Only those who read product labels, because this definitely hasn't been publicized.
I was just perusing the most recent (12/2008) Sinemet product insert and i found the following paragraph:
"There have been reports of patients experiencing intense urges to gamble, increased sexual urges, and other intense urges, and the inability to control these urges while taking one or more of the medications that increase central dopaminergic tone and that are generally used for the treatment of Parkinson’s disease, including SINEMET. Although it is not proven that the medications caused these events, these urges were reported to have stopped in some cases when the dose was reduced or the medication was stopped. Prescribers should ask patients about the development of new or increased gambling urges, sexual urges or other urges while being treated with SINEMET. Patients should inform their physician if they experience new or increased gambling urges, increased sexual urges, or other intense urges while taking SINEMET. Physicians should consider dose reduction or stopping the medication if a patient develops such urges while taking SINEMET."
The fact that (ballparking) 95% of all cases of gambling that have been blamed on dopamine agonists were also taking levodopa has been consistently disregarded by study authors and not even mentioned in news articles.
AND anyone who has taken the fact that Boehringer Ingelheim, which has come under relentless fire for Mirapex, voluntarily (I believe) put a similar warning on their label a couple of years ago as an admission of guilt must now ask themselves why Merck/Bristol Myers Squibb would do the same, if it was voluntary, or why they would be required to, if it was not (I haven't been able to determine which it was) when they have come under no fire at all.
I would also ask why this hasn't been publicized - *vastly* more people are taking levodopa than are taking dopamine agonists.
Actually, I don’t think there is enough evidence to support either drug, taken as prescribed, causing such behavior – however, if dopamine replacement therapy must be blamed, then they both must be considered possible culprits – reports linking levodopa to hypersexuality, for example, far pre-date the approval of Mirapex.
It looks like they also added language about melanoma...
I haven't seen that in the news, either - has anyone else?
Most disturbing to me is that, if there really is a possible association between Sinemet and gambling, this supports my position that dopamine agonists have been being unfairly maligned.
Thursday, January 14, 2010
Thursday, November 12, 2009
Questions Regarding Mayo Clinic Study Re-Posted to YouTube
I have re-posted my comments and questions regarding the Mayo Clinic video on YouTube.
Wednesday, November 11, 2009
Questions Regarding Mayo Clinic Study Deleted from YouTube Video Post
My friend Bob, who has a terrific blog called Parkinson's Patients: Yes We Can Dance, recently drew my attention to a Mayo Clinic video on YouTube. In it, a physician named J. Michael Bostwick tells us that according to the findings of his recent study, at least one in every five people with Parkinson's who takes a dopamine agonist will experience compulsive behavior as a side effect.
That number is radically higher than any previous estimate, and given that even the lower numbers are completely unsupported by the evidence presented in any of the other papers I've ever read, i was curious. i read the study, something that, in general, i HIGHLY recommend to anyone with Parkinson's who is trying to make treatment-related decisions.
As I expected, there were some very curious aspects of this study, and a day or two ago I posted my observations, questions and criticisms of this study as comments to the YouTube video.
Today, I checked in on the video to find that my comments have been deleted.
So, I'm posting them below. I am planning a more comprehensive critique of the study, but wanted to get these comments back up on the Internet just in case anyone reads my newest post on theYouTube video post, which directs them here, before that comment is deleted, too. Here they are:
(I realize, reading these six items again today, that they probably won't make sense to anyone who hasn't read the study. However, I do want them available while I work on a post that will provide more explanation, so that it is clear that comments, criticisms, and questions that were deleted from the Mayo Clinic video post were rational, logical and posed in a civilized fashion.)
1) I beg everyone who sees this to read the actual study - not just the abstract, the whole study – it can be found here: http://www.ncbi.nlm.nih.gov/pmc/issues/177782/ - just scroll down a little – the pramipexole (Mirapex) package insert can be found here: http://www.accessdata.fda.gov/Scripts/cder/DrugsatFDA/index.cfm?fuseaction=Search.Label_ApprovalHistory - check my facts, please!!
