to pay for holistic approaches,” the statement added.

Clinical evidence for the benefits of homeopathy, including research from the University of Bristol, shows that doctors trained in homeopathy prescribe fewer antibiotics and could save the NHS money, it added.

The Society of Homeopaths also expressed its disappointment at the decision and said homeopathy had much to contribute to the wellness agenda now coming to the fore.

“Homeopathy offers a holistic model which can play an important role in helping patients to get well and stay well,” said Sue Crump, chair of the Public Affairs Committee, adding that, at a time of increasing concern about the costs, availability and side-effects of many drug treatments, there is growing evidence that homeopathy can save the NHS money.

“We regret that the NHS has now decided to reduce patient choice and effectively turned its back on homeopathy’s contribution to healthcare.”

The British Homeopathic Association (BHA) argued that the change would not help to improve patient health or balance the books.

“It will have a negative impact on the lives of those in the care of Bristol CCG as most of the referral patients have chronic conditions which have not been helped through conventional treatment and now have to go back to treatments that do not work for them and cost more,” the BHA said in a statement. “The highly-rated, doctor-led service at Portland will continue to be available to paying patients but, sadly, will now be unavailable to those without funds and often in most need who were being helped through the referral service.”

The Portland Centre is to create a new ‘access fund’ for patients in Bristol with support from the BHA.

Dr Jonathan Hayes, Bristol CCG chairman, said: “We are working hard to become an evidence-informed organisation because we need to make the best use of all resources to offer treatment and care to the widest range of people. The decision on homeopathy funding today is a step towards this and brings us in line with national guidelines.”

Is an allopathic qualification essential to being a good homoeopathic practitioner?

 

 

 

 

 

 

 

E-mail: education@instituteforhomoeopathicmedicine.com

Website: https://instituteforhomoeopathicmedicine.wordpress.com

Please feel free to contact us on the email above.

Dear Colleagues.

Is an allopathic qualification essential to being a good homoeopathic practitioner?

After much discussion ~ and based on the reality that most allopathically trained physicians do NOT have a good grasp on the correct practice of homoeopathy, we at the IHM have concluded that it is not, and moreover, that bridging the gap between medical and non-medical homoeopaths is an integral part of the therapy’s future.

To this end, we have decided on the following:

  • We aim to strengthen the IHM’s presence worldwide, and especially in Spain where its headquarters are currently located, by continuing as an independent homoeopathic research and teaching association offering international seminars, practitioner training and master classes. We have presented Seminars since 1987 and formed 5 teaching colleges.
  • To offer IHM membership to medical and non-medical practitioners, according to IHM’s membership requirements, which will endorse a practitioner as a well trained specialist in homoeopathic medicine regardless of allopathic qualifications. We only teach the therapy as per the Organon and do not overlay the writings of Kent or any modern thinking regarding what homoeopathy is.

The IHM Association will comprise of

  • Support members. (Non practitioners.)
  • Student Homoeopaths
  • H.M licentiate Homoeopaths (medical and non medical)

Only Licentiate Practitioners, those who have trained with the IHM and have passed the requisite entry requirements for endorsement, will be promoted on the IHM’s official register.

What we offer:

Based on the writings and thoughts of Samuel Hahnemann,

 “…I have decided to open here in Leipsic, at the beginning of April, an Institute for Graduated Physicians. In this Institute I shall elucidate in every respect the entire homoeopathic system of healing as taught in the “Organon,” and shall make a practical application of it with patients treated in their presence, and thus place my pupils in a condition to be able to practise this system in all cases themselves. A six months’ course will be sufficient to enable any intelligent mind to grasp the principles of this most helpful science of healing. More detailed conditions will be sent on receipt of a prepaid envelope. Dr. Samuel Hahnemann.Leipsic. 4th December, 1811.”

We took a look at the procedure to train persons to become a homoeopathic physician. Knowing that most people cannot take a 6 months sabbatical (as per Hahnemanns proposal) we have devised a method of seminar attendance and home study that spans one year. This will include:

Details pertaining to the professional one year training course. Leading to Licenciateship with the IHM

  • An initial 4 day intensive training session at our Seville Spain faculty. This training is for both neophytes and practicing consultants.
  • A further period of guided home study.Online discussions.Another day 5 training session in our Seville faculty with emphasis on case management.
  • A final assessment by the IHM officers and moderators as to readiness to be placed on the IHM register as a licentiate of the Institute.

