The author Rudyard Kipling once said: “Words are, of course, the most powerful drug used by mankind.” And, we know that different ways of expressing things can have an impact on patients. It is said that ‘people experience diabetes and the language of diabetes in context.’ This goes for many acute and chronic conditions. We are moving more and more into the realm of patient-centered care, with the result being that we are (and should be) viewing patients more as individuals than in bygone days when patients in hospitals were often referred to by their disease…”the heart failure in 3B’ or the ‘lupus nephritis in 12A’. And while that has happened less and less over the years, there are still many communications with and about patients that are problematic. We often hear about what to do when patients ‘fail on metformin’, or during an office visit their diabetes is labeled as ‘uncontrolled.’ These labels of failure and lack of control when shared with or in front of a patient can have a lasting impact on their attitude and/or feelings of self-efficacy. A number of diabetes related organizations addressed the language of diabetes (1-3). Patients are decisionmakers in many medical interactions, and how the decision is framed can have a huge impact on those decisions. The words used can trigger biases, heuristics and affect the direction of therapy in nearly all medical decisions patients make (4). Community based Pharmacists continue to shift in their roles from dispensing to patient education and counseling. As community-based pharmacists and hospital or clinic-based pharmacists expand their education and counseling roles to increasingly involve, medication reconciliation, and even home visits the words used in various situations make a difference (5). This is true, of course for pharmacists practicing in the clinical environment as patient encounters related to drugs (MTM, Med Reconciliation, TCM, etc) are an ever-increasing part of the pharmacists role in clinics, hospitals and medical offices as well. Patient-centered communications or communications about patients should avoid labels either as a noun (eg “are you diabetic”) or an adjective (“that’s a diabetic foot ulcer”), should avoid designations related to control either as a noun or verb (“he has poor glucose control”). Communications of should avoid imperatives (“you really must take this medication each morning”), and should avoid terms like “non-compliant” or “non-adherent” (1). While these terms are applied to diabetes patients in these examples it is easy to see how they can translate to other conditions. In a recent study (5) that looked at home visits as a venue for patient-pharmacist communication, the most discussed topics aligned with the challenges found in other studies such as patients’ lack of knowledge about their medications and medication regimens. These discussions are potential entrees into the use of motivational interviewing as a tool to enhance patients’ motivation…key to many chronic conditions including diabetes [shameless plug: Motivational Interviewing in Diabetes Care. Steinberg MP & Miller WR. Available in the ACCP Bookstore]. Changing our words is hard, but being more conscious of how we speak to and about patients is vital to patient-centered care. Let’s all commit to making a conscious effort to observe the language we use and change it where we need to!

1) The Use of Language in Diabetes Care and Education. Dickinson J, et al Diabetes Care 2017;40:1790-1799

2) International Diabetes Federation campaign on the language around diabetes. https://www.idf.org/our-activities/advocacy-awareness/campaigns/language.html (accessed 12/12/18)

3) Diabetes Australia position statement: A new language for diabetes: improving communications with and about people with diabetes. Speight J, et al. Diabetes Research and Clinical Practice 2012;97:425–431

4) Cognitive biases and heuristics in medical decision making: a critical review using a systematic search strategy. Blumenthal-Barby JS, Krieger H. Medical Decision Making 2015;35:539-557

5) Patient‑pharmacist communication during a post‑discharge pharmacist home visit Ensing HT, et al. International Journal of Clinical Pharmacy 2018;40:712-720


