This post returns to the main subject of the blog: LDN. The concentration so far has been pretty much on autoimmune diseases where low dose naltrexone has helped, in some cases dramatically, those who suffer (including this author) from a wide range of diseases associated with the immune system. Today I want to provide a brief suggestive description of how LDN can help in the treatment of cancer because this part of the story is not widely understood. In addition, you’ll find some links that will take you to other sites with more detailed information and bibliographies that lead to still more. In future posts I’ll definitely be returning to antidepressants, antipsychotics and related industries including psychiatry and the pharmaceutical manufacturers.
At bottom, cancer is cell division out of control. If untreated, cancer cell masses – tumors – can choke off vital bodily processes and can lead to death. Without a constant supply of nutrients, however, tumors would be self-limiting. But cancer cells can generate blood vessels that will carry the necessary nutrients to the cell masses, a process known as angiogenesis. These basic facts suggest targets where the vulnerability of cancer can be exploited in treatment. It happens that LDN is well suited to exploit these vulnerabilities.
First, a reminder: LDN is not a direct therapeutic agent. It is not like, say, antibacterial agents that treat infection directly by making it impossible for bacteria to reproduce. LDN works indirectly. It precipitates changes in the body, the microbiology, of the patient. These changes are what produce the therapeutic effect. As one article recently put it, low dose naltrexone tricks the body into healing itself, bringing the body back into balance, into homeostasis. LDN, then does not treat cancer directly: it produces effects that allow the body to better defeat an attack by cancer cells.
The effects of low dose naltrexone can fight cancer on a number of fronts: by interfering with cell division, by killing individual cancer cells and by inhibiting the process through which cancer cells receive the nutrients they need.
The theory: basically (and my microbiology is primitive), cancer cells have been shown to have Opioid Growth Factor receptors (OGFr). When these receptors are coupled with an Opioid Growth Factor (OGF) peptide molecule, this sends a "don't divide" signal to the cancer cell. When the receptor is uncovered or blocked, that sends a "divide" signal to the cancer cell. Low dose naltrexone causes a 200-300% increase in endorphin production (endorphin = endogenous morphine – one kind of endogenous morphine is Opioid Growth Factor, also known as met-enkephalin). By making additional OGF available to be coupled with OGFr, cancer cell division is inhibited.
In a related process that is not well understood, the natural killer (NK) cell production is enhanced by OGF. These are the cells that hunt and kill foreign cells, including cancer cells, in the body.
Third, the increased supply of OGF will inhibit the process of angiogenesis, by which cancer cells generate blood vessels to carry nutrients to the tumor.
These three processes working together may slow or entirely reverse the multiplication of cancer cells. So LDN, by increasing the supply of OGF in the body, could be very promising in the fight against cancer. This value is further enhanced because LDN has no negative side effects, unlike the cell-destroying consequence of more common treatments for cancer.
Worthy of special note, Dr. Burt Berkson uses LDN in combination with intravenous alpha lipoic acid to treat cancer, especially pancreatic cancer with metastaces to the liver: one of the toughest cancers to treat successfully. His keynote address with reviews of several case histories at the 2009 Low Dose Naltrexone Conference at the NIH has been compiled into a single video and can be found here: www.youtube.com/watch?v=o48MgBi44XM
The largest source of information for all applications of low dose naltrexone (LDN) to be found on the web is at www.lowdosenaltrexone.org and at www.ldnscience.org . There are several applications against cancer that you will find there. I found a summary to be of particular value in preparing this post: http://www.medvision.org/mihpf/medinsight%20-%20ogf%20review.pdf . Other information is available mostly on non-cancer applications of LDN and some theory, elsewhere on this blog. I invite you to give it a browse.
Readers of this blog have watched as I’ve been learning about the conceptual muddle in which the idea of depression is mired, discovered that antidepressants aren’t nearly the success story that big pharma has invested so much in having us believe, and become disgusted by the harm these drugs do, including causing depression. I’ve encountered wholesale conflict of interest in the psychiatric community as it has systematically destroyed its own credibility. And, to tell the simple truth, I’ve been pretty angry about what I’ve found as the overall picture gets worse with every new glance in its direction.
In trying to tell you about all this I find that I may have hurt some people for whom I have nothing but love and respect: the people who are depressed and who need support and all the help it is possible to provide. So this post is to clear up a misunderstanding, perhaps overdue, that I am critical of those who are depressed or doubt the reality of their suffering.
Yesterday, I received a comment from a friend named Debbie on Facebook, following one of my Twitter-length criticisms of the conflict of interest in the production of the DSM-IV (Diagnostic and Statistical Manual) and the forthcoming DSM-V. Debbie asked:
“David, I have to say this, and I mean no disrespect because I love your posts, but do you believe that there is truly no such thing as depression? That those of us that have been so deep in a black hole (I'm not saying laying around trying to get out of working, I'm saying trying to keep it together, going to work, struggling not to drive off an overpass) depressed, that we really have a fake illness??? Confused.”
My response appears below. I reproduce it here because I want very much to avoid anyone else concluding that I think they have a “fake illness”.
No problem, Debbie, yours is a very reasonable question that deserves an answer.
Although the conceptual basis for depression that is found in much of the scientific literature is a muddle, especially the folkloric nonsense about a chemical imbalance as the cause of depression, I do believe that there is an underlying reality to what we call "depression". It can be serious, debilitating, painful and can bring a rational person to actually consider suicide as the remedy-of-last-resort. Many have taken their own lives. I've had depression myself, whatever it is, and was unable to work for three years. I was among the earliest patients to be prescribed Prozac when it first came out some twentyish years ago. After that, I was given and did take other antidepressants singly or in combination. They were all SSRIs except for a brief dance with lithium which made me feel like I was walking through a vat of syrup. So I don't think we have a "fake illness". (You can find much of my view detailed in the last few posts on my blog at http://davidnixon.posterous.com/ )
The problems lie with the clinical and institutional responses to this disorder. A few of them are:
- American psychiatry has painted itself into a corner. Having largely given up psychotherapy, it has opted for prescribing drugs. So when you sit down in front of a psychiatrist, you know that you are talking to a person who will either prescribe drugs or will put him- or her-self out of business.
- The pharmaceutical industry spends a mountain of money (twice what they spend on R&D) to convince you and doctors of all kinds to ask for, take and prescribe their products. In 2004, a study published in 2008 estimated the pharmaceutical industry spent a total of $57.5 billion in the US on promotion and advertising: that's $61,000 for each doctor in the United States.
- There is increasing evidence that antidepressants, when they work at all, work as "active placebos". That is, they produce side effects that act as cues to the patient, suggesting that they are powerful drugs, doing their work to fight depression when, in fact, they may be utterly without therapeutic effect. (The Kirsch book, cited elsewhere on my blog is particularly good in making this argument).
