Category Archives: Clinics

August 2019 Four day course for entry to IHM register.

This August, as for the last 6 years, we offer the intensive 4-day enrolment to the IHM Register for successful practitioners. Membership is not automatic. However, the training is of superior quality and will benefit all participants.

The course is held at one of our clinics in Seville Spain and will be conducted by one of the creators of the OPENREP SYNOPSIS computer repertory program Gary Weaver (Dhom med) utilising the updated and corrected manuscript of the original (not Allens version) Therapeutic Pocketbook 1846 version.

You will learn Solely from Hahnemanns thoughts and writings. You will see how to view a case from his perspective and how to analyse the case using Boenninghausens repertory for a successful prescription.

For August only, we include the OPENREP program($799)  in the training fee of €1000 Euros.  Never done before.(Windows only)  300 texts and Materia Medicas. 17 Repertories.

 

You will learn:

  • Casetaking
  • Case management
  • SX selection
  • Observation skills and hints
  • What is a miasm and when to use in case analysis
  • LM medicines.
  • multiple case examples and breakdown
  • Use of remedies
  • How to read a remedy
  • etc.

Help Desk <education@instituteforhomoeopathicmedicine.com>

 

 

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

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

ihm-letterhead-logo

I.H.M. Office: Antonio Gil Ortega. Calle Guadeloupe 5, 1B. 41003. Sevilla. Telephone: 619 956365. E-mail: education@instituteforhomoeopathicmedicine.com Website:https://instituteforhomoeopathicmedicine.wordpress.com

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 Hahnemannian 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 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 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
  • I.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: http://ihmstaff.boards.net/board/5/licentiate-practitioners

 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.”

P1060304We 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 5 day intensive training session at our Seville Spain faculty. This training will be individualised for new students and practicing consultants.
  • A further period of guided home study for several months will follow. There will be Tutor involvement and online meetings. A Final day 5 training session in our Seville faculty with emphasis on case management will conclude the training and lead to registration with the I.H.M. as a licentiate if all requirements are fulfilled.

For Practising consultants:

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 intensive course.

What we cover in the 5 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 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 5 day intensive. Contact us to discuss.

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

laptop2The 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 and Hebrew. 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.

manuelManuel 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
antonioAntonio 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

isidre-1Isidre Lara i Llobet

Licenciado en Medicina y Cirugía por la Universitat Autònoma de Barcelona en 1980.

Formación en Homeopatía con Homoeopathia Europea con Jacques Imberechts desde 1978, y en cursos de la escuela argentina (Tomás Pablo Paschero, Eugenio Candebabe, …) y mexicana (Proceso Sánchez Ortega). Formación en el método de Alfonso Masi Elizalde en San Sebastián, 1987-1992.
Práctica clínica de medicina homeopática desde 1980; en Palma de Mallorca desde 1984.
Centre de Medicina Homeopàtica de Mallorca. Av. Joan March, nº 8, 5-1. Palma de Mallorca –España.
Tlf.: +34 971 20 65 66 /  658 810 910
Email: islara@homeopatiamallorca.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.

verapicwordpressVera 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.

 

garywDr. Gary Weaver D.O. rM.D., 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, Finland Spain and England.

Consulta: Barriada los Príncipes Parcela 7 Bloque 8, Sevilla. English only but have Spanish translator.  gary@garyweaver.org.

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

Realities of practice.

For additional insight, Please read the comments attached to this post.

 

For whatever reason, a lot of people who have joined the ranks of homoeopathic practitioners over the last 25 years  (in the West especially)  have a strange view and understanding of homoeopathy. I read a lot of case reports detaining the ‘cure’ of individuals who have received some weird medicine and whom had been prescribed for on symptoms related to their “inner state or delusional view of life” or “their relationship to the universe” after several hours of interviewing.

Over the years, it has been a source of amusement and annoyance that these people exude an inner smugness and a condescending attitude towards the rest of us, and who themselves truly believe they are the real deal and have insight into healing. They talk of “healing” and give quasi spiritual psychological explanations for a patients state of being, and onlyconsult maybe 3 or 4 times a month. They will attend conferences and seminars having paid lots of money and listen to gurus telling their wonderful stories, and during the breaks these people discuss their own wonderful cures with people who are waiting their turn to tell of their own wonderful tales of cures.