(If in the opinion of the training officers, if is thought that a practitioner is of sufficient knowledge and expertise and practices according to Hahnemanns methods, the IHM will consider awarding a licentiateship after the primary one week training.)

What we cover in the 4 day intensive.

  • A thorough grounding in Hahnemanns methodology and teachings.
  • You will see through case analysis how his method of understanding the disease state is superior to any other and allows for an accurate case management program.
  • You will see what a ‘miasm’ is and how to take it into account if required.
  • You will learn LM or Q potencies and how to use them.
  • You will learn rubric understanding of the Therapeutic Pocket Book and see its superiority in case analysis.
  • You will have more success in your practice utilizing Hahnemanns directions.

The languages used for teaching are English or Spanish.

(For those in South America, we also have a IHM teaching course in operation: https://institutodemedicinahomoeopaticaamericalatina.wordpress.com/2016/09/12/curso-de-capacitacion-homeopatica-para-principiantes-online-o-semipresencial/

For those in Asia, we have a course for beginners based in Hong kong. http://homeopathyhk.academy/

For those in Israel we have a practitioner training. Contact vera.homeopath@gmail . com

We will consider traveling to a location and conducting the teaching on site for 6 or more students for the 4 day intensive. Contact us to discuss.

We also conduct 2 day seminars in Spain. Contact us to discuss.

The IHM uses primary source materials for all of its teachings. Gary Weaver and Vladimir Polony compiled the SYNOPSIS computer program and spent 3 years working on updating the 1846 Therapeutic Pocket Book by Boenninghausen, to correct errors of insertion, gradings and removing the incorrect additions by Allen. P & W also clarified the outdated English language and revised the terminology yet remained true to the original meaning. The repertory has been translated from the original German (included in the program) to English, Spanish, Italian, Hebrew and Polish. More languages will be added as and when.

http://homeopathyonline.org/repertories.php

http://homeopathyonline.org/materia_medicas.php

The officers of the IHM are also the teachers.

Manuel Gutiérrez Ontiveros

Licenciado en Medicina por la Universidad de Sevilla, año 1983

Formación en Homeopatía

Estudios en Homeopatía de México

Máster en Homeoptía por la Universidad de Sevilla

Cursos de especialización en Homeopatía con diversos profesores internacionales

Ejercicio en Homeopatía desde el año 1983

Contacto

Consulta: Barriada los Príncipes Parcela 7 Bloque 8, Sevilla

Tlf 606 207 345

e-mail:  mgo1712@yahoo.es

 

Antonio Gil Ortega

Licenciado en Medicina por la Universidad de Sevilla en 1982

Formacion en Homeopatia en Mexico D.F. en 1984-85 por el IMHAC

Formación continuada en Homeopatia por diferentes Profesores Internacionales reconocidos.

Acreditación en Medicina Homeopatica por el Real e Ilustre Colegio Oficial de Médicos de Sevilla

Ejercicio Clínico-Homeopatico desde 1983

Consulta: C/ Guadalupe, 5, 1ºB, Sevilla

Tfno.: 619956365

e-mail: pranada11@gmail.com

 

 

Ed Nunnery

Dhom med (Lic) IHM Licencia de Homeopatia Institute for Homoeopathic Medicina U.S.A. 2010.

Degree in Art.

Degree in Music Theory.

Studied Homoeopathy in the Vithoulkas method 1988.

Studied and practiced the Andre Saine method for 8 years.

Trained with the Institute for Homoeopathic Medicine for 4 years.

Semi retired private Practice in Pasadena California. Works for the I.H.M. Administration.