How Sweet it Ain’t

Ah, it’s that time of year again. Turkeys getting stuffed, people getting stuffed and “leave room for dessert.” We love our sweets, and over time our sweet tooth has increased to where the average American eats 15-20 grams of sugar a day, primarily as sweet snacks or sugar sweetened beverages (Carbonated Soft Drinks -CSDs). (1) When we were young we worried about getting cavities, as we got older we worried about getting fat, but we still increased our sugar intake as we aged, and overall as our society aged. Over the years, children and adolescents increased their consumption of sugar sweetened beverages as more of them became available and more readily available in the ubiquitous ‘soda machines’. (2) Of course, ‘sugars’ are of different types, and how the body metabolizes the sugar in fruit and milk differs from how it metabolizes the refined sugar added to processed foods. For the sake of this discussion, ‘sugar’ (sucrose) is refined from sugar cane (to remove the molasses) or a sugar-like sweetener (High Fructose Corn Syrup -HFCS)produced as starch in corn is digested with heat and enzymes to make corn syrup. This process is very involved, requires heat, acid, multiple enzymes and a small amount of mercuric chloride. (3) The sweet syrup still contains some undigested oligosaccharides as well as 5-hydroxymethyl-2-furfural (HMF) which is a known toxin. HMF contents in both sucrose and HFCS are very high (406.6-2121.3 mg/kg for corn syrup and 109.2-893.1 mg/kg for cane syrup), which arouses concern about food safety of these products. (4) In addition, analysis of carbonated soft drinks (CSD) has shown significant degradation products of sugar components, namely -dicarbonyl compounds (5) which most of us associate with diabetes. There is clear evidence that dicarbonyl stress is a contributing mediator of obesity and vascular complications of diabetes. (6,7) While sucrose contains glucose and fructose, it seems that spiking additional fructose (as in HFCS) may not be a good idea since it has been associated with fatty liver and other biochemical changes. (8) We also know, that in many common CSDs there is even more fructose than you might believe from the use of HFCS as a sweetener (as high as 65%). (9) So now we know that the ‘sweetness’ we seek, may have some downsides, but is this new? It turns out that some of the issues uncovered with sugar experiments in rodents were somehow never fully completed in experiments or published. A recent article in JAMA Internal Medicine exposes a 1960s study, which suggests a link between a high-sugar diet and high blood cholesterol levels and cancer in rats, was sponsored by the sugar industry, and when initial findings were presented to the sponsor, the funding disappeared. (10). A more recent article from the same authors suggested that the Sugar Research Foundation sponsored a research program that successfully cast doubt about the health hazards of a high-sugar diet and rather promoted fat “as the dietary culprit” in health concerns such as heart disease. (11) So, there you have it! That is part of the reason the new dietary guidelines call for reducing sugar intake roughly in half. (12) Coca-Cola anyone?



2) Sugar sweetened Beverage Consumption Among U.S. Youth 2011-2014. Rosinger A, Herrick K, Gahche J, Park S. National Center for Health Statistics Data Brief No. 271, January 2017

3) High Fructose Corn Syrup

4) In house validation fro direct determination of 5-hydrosymethyl-2-furfural in corn and cane syrups samples by HPLC-UV. deAndrade JK, Komatsu E, Perreault H, Torres YR, daRosa MR, Felsner ML. Food Chem. 2016;190:481-486

5) Analysis of sugar degradation products with -dicarbonyl structure in carbonated soft drinks by UHPLC-DAD-MS/MS. Gensberger S, Glomb MA, Pischetsrieder M. J. Agri. Food Chem. 2013;61:10238-10245

6) Post-Glucose Load Plasma α-Dicarbonyl Concentrations Are Increased in Individuals With Impaired Glucose Metabolism and Type 2 Diabetes: The CODAM Study. Maessen DE, Hanssen NM, Scheijen JL, van der Kallen CJ, van Greevenbroek MM, Stehouwer CD, Schalkwijk CG. Diabetes Care. 2015;38:913-20

7) Dicarbonyls and glyoxalase in disease mechanisms and clinical therapeutics. Rabbani N, Xue M, Thornalley PJ. Glycoconj J. 2016;33:513-25.

8) Added fructose as a principal driver of non-alcoholic fatty liver disease: a public health crisis. DiNicolantonio JJ, Subramonian AM, O’Keefe JA. Open Heart. 2017; 4(2): e000631

9) Sugar Context of Popular Sweetened Beverages Based on Objective Laboratory Analysis: Focus on Fructose Content. Ventura EE, Davis JN, Goran MI. Obesity 2010;19:868-874

10)Sugar Industry and Coronary Heart Disease research: A historical analysis of internal industry documents. Kearns CE, Schmidt LA, Glantz SA. JAMA Intern. Med. 2016;176:1680-1685

11) Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents. Kearns CE, Appolonio D, Glantz SA. PLoS Biol. 2017;15:e2003460

12) Dietary Guidelines for Americans: 2015-2020
https://health.gov/dietaryguidelines/2015/guidelines/ (Accessed 11/25/17)

Single Payer Healthcare: Case study in running out of The People’s money

Currently there is significant and contentious debate about providing and paying for healthcare in America. In 2010, the Affordable Care Act (ACA) was passed by Congress and included a dozen different new taxes, a specific cadre of policy designs, and mandates for employer participation as well as mandates for individuals to carry insurance. Penalties went along with the mandates, of course. A full discussion of the ACA is beyond the scope of this blog, but suffice it to say that a major issue was how to pay for the expansion of healthcare services. Insurance companies signed up to provide healthcare policies to many individuals, Medicaid rolls were expanded in many states, and a unique provision was made to ‘bail out’ insurance companies if they sustained significant losses.

In short, with its continued funding of Medicare, and its role in partially funding Medicaid and [through bailouts] insurance companies, the extensive role of the federal government makes the United States almost a ‘pseudo’ single payer system with many of the provisions found in other single payer systems (SPSs).

While various factions continue to argue about the future of the ACA, and whether or not it was designed to devolve into a SPS, it would be prudent to look at well-established SPSs to see if there are lessons to be learned. The National Health Service (NHS) in the United Kingdom is a classic and longstanding example of a SPS. The NHS has separate bodies to handle the separate countries in the system. England, Wales, Ireland and Scotland each have separate, very complex organizational systems (1).

From the development of the NHS until now, the evolution of the system in England has devolved to decision-making bodies called Clinical Commissioning Groups, which are regional groups of general practitioners, nurses and consultants that plan and commission the best services for their local patients and population, and collectively have a fiduciary responsibility to the NHS in doing so. (1,2). Over the years, the National Institute for Health and Care Excellence (NICE) has evaluated new therapies and technologies to see if they are worthy to be reimbursed by the NHS. (3)

NICE is not known for readily adopting new medications and technologies. It withdrew NHS funding for newer and more expensive modalities that could potentially impact over 20,000 cancer patients, and more recently rationed treatments for Hepatitis C treatments (4,5,6,7)

No coverage for some products or rationing of others is just the tip of the iceberg in England. Surgery for cataracts is not permitted until the patient is nearly blind (x), knee and hip replacements are denied until “pain is so severe that it interferes with your quality of life and sleep….everyday tasks, such as shopping or getting out of the bath, are difficult or impossible.”(8, 9) And most recently, the “most severe [rationing] ever” by NHS, already adopted by several Clinical Commissioning Groups, is the ban of obese patients and smokers from ‘routine’ surgery. (10)

In addition to these specific issues, there is a movement within the NHS/NICE system to establish a new (lower) financial cap for costs per Quality Adjusted Life Year (QALY) as well as a potentially not approving any treatment that will cost the system more than 20 million pounds during the first three years. (10)

Rationing is the unseemly underbelly of Single Payer healthcare, and when discussed in abstract terms tends to lose its true meaning for the individual. If it is your mothers pain awaiting a new hip, your grandmothers inability to read her romance novels, or even your fathers heart attack while awaiting surgery because he is overweight or some other of the myriad possibilities these very real possibilities need to be discussed openly in light of what is going on with the NHS .

Despite these measures, the NHS is still several billions of dollars in the hole. Clearly these draconian measures are an attempt at slowing the rising healthcare debt, yet they haven’t cut any of the huge bureaucracy that adds to these costs. (12) Think the US government can do a better job? I have a bridge I’d like to sell you…

1. The organisation of the NHS in the UK: comparing structures in the four countries. Doheny S., National Assembly for Wales – Research Service. May 2015. http://www.assemblywales.org/research

2. The NHS in England

3. NHS Commissioning https://www.england.nhs.uk/commissioning/

4. National Institute for Health and Care Excellence https://www.nice.org.uk

5. Betrayal of 20,000 cancer patients: Rationing body rejects ten drugs (allowed in Europe) that could have extended lives