2) For 4 out of 7 patients, there is no stated temporal relationship btw initiation/increase or cessation/decrease in dopamine agonists & certain behavior – in the absence of a temporal relationship, on what basis are you claiming the existence of an association between the drug and the behavior?
3) 2 out of those 4, in addition to having no stated temporal relationship, are footnoted as “not clearly pathologic” – well, you cant’ have your cake and eat it too – if they aren’t pathologic, then they are not eligible for inclusion in a study with pathological as an inclusion criterion
4) you define 2mg/day or greater as therapeutic dosage of pramipexole – but according to the package insert, “doses of 3 mg, 4.5 mg, and 6 mg per day of MIRAPEX tablets were not shown to provide any significant benefit beyond that achieved at a daily dose of 1.5 mg/day.” So, actually, less than 2mg/day is definitely therapeutic.
5) You exclude 28 of the 66 people taking agonists on the basis of this never before heard and according to the package insert completely erroneous categorization of their agonist dosage as subtherapeutic.
6) If you remove the patients who were included without any basis for inclusion, and include those who were excluded without any basis for exclusion, you get 3 patients out of 66 taking dopamine agonists who experienced compulsive behavior, which indicates a prevalence of 4.5%, or approximately ¼ that which you are claiming to have found.
That number is radically higher than any previous estimate, and given that even the lower numbers are completely unsupported by the evidence presented in any of the other papers I've ever read, i was curious. i read the study, something that, in general, i HIGHLY recommend to anyone with Parkinson's who is trying to make treatment-related decisions.
As I expected, there were some very curious aspects of this study, and a day or two ago I posted my observations, questions and criticisms of this study as comments to the YouTube video.
Today, I checked in on the video to find that my comments have been deleted.
So, I'm posting them below. I am planning a more comprehensive critique of the study, but wanted to get these comments back up on the Internet just in case anyone reads my newest post on theYouTube video post, which directs them here, before that comment is deleted, too. Here they are:
(I realize, reading these six items again today, that they probably won't make sense to anyone who hasn't read the study. However, I do want them available while I work on a post that will provide more explanation, so that it is clear that comments, criticisms, and questions that were deleted from the Mayo Clinic video post were rational, logical and posed in a civilized fashion.)
1) I beg everyone who sees this to read the actual study - not just the abstract, the whole study – it can be found here: http://www.ncbi.nlm.nih.gov/pmc/issues/177782/ - just scroll down a little – the pramipexole (Mirapex) package insert can be found here: http://www.accessdata.fda.gov/Scripts/cder/DrugsatFDA/index.cfm?fuseaction=Search.Label_ApprovalHistory - check my facts, please!!
2) For 4 out of 7 patients, there is no stated temporal relationship btw initiation/increase or cessation/decrease in dopamine agonists & certain behavior – in the absence of a temporal relationship, on what basis are you claiming the existence of an association between the drug and the behavior?
3) 2 out of those 4, in addition to having no stated temporal relationship, are footnoted as “not clearly pathologic” – well, you cant’ have your cake and eat it too – if they aren’t pathologic, then they are not eligible for inclusion in a study with pathological as an inclusion criterion
4) you define 2mg/day or greater as therapeutic dosage of pramipexole – but according to the package insert, “doses of 3 mg, 4.5 mg, and 6 mg per day of MIRAPEX tablets were not shown to provide any significant benefit beyond that achieved at a daily dose of 1.5 mg/day.” So, actually, less than 2mg/day is definitely therapeutic.
5) You exclude 28 of the 66 people taking agonists on the basis of this never before heard and according to the package insert completely erroneous categorization of their agonist dosage as subtherapeutic.
6) If you remove the patients who were included without any basis for inclusion, and include those who were excluded without any basis for exclusion, you get 3 patients out of 66 taking dopamine agonists who experienced compulsive behavior, which indicates a prevalence of 4.5%, or approximately ¼ that which you are claiming to have found.
Monday, May 11, 2009
*Is* dopamine agonist therapy associated with pathological gambling?
Well, folks, I finally have corroboration from a doctor, published in a peer-reviewed journal (not that I think that means much, but others might) for my assertion that none of the gambling studies to date (which means as of 2007, or early 2008 at the latest), demonstrates the extent of risk of development of pathological gambling when taking dopaminergic meds. Dr. Zand says:
I wonder why this paper didn't get any press whatsoever?
