The findings associating height and amputation risk come from a secondary analysis of the large Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. One of the lead investigators presented the findings at the American Heart Association’s annual scientific sessions in Orlando. He reported that height was an independent risk factor for amputation during the 5 years that nearly 10,000 type 2 diabetic patients were followed. (During the study period, there were 190 amputations among 115 patients.) Further, every 10 centimeters of increased height corresponded to a 60% increased risk of lower-limb amputation.

This is not the first report that height may play a role in amputation outcomes. A large cross-sectional study of more than 93,000 patients with type 1 or type 2 diabetes in Taiwan concluded the same thing: greater height independently predicted lower-limb amputations. This makes some sense, as taller patients are at a greater risk for peripheral sensory loss than shorter patients, owing to the longer nerve fibers. This, in turn, places taller patients at risk for delayed treatment of diabetic foot and lower extremity ulcers and infections. Still, the association between height and amputation risk is not well-defined.

The FIELD study also found that, in addition to height, prior skin ulcers, previous amputations, neuropathy, peripheral vascular disease, and age were important predictors of amputation risk. Many large-scale, well-publicized studies have shown that many of these risk factors can be controlled through intense glucose control, especially when diagnosis is made and therapy is initiated early in the course of diabetes. However, other similarly large and well-respected studies showed that intense glucose control did not alleviate all of the micro- and macrovascular risks associated with diabetes. Still, all of the research instructs that patients should institute lifestyle modifications and medical treatment as soon as possible for the best chance of long-term positive outcomes.

Patients with chronic diseases like diabetes are bombarded with calls to modify their risk factors: stop smoking, lose weight, get more exercise, lower your cholesterol, or eat a healthier diet. Now, they are told that one significant predictor of serious outcomes is their height, something that is completely unmodifiable. While the researchers are proud to have found yet another group (tall people with diabetes) that need intense monitoring to promote early intervention and treatment, patients may be left wondering, “Is there anything I can really do?” No one can make him- or herself shorter, lifestyle modifications can only do so much, and everyone seems to fall in to one category or another that puts them at increased risk for something and calls for them to be at the front of the more-monitoring line. Maybe all anyone can really do is try to take care of the body he or she has been given and hope for the best.

References

Huysman E, Mathieu C. Diabetes and peripheral vascular disease. Acta Chir Belg. Oct 2009;109(5):587-594.

Tseng, C. (2006). Prevalence of lower-extremity amputation among patients with diabetes mellitus: Is height a factor? Canadian Medical Association Journal, 174 (3), 319-323 DOI: 10.1503/cmaj.050680

Rajamani, K., Colman, P., Li, L., Best, J., Voysey, M., D’Emden, M., Laakso, M., Baker, J., & Keech, A. (2009). Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial The Lancet, 373 (9677), 1780-1788 DOI: 10.1016/S0140-6736(09)60698-X

Rajamani K, Li LP, Kesaniemi YA, et al. Astract 1040: Lower-Limb Amputation in Patients With Type 2 Diabetes Mellitus: Factors Predicting Risk in the FIELD study. Circulation. November 2009;120:S431.

The authors of the JAMA study analyzed the performance of nearly 72,000 primary care physicians among more than 30,000 practices. More than 60% of the physicians were solo practitioners. The physicians were selected from the 2005 Medicare Part B 20% sample and the Healthcare Organization Services database. The researchers aimed to analyze the percentage of these primary care physicians who saw enough patients to detect a 10% difference between practices in 5 performance measures: average ambulatory Medicare spending, rate of mammography for women aged 66 to 69 years, rate of Hemoglobin A1C (HbA1C) testing for diabetics aged 66 to 75 years, rate of preventable hospitalizations, and 30-day readmission rate after discharge for congestive heart failure (CHF).

Overall, the physicians had a median Medicare caseload of 260 patients. Of these, 25 women were eligible for mammography, 30 diabetic patients were eligible for HbA1C testing, and 0 patients were hospitalized for CHF. Very few practices had a sufficient caseload to detect a 10% difference in performance, as measured by cost and quality outcomes. Less than 10% of small practices — those with less than 11 physicians — saw enough patients to accurately detect a difference in ambulatory costs or rate of mammography or HbA1C testing. Conversely, all of the large practices — those with more than 50 physicians — saw enough patients to precisely detect a difference in the same measures. However, none of the practices saw enough patients to detect a 10% difference in preventable hospitalizations or CHF readmission outcomes.

Payment of physicians is believed to influence their clinical practice. Several strategies are being discussed to provide payment or reimbursement to physicians, but no new standard is yet established and the impact on clinical behavior and decision-making is unclear. Fee-for-service payment, the most widely used payment method currently, does not relate to outcome measures or physician performance. Capitation provides a set reimbursement per patient and makes the physician ultimately responsible for costs. Payment with a direct salary does not take into account number of patients, quality of care, or cost, while pay-for-performance programs allocate payment based on patient results. Most of these scenarios require a measurement of healthcare quality and outcomes to guarantee fair and adequate payment. If physicians are not seeing enough patients to accurately measure quality outcomes, how can physician payment be determined? How can we pay for something that we cannot measure?

Many people argue that physicians already have caseloads that are too large, and those caseloads will likely get larger in the years to come.  This may provide enough data to evaluate outcome measures, but will the results be favorable? Will more patients lead to lower quality healthcare? Can quality ever be measured accurately across all patient populations, payment providers, and physicians?  With the changing landscape of healthcare, the wisdom of the different payment methods and the methods to measure performance need to be considered.

References

Tu K, Cauch-Dudek K, Chen Z. Comparison of primary care physician payment models in the management of hypertension. Can Fam Physician. Jul 2009;55(7):719-727.

