Student BMJ is a journal for medical students from the BMJ publishing group. In the November 2005 issue is an article on an alternative modality called Ayurvedic medicine. Ayruveda, the article says, is an ancient healing tradition with roots in India. It goes on to say that Ayruvedic tradition describes health and disease in terms of three fundamental constitutional principles called the doshas. Stephen Barrett’s expose on Ayruveda reports that “Ayurvedic proponents have claimed that the symptoms of disease are always related to the balance of the doshas, which can be determined by feeling the patient's wrist pulse or completing a questionnaire. Some proponents claim (incorrectly) that the pulse can be used to detect diabetes, cancer, musculoskeletal disease, asthma, and ‘imbalances at early stages when there may be no other clinical signs and when mild forms of intervention may suffice.’”
The BMJ publishing group, a division of the British Medical Association, says its mission is "To publish intellectually sound material that will serve the needs of doctors, members, other health professionals, the scientific community, and the public." Its premier journal, BMJ, is widely regarded as a champion of evidence based medicine. So why might a paper on an ancient healing art be published in Student BMJ? To increase students’ cultural awareness, or to alert them to the alternative treatments patients are seeking, perhaps? No. This article in SBMJ actually promotes Ayruveda. The article asks “Is scientific medicine the only way?” The author notes “Studying Ayurveda provided me with an alternative system for categorising and describing states of health and disease.”
So much for intellectually sound material.
Wednesday, November 30, 2005
Heparin induced thrombocytopenia and open heart surgery—news from Chest 2005
The annual meeting of the American College of Chest Physicians recently took place in Montreal. One of the presentations (reported in eMedicine news) concerned the prevalence of heparin-platelet factor 4 (HPF4) antibodies in patients about to undergo open heart surgery. HPF4 antibodies are found in patients with heparin induced thrombocytopenia (HIT) and are instrumental in its pathogenesis. The Milwaukee investigators screened patients before surgery and found antibodies in 5.4%. Antibody positivity was associated with longer ICU stays and a higher incidence of prolonged mechanical ventilation, limb ischemia, renal dialysis and gastrointestinal complications. These findings raise the question of whether all cardiac surgery candidates should be screened.
I’m anxious for some details not available in this sound bite version. What was the mechanism of the bad outcomes associated with antibody positivity? How many of those patients actually met criteria for HIT?
We previously knew that many cardiac surgery patients (up to 50 %!) treated with unfractionated heparin (UFH) test positive for antibodies during their perioperative course but of those only 2% develop HIT. In contrast, fewer orthopedic surgery patients treated with UFH develop antibodies but substantially more antibody positive patients in the orthopedic group develop HIT. Thus the presence of antibodies is more predictive in orthopedic patients than in cardiac surgery patients. [1]
An iceberg model has been proposed for HIT. [2] At the base of the iceberg is a relatively large number of patients who have antibodies. Toward the surface is a smaller number who develop a drop in the platelet count, and at the tip of the iceberg are those who develop thrombosis. The interacting risk factors are complex and the actual number of antibody positive patients who develop HIT seems to vary with the patient population, as the above data suggest.
I’m anxious for some details not available in this sound bite version. What was the mechanism of the bad outcomes associated with antibody positivity? How many of those patients actually met criteria for HIT?
We previously knew that many cardiac surgery patients (up to 50 %!) treated with unfractionated heparin (UFH) test positive for antibodies during their perioperative course but of those only 2% develop HIT. In contrast, fewer orthopedic surgery patients treated with UFH develop antibodies but substantially more antibody positive patients in the orthopedic group develop HIT. Thus the presence of antibodies is more predictive in orthopedic patients than in cardiac surgery patients. [1]
An iceberg model has been proposed for HIT. [2] At the base of the iceberg is a relatively large number of patients who have antibodies. Toward the surface is a smaller number who develop a drop in the platelet count, and at the tip of the iceberg are those who develop thrombosis. The interacting risk factors are complex and the actual number of antibody positive patients who develop HIT seems to vary with the patient population, as the above data suggest.