6. 25 cancer drugs to be denied on NHS http://www.telegraph.co.uk/news/politics/11340860/25-cancer-drugs-to-be-denied-on-NHS.html

7. NHS ‘abandoning’ thousands by rationing hepatitis C drugs https://www.theguardian.com/society/2016/jul/28/nhs-abandoning-thousands-by-rationing-hepatitis-c-drugs

8. Thousands of elderly are losing their sight as NHS rations cataract surgery

9. Pain-level rationing of hip and knee surgery due to cash crisis, admits NHS

10. Obese patients and smokers banned from routine surgery in ‘most severe ever’ rationing in the NHS

11. Daniel Zeichner MP: Proposed changes to NICE & NHS England must not be implemented without a real debate

12. Perspectives on the European Health Care Systems: Some Lessons for America http://www.heritage.org/health-care-reform/report/perspectives-the-european-health-care-systems-some-lessons-america

The Rodney Dangerfield of Cardiovascular Risk Factors in Diabetes

Some of you may remember the great comedian Rodney Dangerfield who passed away in 2004. While some may remember his roles in Caddy Shack or Back to School (my favorite), he was best known for his catchphrase “I don’t get no respect” which was the basis for many comedy monologues.

When we speak of cardiovascular risk in diabetes, we invoke cholesterol, chronic hyperglycemia, reactive oxygen species (ROS), AGE’s, the presence of kidney disease and perhaps others. But almost no one talks about, measures, or attempts to treat one risk factor that is well recognized and treatable (or at least the effects of it seem to be). Have you guessed it yet?

Haptoglobin (Hp) was first described in 1938. It is an α2-sialoglycoprotein coming mainly from hepatocytes in response to the secretion of cytokines such as IL-6, IL-1 and TNF. Haptoglobin is a tetrameric protein that structurally resembles immunoglobulins because it has two light chains (α) and two heavy chains (β) covalently bound to each other by disulfide bridges (S-S). Its main function is to rapidly bind free hemoglobin from intravascular hemolysis to keep it from oxidatively damaging the vascular endothelium. Although present in all vertebrates, in humans Hp is characterized by molecular heterogeneity caused by genetic polymorphism. In the 1940s and 1950s structural heterogeneity was establish when alleles of different structures and lengths were identified, categorized as Hp 1-1, Hp 2-1, and Hp2-2. While these variants can be found in patients without diabetes, much of the work on their role as risk factors has been done in the context of diabetes (both type 1 and type 2). Biologic functions of Hp include prevention of renal damage from intravascular hemolysis, protection against ‘toxic radicals’, and sparing of nitric oxide when unbound to hemoglobin. It has also been found to have a variety of different effects comprising an immune-modulating action. All of these effects seem to differ with the haptoglobin phenotype, and in general a protective role is seen in patients with the Hp 1-1 variant, and a lack of protective effect or more pathological role is seen with the Hp 2-2 variant. Approximately 40% of patients with diabetes carry the Haptoglobin 2-2 gene variant (1)

Increased oxidative stress in diabetic patients results from oxidation of glucose and the modification of low-density lipoproteins (LDL). These changes may stimulate the production of inflammatory cytokines that have been implicated in the morphological and pathological changes found in macrovascular and microvascular complications, and different degrees of susceptibility to the development of vascular problems have been observed in studies of the antioxidant properties of Hp. In diabetic patients, those with Hp 1-1 show better protection against complications than Hp 2-1 and Hp 2-2 individuals. The Hp 2-2 phenotype has been found more frequently in people developing type 2 diabetes (2). Hp 2-2 has been shown to be a major risk factor in diabetic vascular disease (3), an increased risk of Coronary Heart Disease (4) an increased cardiovascular mortality in type 1 diabetes (5), an increased risk of renal function decline (6), an increased risk of death following stroke (7), retinopathy (8) and many other risks of complications in people with diabetes.