Gosden T, Forland F, Kristiansen IS, Sutton M, Leese B, Giuffrida A, Sergison M, & Pedersen L (2000). Capitation, salary, fee-for-service and mixed systems of payment: effects on the behaviour of primary care physicians. Cochrane database of systematic reviews (Online) (3) PMID: 10908531

Landon, B., O’Malley, A., & Keegan, T. (2009). Can Choice of the Sample Population Affect Perceived Performance: Implications for Performance Assessment Journal of General Internal Medicine DOI: 10.1007/s11606-009-1153-z

Gosden, T., Forland, F., Kristiansen, I., Sutton, M., Leese, B., Giuffrida, A., Sergison, M., & Pedersen, L. (2001). Impact of payment method on behaviour of primary care physicians: a systematic review Journal of Health Services Research and Policy, 6 (1), 44-55 DOI: 10.1258/1355819011927198

Nyweide DJ, Weeks WB, Gottlieb DJ, Casalino LP, Fisher ES. Relationship of primary care physicians’ patient caseload with measurement of quality and cost performance. Jama. Dec 9 2009;302(22):2444-2450.

Satin DJ, Miles J. Performance-based bundled payments: potential benefits and burdens. Minn Med. Oct 2009;92(10):33-35.

Without telomeres, chromosomes are damaged each time they replicate and divide. Each replication would lead to shorter and shorter DNA, eroding the genetic material and damaging the chromosome. However, telomeres protect the end of the chromosome, allowing the entire length to be replicated, without losing precious genetic codes. Telomeres contain a unique, repeated, DNA sequence that functions like a little cap on the end of each chromosome. Telomeres are formed by an enzyme called telomerase. Telomerase extends the DNA of the telomere, thus providing even more protection for the delicate ends of the strands of DNA. Therefore, if telomerase activity is high, telomere length is maintained and chromosomes are protected and continue to live productive, healthy lives, as cells go. If, however, telomerase activity is low, the telomeres are shortened and the cells are not protected, leading to cellular aging and cell death. And more cell death leads to more overall aging, and reduced life expectancy.

Since the 1930s, scientists have known about the existence of telomeres, but only recently have they understood the role these structures may play in the course of natural aging or disease processes. Cancer cells, for instance, have increased telomerase activity, guaranteeing near-eternal life for cancer cells. Telomerase defects, on the other hand, lead to inherited diseases, such as types of anemia, and diseases of the skin and cardiovascular system, since cells age and die before they can sufficiently reproduce. Now that scientists understand the role of telomeres in natural aging, as well as disease, telomerase is a new target for therapeutic development. A telomerase antagonist was recently studied in human glioblastoma and revealed promising results. Also, numerous cardiovascular risk factors are associated with telomere length, exposing the possibility of protective therapies in the future.

Even before their role was completely understood, telomeres were markers of human aging and stress. To some extent, telomere length is genetically predetermined at birth. Telomerase activity and telomere length, however, are influenced by a variety of factors, including environmental exposures, oxidative stress, and, to some extent, lifestyle. The Nobel Laureates, who have spent their careers studying telomeres and telomerase activity, report that simply reducing stress can help to lengthen telomeres and delay cellular aging, prolonging overall life. Telomeres might be a more important indicator of longevity, equating to a biological age, rather than a chronological one. So, relax, lengthen those telomeres and enjoy a long life!

References

Bize, P., Criscuolo, F., Metcalfe, N., Nasir, L., & Monaghan, P. (2009). Telomere dynamics rather than age predict life expectancy in the wild Proceedings of the Royal Society B: Biological Sciences, 276 (1662), 1679-1683 DOI: 10.1098/rspb.2008.1817

Das, B., Saini, D., & Seshadri, M. (2009). Telomere Length in Human Adults and High Level Natural Background Radiation PLoS ONE, 4 (12) DOI: 10.1371/journal.pone.0008440

Huzen, J. (2010). The emerging role of telomere biology in cardiovascular disease Frontiers in Bioscience, 15 (1) DOI: 10.2741/3604

Marian, C., Cho, S., Mcellin, B., Maher, E., Hatanpaa, K., Madden, C., Mickey, B., Wright, W., Shay, J., & Bachoo, R. (2010). The Telomerase Antagonist, Imetelstat, Efficiently Targets Glioblastoma Tumor-Initiating Cells Leading to Decreased Proliferation and Tumor Growth Clinical Cancer Research, 16 (1), 154-163 DOI: 10.1158/1078-0432.CCR-09-2850

Nobel Assembly at Karolinska Institutet (15 October 2009). “The Nobel Assembly at Karolinska Institutet has today decided to award The Nobel Prize in Physiology or Medicine jointly to Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak for the discovery of ‘how chromosomes are protected by telomeres and the enzyme telomerase.’” Press release.

Recently, the United Kingdom’s General Medical Council (GMC) determined that several elements of the original publication “Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children,” authored by Dr. Andrew Wakefield, are incorrect. Specifically, the GMC found evidence that the authors did not receive the necessary ethical approval for the investigation and they misrepresented the children’s diseases. The GMC issued a startling reprimand that asserted Dr. Wakefield and colleagues showed a “callous disregard” for children and acted “dishonestly” when conducting the research. It turns out that Dr. Wakefield was being paid by a group of parents who believed their children had been harmed by the MMR vaccine. Dr. Wakefield insists that he was motivated by a genuine concern for the welfare of the children.