Tuesday, November 29, 2005
A warning form the Infectious Disease Society of America
The Infectious Disease Society of America (IDSA) has written a white paper about the rising problem of antimicrobial resistance. Compounding the problem is an alarming trend: research and development for antibiotics is waning. After investigating the problem for over a year the IDSA concluded that antibiotic development is not profitable in today’s environment. The executive summary warns “The pipeline of new antibiotics is drying up. Major pharmaceutical companies are losing interest in the antibiotics market because these drugs simply are not as profitable as drugs that treat chronic (long-term) conditions and lifestyle issues. Drug R&D is expensive, risky, and time-consuming. An aggressive R&D program initiated today would likely require 10 or more years and an investment of $800 million to $1.7 billion to bring a new drug to market.”
The report recommends incentives such as patent extensions, liability protection, and relaxation of FDA requirements for clinical studies. It warns of emerging serious infections without effective treatments unless there is prompt action to promote antibiotic development.
The report recommends incentives such as patent extensions, liability protection, and relaxation of FDA requirements for clinical studies. It warns of emerging serious infections without effective treatments unless there is prompt action to promote antibiotic development.
Elevated troponin in non-cardiac critical illness---what does it mean?
This is a controversial situation that comes up frequently in the ICU, especially in patients with sepsis. It was the subject of a prospective study published September 28 in Critical Care. Earlier literature has suggested that elevated troponin in the setting of sepsis is associated with left ventricular dysfunction [1] [2] [3] [4] [5] and mortality [2] [6] [3] [4] [5]. These same studies demonstrate elevated troponin in close to half of sepsis patients.
In keeping with previous reports, the Critical Care paper found troponin elevation in almost half of their population of ICU patients. About half of those with elevated troponin were found to meet previously defined criteria for myocardial infarction. The new finding in this study was that among patients with elevated troponin only those meeting criteria for myocardial infarction had a worse outcome. Troponin elevation absent other criteria for MI was not associated with a worse prognosis.
Although the mechanism of elevated troponin is non-cardiac critical illness remains uncertain this study adds significantly to our understanding of the problem.
In keeping with previous reports, the Critical Care paper found troponin elevation in almost half of their population of ICU patients. About half of those with elevated troponin were found to meet previously defined criteria for myocardial infarction. The new finding in this study was that among patients with elevated troponin only those meeting criteria for myocardial infarction had a worse outcome. Troponin elevation absent other criteria for MI was not associated with a worse prognosis.
Although the mechanism of elevated troponin is non-cardiac critical illness remains uncertain this study adds significantly to our understanding of the problem.
Monday, November 28, 2005
Another paper challenges metformin’s contraindications
This time it’s specifically in reference to heart failure, which is listed as a contraindication in the product labeling. As I recently blogged, the vast post marketing experience with metformin indicates that it is safe, and that lactic acidosis has been difficult to attribute to it despite widespread contraindicated prescribing.
This large observational study from Diabetes Care showed that heart failure patients treated with metformin, as monotherapy or in combination with sulfonylureas, had significantly lower rates of mortality and hospitalization than those treated with sulfonylurea monotherapy. The average follow up period was 2.5 years. The mechanism may be the alleviation of hyperinsulinemia.
The authors suggest that the strict labeling of metformin may represent unfounded concerns which have deprived patients of beneficial treatment, and challenge the precautionary principle with this statement: Although "patient safety" studies often seem to focus on finding and reducing the use of previously widely prescribed medications that are of unproven benefit or even harmful, our study should serve as a reminder that there is another side to the patient safety coin—some medications that are currently considered contraindicated may have been defined as such on the basis of little or no evidence beyond pathophysiological rationale. Since this rationale alone is considered insufficient evidence for efficacy, it should also be insufficient to declare harm. We believe that the onus in the patient safety literature should shift to acknowledge that both types of patient safety issues can lead to suboptimal prescribing practices.
Well said.
This large observational study from Diabetes Care showed that heart failure patients treated with metformin, as monotherapy or in combination with sulfonylureas, had significantly lower rates of mortality and hospitalization than those treated with sulfonylurea monotherapy. The average follow up period was 2.5 years. The mechanism may be the alleviation of hyperinsulinemia.
The authors suggest that the strict labeling of metformin may represent unfounded concerns which have deprived patients of beneficial treatment, and challenge the precautionary principle with this statement: Although "patient safety" studies often seem to focus on finding and reducing the use of previously widely prescribed medications that are of unproven benefit or even harmful, our study should serve as a reminder that there is another side to the patient safety coin—some medications that are currently considered contraindicated may have been defined as such on the basis of little or no evidence beyond pathophysiological rationale. Since this rationale alone is considered insufficient evidence for efficacy, it should also be insufficient to declare harm. We believe that the onus in the patient safety literature should shift to acknowledge that both types of patient safety issues can lead to suboptimal prescribing practices.