- Given the huge financial incentives for prescribing antidepressants and, more lately, antipsychotics, effective alternative treatments for depression are systematically understated or ignored entirely. Psychotherapy has been shown to be at least as effective as antidepressants (whatever the agency through which they work) in successfully treating the symptoms of depression. The same is true for programs of vigorous exercise. And the claim that combinations of these treatments with drugs is even more effective is not borne out by the evidence. In fact, a recent study at Duke University showed that the depression relapse rate for those taking drugs and engaging in vigorous exercise was more than three times greater than those in the exercise plan alone. And, while psychotherapy may be expensive, a vigorous exercise plan is not.
- As late as the 1970s, depression was thought to be episodic (not chronic) and self-limiting. Without treatment of any kind it was likely to pass within a year. Today, it is a chronic condition claimed to require medication throughout a lifetime. More than 10% of all persons in the United States over the age of 12 are now taking antidepressants. Does this sound like a clinical success story to you? It certainly doesn’t seem so to me. Professionals and researchers are asking the same question. Could antidepressants be doing more harm than good? It is known, for example, that antidepressants CAUSE depression. When that happens, it’s called tardive disphoria. Is it possible that the skyrocketing incidence of mental illness is iatrogenic, that is, caused by treatment? Giovanni Fava has been editorializing in medical journals that antidepressants may be irreversibly changing fundamental brain chemistry, making depression relapse more, rather than less, common, and that "[u]se of antidepressant drugs may propel the illness to a more malignant and treatment unresponsive course".
- Finally, and to return to the place where my initial post began, the degree of corruption among the psychiatric community is breathtaking. Keep in mind, psychiatric diseases are not discovered, they are invented: there is no blood test, no urine test, nothing that could be confused with legitimate science. Disorders are made up and voted upon: if the condition gets enough votes it is a disorder, like "oppositional defiant disorder". You know, a young person, defiant of authority, a troublemaker; in short, a teenager, has now been given the status of a disorder and a four or five digit number assigned that will be written in the insurance claim form causing the claim to be paid and the money machine to roll on and a young life begins a long course of powerful medication. And who are the people who invent these diseases? Well, for the current version, the DSM-IV, 56% of the psychiatrists had direct financial ties to at least one pharmaceutical company. The DSM-V is now being put together and is due out in 2012. No less than 68% of these psychiatrists have direct financial ties to at least one pharmaceutical company.
To be fair, the DSM-V committee has been the object of harsh criticism from within the psychiatric community. Only yesterday, Allen Frances, M.D., the former chair of the DSM-IV Task Force, wrote in Psychology Today that to have any credibility, the DSM-V must be given a critical scientific review that is open, independent, systematic and rigorous. The current task force provides none of these essential requirements, he wrote. It is suggestive of just how bad things are in American psychiatry that Dr. Frances, didn’t even mention that having 68% of the task force members getting kick-backs and bribes from the pharmaceutical industry might also have something to do with its credibility.
Again, Debbie, I don't think you or I have a fake illness. However, getting treatment that isn't fake could be something of a challenge.
The following open letter is directed to a depressed man who had been referred to a psychiatrist by his psychotherapist, a common pattern. The psychiatrist wants him to take SSRIs. He had prior, unpleasant experience with this type of drug because of its side effects. Moreover, he felt it had not helped with the depression. He had gotten away from these drugs and did not want to start them or similar drugs again. Isn’t there something else I can do?, he wondered.
This is what I would have told him if I could. But the space on the website where he left his plea for help was insufficient for what I wanted to say. So I’m posting it here, on my blog that has been devoted mostly to the subject of low dose naltrexone. Readers of the blog know that I have become interested in the possible use of LDN as an antidepressant, that this led to my research into depression in general and, today, to this open letter. It is especially important to remind you that I have no special training in this field. I don’t claim to be an expert and advise the reader to treat what I have to say as the expression of a layman.
Dear Uncooperative Patient:
I applaud your courage and urge you to hold your ground and use means other than antidepressant drugs for treating your depression.
In justification of prescribing SSRIs, psychiatrists will frequently cite what’s called the monoamine hypothesis: there is a chemical imbalance in your brain and these drugs can set it right. Neurotransmitters like serotonin and norepinephrine, they say, are in short supply in your brain and these antidepressants can set the balance back to its natural and proper state. In fact, the name SSRI, selective serotonin reuptake inhibitor, creates a mental picture of the drug doing just that: keeping your serotonin levels from being depleted.
The problem with this hypothesis is that it is false and has been known to be false since 1974. In that year, Bowers drew cerebrospinal fluid from groups of depressed and normal participants, testing for the metabolite of serotonin. If the monoamine hypothesis were true, the depressed patients should have had a lower level of the serotonin metabolite than the normal group. In fact, the two groups had virtually identical serotonin levels. This was an out-and-out falsification of the chemical imbalance theory of depression. http://psycnet.apa.org/psycinfo/1974-27819-001 (“In unipolar depressives pretreatment values for 5-HIAA were not different from controls”)
In the intervening years, this hypothesis has been disproved again and again. Consider these views from leaders in the psychiatric and research community:
1. “The serotonin theory of depression is comparable to the masturbatory theory of insanity.” David Healy, psychiatrist.
2. "A serotonin deficiency for depression has not been found" Joseph Glenmullen , Harvard Medical School.
3. "Indeed, no abnormality of serotonin in depression has ever been demonstrated" David Healy, Psychiatrist.
4. "We have hunted for big simple neurochemical explanations for psychiatric disorders and have not found them." Kenneth Kendler, Psychiatrist.
5. "there is no clear and convincing evidence that monoamine [e.g., serotonin] deficiency accounts for depression" Stephen M. Stahl, Psychiatrist
In Ireland, where drug regulators have not been captured by drug makers, if a pharmaceutical company made this claim, that their drug treats depression by repairing a chemical imbalance in the brain, they would have broken the law. Why? Because the evidence does not support it. Even the FDA admits as much: “‘Biological psychiatrists have looked very closely for a serotonin imbalance or dysfunction in patients with depression or obsessive compulsive disorder and, to date, it has been elusive,’ says Dr. Wayne Goodman, Chair of the US Food and Drug Administration (FDA) Psychopharmacologic Drugs Advisory Committee. Although an SSRI may work well in an individual, this ‘doesn't prove that there is an underlying imbalance, defect or dysfunction in the person's serotonin system,’ he added.” (Colin Meek, “SSRI ads questioned” CMAJ. 2006 March 14; 174(6): 754.) Found online here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1402373/. It is a measure of the disingenuousness of the FDA that having admitted there is no evidence for the imbalance theory, he goes on to say, “I think that is reasonable shorthand for expressing that this is a chemically or brain-based problem and that the medications are normalizing function.” As long as words have meaning, he can’t have it both ways: once he admits there is not evidence for the imbalance theory (“it has been elusive”), what can it possibly mean to say that claims to the contrary are a “reasonable shorthand”? I think it means the FDA is less than fully independent of big pharma.