The original research involved 12 children ranging in age from 3 to 10 years. Eleven of them were boys. Parents of 8 of the children linked the MMR vaccine to the onset of behavioral symptoms associated with autism, psychosis, or encephalitis. The authors concluded that the exposure to the MMR vaccine could not be ruled out as a cause for developmental regression in previously normal children. In 2004, The Lancet issued a partial retraction of the research, but argued they were right to publish the research to promote new ideas and new ways of thinking. In doing so, they sparked a decade of intense controversy and a decline in vaccination rates around the developed world. Now, The Lancet goes further and fully retracts the paper from its published record. Hindsight has led them to rethink their original motives.

No one yet knows exactly what causes autism, or any of the related spectrum of disorders. There is strong evidence for a genetic link, but environmental exposure to toxins cannot be ruled out. New reports of exposure to known mutagens and environmental risk factors before conception appear to be related to an increased risk for autism. A new hypothesis claims that living in urban areas, at higher altitudes, or with high levels of precipitation may decrease sun exposure, increase risk for Vitamin D deficiency, and, therefore, increase the risk for autism. Until large-scale, ethically-compliant, scientifically-sound research in confirmed, the causes and implications of autism will never be known. Until then, everyone should take heed not to believe everything they read – even in prestigious medical journals.

References

Herbert MR (2010). Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders. Current opinion in neurology PMID: 20087183

Kinney, D., Barch, D., Chayka, B., Napoleon, S., & Munir, K. (2010). Environmental risk factors for autism: Do they help cause de novo genetic mutations that contribute to the disorder? Medical Hypotheses, 74 (1), 102-106 DOI: 10.1016/j.mehy.2009.07.052

WAKEFIELD, A., MURCH, S., ANTHONY, A., LINNELL, J., CASSON, D., MALIK, M., BERELOWITZ, M., DHILLON, A., THOMSON, M., & HARVEY, P. (1998). Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children The Lancet, 351 (9103), 637-641 DOI: 10.1016/S0140-6736(97)11096-0

Retraction – Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. The Lancet.

WAKEFIELD, A., MURCH, S., ANTHONY, A., LINNELL, J., CASSON, D., MALIK, M., BERELOWITZ, M., DHILLON, A., THOMSON, M., & HARVEY, P. (1998). Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children The Lancet, 351 (9103), 637-641 DOI: 10.1016/S0140-6736(97)11096-0

For decades, there has been an increased interest in and awareness of the need for physicians and the medical community to work more closely with journalists and the mass media to guarantee the accurate and appropriate dissemination of health information. Training programs for both physicians and journalists now include innovative curriculum to promote collaboration and build a mutual respect between the professions that, in the end, promotes public health and safety. Publishing or broadcasting clear, consistent and contemporary health and medical information to the general public is a shared responsibility of physicians and journalists. But, what happens when the physician and the journalist is the same person?

The advents of 24-hour news, numerous magazines and blogs galore have opened the flood gates for professionals who want to share their knowledge with the public. And gain a little fame in the process. The world does need health care professionals with better-than-average communication skills to share the latest research or medical news in layman’s terms. But, the world does not need physicians who have more experience holding a microphone than a scalpel. Case after case of physician-journalists helping Haitian victims were broadcast on television over the last few weeks, making the physician the story rather than the Haitians in need of help. One would hope that the physicians were simply overcome by their desire to help, and forgot that there were cameras rolling. But, a cynical eye would notice that every network seemed to “one-up” the others with broadcasts of “our doctor did this” and “our medical correspondent did that.” If the physicians really wanted to help the devastated population, they could easily travel to Haiti with a volunteer medical staff, rather than with a producer and a camera crew.  Plus, if viewers wanted to see surgery performed on television, they could watch any of a number of reality series that depict medical procedures.

The sensationalizing of the story is hardly the only downside to this type of reporting. What happens if there are complications from the treatment provided by the physician-journalists? What about patient privacy? What happens when every reporter decides to jump into the story? What happens to the just-the-facts reporting that the public needs?

The public increasingly turns to the media for health information, and inaccurate or inappropriate medical reporting damages public welfare, as well as perception and opinion about the health care community. All reporters — trained journalists and physicians-turned-correspondents alike — have the responsibility to remain objective and report facts of stories, be it medical information or news of death and destruction in crisis-stricken areas.

References

Anthony, S., Lozano-Calderon, S., & Ring, D. (2007). Stigmatization of Repetitive Hand Use in Newspaper Reports of Hand Illness HAND, 3 (1), 30-33 DOI: 10.1007/s11552-007-9052-4

Campbell, N., Heath, J., Bouknight, J., Rudd, K., & Pender, J. (2009). Speaking Out For Mental Health: Collaboration of Future Journalists and Psychiatrists Academic Psychiatry, 33 (2), 166-168 DOI: 10.1176/appi.ap.33.2.166

Catherine, N., Ko, J., & Barr, R. (2008). Getting the Word Out: Advice on Crying and Colic in Popular Parenting Magazines Journal of Developmental & Behavioral Pediatrics, 29 (6), 508-511 DOI: 10.1097/DBP.0b013e31818d0c0c

Strasser T, Gallagher J. The ethics of health communication. World Health Forum. 1994;15(2):175-177.

The study presents the results of the largest-scale clinical trial conducted with Ginkgo biloba, assessing more than 3000 adults aged 72 to 96 years. (The investigators have used the same population to investigate other aspects of Gingko treatment, with results published in several journals.) The current study focuses on the prevention of cognitive decline in older adults. The participants received a twice-daily dose of 120 mg of Ginkgo biloba or placebo. Over the 6-year follow-up period, the rate of decline of cognitive function, as assessed by standard cognitive and psychoneurological function exams, was calculated. Overall, there was no difference in the rate of cognitive decline between participants receiving Ginkgo biloba or placebo. These results did not change when modifying factors, such as age, sex, race, education, genetic variations, or baseline cognitive impairment, were considered.