Well said.
Hemostatic risk factors for arterial thrombosis
Although venous thrombophilic states have recently been well defined the hemostatic (non-atherosclerotic) risks for arterial clotting have been less clear. The topic is reviewed here in Atherosclerosis, Thrombosis and Vascular Biology. The review points out that homocysteine, fibrinogen, C-reactive protein, lupus anticoagulant and anticardiolipin antibody assays are justifiable tests. Somewhat surprisingly, in those patients with concomitant vascular risk factors, in those <55 years old, and in women, testing for factor V leiden and prothrombin mutation may be justifiable.
Saturday, November 26, 2005
More evidence regarding panic disorder and heart disease
I recently posted this regarding myocardial perfusion changes during panic attacks. Now this study (Psychosomatic Medicine) suggests an epidemiologic association (almost two fold risk of coronary disease in patients with panic disorder) which is even worse if depression coexists.
Friday, November 25, 2005
The emerging threat of community acquired methicillin resistant Staphylococcus aureus
Methicillin resistant Staphylococcus aureus (MRSA) has been well known for decades as a nosocomial pathogen. More recently MRSA has been increasingly reported in the community. Community acquired MRSA (CA-MRSA) tends to present as a new strain with features which distinguish it from the more familiar nosocomial MRSA. I found this helpful review in September’s Mayo Clinic Proceedings. (The abstract is linked here. Full text open access will be available in March 2006).
Although some community isolates appear to have escaped from hospitals, the new strains (“true” CA-MRSA) arise de novo in the community. Here are some important distinctions pointed out in the review:
1) CA-MRSA has a unique genetic determinant of resistance---the type IV Staphylococcal cassette cartridge (SCC).
2) Unlike the “old” MRSA which has multiple drug resistance, CA-MRSA is typically sensitive to many non beta lactam antibiotics. Sensitivity patterns have regional variation and tend to show a typical pattern in a given region, which may be the clinician’s principal clue that CA-MRSA rather than the older strain is present.
3) CA-MRSA appears to be more virulent than other S. aureus strains, in part due to expression of the Panton-Valentine leukocidin.
4) CA-MRSA appears to have increased transmissibility and infectivity compared to other S. aureus strains.
5) Skin infections, soft tissue infections and necrotizing pneumonia are characteristic compared to other strains, and necrotizing fasciitis has been reported. Bacteremia and endocarditis are less characteristic.
Perhaps the most troubling aspect of CA-MRSA is its emergence as a cause of community acquired pneumonia. The authors state: “It is now prudent to consider CA-MRSA as an etiology of severe CAP in the correct clinical context. Severe necrotizing pneumonia with or without hemoptysis after an influenzalike illness in high-risk patients warrants therapy directed against MRSA.” The antibiotics of choice for pneumonia are vancomycin and linezolid.
Medical journals promote pseudoscience
Recently I picked on medical schools for promoting unscientific health claims [1] [2]. Today a medical journal got my attention and reminded me that the compromise of science by “mainstream” medicine is pervasive, and not confined to medical schools. What’s ironic is that the journal is BMJ, supposedly a champion of evidence based medicine. This week’s issue contains a review of the homeopathy promoting book “Passionate Medicine: Making the Transition from Conventional Medicine to Homeopathy.” Trouble is, the review is favorable to the book, giving it a four star (the highest) rating. Worse, four homeopathy promoting links are posted on the same page as the review.
BMJ has been taken to task for this sort of thing before and Quackwatch has BMJ on its list of nonrecommended periodicals.
BMJ has been taken to task for this sort of thing before and Quackwatch has BMJ on its list of nonrecommended periodicals.
Controversy in treatment of deep vein thrombosis
The treatment of deep vein thrombosis (DVT) has been controversial concerning prevention of the post thrombotic syndrome (PTS). Although systemic thrombolytic therapy is superior to conventional anticoagulation in restoring venous flow and preserving the function of the venous valves, it is associated with greater risk of hemorrhage and its effect on meaningful clinical outcomes has been disputed.