Zand R. Is dopamine agonist therapy associated with developing pathological gambling in Parkinson's disease patients? Eur Neurol. 2008;59(3-4):183-6. Epub 2008 Jan 29.
"Thus far, published reports have been able to neither demonstrate the extent of risk for gambling-related problems nor study the correlation of dosage with this potential adverse effect among Parkinson’s disease patients treated with dopaminergic medications."My absolute favorite bit is this, with reference to the 2005 study by Dodd, et. al.:
"This report, however, did not include the total number of patients exposed to pramipexole, ropinirole or other dopamine agonist agents, so the incidence of pathological gambling could not be estimated."Which is exactly what i said in my May, 5, 2008 blog entry Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease: Yet Another Closer Look, Part Two, albeit not nearly so concisely.
I wonder why this paper didn't get any press whatsoever?
Zand R. Is dopamine agonist therapy associated with developing pathological gambling in Parkinson's disease patients? Eur Neurol. 2008;59(3-4):183-6. Epub 2008 Jan 29.
Saturday, October 25, 2008
Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease: Yet Another Closer Look, Part Three(a)
Welcome to Part Three(a) of a three part series.
To recap the background provided in Part One, in the 2005 study entitled “Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease,” the authors mine records of Parkinson’s patients seen at the Mayo Clinic in Rochester, MN (MCR), between 2002 and 2004, and find 11 people who had developed pathological gambling (PG) - they conclude that the PG was caused by Parkinson's drugs. The authors so completely fail to provide evidence compelling enough to support this conclusion that the fact that this study was published in a peer-reviewed journal boggles the mind. It is available online for free at the Archives of Neurology, if you are interested. It may actually be necessary to read the study for what I am about to say to make sense – I don’t know.
According to the authors of this study, the 11 people who gambled fit the DSM-IV-TR criteria for PG.* They also say that the PG was temporally associated with the commencement, increase, and/or cessation of dopamine agonist (DA) therapy, a type of drug used to treat Parkinson’s disease (PD), and, for a disproportionate percentage of these people, the culprit was a DA called pramipexole.
Finally, the authors provide the results of their survey of the field of literature, and present in a table six studies in support of their conclusion that Parkinson’s drugs cause – not just “are associated with,” but cause PG.
In Part One, I addressed the authors’ failure to adequately support their central assertion, that DAs cause PG, in the context of what criteria must be met to identify a causal relationship. In Part Two, I addressed specifically the authors’ failure to provide any indication of the prevalence of this phenomenon and show how that pretty much single handedly invalidates the study. And in Part Three(a), I will address the authors’ failure to delineate the parameters of what they call a temporal relationship, and question the resultant inclusion of two of the 11 PGers.
I apologize for the enormous gaps between my posts but I write these things at night, and my meds are only carrying me through the work day in terms of typing. So, I may have to finish Dodd in more bite-sized bits.
Dodd et. al. base their assertion that there is a causal association between dopamine agonist (DA) therapy and pathological gambling (PG) on the presence of what they call a temporal relationship. A temporal relationship exists when Outcome Y follows the introduction of Variable X within a period of time that is considered plausible for a connection. Plausibility is determined by the natures of variable and the outcome – for example, if Outcome Y is deemed to be an allergic reaction and Variable X is a bee sting, the plausibility of their being related remains intact for a far shorter period of time than if Outcome Y is lung cancer and Variable X is smoking.
It should come as no surprise at this point that Dodd et. al. fail to delineate the parameters they use to identify the purported temporal relationship between DA therapy and PG. If we are curious, however, we should be able to infer them from the data provided, which is summarized in the table below:
With the help of common sense, it would seem reasonable to me to infer from the above that as long as either the latency of DA therapy initiation to gambling addiction (3rd column) or the latency of the discontinuation of DA therapy to the resolution of gambling (4th column) is less than or equal to 3months, the authors consider the possibility of a temporal relationship to be plausible – well, for most of the patients listed, anyway.
Patients 8 and 10 are different.
