In January, I discussed growing skepticism about the benefits of oral glucosamine and chondroitin as a treatment for arthritis in dogs and cats. In that post, I made reference to a short feature I wrote which appeared in the Journal of the American Veterinary Medical Association (JAVMA) examining the clinical trial evidence for the use of glucosamine and chondroitin. In this article, I stated:
Oral administration of glucosamine and chondroitin is often used for prevention and treatment of osteoarthritis in dogs, and there is widespread belief in the safety and efficacy of this practice. However, it is important to base recommendations to clients on the best possible research evidence and not solely on the popularity of a practice or anecdotal reports of positive outcomes…
[T]here was insufficient evidence to support a recommendation of glucosamine and chondroitin as an alternative to NSAID medication for treatment of clinical signs attributed to osteoarthritis in dogs…Glucosamine and chondroitin are perhaps the most widely used nutraceuticals for treatment of osteoarthritis in human and veterinary patients. It is worth considering, however, that there is only very weak clinical trial evidence to support this practice and that it is appropriate for veterinarians to temper their recommendations to their clients accordingly.
A recent commentary in Veterinary Practice News by Dr. Narda Robinson, a professor of “integrative” veterinary medicine at the Colorado State University, and occasional participant in discussions here, takes issue with the conclusions of my review. I have a lot of respect for Dr. Robinson, and I think we agree on many issues associated with evidence-based veterinary medicine, but there are some fundamental disagreements I think are uncovered by her approach to evaluating the evidence concerning the use of oral glucosamine and chondroitin for arthritis.
She begins by referring to recent analyses and clinical trials in humans, which add to the already existing data, that seem to indicate glucosamine and chondroitin are no better than placebos in treating arthritis pain. However, even in referring to these results, Dr. Robinson begins to lay the foundations of her ultimate conclusions, citing authors of glucosamine studies to illustrate that no one other than “skeptics” such as myself seems to care what the evidence says. This seems distinctly at odds with her claims to an evidence-based approach.
After finding no clinically relevant effects on perceived joint pain or joint space narrowing, the authors wrote, “We are confident that neither of the preparations [glucosamine or chondroitin] is dangerous. Therefore, we see no harm in having patients continue these preparations as long as they perceive a benefit and cover the costs of treatment themselves.”
From another glucosamine review, “[I]t is likely that most consumers find the presence or absence of clinical evidence demonstrating efficacy to be irrelevant.”
According to Dr. Robinson, while “unsure of glucosamine’s benefits, many veterinarians nevertheless err on the side of hope…” and prescribe one of the plethora of possible glucosamine and chondroitin containing products on the market. She then refutes a couple of possible objections to the claims that oral glucosamine and chondroitin are beneficial for arthritis treatment. In my opinion, these refutations vary in quality from clearly correct, to correct but unbalanced, to outright misleading. I will address each briefly.
Specific Factual Points
1. Oral absorption of Glucosamine:
Dr. Robinson- Measurable amounts of glucosamine can be absorbed and reach the blood and the joints after oral administration at clinically reasonable doses.
SkeptVet- I agree. While the study cited was conducted in horses, which would not necessarily be relevant in dogs and cats, similar studies suggest low but measurable bioavailability for these species. This establishes the plausibility of oral glucosamine, though of course it doesn’t directly demonstrate any meaningful clinical effects.
The levels found in plasma and joint fluid after oral administration in these studies are often significantly lower than in many of the in vitro studies that show effects of glucosamine and chondroitin of the synthesis, degradation, or metabolic activity of cartilage cells (for an excellent review, see the introduction to this study). So the clinical relevance of the bioavailability of these substances remains to be demonstrated.
2. Glucosamine Doesn’t Build Cartilage
Dr. Robinson- “Glucosamine serves as a precursor for glycosoaminoglycans, the main component of joint cartilage.”
SkeptVet- I agree, sort of. Though glycosoaminoglycans are made naturally starting with glucose, glucosamine is an intermediate in the pathway to synthesizing them, and it appears that providing cartilage cells in vitro with extra glucosamine can affect this synthesis. It is far less clear, however, whether this actually happens in the joints of living animals given oral glucosamine. This is really what matters, of course, so referring to glucosamine as a precursor in cartilage production can be a bit misleading because it implies that taking glucosamine stimulates cartilage production in patients with arthritis, which may not be true.