Also, as many of you know, both type 1 and type 2 diabetes are associated with the so called ‘leaky gut’. In type 1 diabetes various antigens are presented to the maturing gut which can stimulate the development of activated T-cells which, over time, destroy pancreatic beta cells. In type 2 diabetes, the ‘leaky gut’ allows lipopolysaccharides into the circulation, releasing cytokines and adipokines causing inflammation, insulin resistance and eventually diabetes with loss of beta cell mass due to glucose and lipid toxicity. A major factor associated with ‘leaky gut’ is zonulin, discovered in 2000 by Fasano. Zonulin is pre-haptoglobin-2. (9) It is fascinating that the haptoglobin 2 allele (especially in those individuals who are homozygous [hp 2-2] would confer risk of diabetes, and risk within diabetes likely due to its role in gut permeability and ongoing inflammation…

The risk associated with the presence of the Hp 2-2 genotype can be mitigated with vitamin E treatment to a striking degree. While vitamin E has not been shown to affect surrogates of risk in individuals with Hp 1-1, its effect is clear for those with Hp 2-2. The summary abstract below speaks for itself:

Clinical trial data from the HOPE, ICARE, and WHS studies is presented showing a pharmacogenomic interaction between the Hp genotype and vitamin E on the development of CVD. Specifically, in individuals with diabetes and the Hp2-2 genotype, vitamin E has been shown to be associated with an approximately 35% reduction in CVD. Cardioprotection by vitamin E in individuals with the Hp2-2 genotype appears to be mediated in part by an improvement in HDL functionality as demonstrated in three independent trials in both type 1 diabetes and type 2 diabetes. (10)

Despite this positive review, and others like it, over 300 articles in PubMed regarding haptoglobin in diabetes, and several presentations at ADA Annual meetings, the current ADA Standards of Medical Care don’t even mention haptoglobin.(11) It truly is the ‘Rodney Dangerfield of risk factors in diabetes’!

So my question to all of you is: With the clear role of haptoglobin genotype 2-2 in the risk of micro and macrovascular complications AND with the clear indication that treatment with Vitamin E can substantially reduce that risk…when was the last time you suggested obtaining a haptoglobin genotype for your patient with diabetes?

1) Changing the Face of Diabetic Care with Haptoglobin Genotype Selection and Vitamin E Nina S. Levy, Ph.D. and Andrew P. Levy, M.D., Ph.D. Rambam Maimonides Med J. 2011 Apr; 2(2): e0047

2) Shi X, et al. Haptoglobin 2-2 Genotype Is Associated with Increased Risk of Type 2 Diabetes Mellitus in Northern Chinese. Genetic Testing and Molecular Biomarkers 2012;16:563-568

3) Asleh R. and Levy AP. In vivo and in vitro studies establishing haptoglobin as a major susceptibility gene for diabetic vascular disease. Vascular Health and Risk Management 2005;1:19–28

4) Cahill LE, et al. The Risk of Coronary Heart Disease Associated With Glycosylated Hemoglobin of 6.5% or Greater Is Pronounced in the Haptoglobin 2-2 Genotype. Journal of the American College of Cardiology 2015;66:1791-9

5) Costacou T. and Orchard TJ. The Haptoglobin genotype predicts cardio-renal mortality in type 1 diabetes. J. Diabetes Complications. 2016;30:221-6

6) Costacou, T, et al. Haptoglobin Genotype and Renal Function Decline in Type 1 Diabetes. Diabetes 58:2904–2909, 2009

7) Ijas P, et al. Haptoglobin Hp2 Variant Promotes Premature Cardiovascular Death in Stroke Survivors. Stroke. 2017;48:1463-1469

8) Mukund R, et al. Haptoglobin2-2 phenotype is an additional risk factor of retinopathy in type 2 diabetes mellitus. Indian Journal of Human Genetic. 2013 Apr-Jun; 19(2): 154–8.

