RSS Feeds
Published letters
Displaying 1-10 letters out of 2411 published
-
Complexities of Defibrillator Deactivation
Submit responseWe strongly agree with the authors' conclusions that hospices may improve quality of care if they routinely identify patients with implantable defibrillators (ICDs) and to address ICD deactivation. In our own hospital-based heart failure cardiology and palliative care practices, we always address ICD deactivation prior to discharging patients to hospice care. However, given the complexity and difficulty of decision- making for families and caregivers during transitions in care, we have observed the occasional patient who is not ready to deactivate their ICD at time of hospital discharge. We appreciate that hospices do accept patients with functioning ICDs with the presumed goal of addressing deactivation after enrollment in hospice. We would like to highlight the study limitation noted by the authors that this study does not directly address patient-level preferences about ICD inactivation. Goldstein et al have reported in a small study that ICD recipients have not discussed ICD deactivation and are unaware that deactivation is an option(1). In our experience, we also have observed that most patients are not made aware of the possible future burden of the ICD at the time of device implantation. We have occasionally noticed a paradox in which patients, despite preferring palliative care or hospice, remain unwilling to undergo deactivation of their ICDs. Furthermore, it is possible that hospices nurses are appropriately querying hospice patients about their preferences for ICD deactivation, irrespective of the presence of a hospice ICD deactivation policy. Further, we want to make note that the median hospice length of stay in a large sample of Medicare heart failure patients was reported at only 17 days with nearly 1/3 of patients staying less than 8 days(2. Thus, a short enrollment in hospice at end of life may be an additional barrier to establishment of highest quality conversations between cardiac patients and hospice care providers. Finally, clinicians need to be aware that, unlike cancer patients, 19% of HF patients are discharged from hospice and nearly 1 in 4 patients survive more than 180 days after hospice enrollment. Thus, admission to hospice care is not a certain indication of terminal HF, which adds to the complexity of prognostication and decision-making with this disease.
References:
1. Bain, K. T., T. L. Maxwell, et al. (2009). "Hospice use among patients with heart failure." American Heart Journal 158(1): 118-125.
2. Goldstein, N., D. Mehta, et al. (2008). "That's Like an Act of Suicide" Patients' Attitudes Toward Deactivation of Implantable Defibrillators." Journal of General Internal Medicine 23(0): 7-12.
Conflict of Interest:
None declared
-
Re: Author's response: Overdose can occur at a patient's usual opioid dose
Submit responseBecker and Nahata raise valuable points regarding our paper (1). Becker makes an important observation in noting that risks of adverse effects of opioids may differ depending on changes in intercurrent illness, particularly among older patients with multiple comorbidities. About 6-7 percent of all adults age 65 or older use opioids long-term for chronic non-cancer pain (2). There is remarkably little research evaluating risks of and risk factors for adverse medical and behavioral effects of long-term opioid use, particularly among elderly patients. Possible adverse effects of opioids include: serious fractures due to falls (3), acetaminophen toxicity (4); hyperalgesia; aspiration pneumonia; complications of chronic constipation; apathy, de-activation and depression; and cognitive impairment, among others. Careful evaluation of patient suitability for long-term opioid use, cautious prescribing, clear explanation of how to use opioids safely and potential risks, close medical monitoring of patients using opioids long-term, safety reminders, and other universal precautions could conceivably reduce risks of adverse effects. However, research evaluating harm reduction interventions among patients using opioids for chronic non-cancer pain is sparse, as is research weighing long-term benefits against the full range of medical and behavioral risks.
Nahata correctly identifies a limitation of our research. We assessed overdose risk relative to estimated average daily dose. Risks could potentially differ markedly depending on the actual pattern of opioid consumption. In fact, we know little about how physicians prescribe and patients use opioids for chronic pain in community practice. Since millions of U.S. adults use opioids long-term, research is needed concerning how opioids are actually used by chronic pain patients, risks and benefits of alternative opioid treatment regimens, and the effectiveness of universal precautions for preventing adverse effects. In the absence of an adequate evidence base for current prescribing practices, a cautious and vigilant stance toward long-term opioid prescribing for chronic non-cancer pain patients seems prudent.
References 1. Dunn KM, Saunders KW, Rutter CM, Banta-Green CJ, Merrill JO, Sullivan MD, Weisner CM, Silverberg MJ, Campbell CI, Psaty BM, Von Korff M. Opioid prescriptions for chronic pain and overdose: a cohort study. Annals of Internal Medicine 2010; 152:85-92.
2. Campbell CI, Weisner C, LeResche L, Ray T, Saunders K, Sullivan MD, Banta-Green C, Merrill JO, Silverberg MJ, Boudreau D, Satre DD, Von Korff M. Age and sex trends in long-term opioid analgesic use for non- cancer pain. Am J Public Health, In press.