Email: ed@instituteforhomoeopathicmedicine.com

 

Vera Resnick. Dhom med (Lic) IHM.
BA International Relations, Hebrew University, Jerusalem, Israel 1986
Qualified from Madicin, Tel Aviv, Israel (Homoeopathy) in 2004
Post Graduate studies with David Little 2004-2006
Advanced Clinical Studies with the IHM 2010-
Clinic: 43 Emek Refaim, Jerusalem, Israel
email: vera.homeopath@gmail.com
phone: 972-54-4640736
SKYPE available.

English and Hebrew speaker.

 

Dr. Gary Weaver D.O., Dhommed I.H.M., H.A.Delhi., M.C.C.H (England), H.B.C.C. (India)., Dgrad H.I.Sydney.Dr. Weaver began his studies in Homoeopathy in 1979 training in England and India. In 1987 he became the co-founder of the Manchester College of Classical Homoeopathy and in 1989 founded the Leeds College of Classical Homoeopathy. In 1990 he founded the Institute for Homoeopathic Medicine in Dublin Ireland. In 1990 he opened the Kuopio Homoeopathic Education and Research Association in Finland. From 2003-2007 he conducted research into the original repertory of Boenninhausen, and is co- director of OpenRep SYNOPSIS the specialist Boenninghausen software.  Gary Weaver has presented seminars in Australia, India, Hong Kong, Finland Spain and England.

 

Guillermo Zamora.
Médico Cirujano UAG., Dhom med (Lic) IHM
Clinic: Pino Suarez 464 ext. 2 Zamora Michoacán, México
Skype: dr.guillermo.zamora
E-mail: homeopathy5@hotmail.com
Cel: 351-134-7331
Spanish and English spoken

 

 

 

Thoughts.

Homeopathy and Microorganisms Producing Exotoxines

The IHM is posting a wonderful and informative article by Dr. Guillermo Zamora, MD , Homeopath written in 2010.

As Homoeopathic physicians, we are often asked if usage is made of antibiotics in cases of infection, and I have long held that at times, judicious application of them may be necessary.  This article will give food for thought. (Editor G.W.)

****************************************************************

It is clear that at Dr. Hahnemann´s times, was unknown the existence of microbial life, however, it seems to be that Dr. Hahemann in some way alluded to the possibility that something else could cause illness. We can see this in the following paragraphs of the Organon:

Paragraph 31, Organon, 6th ed:

The inimical forces, partly psychical, partly physical, to which our terrestrial existence is exposed, which are termed morbific noxious agents, do not possess the power of morbidly deranging the health of man unconditionally1; but we are made ill by them only when our organism is sufficiently disposed and susceptible to attack of the morbific cause that may be present, and to be altered in its health, deranged and made to undergo abnormal sensations and functions – hence they do not produce disease in every one nor at all times.”

In the next paragraph, Dr Hahnemann refers to the infectious miasmas:

  • 78 Sixth Edition

“The true natural chronic diseases are those that arise from a chronic miasm, which when left to themselves, and unchecked by the employment of those remedies that are specific for them, always go on increasing and growing worse, notwithstanding the best mental and corporeal regimen, and torment the patient to the end of his life with ever aggravated sufferings. These, excepting those produced by medical malpractice (§ 74), are the most numerous and greatest scourges of the human race; for the most robust constitution, the best regulated mode of living and the most vigorous energy of the vital force are insufficient for their eradication.1”

Please read the footnote.

“1 During the flourishing years of youth and with the commencement of regular menstruation joined to a mode of life beneficial to soul, heart and body, they remain unrecognized for years. Those afflicted appeal in perfect health to their relatives and acquaintances and the disease that was received by infection or inheritance seems to have wholly disappeared. But in later years, after adverse events and conditions of life, they are sure to appear anew and develop the more rapidly and assume a more serious character in proportion as the vital principle has become disturbed by debilitating passions, worry and care, but especially when disordered by inappropriate medicinal treatment”.

Often come to mind the famous quotes of the famous Dr. Kent:

“I wonder if scientists reflect when they make statements about bacteria. Naturally they would say that the more bacteria the more danger, but this is not so.”

“Save the life of the patient first and don’t worry about the bacteria. They are useless things.”

“The Bacterium is an innocent feller, and if he carries disease he carries the Simple Substance which causes disease, just as an elephant would.”