9) Fasano A., Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation. The American Journal of Pathology 2008;173:1243-1252

10) Hochberg I, et al. Interaction Between the Haptoglobin Genotype and Vitamin E on Cardiovascular Disease in Diabetes. Current Diabetes Reports 2017_online Jun 17

11) American Diabetes Association. Standards of Medical Care in Diabetes. Diabetes Care 2017; 40: Supplement 1

Metformin: Stepchild of Diabetes Care

The Merriam Webster definition of Stepchild is: “one that fails to receive proper care or attention”. We all know that metformin is pretty much a ‘given’ when we initiate care for diabetes based on nearly all type 2 diabetes treatment guidelines. We also know that metformin has been used effectively in diabetes prevention in patients with prediabetes with long-term effectiveness (1) and that this effect was dose and adherence related (2). Yet despite this, one survey suggested that only 36% of primary care providers prescribe metformin for patients with prediabetes at all (3). Combine this with the fact that we that there is a relationship of dose to the intensity of the hypoglycemic effect in diabetes in clinical trials (4) and that there is an association of glucose control in early treatment with ‘regression’ of pre-diabetes (5).

Guidelines are clear on the need to aggressively intensify therapy in patients with newly diagnosed type 2 diabetes to get to the A1C goal, but patients and physicians may feel less urgency early in the course of the disease, and ‘clinical inertia’ or lack of appreciation of the benefits of early control mean that many patients will be at increased risk of later cardiovascular complications from inadequate intensity of metformin dosing even in the few years subsequent to diagnosis (6). With more recent publications suggesting more flexibility in dosing metformin in patients with impaired renal function, we have even more reason to be comfortable with dosing this important medication (7). When was the last time you recommended metformin for a patient with prediabetes? When was the last time your reviewed your type 2 diabetes patients’ doses of metformin and pushed the envelope on dosing? Sounds like there’s a need to me!

1. Diabetes Prevention Program Research Group. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study Lancet. 2009 November 14; 374(9702): 1677

2. The Diabetes Prevention Program Research Group. Long-Term Safety, Tolerability, and Weight Loss Associated With Metformin in the Diabetes Prevention Program Outcomes Study. Diabetes Care 2012;35:731

3. Mainous AG, et al. Prediabetes Screening and Treatment in Diabetes
Prevention: The Impact of Physician Attitudes. J Am Board Fam Med 2016;29:663

4. Hirst JA, et al. Quantifying the Effect of Metformin Treatment and Dose on Glycemic Control. Diabetes Care 2012;35:446

5. Perreault L, et al. Effect of regression from prediabetes to normal glucose regulation on long-term reduction in diabetes risk: results from the Diabetes Prevention Program Outcomes Study. Lancet 2012;379:2243

6. Svensson E, et al. Early Glycemic Control and Magnitude of HbA1c Reduction
Predict Cardiovascular Events and Mortality: Population-Based Cohort Study of 24,752 Metformin Initiators. Diabetes Care 2017;40_online April 17

7. Inzucchi, SE, et al. Metformin in Patients With Type 2 Diabetes and Kidney Disease: A Systematic Review. JAMA. 2014;312:2668

Laugh and the World Laughs With You… …Snore and You Sleep Alone!


Of course, all snoring isn’t necessarily bad (unless you are a sleep partner), but most of us have heard about Obstructive Sleep Apnea (OSA) and have pre-conceived notions about risk factors, prevalence and outcomes. It is safe to say, however, that obstructive sleep apnea is the  ‘elephant in the room’ of cardiovascular risk.  It is true that most individuals who have OSA are overweight or obese, as that is the most common risk factor.  We know that the upper airway collapses in some people who have more tissue in the upper airway (tonsils, adenoids, tongue, palate and uvula).  When the OSA sleeper lays in his/her back, gravity is not in their favor as muscles relax during sleep.  When the sleeper attempts to breath in, the tissue obstructs resulting in snoring or gasping sounds and either a decrease in flow (hypopnea) or a cessation of airflow into the lungs (apnea).  The more often this happens the more likely the sleeper is to develop the consequences of chronic intermittent hypoxia.  OSA affects men about 2-3 times more commonly than women. An older study suggested that roughly 26% of a primary care population was potentially at risk of OSA, yet screen was very rare (1,2). If we look at one specific population, among an estimated 14 million US commercial drivers, 17–28% or 2.4 to 3.9 million are expected to have OSA (3).  In this population the effects of sleep deprivation secondary to OSA can be disastrous.