In spite of a mountain of research and monographs to the contrary many psychiatrists sing the same old tune. People are depressed because of a chemical imbalance. Well, it just ain’t so. Or, if it is, nobody has shown it to be so. And the burden of proof lies with the companies that have about 50 million Americans taking antidepressants for one reason or another, drugs that can have serious, long-term negative consequences on their lives and those of the yet unborn: Drugs, moreover that can be very difficult to stop taking, once started.
Those interested in the simple truth of the matter, might look at some of the major recent books on the subject:
1. Joanna Moncrieff, The Myth of the Chemical Cure: A Critique of Psychiatric Drug Treatment, 2008, 2009.
2. Irving Kirsch, The Emperor’s New Drugs: Exploding the Antidepressant Myth, 2010.
3. Robert Whitaker, Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing rise of Mental Illness in America, 2010.
4. Gary Greenberg, Manufacturing Depression: The Secret History of a Modern Disease, 2010.
5. John Abramson, Overdosed America, 2004.
The Kirsch book is particularly good in summarizing research, some of it his own, that shows that the so-called efficacy of antidepressants is due primarily to the placebo effect.
If not antidepressants, what can you do? Well, you are already doing one of the best things you can do: you are doing psychotherapy. Many will say that a combination of antidepressants and psychotherapy is even better but this is misleading. Better than what? A combination of antidepressants and psychotherapy is better for people who have been on drugs alone but it is not better for people who are doing psychotherapy alone. http://www.elisedusseldorp.nl/pdf/BlomJonkerDusseldorpPTPS2007.pdf
A program of exercise has also been shown to be at least as efficacious as antidepressants in treating depression. Again, there are those who will tell you that a combination of exercise and antidepressants would be even better. But they would be wrong. A Duke University study of depression relapse shows the opposite, in fact. Following participants for six months, the exercise-only group had a relapse rate of only 8 percent; the drug-only (Zoloft) group had a 38 percent relapse rate; the exercise-plus-drug group had a 31 percent relapse rate. (A no-cost access to these findings can be found at: http://www.dukehealth.org/health_library/news/119)
Finally, the side effects of psychotherapy and an exercise program are all good. They’ll give you self-knowledge and a great, healthy body. Not a bad deal. Just as important, both of these activities carry with them a feeling of self-empowerment. You’re not just a passive receptacle with unbalanced brain chemistry into which somebody wants to pour drugs. You will have a sense of control over your own life and a fully justified belief that, through your own action, you can and will get better.
“Doctors prescribe medicines of which they know little, to cure diseases of which they know less, for human beings of whom they know nothing.” – Voltaire
Hello again, everyone.
(This revision reflects the correction of a mistaken claim about diagnostic tests that was pointed out to me by a senior research fellow at a major university. He has my thanks for his kindness and encouragement but I will do him the favor of not identifying him here. I have taken the opportunity to expand my remarks on the basic concept of depression as well as correcting the earlier remarks about diagnostic testing. The second half of the post is unchanged. September 20, 2011)
Most would agree that the practice of medicine has come a long way since Voltaire penned those words. Yet, when it comes to depression, antidepressants, and psychiatry the progress has been much more modest.
This post is a continuation of a question I took up last time about unexpected, beneficial consequences of taking low dose naltrexone: consequences that, however much valued and beneficial, are not the reason for which low dose naltrexone (LDN) was taken in the first place. There are a range of these desirable by-products (and I hope to discuss these in greater detail in future posts) but the focus of interest in the last post was the improvement in mood, the sense of well-being, that frequently attends a regular ingestion of low dose naltrexone. I wondered, could LDN be used as an antidepressant? This question seemed to resolve into two others. First, how well do the existing antidepressants work? The case for LDN would be stronger, I thought, if currently prescribed medications didn’t work all that well. Second, what evidence is there, other than with myself and the members of my family, that LDN generally does help with depression? That will be the subject of the next post. For the moment, this post is about the effectiveness of currently prescribed antidepressant medications.
So, off I went to work on the next part of my research. Speaking as a layman, I was both surprised and disappointed by what I found. First, the very concept of depression is a muddle.
Gary Greenberg (Manufacturing Depression) calls attention to a fundamental question of self-appraisal: “Am I happy enough?” This is an old question and one we ourselves entertain. Another way of asking the same question will give rise to an entire industry: “Am I not happy enough because I have a disease?”
This is the sense in which depression has been manufactured – not as an illness, but as an idea about our suffering, its source, and its relief, about who we are that we suffer this way and who we will be when we are cured. Without this idea, the antidepressant market is too small to bother about.With it, the antidepressant market is virtually unlimited.
In the 1950s and 60s, before rigorous randomized, double-blind, placebo-controlled trials had been invented, the basic structure of today’s conception of depression was being put together. An antitubercular drug called iproniazid was thought to increase norepinepherine and serotonin in the brain. It did this by reducing the rate at which these monoamine molecules were oxidized in the synapse between neurons. It thus became known as a monoamine oxidase inhibitor (MAOI). When depressed people take iproniazid, they get better. Hence, depression must be caused by having too little neurotransmitters in the brain. This conception of depression seemed to draw confirmation from the action of another drug, called reserpine. Reserpine decreased the levels of these same neurotransmitters in the brain. Clinicians thought that reserpine produced a depressive effect on their patients. Depression, then, had to be a disorder caused by an inadequate supply of neurotransmitters, i.e., a chemical imbalance, in the brain.
There are at least two problems with this theory. First, when better research techniques were introduced, it turned out that reserpine did not induce depression. In fact, when depressed people were given reserpine in a controlled study, almost all of them got better, not worse.
Second, this entire approach to the phenomenon of depression is circular. You start out with no clear idea of what depression is but you notice that when you give people a drug that increases neurotransmitters in the brain, they get better, so you conclude that depression must be the opposite of what the drug does. This amounts to creating a disease for which these drugs are the cures. Applying this logic to a headache, when I take an aspirin for my headache and it goes away, I conclude that my headache was caused by too little aspirin in my brain. This is what happens if you have no independently articulated, physiological conception of a disease to start with. We still await such a definition of depression. (The discussion of the last three paragraphs rely heavily on Irving Kirsch’s The Emperor’s New Drugs: Exploding the Antidepressant Myth)
What of diagnostic and other tests for depression? It is not too much to say that tests, like the Structured Clinical Interview for DSM-IV (SCID), are ways of not seeing the wide range of characteristics presented to a clinician when a patient sits down in his or her office. Or, it is a way for all clinicians to see the same things, to focus on the same questions, and record answers that can be tallied. Absent an independent definition of the disorder of depression, these tests measure something but it is not clear what that something is: it is to mimic the form of science without its content.