For Patient 10, even if we disregard the 2.5 year latency to PG onset, the authors ask us to stretch plausibility a minimum of 3 months in considering a latency to cessation of PG of up to 6 months after discontinuing DA therapy.
And – I am just going to say it – the inclusion of Patient 8, with her year-long latency to onset and the fact that they have no evidence that she ever stopped, is ludicrous.
And that brings the total number of people found to have started PG while taking PD meds down from 11 to 9, for whatever that is worth.
I think I will wrap up with a summary of what the studies Dodd et. al. cite in support of their conclusion really say but that will have to wait for another day.
*************************
* Pathological gambling is defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DMS-IV-TR) as follows, and the study does not describe in which five each patient has engaged:
A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:
B. The gambling behavior is not better accounted for by a manic episode
To recap the background provided in Part One, in the 2005 study entitled “Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease,” the authors mine records of Parkinson’s patients seen at the Mayo Clinic in Rochester, MN (MCR), between 2002 and 2004, and find 11 people who had developed pathological gambling (PG) - they conclude that the PG was caused by Parkinson's drugs. The authors so completely fail to provide evidence compelling enough to support this conclusion that the fact that this study was published in a peer-reviewed journal boggles the mind. It is available online for free at the Archives of Neurology, if you are interested. It may actually be necessary to read the study for what I am about to say to make sense – I don’t know.
According to the authors of this study, the 11 people who gambled fit the DSM-IV-TR criteria for PG.* They also say that the PG was temporally associated with the commencement, increase, and/or cessation of dopamine agonist (DA) therapy, a type of drug used to treat Parkinson’s disease (PD), and, for a disproportionate percentage of these people, the culprit was a DA called pramipexole.
Finally, the authors provide the results of their survey of the field of literature, and present in a table six studies in support of their conclusion that Parkinson’s drugs cause – not just “are associated with,” but cause PG.
In Part One, I addressed the authors’ failure to adequately support their central assertion, that DAs cause PG, in the context of what criteria must be met to identify a causal relationship. In Part Two, I addressed specifically the authors’ failure to provide any indication of the prevalence of this phenomenon and show how that pretty much single handedly invalidates the study. And in Part Three(a), I will address the authors’ failure to delineate the parameters of what they call a temporal relationship, and question the resultant inclusion of two of the 11 PGers.
I apologize for the enormous gaps between my posts but I write these things at night, and my meds are only carrying me through the work day in terms of typing. So, I may have to finish Dodd in more bite-sized bits.
Dodd et. al. base their assertion that there is a causal association between dopamine agonist (DA) therapy and pathological gambling (PG) on the presence of what they call a temporal relationship. A temporal relationship exists when Outcome Y follows the introduction of Variable X within a period of time that is considered plausible for a connection. Plausibility is determined by the natures of variable and the outcome – for example, if Outcome Y is deemed to be an allergic reaction and Variable X is a bee sting, the plausibility of their being related remains intact for a far shorter period of time than if Outcome Y is lung cancer and Variable X is smoking.
It should come as no surprise at this point that Dodd et. al. fail to delineate the parameters they use to identify the purported temporal relationship between DA therapy and PG. If we are curious, however, we should be able to infer them from the data provided, which is summarized in the table below:
With the help of common sense, it would seem reasonable to me to infer from the above that as long as either the latency of DA therapy initiation to gambling addiction (3rd column) or the latency of the discontinuation of DA therapy to the resolution of gambling (4th column) is less than or equal to 3months, the authors consider the possibility of a temporal relationship to be plausible – well, for most of the patients listed, anyway.
Patients 8 and 10 are different.
For Patient 10, even if we disregard the 2.5 year latency to PG onset, the authors ask us to stretch plausibility a minimum of 3 months in considering a latency to cessation of PG of up to 6 months after discontinuing DA therapy.
And – I am just going to say it – the inclusion of Patient 8, with her year-long latency to onset and the fact that they have no evidence that she ever stopped, is ludicrous.
And that brings the total number of people found to have started PG while taking PD meds down from 11 to 9, for whatever that is worth.
I think I will wrap up with a summary of what the studies Dodd et. al. cite in support of their conclusion really say but that will have to wait for another day.