The rat model study she refers to did find some observable effect on cartilage damage and metabolism in rats given glucosamine, and a similar rabbit study also found some effects. Both studies, however, also found no significant change in some measures of cartilage loss, and the subjects had extensive cartilage damage even when given glucosamine, so whether the supplement would have a meaningful clinical benefit even in these models, much less the very different environment of a cat or dog joint with naturally occurring arthritis, is hard to say. Human trials are also mixed, with some showing a beneficial effect on cartilage and others not. So a real benefit is possible, but certainly not proven.
4. Glucosamine Doesn’t Reduce Inflammation
Dr. Robinson- “[glucosamine] reduces release of inflammatory mediators. Glucosamine appears to penetrate inflamed joints more readily than healthy ones…”
SkeptVet- I agree, sort of. Certainly, glucosamine given orally and absorbed at low levels into the bloodstream is likely to penetrate inflamed joints more readily than healthy ones. This is just a function of the increased permeability of capillaries in areas of inflammation, and it is true for most substances in the blood stream. It doesn’t tell us if the glucosamine is doing anything useful in these joints. And, of course, it actually argues against the notion sometimes advanced that glucosamine may have a protective benefit for joints not yet affected by arthritis, since apparently even less of the absorbed glucosamine is likely to penetrate into such joints.
As far as the anti-inflammatory effects of glucosamine and chondroitin, they are certainly established in vitro. There is some debate about whether or not they are clinically relevant effects at the concentrations actually achieved in joints when they are given orally. Much of the in vitro research involves either amounts of these agents that are much greater than achieved in actual patients or study of individual inflammatory markers or chemicals, which may or may not tell us much about the effects in the “real-world” environment of an arthritic joint.
6. Glucosamine and Diabetes:
Dr. Robinson- “oral glucosamine/chondroitin does not affect glycemic control or lead to diabetes in the short term. But this research does not answer the question of whether glucosamine is safe for diabetic dogs.
SkeptVet- I agree, and I would probably state the case even more strongly. Given the extensive evidence in human diabetic, and the much more limited research in cats and dogs, I think it very unlikely that glucosamine would cause clinically meaningful problems for diabetic pets. Just as early studies on the benefits of glucosamine were not supported by later, better research, so many of the early studies on the risks of the supplement have not been sustained. The research in pets is not definitive, but the balance of the evidence available is pretty clear.
7. Clinical Benefits of Glucosamine
This is one area in which Dr. Robinson and I pretty clearly disagree. I think she is correct that the results of clinical trials are conflicting, but I think it is a mistake to believe that this means no firm conclusion on efficacy can be drawn. In his book Snake Oil Science, published in 2007, R. Barker Bausell reviewed the clinical research on glucosamine in humans exhaustively, and the balance of the evidence was clearly against any meaningful clinical effects. The larger and better designed or controlled the study, the less likely it is that a benefit will be seen. Studies funded by companies marketing glucosamine products are much more likely to be positive than studies funded by more neutral parties. And since this book was published the studies and reviews I provided links to above have continued to produce mostly negative results.
The evidence concerning the clinical effect of glucosamine in humans is not absolutely uniform, of course. But it never is. There is a well-known process, sometimes called “the decline effect,” by which early studies, often small and poorly designed and often funded and or run by companies or individuals with vested interests in a given hypothesis, and later studies by other researchers with better samples and designs fail to confirm the initial findings. This is not a flaw in science but rather an example of why methodological quality and independent replication of results are so crucial in separating the wheat of truth from the chaff of all the great idea that ultimately turn out to be wrong. Glucosamine research is almost a paradigm of this process, so it is misleading to point to the inconsistency in clinical research results as if it indicated deep uncertainty, when in fact it indicates a gradual refining of the data leading to the conclusion that a meaningful clinical benefit in humans is quite unlikely.