Stepping away from the conception of depression and moving to the economics of depression, the SCID has huge significance. It provides the linkage between the patient in the clinician’s office and the recognized conditions listed in the Diagnostic and Statistical Manual of Mental Disorders, each of which is given a numeric code, usually five digits. These numbers are literal gold mines for the drug industry. When a patient’s diagnosis is given one of those code numbers, it becomes possible to fill out an insurance company claim form and the company in question will have to pay the claim, consistent with the terms of the policy. Without this number, no claim and no money. With a number, the money flows. Given the economic importance of these codes, it is not surprising that the number of recognized mental disorders is increasing. DSM-III (1980) recognized 265 diagnostic categories. DSM-IV (1994), the current version, lists 297 disorders. DSM-V is due out in 2012 and will further expand the number of disorders for which drugs may be prescribed.
Some of these categories are scandalous. For example, a head-strong, defiant, non-conforming kid in school can now be diagnosed to have “oppositional defiant disorder” and be prescribed heavy medication as a result. These medications can begin a lifetime of diagnosis and medication. But that’s the subject of another day.
In my search for indications of how well antidepressants work (however depression is defined), particularly the new generation of selective serotonin reuptake inhibitors (SSRIs) that include Prozac, Zoloft, Paxil, Effexor, Serzone, Remeron and Wellbutrin SR, my first stop was Overdosed America by John Abramson, MD. (See especially, pp. 114-117 and 232-234.)
SSRI’s popular acceptance is attributable in large part to “publication bias”, Abramson argues. News that favors the adoption of a drug, i.e., that shows it is efficacious, is far more likely to be published than trials that show the drug to be no better or even worse than a placebo. He gives the example of the Swedish Drug Authority when application was made for its approval for five antidepressant drugs. There were 28 published studies of which 22 showed the drugs to be significantly better than placebos. The problem was that a total of 42 studies had actually been done, half showing the drugs to be efficacious and half not. Only six of the negative studies were published. This prompts the question, how is a physician to inform himself of what to prescribe? Abramson quotes the Swedish researchers:
[F]or anyone who relies on published data alone to choose a specific drug, our results should be cause for concern.... Any attempt to recommend a specific drug is likely to be based on biased evidence.
Another study, made in 2000, was based on a review of all documents received by the FDA with regard to the seven SSRIs listed above, whether published or not. The data was received through a Freedom of Information Act suit that neatly solved the publication bias problem. In all, some 5200 pages of documents were reviewed. In summary form, the findings of this review are:
1.SSRIs are no more effective than the tricyclic drugs they replaced
2.SSRIs were found to be slightly less than 10 percent more effective than placebos (“Symptoms of depression improved by 30.9 percent in the people who took placebos; 40.7 percent in the people who took the new antidepressants; and by 41.7 percent in the people who took the older antidepressants.”)
3.In cases of mild or medium depression, “nine out of 10 studies showed that the new drugs are no more effective than placebos.”
4.“[T]he actual rate of death from suicide is higher in patients who take the new antidepressants than in those who take the older tricyclics” and
5.“[T]wice as many people taking the new antidepressants successfully committed suicide than did the people who took placebos.”
In 2005, Joanna Moncrieff and Irving Kirsch wrote an article for the BMJ (British Medical Journal) titled “Efficacy of antidepressants in adults”. Their concern was this:
“Most people with depression are initially treated with antidepressants. But how well do the data support their use, and should we reconsider our strategy?”
Basically, they argued that the embrace of these drugs as efficacious treatments went well beyond what the data warranted. They expressed concern that SSRIs may increase the risk of suicidal behavior in adults as well as children. Although “placebo controlled trials of serotonin reuptake inhibitors found significant [statistical]differences in levels of symptoms, these were so small that the effects were deemed unlikely to be clinically important.” (Emphasis added) As unimpressive as the evidence was, they found, it was still weaker than it was made to appear because of questionable methodology used in representing the data.
The reaction to their article came quickly. The reader may find them all via the link just provided. Not all was negative, by any means. Several commentators appeared to take the opportunity created by the article to vent long-held doubts about the effectiveness of SSRIs and the evidence used in their support.
One of the sharpest critiques of Moncrieff and Kirsch is interesting to me in large part because of the people who made it. I’m not making the ad hominem argument that what they say cannot be true because of who they are. It is enough to note that they have strong ties to the drug industry and, on that ground, lack credibility. One of the things that you must do these days if you want to publish your ideas and research in a scientific journal is to disclose what “competing interests” you may have. If you want to write an article that praises, say, Pfizer, you have to disclose that you own shares in the company or are a paid spokesman for the company. I want you to see what these critics listed:
Competing interests: FMQ has served as a consultant for Organon, Inc., Sepracor, and Bristol-Myers, has received honoraria from Pfizer, has been reimbursed by Eli Lilly for serving as a speaker, has shares in Cyberonics, and has offered expert testimony for Sedgwick, Detert, Moran and Arnold, Sterne, Kessler, Goldstein and Fox, McKinsey and Company, and Gerson Lehman Group. JWS has served as a consultant for Organon, Inc., Shire, and Somerset, has received research support from Lilly, Pfizer, Glaxo, Organon, Inc. and Bristol-Myers, has received honoraria from Eli Lilly, Pfizer, and Organon, Inc., and has been reimbursed by Eli Lily, Pfizer, Organon, Inc. and Glaxo for serving as a speaker or on an advisory board. DFK has be reimbursed for scientific advisory to Eli Lilly, Glaxo, Pfizer, Roche Laboratories, Smithkline Beecham, Upjohn, Vela Pharmaceutical and VivoMetrics, Inc., has served on Speaker’s Bureau at Eli Lilly, Glaxo, Pfizer, Roche Laboratories, Smithkline Beecham and Upjohn, has served as a consultant to Eli Lilly, Roche Laboratories, Smithkline Beecham, and Upjohn, and is a stockholder in Forrest Laboratories and Interneuron Pharmaceuticals, Inc. PJM has no competing financial interests.
One wonders how PJM, with no competing interests, found himself in such company.
One critic argued that, if SSRIs were abandoned, patients would have nowhere to go, given long waits for psychotherapy; that it doesn’t really matter whether the SSRI works by altering brain chemistry or whether it is by placebo effect – the patient is helped in either event. This may be true but it is faint praise indeed for the efficacy of the SSRIs.
A telling comment, concerning the Moncrieff and Kirsch article was the following from Steven Taylor, Professor, Dept of Psychiatry, Univ of British Columbia:
[R]egardless of whether one agrees with the conclusions of Kirsch and colleagues, the controversy over the efficacy of SSRIs would never have arisen if these medications were highly powerful treatments for depression. Clearly, these drugs are not satisfactory and there is a pressing need to develop more potent treatments.