3. Saunders KW, Dunn KM, Merrill JO, Sullivan MD, Weisner CM, Braden JB, Psaty BM, Von Korff M. Relationship of opioid use and dosage levels to fractures in older chronic pain patients. Journal of General Internal Medicine, Published online, January 5,2010.
4. Committee on the Safety of Medicines of the UK. Overdose risk prompts UK withdrawal of propoxyphene combination. J Pain Palliat Care Pharmacother. 2006;20:49-50.
Conflict of Interest:
None declared
-
Does reducing salt intake really reduce health care spending in the long term?
Submit responseMarch 9, 2010
Smith-Spangler et al. (1) argue that a reduction in the sodium content of food will prevent many cases of hearts attack and strokes. Population health strategies and policy approaches such as this can undoubtedly be highly cost-effective (i.e., they prevent disease at low cost). The authors also argue that this action will lead to a reduction in health-care spending. This claim is repeated in the accompanying editorial by Frieden and Briss (2). Unfortunately, their claim is erroneous.
Smith-Spangler et al. (1) appear to have considered only the reduced health-care spending as a result of fewer cases of hearts attack and strokes. They state that their analysis predicts an increase in "life-years lived by more than 1.3 million over the lifetime of U.S. adults aged 40 to 85 years alive today." However, they do not appear to have deducted the health-care costs for continuing to care for these people over time. These costs could easily cancel out the estimated savings of $32.1 billion in direct medical costs resulting from fewer cardiovascular cases.
Quite apart from actual health-care spending, the inevitable result of people living longer is increased government spending on social security and other social programs. When this is factored in, the bottom line will most certainly reveal that the "savings" have turned into higher spending. If people wish to make financial estimates based on various policy options, then it is essential that they provide the whole story.
There have been many previous analyses of the likely result of implementation of interventions designed to prevent disease or improve health. Overall, most such medical interventions result in an increase in health-care spending (3). This is especially likely to be the case when dealing with diseases that are commonly fatal and the analysis extends far enough into old age (4). It is unavoidable that the extra years of life generated inevitably result in an increased need for the treatment of chronic conditions and for long-term nursing care. For example, when people quit smoking, there is eventually an increase in health-care spending (5-7). Surprisingly, this is even seen with the prevention of obesity (8).
Of course, the prevention of fatal diseases is undeniably of great value with regard to population health. If we consider the impact of salt reduction strategies on improved quality of life, the benefits are obvious; people with strokes and heart attacks experience considerable suffering, disability and frequently death. If this can be avoided any preventative strategies may be worthwhile in terms of the health benefits. However, this is altogether different from decreasing health-care spending.
Should the government therefore implement policies that target the excessive salt content of food and thereby help to reduce the incidence of hearts attacks and strokes even if the intervention fails to save health care dollars over time? To do anything else would be heartless and a no- brainer!
REFERENCES
1. Smith-Spangler CM, Juusola JL, Enns EA, Owens DK, Garber AM. Population strategies to decrease sodium intake and the burden of cardiovascular disease in the United States. A cost-effectiveness analysis. Ann Intern Med. 2010;152.
2. FriedenTR, Briss PA. We can reduce dietary sodium, save money, and save lives. Ann Intern Med. 2010.
3. Cohen JT, Neumann PJ, Weinstein MC. Does preventive care save money? Health economics and the presidential candidates. N Engl J Med. 2008;358:661-3.
4. Bonneux L, Barendregt JJ, Nusselder WJ, der Maas PJ. Preventing fatal diseases increases healthcare costs: cause elimination life table approach. BMJ. 1998;316:26-9.
5. Rasmussen SR, Prescott E, S rensen TIA, S, gaard J. The total lifetime health cost savings of smoking cessation to society. Eur J Public Health. 2005;15:601-6.
6. Elixhauser A. The costs of smoking and the cost effectiveness of smoking-cessation programs. J Public Health Policy. 1990;11:218-37.
7. Barendregt JJ, Bonneux L, van der Maas PJ. The health care costs of smoking. N Engl J Med. 1997;337:1052-7.
8. van Baal PH, Polder JJ, de Wit GA, et al. Lifetime medical costs of obesity: prevention no cure for increasing health expenditure. PLoS Med. 2008;5:e29.
Conflict of Interest:
None declared
-
National ECG screening is feasible.
Submit responseDear Editor,
I read with interest the editorial by Dr. Maron, however I take serious issue with many of his assertions and I am in fundamental disagreement with his conclusions.(1) I believe his efforts to relate the Italian system of ECG athlete screening to the U.S. are meaningfully flawed in fact and logic.