*************************
* Pathological gambling is defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DMS-IV-TR) as follows, and the study does not describe in which five each patient has engaged:
A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:
- is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble)
- needs to gamble with increasing amounts of money in order to achieve the desired excitement
- has repeated unsuccessful efforts to control, cut back, or stop gambling
- is restless or irritable when attempting to cut down or stop gambling
- gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)
- after losing money gambling, often returns another day to get even ("chasing" one's losses)
- lies to family members, therapist, or others to conceal the extent of involvement with gambling
- has committed illegal acts such as forgery, fraud, theft, or embezzlement to finance gambling
- has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling
- relies on others to provide money to relieve a desperate financial situation caused by gambling
B. The gambling behavior is not better accounted for by a manic episode
Wednesday, July 02, 2008
Evidence-based Medicine - Is This New?
I am hearing this catch phrase fairly regularly recently, and I have to ask - is this actually something new? i mean, newer than, say, 50 years old, at least? Because if it is, good lord what has medicine been based on up until now? Tea leaves? Magic 8 balls? The whims of medical practitioners? Old wives' tales? All those millions of research studies that have been undertaken in the last half century - were they done purely for their entertainment value?
I must be missing something.
I must be missing something.
Monday, May 05, 2008
Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease: Yet Another Closer Look, Part Two
Welcome to Part Two of a three part series.
To recap the background provided in Part One, in the 2005 study entitled “Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease,” the authors mine records of Parkinson’s patients seen at the Mayo Clinic in Rochester, MN (MCR), between 2002 and 2004, and find 11 people who had developed pathological gambling (PG) - they conclude that the PG was caused by Parkinson's drugs. The authors so completely fail to provide evidence compelling enough to support this conclusion that the fact that this study was published in a peer-reviewed journal boggles the mind. It is available online for free at the Archives of Neurology, if you are interested. It may actually be necessary to read the study for what I am about to say to make sense – I don’t know.
According to the authors of this study, the 11 people who gambled fit the DSM-IV-TR criteria for PG.* They also say that the PG was temporally associated with the commencement, increase, and/or cessation of dopamine agonist (DA) therapy, a type of drug used to treat Parkinson’s disease (PD), and, for a disproportionate percentage of these people, the culprit was a DA called pramipexole.
Finally, the authors provide the results of their survey of the field of literature, and present in a table six studies in support of their conclusion that Parkinson’s drugs cause – not just “are associated with,” but cause PG.
In Part One, I addressed the authors’ failure to adequately support their central assertion, that DAs cause PG, in the context of what criteria must be met to identify a causal relationship. In Part Two, I will address specifically the authors’ failure to provide any indication of the prevalence of this phenomenon and show how that pretty much single handedly invalidates the study. And in Part Three, I will address several other questions that come up when one actually reads the study rather than the press coverage it received.
Prevalence is defined by the Centers for Disease Control as “the number of existing disease cases [or, in this case, adverse events of a specific nature] in a defined group of people during a specific time period.”
So there are three parts to prevalence, each of which consists of a number – (1) the number of existing cases; (2) a defined [read: finite, i.e., quantifiable] group of people among whom those cases are found; and (3) a specific time period.
Prevalence is calculated by dividing the number of existing cases by the quantity of people in the specific population in which those cases were found, which yields a percent of people affected. In this study, the authors provide the number of existing cases, which is 11, and they denote a specific time period, which is 2002 to 2004. However, the authors omit (2), the total number of people with Parkinson’s (PWP) being treated at MCR and taking DAs between 2002 and 2004, and that really makes the claim that an association was found groundless.
In order to illustrate why this is true, and because I was unable to find any relevant stats regarding the MCR, I extrapolated a value for the missing piece of data from information found in various places on the internet, and using this method (which I have detailed below, in case you are interested)** I came up with the number 1195 for the total number of PWP taking DAs that were seen at MCR between 2002 and 2004. 11/1195 returns a prevalence of PG of 0.09% among those who were taking DAs.