This hardly seems like newsworthy information, given the plethora of studies that say the same thing. To date, there are no large-scale, definitive studies demonstrating that Ginkgo biloba has much of an effect on anything.  Most studies that do report benefits of Ginkgo biloba therapy are not comprehensive and obtained limited data regarding cognitive function. The results lend themselves to statistical misinterpretation and inappropriate extrapolation of the data.

Still, Ginkgo biloba sales are in the hundreds of millions of dollars worldwide every year. It is commonly used in European medicine to improve memory and treat neuronal disorders and improve brain metabolism. In the United States, it enjoys widespread use as a botanical dietary supplement. The current study should leave consumers asking, “Why?” Once again, Ginkgo biloba is verifiably ineffective for preventing a decline in cognitive function. Plus, as with many unregulated over-the-counter supplements, Ginkgo biloba places patients at increased risk for possible side effects and drug interactions.

Growing old gracefully and successfully is of paramount importance with an ever-older population. It is natural to strive for maintaining, and even enhancing, cognitive reserves. But, there is no evidence that proves Ginkgo biloba will help to achieve those goals. Clinicians and patients are better served by identifying and treating known conditions that may reduce brain capacity and cognitive function, including vascular risk factors, diabetes, and sleep disorders, and promote activities and lifestyles that build cognitive reserve.

… And we don’t want to have to tell you again!

References

Canis, M., Olzowy, B., Welz, C., Suckfüll, M., & Stelter, K. (2009). Simvastatin and Ginkgo biloba in the treatment of subacute tinnitus: a retrospective study of 94 patients American Journal of Otolaryngology DOI: 10.1016/j.amjoto.2009.09.004

Daffner KR. Promoting Successful Cognitive Aging: A Comprehensive Review. J Alzheimers Dis. Dec 14 2009.

Kaschel, R. (2009). Ginkgo biloba: specificity of neuropsychological improvement-a selective review in search of differential effects Human Psychopharmacology: Clinical and Experimental, 24 (5), 345-370 DOI: 10.1002/hup.1037

Leistner, E., & Drewke, C. (2010). Ginkgo biloba and Ginkgotoxin. Journal of Natural Products, 73 (1), 86-92 DOI: 10.1021/np9005019

Snitz, B., O’Meara, E., Carlson, M., Arnold, A., Ives, D., Rapp, S., Saxton, J., Lopez, O., Dunn, L., Sink, K., DeKosky, S., & , . (2009). Ginkgo biloba for Preventing Cognitive Decline in Older Adults: A Randomized Trial JAMA: The Journal of the American Medical Association, 302 (24), 2663-2670 DOI: 10.1001/jama.2009.1913

Many studies have shown similar associations between adult IQ and mortality, but the Swedish study is one of only a handful to link intelligence and cognitive performance at a young age — 10 years in this study — to decreased mortality in adulthood. Many similar studies have been inconclusive to date; the brain continues to develop and change in emotional and cognitive ability and performance until approximately 20 years of age, making early IQ tests somewhat difficult to interpret. However, the newest study published in the BMJ followed more than 1500 children for 65 years and found a significant association between high intelligence at age 10 and education attainment and decreased risk of all-cause mortality. Interestingly, this association was strongest in males, and high IQ was associated with decreased mortality, even after adjusting for education attainment and paternal education — 2 other indicators of mortality. Women, however, did not experience the same association. Women with an above average IQ actually had a higher risk of mortality, after adjusting for other factors, but only after age 60.

Noting the gender differences in the findings, the authors speculate that mortality cannot simply be explained by IQ, but involves the social and physical environment as well. Most other studies investigating a link between IQ and mortality have offered similar remarks. From a very early age, even before birth, parental education, socioeconomic status, and lifestyle choices influence the cognitive ability of children. For example, mothers with more education are more likely to breastfeed their children, and breast milk correlates significantly with total brain volume and high IQ scores.  Education and nutrition during the preschool years are also associated with increased IQ. Similarly, children with parents who were more involved in their education and social choices have a decreased risk of mortality in adulthood. To the same point, children with disengaged and uninvolved parents are more likely to engage in risky behavior and delinquency, which accounts for some of the association between increased risk of mortality and lower IQ.

Still, it is impossible to say that scoring well on an IQ test has a direct link to mortality risk. While high IQ is associated with decreased risk factors for early mortality and unhealthy lifestyle choices, including smoking, heavy alcohol consumption, and overweight and obesity, the association is weakened after adjusting for socioeconomic status. Still, increased physical fitness is linked to high IQ, and improving fitness leads to increased cognitive performance. Adults with high IQ are also less likely to experience depression, and have a significantly reduced risk of many diseases and health conditions. Further, as adults, those with lower IQ are more likely to die from injuries such as poisonings, fire, falls, drowning, and road injuries than those with higher IQ. Quite possibly, childhood IQ is not a cause, per se, of mortality, but a marker for social status and class later in life, which is an indicator of risk of death and illness. The socioeconomic inequalities in access to healthcare may explain a portion of the increased mortality among lower IQ adults.

Or, the association between high intelligence and decreased mortality could be real and causative. Is it another case of survival of the fittest? Is nature getting rid of those who swim in the shallow end of the proverbial gene pool? Probably not. While high IQ at an early age may be an indication of a strong, fit body to begin with, cognitive skills should be fostered and nourishing childhood environments should be promoted to encourage healthy behaviors and choices later in life.