The reader may have noticed, as I did, that the trials mentioned here are ones that have been made comparing the efficacy of a drug or drugs with a placebo. Where, I wondered, are the studies that compare these drugs with each other: what about comparative efficacy trials? A major grocery store chain in Pittsburgh, where I live, will fill a prescription for thirty 20 mg Prozac capsules for $4.00. Prozac is now out of patent, like naltrexone, and so is very cheap. A comparable supply of Cymbalta, will cost about $265.00. Some doctors now prescribe Eli Lilly’s Cymbalta in spite of this huge difference in price. What makes them think that the difference is worth paying 66 times more for the new drug (that happens to be patent protected)? Let’s give them the benefit of the doubt and assume that they are relying on more than the expertise of the drug company’s sales reps whose qualifications might include being modeling school graduate or former cheerleader. Where does our caring doctor go to learn about head-to-head comparisons of the effectiveness of Cymbalta with Prozac or other drugs. The simple answer is there is no such place to go.
Earlier this month (June, 2011), Merrill Goozner, in his website, www.gooznews.com argued in favor of comparative effectiveness research (CER); that the FDA should require it whenever approval is sought for a new drug “when there are already FDA-approved therapies for the same condition.” This requirement is about more than just getting the consumer a better deal. It would force drug manufacturers to focus on new medical challenges, to genuinely innovate in the development of drugs rather than the me-too motivation to get a market share of an established therapy without providing anything new and better. Of course, this makes good sense and, of course, it is opposed by the drug manufacturers. The issue will be decided when the FDA’s Prescription Drug User Fee Act comes up for reauthorization next year. We could all do each other a favor by contacting our representatives in Washington and urging that CER be made a required part of the drug approval process.
I’ll conclude this installment by noting that the widespread acceptance of SSRIs has less to do with the effectiveness of these drugs as antidepressants than the strength of the marketing by drug companies. This is not all bad news. There is so much dissatisfaction with the conceptualization of depression and the drugs currently being prescribed to deal with it that opportunities may exist for the introduction of new, broader concepts for understanding depression and the practical and pharmacological measures available to deal with it. For example, research into the efficacy of exercise as a way of coping with depression exposes a conceptualization of the brain chemistry of depression that is much broader and perhaps more promising than the tunnel vision that can see only serotonin and norepinephrine. But that’s beyond the reach of this installment.
With regard to Big Pharma’s marketing effort, I recommend viewing the documentary, Money Talks: Profits Before Patient Safety at
You don’t just wake up one morning with an urge to find out about low dose naltrexone. Your interest in LDN is probably like mine: either you or someone you care about has a disorder or condition from which you seek relief. In my case, it is ulcerative colitis that ultimately led me to investigate this drug and its applications. But it took the passage of time and a great deal of discomfort, and it took the loss of the way I organized my life that I had taken for granted, it took that and the chance suggestion of a friend to look into those three letters – L - D - N, to get my investigation started.
Once started, I focused like a laser on my central question: could low dose naltrexone help me with ulcerative colitis? Inevitably, I discovered that there were a great many people who were doing the very same thing. Some had my condition. Some had MS, or fibromyalgia or Crohn’s or lupus or rheumatoid arthritis or many other disorders. The treatment of these disorders seemed to converge on the use of naltrexone in small doses that would intermittently block opioid receptors, causing the generation of two to three times the normal production of endorphins. This, in turn, caused the symptoms of each of these disorders to ease as treatment with LDN continued and a balanced condition, called homeostasis, was re-established in our bodies.
This part of the LDN story has been told again and again. One of the things that I noticed in my case and in the reports of others was the beneficial effect that LDN was having on other problems, besides the condition for which it was taken in the first place. For example, I recently read a report that a decades-old problem with gingivitis resolved with the taking of LDN for quite different reasons. In my case, it was depression.
Depression is a chronic condition with which I have contended over a thirty year period. I’ve been prescribed Prozac, Wellbutrin, and Lexapro alone and in combination, sometimes with yet other substances. They never really produced dramatic results, although a combination once gave me marginal but noticeable improvement. Most of the time, I’ve relied on the skills picked up in cognitive therapy to recognize and discipline my thought patterns that could otherwise worsen my condition. I have not taken SSRIs (selective serotonin reuptake inhibitors) or any other antidepressants for several years. Episodes come and go and I deal with them as best I can until they pass.
It was by chance that I was in the middle of a depressive episode when I started taking LDN on March 16, 2011. My colitis began improving immediately as the period between bathroom visits increased, making it possible for me to resume something like a normal life again. What I didn’t notice was that my mood was improving: the depression was lifting. My wife was first to notice the difference. I was waking up in the morning, maybe not with a song on my lips but in a plainly good mood. No more of the helpless and hopeless feelings and thoughts that I had been fighting off. Never had an antidepressant worked in anything like this dramatic manner. This was so much the case that my wife, who has her own struggle with depression, began to tease that she didn’t know how much longer she was going to be able to live with the goody-two-shoes that I was becoming.
Now it was her turn to do the investigating. She did. She decided to try low dose naltrexone herself in May. Within a few days, I could see the change in her disposition. Her mood was improving and, by now, is normal. Delightful to see in a person you love
Just yesterday, I had a long conversation with my sister who lives in Colorado Springs. She’s had Crohn’s disease, now in remission. She first told me about the Specific Carbohydrate Diet and how it had helped her. Thanks to her, it helped me too, although not as dramatically as with her. When I’d found out about low dose naltrexone I was able to return the favor. She’s been taking LDN for about a month now. I asked her about her mood. Was LDN helping with her depression? Her answer was an unequivocal “yes!”. She said she noticed an improvement in her mood after about a week. She no longer considers herself to be depressed.
I doubted that our experience was unique. There must be many people for whom the by-product of taking low dose naltrexone, the unintended, gratuitous benefit was also very significant in their lives. If you have also enjoyed such a benefit, I hope you’ll share your story, below, in the comment section.
Also hugely important, I thought, is the potential use of low dose naltrexone as an inexpensive and safe treatment for depression. The post-tri-cyclic antidepressants, known as reuptake inhibitors, are described as working according to a very different model. LDN, used as an antidepressant, would broaden the paradigm, the pattern, of cellular interactions that are used to describe what is happening when an antidepressant does its job.
This is something I’m going to explore further in the blog. As I see it now, my approach will focus on two separate questions: first, how well do the SSRI antidepressants really work? To anticipate, there is reason to believe that they don’t work nearly as well as the TV commercials would have us believe. I’ll be looking at some of that evidence.