Granted, national ECG screening is a complex problem. But it is not insurmountable. I argue that it can be efficiently and successfully achieved with a "can do" problem-solving attitude. I offer these insights based on my first-person experience with screenings in a multi- county region in suburban Chicago. Since 2006 our program, Young Hearts for Life, has screened more than 44,000 high school students.
Dr. Maron contends there is a dramatic disparity in physician resources between Italy and the U.S. I suggest that this is a misinterpretation of the evidence. Of course the absolute number of athletes in this country is larger but in terms of percentage of population, U.S. athletic participation is statistically about half that of Italy, 5% in the U.S. vs.10% in Italy.(1) Moreover, the number of primary care physicians per capita is similar at 1/1000 in the U.S. vs. 0.9/1,000 in Italy. (2) Furthermore current AHA recommendations already expect all young adult athletes to be seen by a physician. (3)
Notably, Dr. Maron exaggerates the magnitude of national ECG screening in the U.S. He cites 75 million as the total population of American persons under the age of 18. In point of fact, testing is recommended for only those 12-25 yrs of age, which puts the total closer to 40 million, according to U.S. census data from 2005.
On the issue of SCD incidence, Dr. Maron's estimates are highly debatable. The <100 athlete deaths/year statistic he references is based not on a scientific registry like the Italian data but rather on a compilation of media reports, which can be a hit or miss approach. (5)
Dr. Maron's concern with excessively high rates of abnormal results does not reflect more contemporary standards of ECG interpretation that report these rates at 5% or less.(6) In our regional screening programs, we have been able to refine our testing with stratified screening to reduce the number of false positives. Our "abnormal" rate of 2.3% is certainly a number manageable by the medical community. (7) Moreover I do not understand the preoccupation with false positives when similar issues have not impeded testing in other areas of medicine (for example, mammography and nuclear stress testing). The approach of the medical community has always been that of pursuing improvement that reduces the false positive rate by refinement in techniques and experience. It should be no different with ECG screening.
As for economic feasibility issues, Dr. Maron mentioned that the American Heart Association's panel estimates a national program would initially cost about $2 billion a year to screen U.S. athletes. I believe this calculation is based on flawed assumptions related to the cost of performing ECGs. Clearly, ECGs done as a screening test can be done at a much lower cost than the $50 figure assumed in the AHA guideline's economic analysis. And even if it is proven to be correct, our government has spent vastly larger sums on medical issues of more suspect value. H1N1 and meningitis vaccination programs come to mind.
Our program strongly maintains that the focus on athletes-only screenings as defined in the AHA guidelines is too restrictive and deserves more consideration. Shouldn't we be concerned about SCD in all young adults and not just the deaths in a restrictively defined subgroup called athletes? The Italians have a more practical definition of athlete in their studies that more accurately reflects the typical active American high school student. Atkins' prospective study on the incidence of SCD in children from 11 U.S. and Canadian cities reported a death rate that is much higher than that claimed by Dr. Maron and would translate to over 2,500 SCDs in young adults annually in the U.S. (4)
Finally, we should not assume that our only choices are either mandated screening as in Italy or no screening at all. America is a country with a tradition of ingenuity. The medical community is at its best when it faces challenges by persistently working to find solutions. We did not abandon PTCA when the initial experience had a 5% emergency surgery rate in the hands of a small number of highly skilled operators. Ingenuity, skill, determination, cooperation with the device industry and physician education brought us to our current standard where emergency surgery is now rare and excellent PTCA service is delivered in most hospitals. Solutions to problems are not found by saying how we can't achieve a worthy goal but rather by asking how we can. Until we change this mindset we will continue to unnecessarily lose too many of our precious youth to potentially preventable causes of sudden death.
References
1. Barry J. Maron National Electrocardiography Screening for Competitive Athletes: Feasible in the United States? Ann Intern Med 2010 152:324-326.
2. OECD Health Data 2009; General practitioners and specialists in OECD countries 2007
3. Maron et al; Recommendations and Considerations Related to Preparticipation Screening for Cardiovascular Abnormalities in Competitive Athletes: 2007 Update Circulation. 2007;115:1643-1655.
4. Atkins et al; Epidemiology and Outcomes From Out-of-Hospital Cardiac Arrest in Children. The Resuscitation Outcomes Consortium Epistry- Cardiac Arrest Circulation. 2009;119:1484-1491.
5. Maron et al; Sudden Deaths in Young Competitive Athletes Analysis of 1866 Deaths in the United States, 1980-2006 Circulation. 2009;119:1085-1092.
6. Pelliccia et al; Prevalence of abnormal ECGs in a large, unselected population undergoing pre-participation cardiovascular screening Europ Heart J. 28: 2006-2010, 2007.