Dr. Robinson raises the issue of heterogeneity to explain the inconsistency in clinical trial results. Heterogeneity simply means that any population of subjects in a clinical trial will, of course, not consist of identical individuals. It is possible that the intervention being tested might work for a subset of individuals with particular characteristics, but if we don’t know what these characteristics are, randomization will scatter these folks evenly between the placebo and treatment groups, and it will look like the treatment doesn’t work. Heterogeneity is a known limitation of clinical trials and population statistics, which can to some extent be controlled for but which will always present the risk of study results which are valid for populations but not for some individuals.
This is a legitimate concern, but unfortunately it is also an easy way to cast doubt on all clinical research and lay the foundations for the argument that clinical trials ultimately can’t tell us anything useful about how to treat individual patients. It is important to be careful that our concerns about the issue of heterogeneity does not become a kind of clinical trial nihilism that leads us to give up entirely on the immense proven value of clinical trials in guiding medical interventions. Put another way, nothing is perfect, including clinical medical research, but we must be careful not to let the perfect become the enemy of the good to the point where we cannot make meaningful conclusions based on the evidence that exists. This is a caution commonly directed at skeptics who challenge the quality and conclusions of CAM research, but it is also applicable to proponents of CAM who argue that the imperfections of science invalidate the conclusions it reaches on their preferred methods. I believe Dr. Robinson herself appreciates the value of clinical research, but the heterogeneity argument she uses is one that can easily be taken to unfortunate extremes, and has been by others.
The clinical research on glucosamine/chondroitin in dogs and cats is far less in quantity and quality than the human clinical trial data. In my JAVMA paper (which, incidentally, was not a complete review of the subject but only an illustration of a practical and efficient use of evidence-based medical reasoning to answer a focused clinical question), I mentioned two clinical studies. One found no benefit for glucosamine and the other showed little benefit. Both showed far greater and more predictable benefit to NSAID therapy, which is a consistent feature of clinical research on glucosamine and chondroitin.
In her commentary, Dr. Robinson mentions another study which I did not address in my JAVMA piece, since this study involves cats and my article only addressed glucosamine for dogs with arthritis. It is not really a direct investigation of glucosamine/chondroitin supplementation for arthritis but rather of dietary therapy with a diet that includes glucosamine and chondroitin along with other ingredients thought to be beneficial for arthritis, but it is an interesting study which deserves a closer look.
The study was a well-designed randomized, blinded trial with a 70-day monitoring period and a mixture of objective and subjective measurements. 40 cats completed the study, evenly divided between the test diet and a control diet identical except for the absence of fish oils, glucosamine, chondroitin, and green-lipped mussel extract. Obviously, one issue with this study is the presence of multiple ingredients aimed at treating the subjects’ arthritis, which makes it impossible to say anything definitive about whether the glucosamine and chondroitin were ore were not beneficial.
Another concern is that there was one significant difference between the control and test cats, namely that the control cats started the study weighing more and, while both groups lost weight during the study (though not very much), the control cats weighed significantly more at the end of the study. Weight is a very important factor in the clinical symptoms of arthritis. Heavier cats would be expected to have worse symptoms and more rapid progression, and weight loss would be expected to improve symptoms all by itself, so this could confound the findings of this particular study.
As usual, the results were mixed, but as I read the paper they strike me as not very impressive. Subjective pain scoring by owners (who may or may not have been effectively blinded to the treatment and placebo allocation, it’s impossible to tell from the report) improved for both groups, but the difference between test and control groups was not significant. This may represent a “placebo” effect of being enrolled in a clinical trial, or less likely and effect of weight loss.
The objective measure, using an automated activity monitor, showed no overall significant difference between the groups. Interestingly, the control group showed significantly less activity overall and at 2 of the four times of day analyzed when 14-day periods at the beginning and end of the study were compared. A complex regression analysis looking at diet, weight at the start of the study, and weight loss during the study seemed to show an increase in the evening activity level of cats on the test diet, and no change in the activity of these cats at any other time. This analysis also showed a decrease in the activity of the cats on the control diet at all times except overnight.
I am not qualified to evaluate the validity of the statistics involved, but it seems odd that if the test diet had a beneficial effect on arthritis it would show up as a decrease in the activity of the cats on the control diet rather than an increase in the activity of the cats on the test diet. The authors suggest that this may mean that the cats on the test diet had less progression of their arthritis, but I am doubtful that such significant changes represent the progression of arthritis symptoms over only 70 days.