The hemorrhage risk of systemic thrombolysis has spurred interest in local interventional modalities including catheter directed local thrombolysis and catheter extraction techniques. This review from the American Journal of Medicine explores such techniques for the prevention of PTS and discusses the complication of venous gangrene (phlegmasia cerula dolens) which may be amenable to such strategies. It draws upon experience from the National Venous Thrombosis Registry suggesting improved health related quality of life outcomes for patients treated with interventional strategies as opposed to conventional anticoagulation alone.
The take home message is that physicians should be aware that such modalities are available and should familiarize themselves with the capabilities at their individual hospitals. Physicians should be prepared to resort to these strategies in the desperate situation of venous gangrene complicating massive DVT and consider offering the techniques to selected patients with DVT for the prevention of PTS.
The paper unfortunately did not mention that the widely accepted modality for prevention of PTS, compression stockings fitted to 30-40 mm Hg, work pretty well for this purpose.
The hemorrhage risk of systemic thrombolysis has spurred interest in local interventional modalities including catheter directed local thrombolysis and catheter extraction techniques. This review from the American Journal of Medicine explores such techniques for the prevention of PTS and discusses the complication of venous gangrene (phlegmasia cerula dolens) which may be amenable to such strategies. It draws upon experience from the National Venous Thrombosis Registry suggesting improved health related quality of life outcomes for patients treated with interventional strategies as opposed to conventional anticoagulation alone.
The take home message is that physicians should be aware that such modalities are available and should familiarize themselves with the capabilities at their individual hospitals. Physicians should be prepared to resort to these strategies in the desperate situation of venous gangrene complicating massive DVT and consider offering the techniques to selected patients with DVT for the prevention of PTS.
The paper unfortunately did not mention that the widely accepted modality for prevention of PTS, compression stockings fitted to 30-40 mm Hg, work pretty well for this purpose.
Tuesday, November 22, 2005
More on the disruptive physician
Medscape General Medicine recently posted a provocative discussion on this topic, which I had blogged about November 5. There appears to be a burgeoning power struggle between hospital administrators (and their lawyers) and some rank and file physicians. It’s an unintended consequence of the Health Care Quality Improvement Act of 1986, which sought to protect hospital peer review. It provides immunities for hospitals in the peer review process, greatly enhancing their power to discipline physicians. Some physician groups are concerned that this has lead to abuses of peer review as hospitals, for a variety of reasons, increasingly seek to control doctors, setting increasingly narrow boundaries for behavior. A related development has been the emerging notion of the “disruptive physician.” Originally conceived with the good intention of addressing the genuine problems of incompetence and abusive physician behavior, the concept has come to be used as a pretext for stifling dissent, eliminating economic competition and abusing the peer review process.
This article and an accompanying editorial discuss the related issues of sham peer review and the abuse of the “disruptive physician” concept.
This article and an accompanying editorial discuss the related issues of sham peer review and the abuse of the “disruptive physician” concept.
Monday, November 21, 2005
Hype versus evidence in patient safety
At last----a refreshingly sober assessment of medical errors and patient safety, here in CMAJ.
Don’t forget the thyroid in chronic urticaria
There is a high prevalence of thyroid autoimmunity in patients with chronic urticaria. The patient with urticaria and anti-thyroid antibodies may be euthyroid, hyperthyroid or hypothyroid. The mechanism of the association is poorly understood. The Thyroid and Urticaria is a review of the topic in the October issue of Current Opinion in Allergy and Clinical Immunology.
Some patients may achieve remission with L-thyroxine, which of course is indicated for those who are hypothyroid. Such treatment of euthyroid patients is not supported by high level evidence and is controversial.
Thyroid testing should be considered in patients with chronic urticaria. Knowledge of this association could help a patient and might come in handy some day on internal medicine boards.
Some patients may achieve remission with L-thyroxine, which of course is indicated for those who are hypothyroid. Such treatment of euthyroid patients is not supported by high level evidence and is controversial.
Thyroid testing should be considered in patients with chronic urticaria. Knowledge of this association could help a patient and might come in handy some day on internal medicine boards.
Sunday, November 20, 2005
Irresponsible diet hype is being offered by the media
Don’t trust popular media for health information
The lay press lacks nuance and perspective in reporting on medicine and health, with the result that the consumer gets served an endless series of hyped up sound bites. These sound bites are often superficially contradictory, leading readers to wonder if medical science can make up its mind about much of anything. Nowhere is this better illustrated than in the popular coverage of diet trends.