Second, what can we say about the efficacy of low dose naltrexone in the treatment of depression? In attempting to give the outline of an answer, I’ll be looking at inferential evidence as well as direct evidence. I’ll be looking at some of the studies that evaluate the importance of exercise in the battle against depression. Exercise, as one of the important triggers for the generation of endorphins in our bodies, the so-called “runner’s high” can be viewed as an indirect indicator of what to expect from low dose naltrexone. At least that is one area that I’ll look at. The other is what direct evidence is there that LDN works as an antidepressant?
If you’ve been following this blog, you know that I don’t break out in a rash at the mention of anecdotal evidence. I will take anecdotal evidence, the story told from the patient’s perspective, medical histories, that is, historical accounts that happen to be written by doctors, and double-blind, randomized trials to be different voices in a conversation. In this conversation, I regard no voice as privileged. Each is valid within its own terms of reference. And all can contribute to a fuller understanding.
So I’ve got my work cut out for me. I hope you’ll stay tuned.
Hello, everyone. This post is about one of those basic, basic things that I see being discussed on the boards time and time again. "How can I get a 3mg dose out a 50 mg tablet?" I hope there will be some utility in offering illustrated - yes, illustrated, ladies and gentlemen! - instructions.
I'm going to assume that you have 50mg naltrexone tablets.
The photo gallery, below, will walk you through what you’ll need.
1, Take one tablet and grind it up with a mortar and pestle if you have one. Otherwise just drop it into a darkened 60ml bottle, into which you have put 50ml of distilled water.
2. Let it sit, shaking occasionally, until dissolved. You will see some fine, undissolved residue in the bottom. This can be seen in the bottle in the photo gallery, keeping in mind that it was photographed while sitting on its side. This is the filler that makes up most of the tablet.
3. Remember, since the pill contains a 50mg dose and you’ve used 50ml of distilled water in your bottle, each ml of solution equals one mg of medication. To dispense your dose, shake the bottle vigorously while holding the flip-cap down with your thumb. (Actually, shaking isn't essential. You're just evenly distributing the filler.) Before inserting the oral syringe, draw out the plunger, as if you were measuring your dose with air. You’ll then lift the flip-cap and insert a 5ml oral syringe into the opening. When inserted firmly into the opening at the top of the bottle, push in the plunger, upend the bottle, and draw out your measured dose. Squirt it into a soft drink or juice and down the hatch.
That's really easy: even I can do it.
Equipment
If you don't have a mortar and pestle, don't buy one unless you really want one. I've had mine for ages. It was made by Coors who used to make all sorts of lab equipment. If you must have one, you can buy them (from other manufacturers) at Amazon for about $10 and Target for about $15. I’m told there are pill crushers that are less expensive. The 5ml oral syringe I got for free from the pharmacist at Walgreen's. Tip: the ink will rub off the syringe with use. While you can still read it, take a sharp knife blade and score the barrel of the syringe at the measures you'll need. For example, I've got score marks clear around the syringe: at the 3ml and 4.5ml amounts. Be careful not to press too hard or you'll cut through the plastic material! The Walgreen's pharmacist also gave me the colored plastic 60ml medicine bottle pictured above. The bottle is colored for a reason: exposure to light will shorten the useful life of the LDN that you have mixed. You'll probably have to buy the stopper. Mine came as a set with other stuff I don't need and cost about $2.80. Finally, keep the bottle in the refrigerator: your medication is less reactive when cold and so will last longer.
I’m working on some long range projects for he blog.
•One thing that interests me is the low esteem that personal medical stories are accorded. It is said that they are only anecdotal as if such a story carried with it an odor that offended more delicate and sophisticated nostrils. I have already indicated that I find this attitude to be offensive. In fact, I believe it can be traced back to a mistaken pattern of thought which I am in the process of writing about. It will be a philosophical blog but I guarantee it won’t actually harm the reader, though it won’t be the sexiest of topics.
•Another work in progress is a piece about resistance to writing prescriptions for low dose naltrexone among many, I rather think, most, doctors. There is the hide-bound, head-in-the-sand attitude that so many patients report, of course. But there is the “off-label” bugaboo that offers cover to both the timid and the bull-headed. The validity of these “off-label” concerns needs to be addressed and I’m working on it. The concern about medical liability is a closely related but not identical issue that will be a part of this effort.
Today, however, I’m taking notice of the price rip-offs by some sellers of naltrexone to those of us who are not able to obtain a prescription. The attribution of motives is risky and I’m not going to do it. I do think that a population of persons without prescriptions is a tempting target for charging sky-high prices for dirt-cheap drugs.
Remember, naltrexone is 30 years old and long out of patent. It never was all that popular in treating addicts and alcoholics. It prevented the high but did little for the craving and, although it caused endorphin production to increase the patient never felt the attending sense of well-being because the opiate receptors were permanently blocked. What a bummer!
But then there was the work by Drs. Zagon in the lab and Bihari in the clinical setting that gave us all some very good news that we all know about. Part of the good news is that the drug is cheap, cheap, cheap. But there are those who will charge whatever the market will bear. I don’t care if they are ashamed or not but their outrageous prices should be shown for what they are.
To do this, I’m starting with the prices charged by the place I buy my naltrexone, All Day Chemist in India. I don’t know if their price is the lowest or their service is the best. I’ll just say I’m happy with both their prices and service. I’ll also add that they’re not paying me to say nice things about them. Anyway, I’m taking what I pay them for naltrexone for ten 50mg tablets (that’s about a 100 day supply at 4.5mg per dose) and comparing to a number of other sellers who’s websites came up when I Googled “buy naltrexone online no prescription”, today, Sunday, May 29, 2011. The table below is the result.
Huge price markups for Naltrexone from some sellers
Prices collected from listed websites on Sunday, May 29, 2011
As bad as these prices are, they are actually a little bit worse. You will note that the listed postage charges for sellers other than All Day Chemist are lower. I have quoted the lowest listed price option for each so there would be no question about putting them in a worse light than I had to. My first order from All Day Chemist was confiscated by US Customs. I eventually got a letter from the FDA saying that the shipment appeared to be narcotics and was improperly labeled and seized. Obviously wrong, but that’s what happened. Long before the FDA letter arrived, All Day Chemist agreed with me that the shipment had probably been seized and they sent another shipment at no charge to me. And that’s their standard policy. These other sellers want to charge $4.95 or $5.95 for insurance to guarantee delivery.
It gets even worse. The postage quoted for sellers other than All Day Chemist are shipped by what is usually called “AirMail”. The Canadian Healthcare site says, in small type, “* AirMail ($10.95) - 2-3 weeks, non-traceable.” They offer another option: “* Courier ($14.95) - 4-7 business days, traceable.” My interpretation of these numbers is that if you don’t stump up the $14.95 for traceable courier delivery and an additional $4.95 for “insurance”, you would simply be out of luck for the $151.01 you paid for an untraceable shipment without insurance if customs grabbed your shipment as it did mine. So, the true shipping cost is $19.90, not $10.95 for shipping, if you’re going to get the same deal that All Day Chemist provides. Pharm Discount will charge you $30.00 for a traceable shipment instead of the $10.00 they charge for “Airmail service”.