7. Nora et al; Preliminary Findings of ECG Screening in 9,125 Young Adults Oral Abstract Presentation; AHA annual scientific session, Circulation. 2007;116:II_845.
Conflict of Interest:
None declared
-
Duration and Timing Effects on Risks and Benefits of Menopausal Hormones
Submit responseWe applaud the efforts of Toh et al. (1) to delve deeper into the still controversial issue of inconsistencies in the cardiovascular disease (CVD) outcomes between the Women's Health Initiative (WHI) E P hormone trial and previous large observational studies. Current evidence supports the concept that both timing of menopausal hormone therapy (MHT) initiation and duration of treatment (2, 3) are important determinants of the risk:benefit ratio. The data presented by Toh et al., suggesting that the slightly higher CVD event risk in the first two years of treatment transitions to a lower risk after six or more years of use only in study drug-compliant WHI women initiating treatment less than ten years postmenopausally, are relevant to both of these questions. We regret that the authors focused on the statistically nonsignificant early increase in risk and discounted possible long-term benefits by stating that, "Because the typical duration of use of hormone therapy is short, most women contemplating estrogen plus progestin therapy for the relief of menopausal symptoms should not expect protection against CHD." On the contrary, before publication of the original WHI report in 2002 (4), MHT was frequently prescribed long-term to reduce both risks of osteoporotic fractures and CVD. Ironically, the WHI conclusion that MHT produced net harm was the primary basis for the change in the FDA official guidance and subsequent clinical practice discouraging long-term MHT use. This change owed precisely to the lack of distinction between risks and benefits for recently vs. remotely menopausal women in the initial report, an issue that WHI investigators and others performing follow-up analyses have attempted to address (5). Thus, it seems to us that an alternative interpretation of the new analysis by Toh et al. would be that recently menopausal women have little to fear in the early period of hormone treatment when incident CVD rates are low, and they may stand to benefit from long-term continuation of MHT into the later postmenopausal years when CVD risk is much higher. This may be seen as simply a matter of perspective (glass half-empty vs. glass half-full), but the health and lives of millions of women will depend on how the results of this and future research are interpreted by the medical community and the public.
References
1. Toh S, Hernandez-Diaz S, Logan R, Rossouw JE, Hernan MA. Coronary heart disease in postmenopausal recipients of estrogen plus progestin therapy: does the increased risk ever disappear? A randomized trial. Ann Intern Med. 2010;152(4):211-7.
2. Grodstein F, Manson JE, Stampfer MJ. Postmenopausal hormone use and secondary prevention of coronary events in the nurses' health study. a prospective, observational study. Ann Intern Med. 2001;135(1):1-8.
3. Chilvers CE, Knibb RC, Armstrong SJ, Woods KL, Logan RF. Post menopausal hormone replacement therapy and risk of acute myocardial infarction--a case control study of women in the East Midlands, UK. Eur Heart J. 2003;24(24):2197-205.
4. WHI Trials Group. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321-33.
5. Manson JE, Hsia J, Johnson KC, et al. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349:523-534.
Conflict of Interest:
Authors are co-PI's of the Kronos Early Estrogen Prevention Study (KEEPS) investigating cardiovascular effects of oral vs. transdermal hormone treatment in recently menopausal women
-
Vitamin D Systematic Reviews
Submit responseEditor: It is exceedingly disappointing to find, in the world's leading journal of internal medicine, two poorly conceived systematic reviews of vitamin D effects on the cardiovascular system (1, 2), accompanied by a largely supportive editorial (3), all three of which exhibit a limited awareness of current vitamin D physiology. For example, the review by Wang et al. (1) identifies a group of six prospective studies, only one of which used actual vitamin D (cholecalciferol). The others all used various 1- hydroxylated derivatives. Nor did the editorial, citing those six, pick up this critical distinction. Presumably the authors of the studies included were operating on the premise that, since calcitriol [1,25(OH)2D] is the ultimate, active form of the vitamin, it made sense to use that compound in their studies. That use, in hindsight, is understandable, even if now recognized to be inappropriate. The authors of the systematic reviews, however, should have been aware of current biology and therefore excluded them. The fact that the authors of the papers concerned used the term "vitamin D as a key word, or explicitly in their titles, simply highlights why individuals doing systematic reviews need to have up-to-date content knowledge of the subject they are reviewing. A very large body of literature, published over the past 10 years, makes clear that the non-calcium effects of vitamin D are autocrine (4), not endocrine, and that the 1- hydroxylated form of the vitamin is synthesized intracellularly