The latest offering is this shocking headline: “Low-Carb Diet: An Alarming, New Danger.” Then, in bold type, the first sentence of the article reads “Low-carbohydrate diets may lead to dramatic weight loss, but dieters pay a big price for their thinner waistlines.” The article goes on to say that the diets lead to reduced myocardial energy storage and impaired cardiac relaxation. This is based on an Oxford University study that was apparently presented at the American Heart Association last week.
In attempting to dig deeper I was unable to find quality reporting on the study. The AHA will have some of the meeting presentations posted on the web later this month. I did find this from the British Heart Foundation, which sponsored the study. Their web page says that myocardial energy storage was measured by magnetic resonance spectroscopy. There were no clinical endpoints studied.
What’s irresponsible about the reporting is this study is far too preliminary and too low-level to warrant prime time. Specifically, the study period was all of two weeks, and the study population consisted of 19 subjects (the investigators themselves along with some of their friends and family!). Not exactly high level evidence. It’s hypothesis generating at best.
Next I did a Google news search and got this. Sure enough, the usual parade of contradictory sound bites appeared. The first few hits tell me low carb is bad (it reduces energy stores in the heart)---but, the next few headlines say it’s good for the heart (it helps improve the metabolic syndrome). So what’s the deal? Is low carb good for us? Yes and no, if you follow the popular press. Good last week, deadly today. What will it be tomorrow?
All this, of course, is rubbish. Science doesn’t move like the daily news. Its progress is gradual, with each new set of observations integrated cautiously with what was known before. There are no pat answers about low carb diets. They are probably good for some patients and bad for others. Basic research paints an enormously complex picture and suggests that it depends on one’s genetic makeup and associated risk factors.
If I were not such a passionate believer in open sharing and expression of ideas I’d be calling for a media ban at scientific sessions. I guess we shouldn’t blame them for being faithful to the interests of their stockholders. After all, hype sells.
The lay press lacks nuance and perspective in reporting on medicine and health, with the result that the consumer gets served an endless series of hyped up sound bites. These sound bites are often superficially contradictory, leading readers to wonder if medical science can make up its mind about much of anything. Nowhere is this better illustrated than in the popular coverage of diet trends.
The latest offering is this shocking headline: “Low-Carb Diet: An Alarming, New Danger.” Then, in bold type, the first sentence of the article reads “Low-carbohydrate diets may lead to dramatic weight loss, but dieters pay a big price for their thinner waistlines.” The article goes on to say that the diets lead to reduced myocardial energy storage and impaired cardiac relaxation. This is based on an Oxford University study that was apparently presented at the American Heart Association last week.
In attempting to dig deeper I was unable to find quality reporting on the study. The AHA will have some of the meeting presentations posted on the web later this month. I did find this from the British Heart Foundation, which sponsored the study. Their web page says that myocardial energy storage was measured by magnetic resonance spectroscopy. There were no clinical endpoints studied.
What’s irresponsible about the reporting is this study is far too preliminary and too low-level to warrant prime time. Specifically, the study period was all of two weeks, and the study population consisted of 19 subjects (the investigators themselves along with some of their friends and family!). Not exactly high level evidence. It’s hypothesis generating at best.
Next I did a Google news search and got this. Sure enough, the usual parade of contradictory sound bites appeared. The first few hits tell me low carb is bad (it reduces energy stores in the heart)---but, the next few headlines say it’s good for the heart (it helps improve the metabolic syndrome). So what’s the deal? Is low carb good for us? Yes and no, if you follow the popular press. Good last week, deadly today. What will it be tomorrow?
All this, of course, is rubbish. Science doesn’t move like the daily news. Its progress is gradual, with each new set of observations integrated cautiously with what was known before. There are no pat answers about low carb diets. They are probably good for some patients and bad for others. Basic research paints an enormously complex picture and suggests that it depends on one’s genetic makeup and associated risk factors.
If I were not such a passionate believer in open sharing and expression of ideas I’d be calling for a media ban at scientific sessions. I guess we shouldn’t blame them for being faithful to the interests of their stockholders. After all, hype sells.
The down and dirty on avian flu
Here’s some information from the infectious disease folks at Vanderbilt (Vanderbilt Reporter, November 4) which cuts through the hype and tells you the essentials.
Saturday, November 19, 2005
Hypertensive headache?
We were traditionally taught that hypertension is a silent killer, and that the notion of hypertensive headache is a myth. This meta-analysis in Circulation reports that antihypertensive treatment prevents headache, NNT=30, without regard to antihypertensive class. Four classes of medication with differing mechanisms of action were studied. Maybe our patients knew what they were talking about all along.