One more thing: Canadian Healthcare will throw in 4 free viagra pills with your order - perhaps as a reminder that somebody is getting screwed.
Well, she’s done it, right on schedule. Julia Schopick has made available a 2002 interview with Dr. Bernard Bihari for the first time on the internet. It comes as a tribute to his lifetime of service on this the first anniversary of his death on May 16, 2010. This is a good day for those who, like me, look forward to a fuller utilization of low dose naltrexone in the fight against HIV/AIDS, Cancer, autoimmune diseases and others. His calm presentation and humble demeanor only add to the credibility of the information he reports from his clinical and research experience.
We all owe Julia a big thank you for making this happen. She was trusted with the video of Dr. Bihari’s interview by his widow, Jackie Young. Julia presents the interview in two formats: the actual video and a transcription with a time line notation keyed to the video.
I urge you all to take the time to view it in full.
Julia’s website is a valuable resource for information about the medical industry and efforts to reform it. She has authored two books of importance to the LDN community. The first is an e-book, available free on the internet, called The Faces of Low Dose Naltrexone that can be found on her website, HonestMedicine.com, at this address. The second, Honest Medicine: Effective, Time-Tested, Inexpensive Treatments for Life-Threatening Diseases, from Innovative Health Publishing (November 1, 2010). Check Amazon to see the five-star reviews.
This post will give you a partial profile of another of the most important people in the advancement of the use of low dose naltrexone (LDN) and alpha lipoic acid (ALA) to treat many disorders safely, effectively and cheaply, Dr. Burt Berkson of the Integrative Medical Center of New Mexico, P.C. in Las Cruces. I’m also going to show you two summaries of Dr. Berkson’s clinical experience in dealing with rheumatoid arthritis and lupus.
Dr. Berkson has been defending the clinical use of LDN and ALA for a long time. He was the FDA’s chief investigator for alpha lipoic acid for 23 years. Very early in his career, he earned a PhD in microbiology and then went on for his degree in medicine.
There is the now famous story of when Dr. Berkson, as an internal medicine resident at a major Cleveland hospital was confronted with two patients, a married couple, who had eaten Destroying Angel mushrooms (Amanita verna) and were in end-stage liver failure.
The chief doctor assigned Dr. Berkson with the sole responsibility for these patients, instructing him there was nothing to be done for them, that he was to watch them die, relieving their suffering as he might and report the case on grand rounds.
But the young Dr. Berkson would not accept that he could do nothing. Instead, he called the NIH where he talked to Dr. Fred Bartter, chief of endocrinology. Berkson wanted to know if there was anything that could regenerate a liver. Dr. Bartter said he should try intravenous alpha lipoic acid and sent him some by private plane. Berkson picked it up at the airport and injected it into the patients.
I administered ALA to both patients that Sunday night, and within a few hours the man, who had been near death, said he was feeling much better. In three days the woman was almost well, and the man was getting out of bed regularly. He was ready to go home within one week. Remarkably, his liver enzymes [that had been in the thousands] returned to normal, and he had regenerated most of his liver.1
Did Dr. Berkson receive plaudits from the hospital staff for saving these patients? He did not. He was reprimanded. He was forbidden to use ALA again. He was forbidden to call NIH again.
But the Destroying Angels were in bloom and two more patients showed up, in even worse shape than the first pair. Dr. Berkson had some ALA left over from the earlier case and he administered it to the patients who then got better, regaining their health and left the hospital.
Berkson recalls that the hospital administration was “furious with me and branded me as a doctor who could not follow orders.” If it had not been for the NIH having sent a team to review these four cases and praising him as a hero, Berkson believes he would have been fired for insubordination.
For me, Dr. Berkson’s story demonstrates:
1.The great good that can result when a dedicated professional has the courage to challenge the inflexibility of institutional medicine,
2.By implication, the necessity for patients to inform themselves and, ultimately, take responsibility for their own health, and
3.That case histories provide a step-by-step demonstration of the efficacy of both LDN and ALA that will encourage interest in both the use and study of these compounds.
On the last point, I’m going to call attention to two summaries of Dr. Berkson’s case histories as delivered by him in his keynote speech at the Fifth Annual LDN Conference at the NIH in Washington DC on November 7, 2009.
I’m not going to try to capture the details of his treatment protocols. As we all know by now, I lack the training that I’d need to fully understand them. Be that as it may, there is an unmistakable impression created by these summaries that Dr. Berkson’s use of LDN and ALA is filled with promise based upon his remarkable achievements.
The first summary is about treatment of rheumatoid arthritis cases. A tool that can be used in the diagnoses of rheumatoid arthritis is a blood test that measures rheumatoid factor. Rheumatoid factor is an antibody that functions in the immune system. It is not typically found in the blood of healthy people, especially those under the age of 65 (it tends to become more common in older people). Rheumatoid factor is found in the blood of 80% of adults with rheumatoid arthritis, hence its use as a diagnostic tool.
Testing for rheumatoid factor in the blood reveals either the presence or the absence of the antibody: the test is either positive or negative. If the test is positive, the blood sample is diluted and retested. If it is still positive, it is diluted again and again until the test is negative. The number of dilutions is the reported test result, for example, 1:1000 is strong and means the blood sample can be diluted 1000 times and antibodies are still found. A test result of 1:10 is week and means the sample can be diluted only ten times and still be positive.
The summary below shows the measured rheumatoid factor at about the time the patient first presented to Dr. Berkson and again after 6 months to one year after treatment began.
Rheumatoid Factor
On presentation and after treatment by Dr. Berkson
Patient
One Month
6 mos to 1 yr
Percent Reduction
SL
26
13
50.00%
LM
600
54
91.00%
KP
22
12
45.45%
SP
358
70
80.45%
TE
969
131
86.48%
PS
1926
10
99.48%
TM
361
48
86.70%
RA
54
11
79.63%
BA
196
70
64.29%
JC
98
15
84.69%
RC
239
0
100.00%
PH
61
39
36.07%
ES
58
7
87.93%
BT
81
3
96.30%
LV
428
224
47.66%
Average Reduction %
75.74%
From keynote speech by Dr. Burt Berkson at the Fifth Annual LDN Conference at NIH in Washington DC on November 7, 2009.
The second summary is based on lupus patients that have gone to Dr. Berkson for help. The data summarized show the results for testing for another kind of antibody, this one associated with lupus disease. The antibody tested for in this instance is called the antinuclear antibody (ANA) test.