References

Aberg, M., Pedersen, N., Toren, K., Svartengren, M., Backstrand, B., Johnsson, T., Cooper-Kuhn, C., Aberg, N., Nilsson, M., & Kuhn, H. (2009). Cardiovascular fitness is associated with cognition in young adulthood Proceedings of the National Academy of Sciences, 106 (49), 20906-20911 DOI: 10.1073/pnas.0905307106

Batty, G., Deary, I., & Macintyre, S. (2007). Childhood IQ in relation to risk factors for premature mortality in middle-aged persons: the Aberdeen Children of the 1950s study Journal of Epidemiology & Community Health, 61 (3), 241-247 DOI: 10.1136/jech.2006.048215

Batty, G., Gale, C., Tynelius, P., Deary, I., & Rasmussen, F. (2008). IQ in Early Adulthood, Socioeconomic Position, and Unintentional Injury Mortality by Middle Age: A Cohort Study of More Than 1 Million Swedish Men American Journal of Epidemiology, 169 (5), 606-615 DOI: 10.1093/aje/kwn381

Batty, G., Shipley, M., Mortensen, L., Boyle, S., Barefoot, J., Gronbaek, M., Gale, C., & Deary, I. (2008). IQ in late adolescence/early adulthood, risk factors in middle age and later all-cause mortality in men: the Vietnam Experience Study Journal of Epidemiology & Community Health, 62 (6), 522-531 DOI: 10.1136/jech.2007.064881

Batty, G., Wennerstad, K., Smith, G., Gunnell, D., Deary, I., Tynelius, P., & Rasmussen, F. (2009). IQ in Early Adulthood and Mortality By Middle Age Epidemiology, 20 (1), 100-109 DOI: 10.1097/EDE.0b013e31818ba076

Der, G., Batty, G., & Deary, I. (2009). The association between IQ in adolescence and a range of health outcomes at 40 in the 1979 US National Longitudinal Study of Youth Intelligence, 37 (6), 573-580 DOI: 10.1016/j.intell.2008.12.002

Hart, C. (2003). Childhood IQ, Social Class, Deprivation, and Their Relationships with Mortality and Morbidity Risk in Later Life: Prospective Observational Study Linking the Scottish Mental Survey 1932 and the Midspan Studies Psychosomatic Medicine, 65 (5), 877-883 DOI: 10.1097/01.PSY.0000088584.82822.86

Isaacs EB, Fischl BR, Quinn BT, Chong WK, Gadian DG, Lucas A. Impact of breast milk on IQ, brain size and white matter development. Pediatr Res. Dec 22 2009.

Gordon, A. (2008). Breastfeeding, Breast-Milk Feeding, Breast Feeding, and IQ: Unknown and Known Knowns Archives of General Psychiatry, 65 (12), 1457-1458 DOI: 10.1001/archpsyc.65.12.1457

Lager, A., Bremberg, S., & Vagero, D. (2009). The association of early IQ and education with mortality: 65 year longitudinal study in Malmo, Sweden BMJ, 339 (dec11 1) DOI: 10.1136/bmj.b5282

Approximately 13% of physician visits every year are for medically unexplained symptoms, and up to 25% of patients report such symptoms during physician visits. Often, patients report persistent physical symptoms, but no somatic origin can be found. Physicians may try to explore the psychological basis of the symptoms, but this is a frustrating and futile prospect that uses valuable time and resources with no satisfactory result for the patient.

Many hypochondriacal patients are taking their concerns to the Internet and making “Google” a diagnostic procedure. Researchers at Microsoft recently examined how people search for medical information on the Internet, and reported on its potential implications. The researchers reviewed logs of 515 individual’s health-related Web search experiences. Not surprisingly, one principal finding was that search engines have the potential to escalate medical concerns. The authors assert that the escalation is related to the amount of medical content viewed by searchers, the existence of escalatory terminology in the Web pages, and the searcher’s predisposition to escalate his or her anxiety versus seeking more sensible explanations for physical symptoms.

The Microsoft researchers also found that post-session anxiety lingers after escalations of medical concerns, often to an extent that interrupts other Web-related activities. The information obtained from the Web also influences people’s decisions about visiting a physician, diagnosing or treating ailments, or engaging in proactive health activities. One worrisome finding of the Microsoft study concluded that some users of search engines interpreted the ranking of the Web search results as the likelihood of the illness. The Web can ultimately be a dangerous place for people to seek advice, with no guidance on deciphering fact from fiction, and everything in between.

Not all who seek Web-based information will be misled, but the potential for the wrong information falling into the wrong hands is considerable. Patients should heed a “let the searcher beware” and always obtain sounds medical advice from a trained health care professional. Physicians, however, should be attentive to the needs of patients and maintain open lines of communication when considering all of a patient’s symptoms.

References

Kappen, T., & van Dulmen, S. (2008). General practitioners’ responses to the initial presentation of medically unexplained symptoms: a quantitative analysis BioPsychoSocial Medicine, 2 (1) DOI: 10.1186/1751-0759-2-22

Wick JY, Zanni GR. Hypochondria: the worried well. Consult Pharm. Mar 2008;23(3):192-194, 196-198, 207-198.

Peters, S., Rogers, A., Salmon, P., Gask, L., Dowrick, C., Towey, M., Clifford, R., & Morriss, R. (2008). What Do Patients Choose to Tell Their Doctors? Qualitative Analysis of Potential Barriers to Reattributing Medically Unexplained Symptoms Journal of General Internal Medicine, 24 (4), 443-449 DOI: 10.1007/s11606-008-0872-x

Salmon, P., Ring, A., Humphris, G., Davies, J., & Dowrick, C. (2009). Primary Care Consultations About Medically Unexplained Symptoms: How Do Patients Indicate What They Want? Journal of General Internal Medicine, 24 (4), 450-456 DOI: 10.1007/s11606-008-0898-0

White RW, Horvitz E. Cyberchondria: Studies of the Escalation of Medical Concerns in Web Search. Redmond, WA: Microsoft Research; November 2008.