by the target tissues concerned and is not derived from circulating calcitriol (5). Available evidence indicates that the concentration of calcitriol required to produce these non-calcium effects is higher than can safely be achieved through the mediation of serum calcitriol (5). Rather, serum 25(OH)D, present in thousand-fold greater concentration than calcitriol, provides the substrate for cells to manufacture as much calcitriol as they need, confined to the tissues concerned. But that works only so long as serum 25(OH)D levels are themselves adequate. Hence the critical importance of sufficient cholecalciferol input. One review hedges its conclusions with the qualifier "the dosages used which, as it turns out, were small. Both the editorial and Wang et al. speak of doses of 700-1000 IU/d as high. True, 700-800 IU is above the 1997 AI for vitamin D, but more than 95% of what is currently known about vitamin D has been published since those 1997 recommendations. It is now clear that outdoor summer workers commonly have serum 25(OH)D values between 120 and 200 nmol/L and that this may well be the primitive human level, as judged by values found in agricultural workers in the tropics (6). Both controlled dosing studies and extensive experience in recent years have established that serum 25(OH)D rises by about 0.6-1.0 nmol/L/ (or 1.5-2.5 nmol/L/100 IU/d) (7). Thus serum levels of 80 nmol/L require continuous inputs from all sources on the order of 4000 IU/d, and 100 nmol/L, 5000 IU/d, etc. Such doses are not only not high but physiological, as they occur in normal individuals under conditions approximating those experienced by our ancestors. Finally, the editorial raises a note of caution by way of comparison with trials of e.g, -carotene. While moving subjects from normal to high vitamin A levels may well produce harm, that is quite different from moving subjects from low to physiological levels of vitamin D. In brief, the systematic reviews were largely non-informative and the cautionary note struck by the editorial has essentially no basis in the evidence.
References
1. Wang L, Manson JE, Song Y, Sesso HD. Systematic review: Vitamin D and calcium supplementation in prevention of cardiovascular events. Ann Intern Med 2010;152:315-323.
2. Pittas AG, Chung M, Trikalinos T, Mitri J, Brendel M, Patel K, et al. Systematic review: Vitamin D and cardiometabolic outcomes. Ann Intern Med 2010;152:307-314.
3. Guallar E, Miller ER III, Ordovas JM, Stranges S. Vitamin D supplementation in the age of lost innocence. Ann Intern Med 2010;152:327- 329.
4. Holick MF. The vitamin D deficiency pandemic and consequences for nonskeletal health: mechanisms of action. Mol Aspects Med 2008;29:361-368.
5. Liu PT, Stenger S, Li H, Wenzel L, Tan BH, Krutzik S, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science 2006;311:1770-1773.
6. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D levels, and safety. Am J Clin Nutr 1999;69:842-856.
7. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25 -hydroxy-cholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr 2003;77:204-210.
Conflict of Interest:
None declared
-
Mammographic Screnning Perspective
Submit responseDear Sirs,
As an internist now practicing as a breast imaging radiologist, I offer the following perspective regarding your recent editorial (1).
The basic decision facing women regarding mammographic screening is whether to follow the recommendations of the USPSTF (biennial age 50-74) or the recommendations of American Cancer Society (ACS) and others (annual begin age 40) (2-4).
Using USPSTF data (3), women electing ACS guidelines would expect a 70.3% improvement in mortality reduction and a 71.6% improvement in life years gained compared to USPSTF guidelines. The mean mortality reduction was 39.5 % vs. 23.2% and for life years gained 189.3 vs. 110.3. These differences are large and equate to thousands fewer American breast cancer deaths each year if ACS guidelines are followed compared to USPSTF.
Especially relevant to women making decisions about their own heath, are the improvements in mortality reduction for women who actually get regular screening mammograms compared to those simply invited to screening in decades old RCTs. The USPSTF models show mortality reduction estimates for women electing annual mammograms to be as high as 54% (range 54-29%). These values do not account for improvements in mammographic technology such as digital mammography since RCTs were undertaken.
Given these benefits, women and physicians may be lead to believe the "harms" of screening mammography are large. But what are the actual quantified harms? Using USPSTF data (3), a woman who is annually screened would be expected to need to return for extra mammographic views or an ultrasound once every 13.3 years (2,250/30,000 screen yrs). These return visit "harms" can be reduced to 0 when women choose same visit screening and diagnostic interpretation currently offered at many breast imaging clinics. How about "unnecessary" biopsies? USPSTF data (3) shows an annually screened woman can expect an "unnecessary" benign biopsy once every 190 years of annual screening (158/30,000 screen -yrs). Most annually screened women will never be recommended for a benign (needle) biopsy.