In this last sentence, I wonder if the bacteria would transport only the simple substance or they are able to carry more than that, for example: Exotoxins.

*Exoenzyme (Taken from wikipedia):

“An exoenzyme, or extracellular enzyme, is an enzyme that is secreted by a cellL and that works outside of that cellL. It is usually used for breaking up large molecules that would not be able to enter the cell otherwise.”

*Exotoxine: (Taken from wikipedia):

“An exotoxin is a toxin excreted by a microorganism , including bacteria, fungi, algae, and protozoa. An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host. Exotoxins may be secreted, or, similar to endotoxins, may be released during lysis of the cell.

Most exotoxins can be destroyed by heating. They may exert their effect locally or produce systemic effects. Well known exotoxins include the botulinum toxin produced by Clostridium botulinum and the Corynebacterium diphtheriae exotoxin which is produced during life threatening symptoms of diphtheria.

Exotoxins are susceptible to antibodies produced by the immune system, but many exotoxins are so toxic that they may be fatal to the host before the immune system has a chance to mount defenses against it.”

It is according to the last paragraph where I would focus more, overall, to mention some of the most dangerous bacteria or bacterial gender in medicine.

Taken from: “ Microbiología Médica de Volk, 3rd edition.”

  • Staphylococcus Aureus:

Gram + bacteria, which produces a light golden pigment, called Polysaccharide A. The ability of these to cause disease depends on its resistance to be phagocytosed and its production of extracellular toxins and enzymes, for example:

Coagulase: This is an extracellular enzyme coagulase-reacting normally present in plasma (perhaps prothrombin) and plasma coagulation by converting fibrinogen into fibrin. The only pathogenic effect has been suggested for this enzyme is covering with fibrin microorganisms to inhibit phagocytosis.

Staphylococcal hemolysins: There are four: Alpha, beta, gamma and delta: It has been shown that alpha toxin, damages the smooth muscle cells and also destroys the skin (it dermonecrotic). It is also toxic to macrophages, platelets, and causes degranulation of PMNs.

Beta toxin is an enzyme that reacts with phosphorylcholine sphingomyelin to separate and further cooling causes cell rupture.

Gamma toxin, produces red blood cell destruction.

The toxin delta: injured a large number of blood cells and the injury apparently is a consequence of the reaction of hydrophobic amino acids in the phospholipids of the cell membrane.

Leukocidin: This toxin is composed of two separable components that act synergistically to cause damage to polymorphonuclear cells and macrophages.

Exfoliatina: This exotoxin, encoded by a plasmid, cause “severe exfoliative dermatitis” (Please see the case at the end); or also called “scalded skin syndrome of Staphylococcal origin”. It is characterized by the formation of wrinkles and exfoliation of the epidermis, resulting in significant loss of fluid through the skin bare. The epidermal sloughing is caused by an exotoxin diffusible, and thus infecting staphyloccocus may be present or absent in the affected skin area.

Staphylococcal enterotoxins: This exotoxin, causes food poisoning characterized by severe diarrhea and committees. Have been described 6 antigenically distinct enterotoxins A, B, C1, C2, D and E. These toxins are not destroyed and can be termoestabiles even if the food is heated sufficiently to destroy viable staphylococci.

Pyrogenic toxins: These toxins intensify the susceptibility to toxic shock (such as that occurs in women using tampons during menstruation) and cause a similar rash of scarlet fever.

Penicillinase: Enzyme capable of destroying penicillin.

  • Excherinchia Coli:
  1. Coli: This produces one or two different toxins, the so-called thermolabile LT and is destroyed by heating at 85 degrees C for 30 minutes, and the thermostable, designated with the letters ST and is not destroyed by heating at 100 degrees C for 30 minutes.

    E. Coli causes gastrointestinal infections in a severe way and sometimes fatal in infants. In adults, the infection is known by many names, for example, “Traveler’s diarrhea.” It can cause cystitis, pyelonephritis, abscesses, even sepsis.