The authors of the NEJM study forecasted life expectancy and quality-adjusted life expectancy for a representative 18-year old, assuming that current trends in obesity and smoking continue. In most of the scenarios examined, the negative effects of overweight and obesity outweighed the positive effects of a decline in the rates of smoking. The average 18-year old today would gain 0.31 years of life expectancy owing to the decline in smoking; at the same time, he will lose more than 1 year owing to the rise in overweight and obesity. Overall, the authors concluded that the average 18-year old today would lose 0.71 years of life, or 0.91 quality-adjusted years, by the year 2020. If all adults in the United States became nonsmokers of healthy weight by 2020, the life expectancy of the average 18-year old would increase by almost 4 years, or more than 5 quality-adjusted years.

The increase in overweight and obesity has increased dramatically in the last 30 years, but the prevalence differs among gender, race, and age cohorts. The prevalence of obesity is approximately 35% among white men, black men, and white women, but is 55% among black women. The mean age of obese men and women is also rising, to 49 years among white and 44 years among blacks. The population of the United States is gaining years and pounds, and the disability and health care burden associated with an aging obese population are significant.

Everyone knows smoking kills; nonsmokers live up to 10 years longer than smokers. However, smoking does not cause the disability that comes with overweight and obesity. While obesity does not lead to quite the same decrease in life expectancy — 6 to 7 years on average, the quality of the life is significantly decreased compared to people of healthy weight. Overweight and obese people will spend 3 to 5 years of their life with significant disability owing to obesity-related conditions and have reduced functioning in their activities of daily living.

Still, one study concluded that unhealthy living is unhealthy living, regardless of whether that living is related to smoking or obesity. People who make unhealthy lifestyle choices will have a lower life expectancy than healthy-living cohorts, even if they eliminate smoking and obesity. Other vices, as well as unmodifiable factors like race, gender, and age, contribute to life expectancy and quality of life.

Both smoking and obesity are unhealthy lifestyle choices and are risk factors for a large burden of disease. By the year 2020, smoking is expected to decline by 21%, but 45% of the population will be obese. Targeted medical and public health interventions to control the obesity epidemic are needed to reclaim the gains made in healthy living through smoking cessation and prevention programs.

References

Lubetkin, E., & Jia, H. (2009). Health-Related Quality of Life, Quality-Adjusted Life Years, and Quality-Adjusted Life Expectancy in New York City from 1995 to 2006 Journal of Urban Health, 86 (4), 551-561 DOI: 10.1007/s11524-009-9344-9

Stewart, S., Cutler, D., & Rosen, A. (2009). Forecasting the Effects of Obesity and Smoking on U.S. Life Expectancy New England Journal of Medicine, 361 (23), 2252-2260 DOI: 10.1056/NEJMsa0900459

Reuser, M., Bonneux, L., & Willekens, F. (2009). Smoking Kills, Obesity Disables: A Multistate Approach of the US Health and Retirement Survey Obesity, 17 (4), 783-789 DOI: 10.1038/oby.2008.640

Wang, Y., Colditz, G., & Kuntz, K. (2007). Forecasting the Obesity Epidemic in the Aging U.S. Population** Obesity, 15 (11), 2855-2865 DOI: 10.1038/oby.2007.339

van Baal, P., Hoogenveen, R., de Wit, G., & Boshuizen, H. (2006). Estimating health-adjusted life expectancy conditional on risk factors: results for smoking and obesity Population Health Metrics, 4 (1) DOI: 10.1186/1478-7954-4-14

Income inequality is measured by the Gini coefficient, a measure of income disparity within a population. The Gini coefficient ranges between 0 and 1, with 0 signifying complete income equality (everyone receives the same income) and 1 signifying complete inequality (one individual receives all the income). Most European countries have a Gini coefficient of approximately 0.3, while the United States has a Gini coefficient close to 0.4. The Gini coefficient of the entire world has been estimated at approximately 0.6.

The BMJ analysis systematically examined 9 cohort and 19 cross-sectional studies involving a total of more than 61 million subjects to describe the association between the Gini coefficient and mortality and self-reported health status. Overall, the investigators concluded that people living in regions with high income inequality (a higher Gini coefficient) had an increased risk of premature death, independent of their individual socioeconomic status, age, or gender. The increase mortality risk amounted to 8% per 0.05 increase in the Gini coefficient. There were stronger associations between income inequality and poor health in samples with a higher Gini coefficient, studies conducted after 1990, and studies with a follow-up duration of more than 7 years.

This study also seems to confirm a theoretical “threshold effect” above which the disparities in health outcomes are seen. By the authors’ estimation, the Gini must be above 0.3 before the adverse health effects are apparent. If the associations and estimations are true, the authors calculate that 1.5 million deaths could be avoided in 30 developed countries if the Gini coefficients were leveled to 0.3 or below. However, very little data is available on income inequality or health outcomes in developing nations, which would likely adjust the findings.

Income inequality is believed to damage health outcomes in two ways. First, an unequal society usually involves a considerable portion of the population that is living in poverty, and many studies have determined that poverty is bad for overall health outcomes. The greater the income inequality, the more impoverished citizens, and the more who are in poor health. The second, less easily defined, explanation is that income inequality is also detrimental to the more affluent members of society, since these citizens experience psychosocial stress from the inequality and loss of social cohesion. The public health burdens of the second situation are obviously broader, but much less quantifiable, and more controversial.