Sophisticated labeling ("whipped up emotional anecdotes politics) used to identify those who disagree with USPSTF positions is the antithesis of evidence based medicine (1). Many Americans simply disagree with the USPSTF judgments and consider the incremental mortality reduction of annual screening beginning at age 40 to more than compensate for the known down sides of mammography. For women electing screening, annual mammography beginning at age 40 has again been shown to offer the best survival strategy.
References:
1. Editorial “ When Evidence Collides with Anecdote, Politics, and Emotion: Breast Cancer Screening. www.annals.org 2/12/2010.
2. Nelson HD, Tyne K, Naik A, Bougatsos C, Chan BK, Humphrey L. Screening for Breast Cancer: An Update for the U.S. Preventive Services Task Force. Ann Intern Med 2009;151:727-737.
3. Mandelblatt JS, Cronin KA, Bailey S, Berry DA, de Koning HJ, Draisma G, Huang H, Lee SJ, Munsell M, Plevritis SK, Ravdin P, Schechter CB, Sigal B, Stoto MA, Stout NK, van Ravsteyn NT, Venier J, Zelen M, Feuer EJ. Effects of Mammography Screening under Different Screening Schedules: Model Estimates of Potential Benefits and Harms. Ann Intern Med 2009;151:738- 747.
4. U.S. Preventive Services Task Force. Screening for Breast Cancer: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med 2009;151:716-726.
Conflict of Interest:
grants - NIH, GE Global Research
-
Comments on Opioid Pain Relievers & Overdose Potential - The Real Danger is Untreated/Undertreated Pain
Submit responseby Heather O. Grace
I am writing in response to Dr. A. Thomas McLellan's editorial online at: www.annals.org/content/152/2/123.full.
I hate having intractable pain, degenerative disc disease and neurological conditions that can prevent me from completing the simplest tasks. However, I can say with confidence that I am in no danger of overdose!
No true pain patient is at risk of overdose when managed via regular visits to a competent doctor. Under 2% of people taking opioids ever overdose. In fact, the study Dr. McLellan references had even lower rates of overdose--and those at risk appear to mainly be patients on low dose therapies.
It took me over five years of severe pain to find a doctor who would do anything and everything to help me. Unfortunately, I was at the end of my rope, suicidal, by that point.
That doctor saved my life. Our system is broken--not serving severe chronic pain patients like me. If Dr. McLellan is truly concerned about pain patients dying, then I ask:
What about the deaths of patients who don't get pain relief because the DEA restrictions have created a climate of fear among doctors? If you consider the deaths due to heart attack or stroke, in addition to those via suicide, the loss of life is far greater than the loss due to overdose.
Access to medication is a constant concern (fear, really) for pain patients. Patients often have a medication that works, then it is suddenly no longer available. The DEA limits access to many opioids. Worse still, the DEA also routinely accesses confidential prescription records of individual patients--without warrants--in order to target doctors treating high-dose opioid patients.
John Stossel, the famed journalist who was also treated for a serious pain condition, spoke on The O'Reilly Factor on Feb 23, and on his own show, Stossel, on Feb 25, 2010.
He said: "The Drug Enforcement Agency's war on drug dealers has led them to watch pain-management doctors like hawks. Drugs like Vicodin and OxyContin provide wonderful pain relief. But because they are also taken by 'recreational' drug users, doctors go to jail for prescribing quantities that the DEA considers 'inappropriate.' As a result, pain specialists are scared into underprescribing painkillers. Sick people suffer horrible pain needlessly." Source: www.creators.com/opinion/john-stossel/whose-body-is-it-2010-02-24.html
"The system is broken, and patients are suffering," said Claudia Schlosberg, from the American Society of Consultant Pharmacists. "Law enforcement concern has to be compatible with meeting patients' needs. Right now it's not." Source: www.painreliefnetwork.org/page/2/
And there are serious health implications: Dr. Forest Tennant, a founder of the American Society of Addiction Medicine has identified Cardiac Adrenal Pain Syndrome: "Severe pain is well-known to stimulate the cardiac and adrenal systems...The tachycardia and hypertension is caused by pain's over-stimulation of the nervous system. It's the root cause of cardiac and adrenal complications." Source: www.healthcentral.com/chronic-pain/c/3388/69308/information
Treating severe pain patients is not the mystery many people might think it is. Doctors can use objective scales to diagnose patients: blood pressure/pulse, visible inspection, MRIs/CAT scans and bloodwork.
If Dr. McLellan wants to truly help prevent deaths of pain patients, then there are 3 things I recommend the current administration focus its' efforts on:
1. Revise DEA mandate that creates prescription fears even for doctors who treat legitimate pain patients. Don't restrict access to any of the FDA-approved opioids.