A much more insidious and common occurrence of OSA is in people with diabetes.  If we look at the type 2 diabetes patient population, the proportion at risk is significantly higher, due to the higher prevalence of older patients, and those with obesity. A recent review suggested the overall prevalence of diagnosed OSA in diabetic patients is approximately 71% based on the average data from five studies including a total number of nearly 1200 patients with type 2 diabetes (4). In 2008, the IDF Taskforce on Epidemiology and Prevention released a consensus statement that recommended a targeted approach to “screen individuals with type 2 diabetes and obesity for sleep disordered breathing (SDB)”. Briefly, the IDF recommended that healthcare professionals should consider the possibility of OSA in patients with type 2 diabetes and work in tandem with the local ‘sleep service’ to provide a clinically appropriate process of assessment, referral and intervention (5).

Several screening tests are available and include the Berlin Questionnaire, the STOP-BANG Questionnaire, and the Epworth Sleepiness Scale.  This last screener may be less effective than the others primarily due to the fact that daytime sleepiness, while common, is not universal, and appears less often in women and in individuals with heart failure. I prefer the “Canadian modifications” of the STOP-BANG screening tool (6).  Further diagnostic tests include the ‘gold standard’ sleep study (polysomnography), and within the last several years more and more products have been introduced that can be used as home diagnostic tests (7).

Studies have shown that cardiac remodeling occurs In OSA patients and that the changes are similar to predisposing changes for heart failure.  There is a significant increase in cardiovascular risk from the downstream consequences of chronic intermittent hypoxia from repeated episodes of apnea or hypopnea during sleep: atherosclerosis, cardiovascular disease including conditions such as myocardial infarction, congestive heart failure, cerebrovascular accident, resistant hypertension, and cardiac arrhythmia, as well as cognitive dysfunction, depression, poor glucose control in diabetes and motor vehicle accidents to name just some of them.

So, the prevalence in people with diabetes is high, and the outcomes of cardiovascular morbidity and mortality are well described.  Yet, the screening rate is abysmally low (in one study around 5%).  Routine screening of diabetes patients should lead many more people to a diagnostic procedure and to CPAP as the most effective treatment.  An old saying about how to eat an elephant is “one bite at a time”.  In the case of OSA, I would submit that some of these bites are up to you.  Pharmacists, involved in screening for OSA you ask (?) Of course! In this era of patient-centered care, how could a credible “diabetes practitioner” [yes, that’s you…] NOT screen patients for Obstructive Sleep Apnea!

  1. Hiestand DM, Britz P, Goldman M, Phillips B. Prevalence of symptoms and risk of sleep apnea in the US population: results from the National Sleep Foundation sleep in America 2005 poll. Chest 2006; 130:780 – 6.
  2. Grover M, et al.  Identifying Patients at Risk for Obstructive Sleep Apnea in a Primary Care Practice. J Am Board Fam Med 2011;24:152–160
  3. Kales S, and Straubel,M. Obstructive Sleep Apnea in North American Commercial Drivers. Industrial Health 2014, 52, 13–24
  4. Pamidi S and Tasali E . Obstructive Sleep Apnea And Diabetes-IsThereALink_Pamidi FrontNeurol_2012_v3_Article128
  5. Seetho I, et al. Obstructive sleep apnoea in diabetes – assessment and awareness. British Journal of Diabetes  2014(3):105-108
  6. http://www.stopbang.ca/osa/screening.php
  7. http://www.sleepreviewmag.com/2016/04/home-sleep-testing-hst-side-side-comparison-guide-april-2016/

Low hanging fruit

Hopefully everyone had a good holiday break, and maybe even the chance to curl up with a good book…or better, with the Federal Register!  Yes, you heard that right, the Federal appleRegister from 2016 has a number of positive developments in areas that are or will soon be ‘ripe’ for pharmacist intervention.  Notices and rulemaking for Medicare are published by CMS in the Federal Register. These notices are often accompanied by CMS’ responses to comments received on proposed rulemaking as well as some interesting background data.  So let’s look at what CMS considers important (i.e. what they are willing to pay for).  First, they recognize that medication misadventures often result in costly adverse effects including ED visits and hospitalizations.  They recognized MTM as needed (Ref 1), and when it was clear that it wasn’t being used as often as they wanted, they expanded the criteria to qualify more patients for MTM.  Realizing that medication misadventures were more likely during care transitions, CMS decided to reimburse for Transitional Care Management (CPT 99495, 99496) that included Medication Reconciliation. (Ref 2) With CMS’ announced aggressive plan to move to a system of more value-based reimbursement, new payment models were recently release as MACRA-MIPS (Ref 3), and medication reconciliation was a key component for the Merit-based Incentive Payment System (Ref 3, see pgs 77225 and 77230).