Community acquired methicillin-resistant staphylococcus aureus: what to tell the family
Many young and otherwise healthy patients are now being hospitalized with community acquired methicillin-resistant staphylococcus aureus (CA-MRSA) infections. Family members, taking notice when we place these patients on contact isolation, naturally want to know if they should take similar precautions when the patient goes home. Here’s a little blurb from Patient Care on how to counsel patients and family at discharge.
This is a big deal for a couple of reasons. First, as pointed out in the Patient Care article, CA-MRSA seems to be more transmissible than the “old” and more familiar MRSA. Worse, at least some CA-MRSA strains are hyper-virulent, associated with severe and rapidly progressive infections such as necrotizing pneumonia, due in part to the Panton-Valentine leukocidin. The issue of CA-MRSA pneumonia was reviewed in last April’s Current Opinion in Infectious Disease (subscription required).
This is a big deal for a couple of reasons. First, as pointed out in the Patient Care article, CA-MRSA seems to be more transmissible than the “old” and more familiar MRSA. Worse, at least some CA-MRSA strains are hyper-virulent, associated with severe and rapidly progressive infections such as necrotizing pneumonia, due in part to the Panton-Valentine leukocidin. The issue of CA-MRSA pneumonia was reviewed in last April’s Current Opinion in Infectious Disease (subscription required).
Friday, November 18, 2005
Giant cell arteritis
Here’s a review on a must not miss diagnosis, giant cell arteritis (GCA). Of particular interest to me are the following points:
1) GCA can have unexpected late extra-cranial manifestations such as aortic aneurysm.
2) Steroids must be started as soon as the diagnosis is suspected and need not await temporal artery (TA) biopsy. Biopsy results are not affected by several days of steroid treatment. (This comes in handy if the patient presents with signs and symptoms of GCA late on a Friday afternoon).
3) Bilateral TA biopsy is sometimes necessary.
4) Combining the erythrocyte sedimentation rate with the C-reactive protein is superior to either test alone. In a population of patients undergoing TA biopsy, combined abnormal results of both tests was associated with a specificity of 97%. *
1) GCA can have unexpected late extra-cranial manifestations such as aortic aneurysm.
2) Steroids must be started as soon as the diagnosis is suspected and need not await temporal artery (TA) biopsy. Biopsy results are not affected by several days of steroid treatment. (This comes in handy if the patient presents with signs and symptoms of GCA late on a Friday afternoon).
3) Bilateral TA biopsy is sometimes necessary.
4) Combining the erythrocyte sedimentation rate with the C-reactive protein is superior to either test alone. In a population of patients undergoing TA biopsy, combined abnormal results of both tests was associated with a specificity of 97%. *
Thursday, November 17, 2005
What is the supposed mechanism of homeopathy?
Where better to find out than from its supporters? Here’s a pro-homeopathy alt med blog found via the Health Fraud List. This post from the blog outlines the “mechanism.”
Concerning the dilution of the remedy it says “Once we reach the 12C potency, according to chemical science, there should be no more physical substance left in the dilution……..Potencies above 12C work very effectively as though there was still a material substance present. Even though there is nothing left of the original physical substance, the medicine acts as though there were.” Then how could there be any biological effect? Reading on----“the vital force in the water, which now holds the impression from the original substance, acts upon the vital force of whoever takes the medicine.”
So, let’s see. The original active ingredient, though diluted so many times that no molecules remain in the water, leaves an “impression.” That impression is held in the vital force of the water, which in turn acts upon some vital force in the patient. Got it? Aren’t you glad this is supported by your tax dollars?
Concerning the dilution of the remedy it says “Once we reach the 12C potency, according to chemical science, there should be no more physical substance left in the dilution……..Potencies above 12C work very effectively as though there was still a material substance present. Even though there is nothing left of the original physical substance, the medicine acts as though there were.” Then how could there be any biological effect? Reading on----“the vital force in the water, which now holds the impression from the original substance, acts upon the vital force of whoever takes the medicine.”
So, let’s see. The original active ingredient, though diluted so many times that no molecules remain in the water, leaves an “impression.” That impression is held in the vital force of the water, which in turn acts upon some vital force in the patient. Got it? Aren’t you glad this is supported by your tax dollars?
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