    So, as these two microorganisms producing lethal exotoxines, there are some more such as the following:

  • Shigella
  • The Clostridium Genre, for exemple, Clostridium Perfringens , C. Boulinum
  • The Bacillus Genre : Bacillus Cereus (Rare and are required high concentrations of microrganisms). Bacillus Anthracis.
  • Pseudomona Aeruginosa.

It seems that the quantity in number of bacteria is also important because for this it will depend the amount of toxins circulating in the body

Furthermore, and as I wrote in my article “How could coexist conventional medicine and homeopathy?”:

“III.-Poisons (i.e. bites of venenous animals, intoxications by known chemical substances), : These cases should not be viewed as dynamic diseases, therefore must be treated with the antidote from conventional medicine and / or supportive measures such as dialysis, antibodies filtration and some immunoglobulin used in immunology for blocking of certain toxins”

Now, I would add “And diseases produced by microorganisms producing lethal exotoxines should not be taken as dynamic diseases; therefore antibiotics should be used on circumstances where lethal toxins are endangering the patient´s life”

Of course, I would like to know about cured cases regarding this matter. Kindly, I invite you to share them with me.

This is a staphylococcus skin case of mine which was treated homeopathically for 5 days. A Lycopodium patient, male, 6 years old (Lycopodium the first two days was improving burning pain, itching, drying vesicles).

4 days of evolution (behind left knee)

Neck.

Behind right knee

After 5 days the patient still was developing new vesicle eruptions and the vesicles that had dried, they were wet again. Furthermore, the patient started to get sloughing and fall of large areas of skin (exfoliation or desquamation) on more than 10% of body surface (As if he were burned). I made several changes: Belladonna (on the third day) and Arsenicum (5th day) … No results. Neither worsening nor improvement.

In this article, I could talk about my successful cases, however, it could be that I had failed (homeopathy never fails), or it could be that there is the need to establish new criteria in order to increase the patient´s safety. I must say that after 5 days, I took the patient to the hospital, and I administered antibiotics against Staphylococcus aureus. Locally, I washed his skin lesions (Three times a day) with soap and water and later I used Cantharis MT (5 drops into a glass water). The patient improved almost 100% in two days, therefore he was taken out of hospital. Doctors were surprised for the quick response and nobody believed that during six years the child had never taken antibiotics, but only homeopathy.

Pimples Pustules and Boenninghausen’s Questions

From: https://pandwisrael.wordpress.com/2017/10/27/pimples-pustules-and-boenninghausens-questions/

Vera Resnick

I was recently asked about Phosphorous in eruptions. Specifically I was asked why Phosphorous doesn’t appear in the TPB symptom Eruption, pustules (symptom no. 1426 in P&W Synopsis), when the word “pustule” appears twice in Hahnemann’s proving.

In the proving “Pustules” appears in the following contexts:

431 – Eruption of pimples in the face
432 – Eruption of pimples on both of the cheeks.
433 – Frequent pustules and scurf from suppuration in the face, after the least lesion of its skin.
434 – Rough, red, mottled eruption of the face, slightly elevated. [Ng.].

459 – Burning pain on the red of the lower lip, with white blisters on the inner side of it, with burning pain (aft. 11 d.).
460 – The lower lip is cracked wide open, in the middle.
461 – An itching spot on the left lower jaw, he had to scratch it raw.
462 – Itching of the upper lip, with pain after rubbing.
463 – Swollen upper lip, every morning.
464 – Eruption on the red of both the lips, at times with stitches.
465 – Pustules on the commissures of the lips.

Trawling through Merriam Webster revealed that although pustules usually refer only to blister-like eruptions, and not always to pus filled ones, it is often used interchangeably with pimples, used to imply a more impressive presence of the eruption.

So bearing in mind that when looking through provings we are dealing with several levels of translation – from sensation to words in German, from words of the prover to Hahnemann’s collated and edited proving in German, and from Hahnemann’s German to modern (fairly) English – we probably have to include pimples in this.  This is P&W’s footnote on the TPB rubric:

[1] Pustules, any type of skin eruptions, which elevate over the skin and can be filled either with pus or pus-like fluid and form crusts that may or may not erode the skin.