But even that is not enough information. The authors also fail to provide the prevalence of PG in the general population or in untreated PD, which is just as crucial as the total number of (PWP) being treated at MCR and taking DAs between 2002 and 2004, because the only way a prevalence in a certain population has meaning is in relation to the prevalence of the same phenomenon in a different population.
So, I looked around and found the following stats for the general population from 1999. Estimates of the lifetime prevalence of PG in the general population in the US in the late 90s range from 1.2-3.9%, while estimates of past year prevalence of PG in the general population range from 0.6-2%.***
As you might have noticed, the prevalence I have extrapolated for the 11 who gambled is far lower than even the lowest estimated prevalence I could find for the general population. One might argue that my method of deriving that prevalence was not scientific, and that may be true.
However, in the absence of the total number of (PWP) being treated at MCR and taking DAs between 2002 and 2004, there is no way of knowing whether the prevalence of PG among those taking DAs is higher or lower than that of the general population.
And if the prevalence really were 0.09%, i.e., significantly lower than that of the general population, then I would think the makers of pramipexole would be doing the victory dance, because they would then be purveyors of a treatment for, not a cause of, PG.
And it is in that way that the authors fail to provide evidence sufficient and compelling enough to support their conclusion.
If I have not explained my thoughts clearly, please let me know and I will try again.
On to Part Three.
*************************
* Pathological gambling is defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DMS-IV-TR) as follows, and the study does not describe in which five each patient has engaged:
A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:
B. The gambling behavior is not better accounted for by a manic episode
**Based on the fact that Ohio State University’s Dept of Neurology’s 28 physicians see 400 PWP annually, I will extrapolate that the 93 neurologists at MCR see 1328 PWP annually, or 3984 PWP over the three year period in question. And according to the website of a law firm selling its services to folks who have gambled while taking a DA, 30% of PWP are prescribed DAs – which would mean 1195 people on DAs were seen at MRC between 2002 and 2004.
*** 3.9% lifetime; 2% past year ~ National Research Council. Pathological Gambling: A Critical Review. Washington, DC: National Academy Press; 1999
1.2% lifetime; 0.6% past year ~ National Opinion Research Center at the University of Chicago, Gemini Research, and The Lewin Group. Gambling Impact and Behavior Study. Report to the National Gambling Impact Study Commission. April 1, 1999. Table 7, p. 26.
To recap the background provided in Part One, in the 2005 study entitled “Pathological Gambling Caused by Drugs Used to Treat Parkinson’s Disease,” the authors mine records of Parkinson’s patients seen at the Mayo Clinic in Rochester, MN (MCR), between 2002 and 2004, and find 11 people who had developed pathological gambling (PG) - they conclude that the PG was caused by Parkinson's drugs. The authors so completely fail to provide evidence compelling enough to support this conclusion that the fact that this study was published in a peer-reviewed journal boggles the mind. It is available online for free at the Archives of Neurology, if you are interested. It may actually be necessary to read the study for what I am about to say to make sense – I don’t know.
According to the authors of this study, the 11 people who gambled fit the DSM-IV-TR criteria for PG.* They also say that the PG was temporally associated with the commencement, increase, and/or cessation of dopamine agonist (DA) therapy, a type of drug used to treat Parkinson’s disease (PD), and, for a disproportionate percentage of these people, the culprit was a DA called pramipexole.
Finally, the authors provide the results of their survey of the field of literature, and present in a table six studies in support of their conclusion that Parkinson’s drugs cause – not just “are associated with,” but cause PG.
In Part One, I addressed the authors’ failure to adequately support their central assertion, that DAs cause PG, in the context of what criteria must be met to identify a causal relationship. In Part Two, I will address specifically the authors’ failure to provide any indication of the prevalence of this phenomenon and show how that pretty much single handedly invalidates the study. And in Part Three, I will address several other questions that come up when one actually reads the study rather than the press coverage it received.
Prevalence is defined by the Centers for Disease Control as “the number of existing disease cases [or, in this case, adverse events of a specific nature] in a defined group of people during a specific time period.”
So there are three parts to prevalence, each of which consists of a number – (1) the number of existing cases; (2) a defined [read: finite, i.e., quantifiable] group of people among whom those cases are found; and (3) a specific time period.