Other subjective measures, such as overall owner-assessed quality of life, improved for both groups with no significant differences between them. A few measures did change significantly in each group from the beginning to the end of the study:
Decreased aggression and eating in control group
Increased sleeping in the control group
Increased jumping and eating in the test group
Decreased sleeping in the test group
There were also some subjective owner assessments of behavior change during the study that differed significantly between the groups. Playing and interaction with other pets increase for both groups, but more for those on the test diet than those on the control diet. Both groups slept less and hid less over the course of the study, but again the change was greater for the test diet group than the control group.
Subjective measures of pain on physical examination by veterinarians in the study showed improvements in both groups but no significant difference between them.
So overall the study shows a lack of significant difference between the groups in most measures but a few differences that do reach statistical significance. The overall pattern is not consistent or compelling, but it may be that the cats on the control diet became less active over the 70 days of the study, which could conceivably suggest some influence of diet on activity. However, most measures improved for both groups, which illustrates the non-specific treatment effects (aka “placebo” effects) that are such a problem in figuring out what are real treatment effects in clinical research studies and what are artifacts of the research process.
In any case, even if the test diet did have real effects on the behavior of the cats in the study, that doesn’t tell us if the effects were clinically meaningful, if they had to do with treatment of arthritis symptoms, or if they were due to glucosamine. Yet the study is cited in Dr. Robinson’s article with the clear implication that it is positive evidence for the benefits of oral glucosamine in the treatment of arthritis. This is a seriously misleading oversimplification which is unfortunately all too common in debates about the merits of medical interventions, particularly those for which the research data is not absolutely unequivocal, which it rarely is.
The Bottom Line
So clearly Dr. Robinson and I agree on many things. We agree that glucosamine can be absorbed in low but measurable amounts when given orally, that some of it reaches joints, and that in vitro at least it can have anti-inflammatory effects. These facts establish the plausibility of glucosamine as a treatment for arthritis, but not that it actually works.
We also agree that it is most likely very safe. There is some risk associated with the poor regulation and quality control of nutraceuticals generally, which often contain dangerous contaminates and other ingredients not on the label. And I have had clients who eschewed proven therapies, such as NSAIDs, because they felt glucosamine alone was sufficient arthritis therapy, which leaves animals with inadequately treated pain. But Dr. Robinson carefully points out that she would not recommend this kind of single-agent use, and overall I think we agree that there is little risk associated with using glucosamine.
Where we disagree, as far as the facts, is in the interpretation of the clinical trial evidence. I think it is solidly against there being any meaningful benefit for oral glucosamine for all the reasons I have indicated. Dr. Robinson appears to believe that benefit is uncertain but possible. While I don’t believe her assessment is correct, it is certainly not irrational or unreasonable. Intelligent, informed, well-intentioned people can certainly disagree over the facts.
However, I think our greater disagreement is not on the question of the interpretation of the evidence but more fundamentally what constitutes evidence-based medicine. She concludes her article this way:
Although the evidence on glucosamine remains contradictory, there does appear to be some value and little risk. Not ready to abandon a product that could very well help and likely not hurt, this evidence-based practitioner will continue to mention glucosamine as one of many options for multimodal analgesia for OA patients and potential disease modifying OA benefits as well.
It seems to me that this amounts to saying, “It’s most likely harmless, and it could help, so why not try it?” I think she most accurately described her position herself when she said, “unsure of glucosamine’s benefits, many veterinarians nevertheless err on the side of hope.” The recommendation of glucosamine as a treatment for arthritis is not a decision based on evidence, but based on hope.
So, as Dr. Robinson asks, is there anything wrong with this? In the case of glucosamine, no not really. But I do worry a lot about the impact of practicing “hope-based medicine” generally, and especially of identifying it as evidence-based medicine. Ten years ago, when the data was less clear, I was hopeful glucosamine might be a useful therapy for my patients. I regularly recommended it, I gave it to my own pets, and I even took it myself. Then, as the data grew clearer, I abandoned the therapy because that ultimately is the approach to medicine that I think is most likely to lead us to the best, most effective practices.