The works in writing of Samuel Hahnemann and colleagues of his era are available for free on Google Books. Therein lies the recorded genesis and struggle and definitions and methodology for homoeopathic treatment. Therein lies how it has to be done, and how it will work consistently and repeatably IF the principles are applied.

Homoeopathy is a medical specialty within the framework of the field of medicine. It is NOT the complete answer for medical treatment. Osteopathy, surgery and physical/mental/emotional nursing healthcare coming to mind. It will not help someone who is dependent on drugs which have altered the body chemistry or killed functionality of an organ or gland. It will not act where in most cases, a natural immune response is lacking or not functioning due to external influences or an immune disorder.

It is however, the better course of treatment where a curative response CAN be elicited. It is the better course of treatment for general therapeutic treatment in primary and ongoing health care.  However, and this is the reality, it is only as good as the therapist prescribing for the problem. It is only good if a standardised methodology is employed based on Hahnemannian directives.

I realise that many people who are reading this will look back on their training and scoff… They ‘know’ it takes hours of painstaking casetaking to reach the real seat of the problem, the delusion or sensation that is the trigger to ALL their ailments. Well your argument is with Hahnemann and ultimately your conscience as the reality bites you.

Sorry to be a killjoy. Disease as individually expressed by a patient in their observable symptoms, are the key to prescribing. The rest is pure speculation. See Organon 5th and 6th editions paras 1-10 and 152-158.

I believe, no, I know, a properly trained homoeopathic physician could run a general practitioners office efficiently and successfully for exactly the SAME daily visits from patients as an allopathic physician has.

In the same knowledge, I also know, 99% of homoeopaths in the West could not do it. There is not the training. There is not the comprehension, there is not the ability to case take and prescribe quickly and efficiently, and there is not the understanding of how to manage cases and when to hand over care to another branch of the medical system for a short while.

I have had this conversation many times with practitioners. They all complain about the therapy of homoeopathy not being accepted or utilised properly within the health systems, and say “we can do so much better”.  Well……. no you cant.

To clarify, the therapeutics, ie the medicines that are prepared in the manner for use within the practice of homoeopathy, are better. They are able to create an artificial disease set of symptoms within the human economy and stimulate or re direct the overpowered immune system to react in a more focused way to restore health to the individual. NO DRUG EVER CURES….. the body does.

We all have to decide through our experience and understanding (and legal liability) when to change therapies or allow the influence of another therapy be utilised for the welfare of patients. I do not mind stating some of my delineated areas of patient concern where I, through experience will not hesitate too long before administering certain anti bacterial infection medications.

One is Tetanus. I have observed the path of the disease in Asian and Middle Eastern countries, and have managed some cases homoeopathically and some, I turned over to the influence of antibacterial treatment because the infection was life threatening. Clostridium tetani acts quickly flooding the body with neurotoxins. I have come to a settled understanding in my thinking that this falls under the sphere of Hahnemanns common sense approach to “removing maintaining causes” and as such, I see the body full of an infecting poison as being a maintaining cause. I will treat along side the A/B giving the patient the appropriate medicine for the individual dis-ease that they experience.

Another one is snake bite. I will immediately give homoeopathic treatment and have the patient monitored carefully. In India, where there are a high casualty rate of 45000 deaths a year from snake bite, there is anti-venom available in most hospitals and out station clinics. The problem with Snake bite is similar to Tetanus, a maintaining and presence of poison in the system, and a short duration of excruciating pain leading to expiry.

Symptoms of neurotoxicity, ranging from ptosis, dysphagia, respiratory distress and unconsciousness are all the result of the spreading poison. In many/most  cases, mechanical help with breathing is required. A polyvant administration of anti venom is administered, which has been culled from usually 4 of the most toxic snakes poisons in India, and this dilutes and flushes out the strong poison administered from the snake bite. (ironically, it works in a homoeopathic manner) I continue individualised homoeopathic treatment when the patient exhibits prescribing symptoms, but would advice continuation of the anti venom treatment until able to breathe unventilated and the poison is flushed from the system.

To get back to “No.. you cant.” A waiting room in a G.P.s clinic will contain people with minor ailments of an acute nature, and undiagnosed ailments of a chronic nature. a homoeopath will have to be able to do the following.

Firstly, a well trained Hahnemannian homoeopath will have a working knowledge of medicines which makes them able to differentiate symptoms from each other as they observe them. They will of course have the memory aid of a repertory to look up symptoms if they need to refresh their memories or direct them to a medicine or group of medicines for consideration on a combination of symptoms not seen before. With practice, an acute disorder can be dealt with in a 10 minute framework. If you have a good student homoeopath or nurse, they could even work with the acute disorders for you, and check with you for patients whom they are unsure about.