2. Ensure pain treaters have access to appropriate documentation on HOW to objectively diagnose pain patients, such as the article written by Dr. Forest Tennant, who has treated pain patients for 25 years. Source: www.pain-topics.org/pdf/Tennant-PainSigns.pdf
3. Create a nationwide Pain Patient's Bill of Rights, similar to the one in California. Include the CA patient rights, plus the objective diagnostic criteria, as noted in #2, above.
By doing all three, a more comprehensive system of care will be in place, throughout the country. People are beginning to open their eyes to the truth about opioids. The Stossel Show is a wonderful step in the right direction. You, Dr. McLellan, as the Deputy Director of the Office of National Drug Control Policy, can be on the forefront of meaningful differences in the quality of care. Plus, with education comes less severe uncontrolled pain and, most certainly, less needless deaths.
I realize it is hard to understand our plight as someone on the outside of all this suffering. I didn't understand use of morphine or methadone until I was suffering and near my own demise. I urge you, Dr McLellan, to look at things from a fresh perspective, talking to pain patients and their doctors, to see what it is to live with pain. We take our opioids just as diabetics take insulin. There really is no difference.
Please, Dr. McLellan, as the #2 Drug Czar working under Director, R. Gil Kerlikowske, you have the power to make positive changes to the way pain patients are treated. I urge you to take a stand in the right direction--to help pain patients--we are counting on you!
Conflict of Interest:
1. I am a pain patient with severe neurologic injury, taking life-saving opioids since 2007. 2. Provide concomitant therapeutic items (nonprescription) via ThePainStore.com.
-
Some "Clarification " Warranted
Submit responseAfter reading the McLellan editorial, I did some further research on the man who holds the Deputy Director position with the Obama White House Office of National Drug Control Policy. We knew at the start that he held a PhD and not a medical degree, so we could judge the comments from his expertise in addiction studies and not from what's medically best for the body hit with the stress burden of pain. But I am more than a little disturbed that his full title was not disclosed at the time of the editorial's first printing. Mr. McLellan's full title is "Deputy Director for DEMAND REDUCTION." I believe that puts a much different spin on his opinions when it becomes known that his very job is to reduce the amount of users of opioids nationally. I hold to this philosophy as a caregiver for my wife who suffers from unrelenting pain when opioid treatment is not available to her: Pain MEDICINE is for Pain PATIENTS, just as Insulin is for Diabetics. If there is to be any reduction in demand, make it come from any other area but the one for which it was made.Conflict of Interest:
None declared
-
Has evidence become redundant in public health policy development?
Submit responseThe salt and health debate is so highly charged that hardly a comment can be made without first being prejudged in light of a potential conflict of interest. That being said, I must note that I am the Technical Director of the Salt Institute. I believe the recent article entitled. "Population Strategies to Decrease Sodium Intake and the Burden of Cardiovascular Disease" by Smith-Spangler et al (1) is important in many ways. It is the latest in a torrent of papers published since the beginning of 2010 advocating population-wide salt reduction, yet like all the others, provides no new clinical or scientific evidence to support that recommendation. It begs the question of whether we have gone beyond the need for actual scientific evidence when recommending public health policy.
Like the Bibbens-Domingo et al publication before it (2), this paper is a statistical computer modeling exercise that is based upon a faulty set of assumptions, none of which are supported by sound scientific or clinical evidence. Unfortunately, these models are often understood, interpreted and reported as if they were actual scientific evidence - they are not. Such models do not discriminate between what is true and what is false because they reflect a flawed view of reality. In real life, salt metabolism and physiology is far more complex then the simplistic assumption that a population-wide reduction in salt consumption will benefit everyone - as the actual scientific evidence has demonstrated.
The clinical evidence has shown the population response to salt reduction to be heterogeneous (3), (4), (5) with about 30% showing a slight reduction in blood pressure (BP), 20-25% showing an increase in blood pressure and the remaining population showing no effect at all. A goal of scientific experiment is to reduce confounding variables to a minimum, yet the data upon which the BP benefits assumption used in the models were not corrected for cohort bias, body mass index, genetics, exercise, diet and all the other variables that critically and collectively contribute to blood pressure. Equally important and as highlighted in the IQWIG review (6), because all studies were of extremely short duration, there is no satisfactory evidence to support the idea that the small drop in blood pressure for a limited portion of the population is sustainable over a long period and will not creep back up after acclimatization to the new level of salt consumption.
Instead, in the case of the Smith-Spengler paper, the authors referred to one Cochrane Collaboration Review paper supporting salt reduction (7), while ignoring the Cochrane Collaboration Review paper (8) and the recent IQWIG meta-review (6), both of which did not assign any significant health outcome benefits to population-wide reduction in salt consumption.