Lots of people hope that homeopathy will help their pets, and many believe it does. And it is certainly harmless in itself, as it is only water. So is it right to use it alone, or even to add it to conventional therapy, “just in case?” I don’t think so. Granted, the evidence against glucosamine is strong but not indisputable, and the evidence against homeopathy is overwhelming. But I’m sure Dr. Robinson, no fan of homeopathy herself, has had exactly the kind of disagreements with proponents of homeopathy that she and I are having here. It is possible to find some positive studies, of poor quality and with high risk of bias, to support the use of homeopathy. Or prayer, or energy healing, or just about any intervention that people hope will benefit themselves or their patients patient. And so it is always possible for intelligent, rational people to be driven by this hope to put the most positive possible spin on the evidence, or at the last resort to say, as I think Dr. Robinson has in her article, “It’s most likely harmless, and it could help, so why not try it?” But that isn’t evidence-based medicine, and even if in individual cases, like that of glucosamine, such an approach may not lead to great harm, overall it undermines the quality and rigor of the reasoning that we use to decide what is truly helpful to our patients and what isn’t.
I regularly tell my clients that the evidence, while incomplete and not entirely consistent, is pretty strongly against any benefit from glucosamine and that the evidence of potential harm is very low, and then I let them decide if they want to use it or not. If I interpreted the existing evidence more positively, as Dr. Robinson does, I might tell them that glucosamine is harmless and might possibly have some benefits though the data is unclear, and again let them decide whether that is sufficient to warrant using it, which is what it sounds like Dr. Robinson does.
So it doesn’t sound like in practice Dr. Robinson and I approach the particular product all that differently with our clients. But the subtle difference in emphasis does seem of some importance to me. Her article gives the distinct impression that her reluctance to abandon the product is based not primarily on the balance of the evidence being positive but simply on the fact that the evidence is not uniformly negative, and if there is any reason to hope it might work it is worth trying (in the absence of clear evidence of harm). As I understand it, truly evidence-based medicine should give the greatest weight to the highest level available evidence and should not give any special weight or importance to our hopes. I understand Dr. Robinson’s perspective, and it makes a kind of sense. But it is all too familiar from many debates I have had with far less reasonable people about far more unlikely, or even ridiculous interventions. Erring on the side of hope is understandable, but it is not evidence-based medicine, and in the long run I don’t think it’s in the best interests of our pursuit of the truth about medical therapies or of our patients.
Thanks for your reflections on my article. Always nice to hear your views!
skeptvet, you are so tactful! I would have thought this would be a good opportunity for Narda to explain her position. Her response, although bizarre, is not unexpected.
Reiki and acupuncture are also on Narda’s hope-list, which doesn’t exactly lend much credence to her self-titled “evidence-based practitioner”.
Ten years ago, when the data was less clear, I was hopeful glucosamine might be a useful therapy for my patients. I regularly recommended it, I gave it to my own pets, and I even took it myself. Then, as the data grew clearer, I abandoned the therapy because that ultimately is the approach to medicine that I think is most likely to lead us to the best, most effective practices.>>>>>
I just checked the computer to see I sold my last bottle 12/16/99. It met my nyt evidence based preacher definition of proven threapy at one time.
The disapline that insist on proof that traditional medical practices really work. Millions of dollars have been spent by the taxpayers to try and repeat the proven studies that got me to start selling it. The initial proven studies were bogus. They took xrays to show the stuff works but the results could not be repeated by anyone not making money selling the stuff. I was making a ton of money selling the stuff. It was hard to tell the client who had spent hundreds of dollars buying the stuff from me that they had wasted their money. I am sure some of the clients were convince it worked and either switched vets or bought the stuff from some from another vet. If i had not been making money selling the stuff and getting free CE credit meals paid for by the company selling the stuff, I might have waited until the first proven study could be repeated.
egg on face
art malernee dvm
fla lic 1820
Interesting that I get attacked for just sending a note of appreciation to my friend Skeptvet for giving some feedback to my article.
Not everything has to be a contentious fight.
Not everything has to be a contentious fight.>>>>>>> As I see it you are at this time promoting unproven medical care and telling people that is science based medicine. But i am willing to start selling the stuff again if you can convince me with data. I like to make money.
art malernee dvm
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Narda, I actually forgot about this and came back to it today.