A chronic or undiagnosed major illness, can be treated in this manner in a busy homoeopathic clinic. I can only offer my own experience and practice methodology so its just an example.

A new patient is taken into a clinic room by a homoeopathic colleague/nurse/advanced student, and case taking is started. What is the complaint? it is written down, how does it affect them? it is written down. Where does it affect them? it is written down. What else are they affected by? It is written down. Some tests are applied to the relevant area, If necessary, blood is extracted for analysis and other tests applied if required. This takes usually 20 minutes. The patient is then shown into my office along with the written details, the practitioner will quickly summarize the patients details and then sit in with us as I go through the case with the patient.. In line with Hahnemanns suggestions, I will ask further clarifying questions based on their statements to the practitioner when being examined. I will double check some reactions or observations noted on the form to be sure, and then will ask any other questions I feel necessary.This should take no more than 15-25 minutes.

I will make a prescription if and only if I am sure of one and then the patient is taken to the dispensary and given medicine and directions for taking and then a return visit booked. In this manner, it is possible for a single practitioner with 2 or 3 nurses or undergraduate student to help to see 40-100 patients a day comfortably.

A common method of patient treatment in India, in some of the free clinics, was for student homoeopaths to walk down a line of patients and take notes of the symptoms. They would then return to the beginning of the line and relate the SX to the prescriber, who would listen and then prescribe and move on.. one minute to 2 minutes per patient. In this manner, there was an ability to get the key symptoms from each patient without the prescriber having to wade through other symptoms or memory lapses and humming and hawing from the patient. When there are 2 or three hundred or more patients to treat, it is the only way.

So for those who sit down and spend up to three hours per patient examining every detail of their life, you will not be able to run a clinic. I would also suggest you will not even be able to cure the patients you have now. Cure is not a relative term. Its an observed change of symptoms expressed. If they come with Asthma do they leave free of Asthma after treatment? Or is a cure considered if they are free of a spiritual issue instead, but still have the asthma?

As a therapy, Homoeopathy is in a dangerous place. Relatively few good practitioners to practice real homoeopathic application of principles left. disease is not an easy thing to work with at the best of times. Better to work with a therapy along guidelines with a proven record of success rather than not.

Practitioner memories.

Several years ago, in one of the I.H.M. colleges, I was approached by one of the teachers regarding her sons health. This particular teacher, was known for her affection and affiliation to a well known “guru” homoeopath on the  scene, and had taken her son to him several times without a successful resolution to the problem. As resolution had not been found, she then took her son to another well known homoeopath who consulted with him and then prescribed the SAME medicine as the previous practitioner with the same negative result.

After listening to her story where she explained that she had been told that her son was “not ready to receive his health back” and that “he was holding on to his sickness”, she was desperate on his behalf. I asked her if she would be willing for him to be a patient in the training clinic with a video link to the class below. She accepted.

Now this college had a complete 3rd year intake from another college. It was a struggle to redirect them from the metaphysical training they had been subjected to, and I wanted to give them a taste of being a practitioner. This particular teacher had come with them from the college, as part of the package deal.

I took the case with a very articulate and precise 13 year old who recounted his problems. I took about an hour to get the details, thanked him and off he went to the kitchens for food and a drink….

I walked down to the classroom and looked at the assembled 16 students, who all had notes and were busily discussing the case with each other….. not the case, more the emotional expression of his comments, more the allegorical extractions from his sentences. I realised what a problem I had on my hands.

“Ok guys, lets do this” I said, “Lets go to the kitchen and have a break and a snack and then come back and discuss it.” As they got to the door I said “oh, one more thing, XXXX (the patient) will be there, please do NOT ask him any questions regarding his health.” So off we all went.

Thirty minutes later we reassembled in the classroom. I set the ground rules for this analysis.

“This young man has been to two of the country’s most admired prescribers. They made a judgement that he is not ready to be cured, and so far he has not been. Here we have a a patient with a skin problem that desperately requires alleviation. As practitioners, do you think we are wasting our time in treating this person as others have said, or do you think we as a class can do something?”