Switching gears to a key condition recognized by CMS, diabetes, it is clear that they value Diabetes Self Management Education (CPT G0108, G0109), and that they have increased the reimbursement for provision of that service. (4) Recently, CMS has announced that it will reimburse diabetes prevention in the proposed Medicare Diabetes Prevention Program (Ref 5, see section III.J)  The preliminary structure proposal is in Ref 5, and establishes how you can be prepared for the final rulemaking in 2017, and implementation in 2018.  In this document you can find links to the proposed standards and to the proposed curriculum developed by CDC. This is a must read if you want to be prepared to offer this service!

Finally, CMS has not only established reimbursement for Chronic Care Management (CPT 99490), but updated their rules with new codes for more complex patients who are involved in CCM (CPT 99487-99489) so that the reimbursement could better reflect the amount of work involved with CCM in highly complex patients (Ref 5, see section E.4 and Table 11).  As most of you already know, CCM can be provided to patients with 2 or more chronic diseases, and thus nearly all your patients with diabetes would qualify.

It is clear that medications, diabetes and chronic care are not only on the CMS’ radar screen, but they are addressing concerns related to expansion of these services as well as augmenting reimbursement.  Members of the ACCP Endocrine & Metabolism PRN are particularly well positioned to take advantage of many of these services!

At the 2016 ACCP Annual Meeting in October, a session discussing TCM and CCM was poorly attended, yet just down the hall a session on PCSK-9 inhibitors was packed.  While being the local guru on pharmacodynamics of PCSK-9 inhibitors may bring personal satisfaction, providing services such as TCM, CCM, DSMT, and soon MDPP brings revenue.  We are fighting for recognition as ‘providers’, and in any fight, you are lucky when the other guy telegraphs his moves.  CMS is not telegraphing, they are shouting it from the rooftops, yet only a few ACCP members are doing any of these services.  My bias is obvious, if you want to be recognized as ‘providers’, then start providing what your customer wants!

  1. The Medicare Prescription Drug, Improvement, and Modernization Act of 2003. Public Law 108-173. December 8, 2003. Available at: http://www.gpo.gov/fdsys/pkg/PLAW-108publ173/content-detail.html. [accessed 12/27/2016]
  2. https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/Transitional-Care-Management-Services-Fact-Sheet-ICN908628.pdf [accessed 12/27/2016]
  3. Medicare Program; Merit-Based Incentive Payment System (MIPS) and Alternative Payment Model (APM) Incentive Under the Physician Fee Schedule, and Criteria for Physician- Focused Payment Models. Federal Register / Vol. 81, No. 214 / Friday, November 4, 2016 / Rules and Regulations. https://www.federalregister.gov/documents/2016/11/04/2016-25240/medicare-program-merit-based-incentive-payment-system-mips-and-alternative-payment-model-apm [accessed 12/27/2016]
  4. Medicare Benefit Policy Manual Chapter 15 – Covered Medical and Other Health Services https://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/downloads/bp102c15.pdf [accessed 12/27/2016]
  5. Medicare Program; Revisions to Payment Policies Under the Physician Fee Schedule and Other Revisions to Part B for CY 2017; Medicare Advantage Bid Pricing Data Release; Medicare Advantage and Part D Medical Loss Ratio Data Release; Medicare Advantage Provider Network Requirements; Expansion of Medicare Diabetes Prevention Program Model; Medicare Shared Savings Program Requirements. https://www.federalregister.gov/documents/2016/11/15/2016-26668/medicare-program-revisions-to-payment-policies-under-the-physician-fee-schedule-and-other-revisions [accessed 12/27/2016]