Nothing is ever a contentious fight, since you refuse to state your position when asked, and you have a habit of such attacks yourself whenever challenged.
Thank you for the informative article. The replies were also helpful. One cannot research enough when it comes to medicines/supplements for one’s family (pets included here) when money is on the line. I’m finding that coming at research on particular topics with initial skepticism seems to yield results more in line with the truth than simply believing the first web page that pops up on a Google term search. The problem with the Internet is that it is really sales-driven, and it shows every time I search for information on a recommended product or therapy. I find it interesting how powerful the advertising dollar is when coupled with individuals belief (read: hope) in a product. I think that the drug industry has known this for quite some time….. Thank you again skepvet.
skepvet, thank you for this article and its companion piece. I have been trying to decide, based on science, whether to reorder the glucosamine product I’ve been using on my aged dogs for some time, and am going to discontinue it, thanks to this review and similar ones I’ve read. One of my older dogs has moderate hip dysplasia and a calcified disk in her neck, and the other has degenerative disk disease in his back. I have found that the very best things for them are: weight management; controlled exercise that increases both strength and flexibility; veterinary NSAIDs when needed.
My biggest fear about the NSAIDs is that I know first-hand how devastating they can be to the GI tract, having been myself hospitalized once for naproxen use (intestinal bleeding), and even once for Celebrex use. Do the same dangers apply to dogs – are they as susceptible to the GI problems with, say Metacam, as humans are with NSAIDs? (Careful examination of the literature shows that even Celebrex is not nearly as safe for humans – long term – as is claimed by the manufacturer. Yet Metacam’s website states: “METACAM Oral Suspension has an unlimited duration of use for the treatment of OA in dogs.”) My apologies if this is a bit rambling, but I wonder about the flip side of the evidence that NSAIDs are the best proven treatment (while not at all disputing that glucosamine is completely unproven, so not making a comparison): are there significant risks with the use of canine NSAIDs?
I have written a little about NSAID use in dogs, so this might be useful for you:
Safety and Efficacy of NSAIDs in Canine Arthritis
The bottom line is that while they work well and are very safe for many animals, there is no benefit without risk in medicine. You can’t tinker with something as complex as a living organism without potentially making changes you don’t want as well as those you do. Currently, the individual factors that make some dogs more susceptible to NSAID side effects than others aren’t well understood. Certainly regular bloodwork and urinalysis to monitor kidney, liver, and GI effects is important. I have had many dogs on NSAIDs for years with no evidence of a problem, some that have showed warning signs and been taken off them as a precaution, and a very few who experienced real harm. The key is to consider the relative weight of the risks and benefits. The majority of dogs will feel less pain with no side effects, and even those that have problems can be protected by careful monitoring. Not treating, or treating with ineffective therapies takes away the risk but leaves the pain, so I think it’s a judgement that has to be made for each individual patient weighing all the information.
All the best
Thank you so much for the link and the info. My post was a bit rambling, but your response really helped with my main question, which involved my lack of scientific knowledge about this risks of NSAIDs in dogs. Being human, I have tended to generalize from my own experience with NSAIDs and to be extremely cautious about using them with my dogs. But I also know that NSAIDs are, in fact, riskier for humans than many people realize, and I didn’t know if that was true for dogs as well. After reading your article, I am going to talk to my vet about increasing the frequency of my dogs’ Metacam dosage (which she was in favor of, but I was reluctant to do). I have a much better sense of how to monitor for problems now.