It is nearly impossible to confirm a causal relationship between income inequality and health outcomes. And no one supports the redistribution of income just to improve health outcomes. Simply improving health education and increasing access to health care of the socially and economically disadvantaged — two issues that could use improvement no matter which end of the Gini spectrum a country falls — could level the proverbial playing field. But, many policy makers support, at the very least, acknowledging the link between macroeconomic conditions and individual health outcomes when drafting economic and health care policy or legislation for local and international communities.

References

Kondo, N., Sembajwe, G., Kawachi, I., van Dam, R., Subramanian, S., & Yamagata, Z. (2009). Income inequality, mortality, and self rated health: meta-analysis of multilevel studies BMJ, 339 (nov10 2) DOI: 10.1136/bmj.b4471

SUBRAMANIAN, S., & KAWACHI, I. (2006). Whose health is affected by income inequality? A multilevel interaction analysis of contemporaneous and lagged effects of state income inequality on individual self-rated health in the United States Health & Place, 12 (2), 141-156 DOI: 10.1016/j.healthplace.2004.11.001

LYNCH, J., SMITH, G., HARPER, S., HILLEMEIER, M., ROSS, N., KAPLAN, G., & WOLFSON, M. (2004). Is Income Inequality a Determinant of Population Health? Part 1. A Systematic Review The Milbank Quarterly, 82 (1), 5-99 DOI: 10.1111/j.0887-378X.2004.00302.x

Ichida, Y., Kondo, K., Hirai, H., Hanibuchi, T., Yoshikawa, G., & Murata, C. (2009). Social capital, income inequality and self-rated health in Chita peninsula, Japan: a multilevel analysis of older people in 25 communities Social Science & Medicine, 69 (4), 489-499 DOI: 10.1016/j.socscimed.2009.05.006

This may not be the traditional image of Santa Claus, but maybe it should be, according to a study published in the British Medical Journal (BMJ). The public health experts conducting the study report that Santa’s history of bad behavior is catching up with him. Supposedly, Santa is promoting obesity, speeding, and drinking and, therefore, damaging millions of young lives. Instead, the authors suggest, Santa should be used to promote healthy lifestyle choices. They go so far as to suggest that Santa give up the cookies in favor of his reindeer’s vegetables, and forgo the sleigh for a bike or a good pair of running shoes. If he keeps his sleigh, Santa definitely needs to give up the brandy, the authors claim, as this makes Santa the poster child for drunk-driving accidents just waiting to happen. Plus, he needs to wear a helmet and a seatbelt. And, slow down. (Santa has to travels at millions of times a safe speed limit to make all his stops on time.)

The BMJ authors deny claims of being akin to Ebenezer Scrooge or the Grinch, but insist they want to open a public debate about advertising and public health. Should Santa be allowed to sell alcohol and unhealthy foods? Should advertisers put Santa next to Ronald McDonald and call it a day?

With all the unhealthy influences in the lives of children, should Santa Claus really be destroyed? By mid-childhood, most kids understand that Santa is not a real person and that he is just a symbol used to promote kindness and giving. The generosity and devotion fulfilled by Santa Claus far outweighs any bad influences that he may present to kids. Besides, participating in charitable giving and philanthropic behaviors makes people healthier.

Granted, Santa is not the best role model of healthy living, but he is also NOT REAL. Santa is an embodiment of the love, devotion, and generosity of the holiday season, and that is very real.

References

Grzywacz JG, Keyes CL. Toward health promotion: physical and social behaviors in complete health. Am J Health Behav. Mar-Apr 2004;28(2):99-111.

Grills, N., & Halyday, B. (2009). Santa Claus: a public health pariah? BMJ, 339 (dec16 1) DOI: 10.1136/bmj.b5261

Cyr C. Do reindeer and children know something that we don’t? Pediatric inpatients’ belief in Santa Claus. Cmaj. Dec 10 2002;167(12):1325-1327.

The authors of a recent study published in the journal Pediatrics evaluated 140 white male children with ADHD over a 10-year period. They assessed the relationship between treatment with stimulants in childhood and adolescence and the later development of psychiatric disorders, as well as grade level retention. The subjects with ADHD were compared to a group of 120 age- and gender-matched children without ADHD. At the beginning of the study, the children were between the ages of 6 and 18 years old; at the 10-year follow-up, the mean age was 22 years. Nearly three-fourths of the children with ADHD had been treated with stimulants sometime during the 10-year study period. The authors reported that these children were significantly less likely to develop anxiety and depressive disorders or exhibit disruptive behavior in young adulthood compared to ADHD children not treated with stimulants. These children were also less likely to repeat a grade level compared with untreated children. Overall, the authors conclude that stimulant treatment decreases the risk for the development of psychiatric disorders and academic failure in children with ADHD.

<Untreated ADHD is associated with the development of significant and potentially dangerous disorders: major depression, anxiety disorders, conduct disorders, oppositional-defiant disorders, and bipolar disorders. In the Pediatrics study, the only disorder for which the risk was not lowered with the use of stimulant medication was bipolar disorder. This is likely due to the fact that bipolar disorder has very different causes than the other ADHD-related conditions.

The same authors of the Pediatrics study published related findings in the American Journal of Psychiatry in 2008. Evaluating the same group of children, the authors reported that there was no statistically significant association between stimulant use in childhood or adolescence and later alcohol, drug, or nicotine abuse. Another study that examined the link between age at initiation of stimulant treatment and later substance abuse also concluded that early treatment with stimulant medication does not increase the risk of substance use disorders. Specifically, the study found that the later the stimulant was initiated, the greater the chance of developing a substance disorder. The hypothesis is that early use of stimulants may actually increase the white matter in the brain of ADHD children, which is often smaller than in children without ADHD, during a period of immense brain growth.