One of the female practitioners said “well we probably are wasting our time. If xxxx (guru practitioner) failed then the boy cannot be cured“. I asked her if she wished to be excused and could go home early, I said to the class, “in fact if any of you think he cannot be cured or think its not worth having a go, then its ok, I would treat the boy privately and we would not worry about it”

Curiousity will always get an enquiring student, plus the desire to be part of a group that might just be good enough to beat the teachers in their own field. So we settled down to take the case. I let them discuss among themselves for 15 minutes until they began looking at me as they ran out of ideas…

“So” I said, “15 minutes has passed and I have not heard one single reference to his problem, just hypothetical assumptions and  a direction that is leading to the same medicine that was prescribed previously……THAT DID NOT WORK! If you want to help this boy then you had better start applying what you have been taught this term and find a medicine that does work”

I split the class in to 3 groups. they appointed a group director and began to look at the case, symptom by symptom. I did not comment on the case. After an hour, each group had begun to establish areas of importance, and were moving on to look at aggravations, at locations, at sensations. We had another break, and this time in the break, it was very much more subdued as each one was thinking and contemplating.

On return, I asked each group what they had come up with. I recall that as the reasoning was brought out, one or two students said ” no, that is not correct, this is what happened and this was the reaction and what has just been stated is an assumption”………. it made me smile as I recall this, because the switch had been turned on for a few of them. Over the next hour, the group honed the choice of medicines down to Two, one of which was the failed prescription. We took a break then again.

On return, I told them to forget the failed prescription, and try and see why the other came up and whether or not they can justify giving it. One of the students, who was a very quiet and shy woman generally, asked if she could say something. She went on to describe in absolute clear and detailed terms the route she had taken to ascertain the prescription, and gave a logical reasoned and well thought out analysis of his reaction to heat resulting in epistaxis every time, and how she could not a find anything in the skin symptoms to contra- indicate it. Another student, described a very clear picture of the skin condition and had come to the same medicine choice. In the next few minutes, the class put together all their notes and collectively came to the same remedy.

I asked them if they were prepared to give the medicine? I was asked if it would be the medicine that I would choose. I told them that this was their case. They needed to be responsible for it. I would not comment or advise. The silence was palpable. The quiet female student who had made such a reasoned diagnosis previously said.. “If it was my child, I think I would give it because I am fairly sure that the reasons to give it outweigh those not to”.

We gave the patients mother the remedy in the 200th potency to be given in water, one dose a day for 3 days and see him again in 4 weeks. I told the class that I would handle any calls from the mother but they would not know until the next appointment.

4 weeks later the boy presented himself again. 90% of the problem had cleared up! during the follow up examination… some of the symptoms had changed, and in repertorising the present state, they came to the previously FAILED prescription only. They did not know what to do. So I asked them if they were satisfied with the previous choice and they were……. so I asked them why they were doubting themselves now. Nervously they decided to give 2 doses of the medicine. He presented himself in 4 weeks after this change of medicine with ALL of the ancilliary symptoms cleared up, and just a few traces of the skin problem left. We represcribed the 2nd medicine again and he cleared up within a few weeks.

I had a long discussion with them regarding the choices of medicine being made on sound observation, and how that the 2nd medicine given, and the same one chosen by the other practitioners was necessary, but only when it was required by a complete symptom picture. It would not work until the core of the problem was dealt with.

As a side note, I just checked a few Registers of practitioners today, and I saw only one name from this group. The sad thing is even though several of them prior to leaving the college had a firm grasp on Hahnemanns principles of practice, they nearly all changed their method of prescribing to Seghal or Sankaran or Sherr.

homeopatiamallorca

The I.H. M. and P&W are pleased to announce an association with 4 experienced homoeopaths on the beautiful Island of Mallorca. Working together in the The Homeopathic Medical Centre Mallorca since 1982. Andreu Forteza, Isidre Lara, Joaquin Peleteiro and Josep Maria Quera.

Dr Isidre Lara is the new Spanish representative for P&W, and the homoeopathic clinic is now on the approved list of practitioners.

The clinic practitioners have been through a variety of training in their careers, but have always stayed true to the basic implementation of the application of homeoopathic principles. the SYNOPSIS program is now installed on their computers for everyday use.

The view from the top of the building. Some of the offices open onto the balcony.

You are welcomed into the clinc at the entrance.

The waiting room.

The practitioners.

Dr Andreu Forteza

Dr Joaquin Peleteiro using the P & W SYNOPSIS program

Dr Josep Queralt

Dr Isidre Lara

Showing the office onto the lovely balcony.

Medicines. The Clinic has a full pharmacy.