Related to that is a secondary concern, poorly stated by me above, which is that I *fully* agree that natural/supplement products often wildly overstate the effectiveness of their products. (Or they do similar things, such as downplay the lack of evidence in various ways. I loved this ad I saw just yesterday for a homeopathic treatment, which stated that because the “philosophy” of homeopathy is “different,” evidence-based science was actually irrelevant in evaluating outcomes. It’s good for a laugh if the consequences weren’t so sad.) Pharmaceutical companies, though, do programmatically downplay risks, even serious risks. It took, for example, a lot of digging on my part to find out what was going on with my problems with Celebrex (my physician had told me that “Celebrex literally cannot injure the intestines”) and how the company has squashed data that showed its comparative GI-protectiveness diminishes over time (after a certain duration of use, it is about as bad for the GI tract as other NSAIDS). Two different doctors were on board with my using high, long-term doses of Celebrex after being hospitalized for intestinal bleeding with naproxen. Neither doctor knew the similar risks of these drugs over time. My point isn’t about Celebrex or about my specific doctors, but about an approach, a stance by pharmaceutical companies that is just as pervasive and determinative as that of supplement companies, and that the misinformation is as bad on both sides. I used to be very into natural products, but have become overwhelmingly, well, skeptical about their usefulness, without being dismissive of possibilities (have had good outcomes with Fortiflora in dogs with long-term diarrhea that wasn’t responding well to metronidazole and other medical treatments – though I also understand that sometimes things just self-limit). But I am equally skeptical of safety claims of pharmaceutical companies. I think that the suppression of harm and risk data by these companies is every bit as extreme and widespread as the exaggeration of benefit by supplement companies, and even doctors and vets don’t always have great risk information. Sadly, I think that this often throws people into the arms of unscrupulous supplement companies; people have an unexpected terrible reaction to a drug and then turn to supplements. If risks were better publicized (and new, less-risk-tested treatments were not so overly pushed by pharmaceutical companies relative to effective older treatments), there would be more realistic expectations about meds and less searching for alternatives.
Much to the surprise of many of my critics, I have no disagreement about the unreliability of much information coming from pharmaceutical companies. The only differences between Big Pharma and the supplement industry is that pharmaceutial companies are much bigger, and they are regulated in a meaningful (though still insufficient) way. They are not in any sense more inherently trustworthy, but we have laws and agencies watching them and protecting us against some of the worst excesses. If the same rules were applied to suppmlements and herbal remedies, we would find out which were safe and effective and which weren’t a lot faster.
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you are too slow compared to the speed of research…
Actually, these articles both predate several of my analyses, and they don’t change them. Believers in glucosamine can point to studies that appear to find a benefit. Skeptics can point to studies that do not, and I could certainly answer these citations with lots that show no effect. The challenge of a critical, objective analysis is to view the literature as a whole, to consider the methodological quality and risk of bias of each study, and develop a global assessment. For all the reasons I’ve discussed many times, the total body of literature supports little to no clinical benefit to oral glucosamine.
Although cancer in humans is a different case, obviously, this article recently published in Seminars in Cancer Biology points to the complexities involved with “evidence” and “hope” based paradigms and the ethics analysis from this:
From evidence-based to hope-based medicine? Ethical aspects on conditional market
authorization of and early access to new cancer drugs
There is a strong patient demand for early access to potentially beneficial
cancer drugs. In line with this authorization agencies like the European
Medicines Agency are providing drugs with conditional market authorisation based
on positive interim analyses. This implies that drugs are used with insecure
evidence of efficacy and adverse side-effects. Several authors have pointed to
ethical problems with such a system but up to date no indepth ethical analysis of
this system is found which is the aim of this article. Drawing of the four
generally accepted principles of medical ethics: beneficence, nonmaleficence,
respect for autonomy and justice the ethical pros and cons of conditional market
authorisation are analysed. From the perspective of beneficence and
non-maleficence it is found that the main problem is not risk of adverse
side-effects to patients, but rather risk of less beneficial outcomes than what
can be expected which could change incentives for patients’ choice of treatment.
This is also related to the extent to which patients might make an autonomous
choice, especially taking into account problematic psychological attitudes and
biases in medical decision-making. However, the main problem is related to
justice and an equitable distribution of scarce health-care resources given the
opportunity cost of drugs treatment. When using resources on cancer treatments
which later might be found to be less efficacious than was first expected, other
patients (in and outside the cancer field) are deprived of potentially more
beneficial treatments even though their needs might be equally or more severe. At
the same time, demanding more evidence has an ethical cost to patients in terms
of depriving them of potential benefits in terms of reduced mortality and
morbidity. In order to handle these ethical conflicts further research and
analyses are required and it is suggested that pricing strategies and information
requirements are alternatives to be further explored.