Prevalence is calculated by dividing the number of existing cases by the quantity of people in the specific population in which those cases were found, which yields a percent of people affected. In this study, the authors provide the number of existing cases, which is 11, and they denote a specific time period, which is 2002 to 2004. However, the authors omit (2), the total number of people with Parkinson’s (PWP) being treated at MCR and taking DAs between 2002 and 2004, and that really makes the claim that an association was found groundless.
In order to illustrate why this is true, and because I was unable to find any relevant stats regarding the MCR, I extrapolated a value for the missing piece of data from information found in various places on the internet, and using this method (which I have detailed below, in case you are interested)** I came up with the number 1195 for the total number of PWP taking DAs that were seen at MCR between 2002 and 2004. 11/1195 returns a prevalence of PG of 0.09% among those who were taking DAs.
But even that is not enough information. The authors also fail to provide the prevalence of PG in the general population or in untreated PD, which is just as crucial as the total number of (PWP) being treated at MCR and taking DAs between 2002 and 2004, because the only way a prevalence in a certain population has meaning is in relation to the prevalence of the same phenomenon in a different population.
So, I looked around and found the following stats for the general population from 1999. Estimates of the lifetime prevalence of PG in the general population in the US in the late 90s range from 1.2-3.9%, while estimates of past year prevalence of PG in the general population range from 0.6-2%.***
As you might have noticed, the prevalence I have extrapolated for the 11 who gambled is far lower than even the lowest estimated prevalence I could find for the general population. One might argue that my method of deriving that prevalence was not scientific, and that may be true.
However, in the absence of the total number of (PWP) being treated at MCR and taking DAs between 2002 and 2004, there is no way of knowing whether the prevalence of PG among those taking DAs is higher or lower than that of the general population.
And if the prevalence really were 0.09%, i.e., significantly lower than that of the general population, then I would think the makers of pramipexole would be doing the victory dance, because they would then be purveyors of a treatment for, not a cause of, PG.
And it is in that way that the authors fail to provide evidence sufficient and compelling enough to support their conclusion.
If I have not explained my thoughts clearly, please let me know and I will try again.
On to Part Three.
*************************
* Pathological gambling is defined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DMS-IV-TR) as follows, and the study does not describe in which five each patient has engaged:
A. Persistent and recurrent maladaptive gambling behavior as indicated by five (or more) of the following:
- is preoccupied with gambling (e.g., preoccupied with reliving past gambling experiences, handicapping or planning the next venture, or thinking of ways to get money with which to gamble)
- needs to gamble with increasing amounts of money in order to achieve the desired excitement
- has repeated unsuccessful efforts to control, cut back, or stop gambling
- is restless or irritable when attempting to cut down or stop gambling
- gambles as a way of escaping from problems or of relieving a dysphoric mood (e.g., feelings of helplessness, guilt, anxiety, depression)
- after losing money gambling, often returns another day to get even ("chasing" one's losses)
- lies to family members, therapist, or others to conceal the extent of involvement with gambling
- has committed illegal acts such as forgery, fraud, theft, or embezzlement to finance gambling
- has jeopardized or lost a significant relationship, job, or educational or career opportunity because of gambling
- relies on others to provide money to relieve a desperate financial situation caused by gambling
B. The gambling behavior is not better accounted for by a manic episode
**Based on the fact that Ohio State University’s Dept of Neurology’s 28 physicians see 400 PWP annually, I will extrapolate that the 93 neurologists at MCR see 1328 PWP annually, or 3984 PWP over the three year period in question. And according to the website of a law firm selling its services to folks who have gambled while taking a DA, 30% of PWP are prescribed DAs – which would mean 1195 people on DAs were seen at MRC between 2002 and 2004.
*** 3.9% lifetime; 2% past year ~ National Research Council. Pathological Gambling: A Critical Review. Washington, DC: National Academy Press; 1999
1.2% lifetime; 0.6% past year ~ National Opinion Research Center at the University of Chicago, Gemini Research, and The Lewin Group. Gambling Impact and Behavior Study. Report to the National Gambling Impact Study Commission. April 1, 1999. Table 7, p. 26.
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