Why have I put you through so many pimples and pustules? Because this kind of question is why so many people miss the point when starting to work with the TPB.

The TPB is essentially a practical manual, a guide to materia medica. It reflects how Boenninghausen used the provings in his clinic, how he searched for information and how he deduced the symptoms to use and the remedies to investigate.

So you may be dealing with pimples. Or pustules. Or pimples which are turning into pustules. In the case I was asked about, the practitioner seemed fairly sure of the Phosphorous for the other symptoms, but found the absence of the remedy in pimples gave him reason to hesitate.

In such cases the issue is not whether the eruption is a pimple or a pustule. The issue is far more about the nature of the pimple/pustule.
– Is it crusted?
– Is there fluid in the pimple/pustule?
– Is there a colour, a texture, a smell?
– Is there pain on touching?
– Is there constant pain, and what is its nature? Burning, aching, stitching?
– Is the patient crippled with embarrassment about the pimple/pustule, much more than usually?
– Is it before/during/after menses?
– Is it after binge eating?

Do you see where I’m going with this? The remedy will become clear not from the question “what is it, pimple or pustule?” but from all the other questions. To remind you of Boenninghausen’s questions:

Quis – Who is the patient, what does he do, what’s his usual state of health
Quid – What is the complaint – sensation
Ubi – Where is the problem – location
Quibus Auxilibus – with what/concomitants
Cur – Why, trigger, maintaining causes
Quomodo – Modalities, aggravations and ameliorations
Quando – Time modalities, occurrence, aggravation and amelioration.

My main point here is that learning to work with Boenninghausen means learning to think very differently about symptoms and case-taking. If you’re starting out with Boenninghausen from a Kentian background – as I did – looking for rubrics can feel like hunting for a tooth which has been pulled out. You will not find the rubric you’re looking for if you’re searching for Face, eruptions, cheeks, pustule, yellow, excoriating. If you’re lucky – as you will be here, you will find Face eruptions cheeks. And you’ll have to look for the rest step by step – Eruptions yellow, eruptions excoriating, pustules (and pimples). My preference is to look more for the smell, the color, the modalities – and then once I’ve narrowed things down to several remedies, to search for the other qualities through the reversed materia medica and through the proving itself.

Why I dont recommend a homoeopath….

………….I live in XXXXX, can you recommend a homoeopath?

We all get asked. I have a policy of not suggesting a name if I dont know anyone personally. I found it to be a fatal error to do so.

……..You look so elegant, a long neck, for these reasons I am going to prescribe SWAN 1m for you….

………..You said you felt like you were drowning in problems, that your business was under water, for these reasons I am only going to look at sea mammal remedies for the similimum….”

At some point I gave up on mainstream homoeopathy. The therapy has lost its way. The people who use the medicines, I am loath to call them homoeopaths, have succumbed to the quasi healer thinking in the schools and never did learn to be physicians, instead relying on disparate teachings of the sensation method and mentalisations rather than solid prescribing symptoms. Most have not read the Organon or understand disease process and prefer to put their trust in the Universe rather than Hahnemanns directions.

A few year ago, a well known female homoeopath, prominent in her public persona and a staunch supporter of Sankaran, got very sick with food poisoning… for some reason she called me. I noted the symptoms, prescribed and waited on the phone with her as the medicine did its work and cleared the system.  She never acknowledged it. Later I saw her lauding the power of the remedy but neglecting to mention me or the help she received. She did not have much to do with me after the episode… too embarrassed I guess that a person who practises in the Hahnemannian way saved her life.

Some of the modern provings are based on dreams, and used even though the person who had the dream NEVER took the remedy! Yet vast swathes of modern prescribers use the remedies and swear by their effectiveness, only to later drop the remedy from their medicine kit and privately admit they were not effective.  This because the proving overseer is a ‘master practitioner’.  This is a another fallacy simply because a well trained homoeopath would never let such a poorly tested and proven remedy see the light of day.

A colleague of mine in another country, is constantly amazed when talking to recently graduated practitioners that they know little or NOTHING of the Organon. “How can they treat people without knowing Hahnemanns instructions? she asked……… I just shrug.

We need to clean up our profession.