As the name implies, these antibodies attack the innermost structures of the body’s cells, the nucleus where the DNA is found. These antibodies tend to be found in the blood of patients with autoimmune diseases in which the immune system turns against and attacks “self” cells. The data show the results from the ANA test at one month and again after treatment for 6 months to one year.
Patients with Lupus (SLE)
Antinuclear Antibody Counts
On presentation and after treatment by Dr. Berkson
Patient
1 Month
6 Months to One Year
Percent Reduction
Alice A
327
0
100.00%
Mona A
1360
260
80.88%
List B
160
0
100.00%
Frances B
146
14
90.41%
Jean B
320
0
100.00%
Mary Beg
320
160
50.00%
Mary Ben
160
0
100.00%
Jean Bil
320
0
100.00%
Eliz O
320
0
100.00%
Toni E
2934
70
97.61%
Bryan E
160
0
100.00%
Barbara D
180
0
100.00%
Elan G
3240
0
100.00%
Glad H
320
40
87.50%
Penny H
1162
11
99.05%
Leila L
678
30
95.58%
Tina M
249
40
83.94%
WW
640
40
93.75%
Janice M
360
0
100.00%
Alice M
320
49
84.69%
Luc M
249
0
100.00%
Ophelia M
242
0
100.00%
From keynote speech by Dr. Burt Berkson at the Fifth Annual LDN Conference at NIH in Washington DC on November 7, 2009.
The impressive results summarized here occupy a key position between so-called anecdotal evidence for the efficacy of LDN and/or ALA, as in my last post, and the holy grail of studies, the randomized double-blind (and very expensive) projects that would end the medical debate once and for all.
Case histories of the like that are summarized above constitute the bricks and mortar for constructing a compelling evidentiary basis that will justify (and make respectable) the studies that must ultimately be made.
Those studies must be done at public institutions and must be funded by grants, both public and private. We cannot expect the big pharmaceutical companies to invest millions in studies that will justify treatment at a cost of $5 to $10 per month, displacing drugs that cost thousands of dollars per month. So our hope must rest with public institutions like Penn State and San Francisco State University, to do what big pharma will not. Case histories by physicians like Dr. Berkson, when reported in the literature, will provide the cover to justify such studies. When that happens, we will all be the beneficiaries.
Endnote:
1The Alpha Lupoic Acid Breakthrough: The Superb Antioxident That May Slow Aging, Repair Liver Damage and Reduce the Risk of Cancer, Heart Disease and Diabetes, Three Rivers Press; 1 edition (September 9, 1998), page xi. If you’ll check this book at Amazon, there is a review written by one of the first patients whose lives were saved by Dr. Berkson. She liked the book.
Note: Julia Schopick, author of the internet book The Faces of Low Dose Naltrexone and Honest Medicine: Effective, Time-Tested, Inexpensive Treatments for Life-Threatening Diseases (check Amazon) has been transcribing an old video of Dr. Bernard Bihari and will be posting it on her site tomorrow, May 16, 2011, the first anniversary of his death. A fitting remembrance of a wonderful man. I’ll give you a link to it as soon as it is up.
"There is a principle which is a bar against all information, which is proof against all arguments and which cannot fail to keep a man in everlasting ignorance - that principle is contempt prior to investigation." -- Herbert Spencer
Some people, including many doctors, say that the evidence for low dose naltrexone's efficacy is merely anecdotal, as if anecdotal implied "untrue" or at least "unsound". I gotta admit, talk like that makes me angry. Anecdotal evidence is, by far, the kind of evidence you rely upon most in your day-to-day life. Let's imagine you described the two or three most important lessons your life experience has taught you, sometimes attended by great pain. Assume further that the person you were talking to said that those stories of yours were only anecdotal and, hence, without much value. Let's say you don't smack the guy. But you would know that you are talking to a hapless boob with no understanding of human experience or maybe some blind devotee of the scientific method who wants to apply it to everything he sees, despairing of the untidiness of human interaction, which amounts to the same thing. Apologies for taking anecdotal evidence seriously are inappropriate. If you are not setting out on a new career as a research scientist, anecdotal evidence will do just fine. So you are not doing scientific research. What you ARE doing is trying to save the quality of your life - or life itself - or that of someone you care about. Whatever you decide to call upon in making decisions is your business because, like it or not, you are the only person who has responsibility for your health. Doctors are there to assist and treat, but you, as president Bush said, are the decider. If we are to properly exercise our responsibility to ourselves we must inform ourselves. Part of what we will take into account are the studies - the supposed gold standard - that are double-blind, randomized and evidence-based. The trouble is that your condition may not be exactly like the one in the study. Your doctor is going to have to interpolate, to guess, based on his or her clinical experience and your medical history how or whether and to what extent those studies apply to you: it’s called the practice of medicine, not the science of medicine. Ultimately, whatever the recommendation, it doesn't count for anything until you decide that it does. In the meantime, you'll be calling upon all sorts of information, including anecdotal reports, that will lead you to accept or reject your physician's recommendation. From my perspective as somebody who has an autoimmune disease (ulcerative colitis), I've seen enough and read enough to decide for myself to take LDN and, when my specialist and PCP wouldn't prescribe it, I didn't hesitate to order it online from All Day Chemist. What I've learned, first, is there is no downside. If it doesn't cure my condition, at least it won't hurt me. (Of course, it did help, quickly and dramatically. See earlier blog, "Low Dose Naltrexone: My Story") Beyond that, there is the reported clinical experience of Drs. Bihari, Burt Berkson and many others showing very positive results. For example, Dr. Berkson, in his keynote speech at the Fifth Annual LDN Conference at the NIH in Washington in November of 2009 reported that he finds the "best LDN results with autoimmune disorders, most improve greatly." Moreover, there is a mountain of anecdotal evidence showing LDN to be efficacious in a wide range of disorders. I just found out about four videos, made in October and November of 2010, that I hope you'll take a look at: photos and stories of people who report significant benefits to themselves from taking LDN. The series, called Global Advocates, is brought to us by the LDN Research Trust, a fine organization deserving our support.
Many of these slides refer to the various forms of multiple sclerosis. So you'll know what they are talking about, here is a list of those forms (taken from The Promise of Low Dose Naltrexone Therapy, Potential Benefits in Cancer, Autoimmune, Neurological and Infectious Disorders – Elaine A. Moore, Samantha Wilkinson)
·Relapsing remitting MS (RRMS) Most common, accounts for 85% of all cases
·Secondary progressive MS (SPMS) Of RRMS group, 50% go on to develop this within 10 yrs of initial diagnosis
·Primary progressive MS (PPMS) About 15% of patients with progressive MS have gradually worsening manifestations from the onset without clinical relapses and are described as having primary progressive MS
·Progressive relapsing (PRMS) This form in about 5% of cases. It is progressive from the onset with superimposed relapses (with or without recovery).