By definition, assumptions are highly subjective, but when the data upon which they are based does not reflect the available evidence, then questioning the assumptions and the model that flows from them is an obligation. Even if flawlessly executed, the best one can hope for from any model based on an slanted view of the evidence is a slanted model.
What is more troubling is the growing dependence upon such models as surrogates for evidence - even when evidence actually exists. The authors make several references to the Food Standards Agency (FSA) program on salt reduction in the UK. The FSA claim success in reducing per capita salt intakes. If this were indeed the case, then the impact of per capita salt reduction should have an immediate measurable effect in the UK. Were there cost savings apparent in the latest UK health budget? Has this population-wide drop in salt consumption positively manifested itself in UK health outcomes? Success cannot be measured on the basis of 24hrUrNa levels - that is neither the promise of the FSA program nor that of the Smith-Spangler model. Success is measured in measurable health outcomes and in dollars saved in health care. Surely, those figures are available, even if only in preliminary form? Unfortunately, metrics to measure success in these terms were never instituted in the UK, where the FSA apparently does not believe in analyzing the true impact of their program upon the population.
Over the last three decades, Finland reduced its salt consumption by a whopping 40% or more (9), yet when its cardiovascular performance over that time period is compared on the WHO Global Cardiovascular Infobase (10) with its neighboring countries and Canada and the United States, all countries that did not reduce their salt intakes, Finland fared poorly.
The urban legend is that salt reduction will benefit most if not all the population, put the popularity of an opinion doesn't make it correct. No poll of activists, physicians, scientists, journalists or consumers has anything to do with the process of science. Science is not a democratic process. I have often heard it said that well-established, widely recognized institutions believe in the urban legend, but we have seen many previous examples where the association of credibility with the stature of institutions has led us astray. We have seen the 1,500 year old belief in spontaneous generation, supported by all the great institutions of the time, trashed by Pasteur; the famous peers and institutions of Copernicus' time all considered the earth to be the center of the solar system; and, closer to home, not long ago, women's hormone replacement therapy was the policy supported by our great institutions.
The role of salt in human physiology is a matter of biology and cannot be trumped by statistics, models or opinions (my own included).
Public health policies must be based upon evidence. Where evidence does not exist, it should be sought and developed through appropriate clinical trials. If anything, this study by Smith-Spangler et al confirms the potential significance of a large trial to determine the health outcomes of population-wide salt reduction. It is time that all sides of the salt debate dispense with the rhetoric and join together in support of a large clinical trial upon which rational public policy can be based.
References
(1) Smith-Spangler, C.M., Juusola,J.L.,Enns, E.A.,Owens, D.K., and Garber,A.M., "Population Strategies to Decrease Sodium Intake and the Burden of Cardiovascular Disease," Ann of Internal Medicine, March 2, 2010, 152 (5).
(2) Bibbins-Domingo,K., Chertow, G.M., Coxon, P.G., Moran, A., Lightwood, J.M., Pletcher, M.J., and Goldman,L., "Projected Effect of Dietary Salt Reductions on Future Cardiovascular Disease," New Eng. J.Med., 2010, 362:590-599, Feb. 18.
(3) Luft, F.C., Rankin, L.I., Block, R. et al. "Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men," Circulation 1979; 60: 697-706.
(4) Miller, J.Z., Weinberger, M.H., Daugherty, S.A. et al. "Heterogeneity of blood pressure responses to dietary sodium restriction in normotensive adults," Journal of Chronic Diseases, 1987; 40: 245-250.
(5) Luft, F.C., McCarron, D.A., "Heterogeneity of hypertension: the diverse role of electrolyte intake," Annual Reviews of Medicine, 1991; 42: 347-355.
(6) Institut fur Qualitat und Wirtschaftlichkeit im Gesundheitswesen, "Benefit assessment of non-drug treatment strategies in patients with essential hypertension: reduction in salt intake," IQWiG Reports - Commission No. A05-21B, June 18, 2009 accessed at http:// www.iqwig.de/download/A05-21B_exec accessed on March 5, 2010.
(7) He FJ, MacGregor GA. "Effect of longer-term modest salt reduction on blood pressure," Cochrane Database Syst Rev. 2004:CD004937. [PMID: 15266549].
(8) Hooper L, Bartlett C, Davey Smith G, Ebrahim S. "Advice to reduce dietary salt for prevention of cardiovascular disease," Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD003656. DOI: 10.1002/14651858.CD003656.pub2.
(9) Karppanen, H. and Mervaala, E., "Sodium intake and hypertension," Progress in Cardiovascular Diseases, 49 (2), 59-75, 2006.
(10) http://www.cvdinfobase.ca/ch
Conflict of Interest:
Employee of Salt Institute