All of these studies, while positive for advocates of the use of stimulants, do not account for the effects of early ADHD diagnosis, referral, and treatment, independent of medication administration. Possibly, any treatment, whether with stimulant medication, non-stimulant medication, or behavioral therapy, contributes to the decreased risk of psychological disorders and academic failures later in life. Perhaps the conditions associated with ADHD are the result of untreated ADHD, and not the ADHD itself. For example, if untreated ADHD leads to failure at school and a loss of self-esteem and self-confidence, children and adolescents may develop depression and turn to drugs and alcohol in order to self-medicate.

Medicating young children, particularly with stimulants, will remain controversial. But, leaving ADHD untreated is also a contentious issue. The latest guidelines issued by the National Institute for Health and Clinical Excellence advises that psychotherapy should be first-line therapy for children with ADHD, causing concern among many health care providers. New information will at least arm parents with the knowledge that stimulants may not cause as much harm in children as once believed, and may actually do a lot of good. Parents, clinicians, and patients must evaluate the risks and benefits of any treatment for their own use.

References

Biederman, J., Monuteaux, M., Spencer, T., Wilens, T., MacPherson, H., & Faraone, S. (2008). Stimulant Therapy and Risk for Subsequent Substance Use Disorders in Male Adults With ADHD: A Naturalistic Controlled 10-Year Follow-Up Study American Journal of Psychiatry, 165 (5), 597-603 DOI: 10.1176/appi.ajp.2007.07091486

Mannuzza, S., Klein, R., Truong, N., Moulton, J., Roizen, E., Howell, K., & Castellanos, F. (2008). Age of Methylphenidate Treatment Initiation in Children With ADHD and Later Substance Abuse: Prospective Follow-Up Into Adulthood American Journal of Psychiatry, 165 (5), 604-609 DOI: 10.1176/appi.ajp.2008.07091465

Brimble MJ. Diagnosis and management of ADHD: a new way forward? Community Pract 2009;82(10):34-7.
Nair R, Moss SB. Management of attention-deficit hyperactivity disorder in adults: focus on methylphenidate hydrochloride. Neuropsychiatric disease and treatment 2009;5:421-32.

Biederman J, Monuteaux MC, Spencer T, Wilens TE, Faraone SV. Do stimulants protect against psychiatric disorders in youth with ADHD? A 10-year follow-up study. Pediatrics 2009;124(1):71-8.

The retrospective analysis examined the frequency, duration, and quality of primary care visits by adults in the United States. The study population included a nationally representative sample of 46,250 adults who visited primary care physicians between 1997 and 2005. Overall, primary care visits increased during the study period from 273 million to 338 million annually, or 10% per capita. The duration of the visits increased from an average of 18 minutes to almost 21 minutes. The increase in duration was significant for general medical exams (3.4 minutes), as well as the 3 most common diagnoses in primary care: diabetes mellitus (4.2 minutes), hypertension (3.7 minutes), and arthropathies (5.9 minutes).

The authors also assessed the quality of counseling and screening, as well as medication therapy. Overall, appropriate counseling or screening took 2.6 to 4.2 minutes per visit. Of the 3 quality indicators measured for counseling and screening, only 1 improved during the study period. Providing appropriate medication therapy was not associated with longer visits. Of the 6 quality indicators for medication therapy, 4 improved during the study period. The authors admit that overall performance, as assessed by the quality indicators, was poor.

The authors report that only modest relationships between visit duration and quality of care were achieved. Providing counseling did take additional time during the visit, but there was no correlation between the time spent in the visit and the appropriateness of the medication therapy. Related studies have actually shown a correlation between inappropriate medication use and shorter visit durations.

The current study did not address racial or ethnic differences in visit frequency, duration, or quality, which is often associated with disparities in health care provision. The study also could not adequately address the severity and complexity of illnesses or conditions and used limited quality measures.

With an aging population, it is not surprising that more time is required to care for more patients with more diseases than ever before. However, other studies have revealed that, while overall lengths of physician visits have increased, the duration of visits is the same across all age groups. Older patients, often with more medical conditions and on more complicated medication regimens, do not spend more time with physicians than younger, healthier patients. This supports the conclusion of the authors of the Archives study that promotes an interdisciplinary approach to improving medical care; particularly older, higher-risk patients may require additional time with nurse practitioners, pharmacists, and other health care providers to optimize medical care.

Substantially improving the efficiency of the provision of health care requires more than simply increased face time between physicians and patients; it will require enhanced electronic medical record keeping, augmented multidisciplinary approaches to care, and adequate reimbursement for providers spending time with patients. But, for now, physicians and patients alike should remember to always use time wisely, for it is a precious commodity. As William Penn understood, “time is what we want most, but what we use worst.”

References

Olfson, M., Cherry, D., & Lewis-Fernandez, R. (2009). Racial Differences in Visit Duration of Outpatient Psychiatric Visits Archives of General Psychiatry, 66 (2), 214-221 DOI: 10.1001/archgenpsychiatry.2008.523

Chen, L., Farwell, W., & Jha, A. (2009). Primary Care Visit Duration and Quality: Does Good Care Take Longer? Archives of Internal Medicine, 169 (20), 1866-1872 DOI: 10.1001/archinternmed.2009.341

Linder, J. (2003). Association between antibiotic prescribing and visit duration in adults with upper respiratory tract infections Clinical Therapeutics, 25 (9), 2419-2430 DOI: 10.1016/S0149-2918(03)80284-9

Lo, A., Ryder, K., & Shorr, R. (2005). Relationship Between Patient Age and Duration of Physician Visit in Ambulatory Setting: Does One Size Fit All? Journal of the American Geriatrics Society, 53 (7), 1162-1167 DOI: 10.1111/j.1532-5415.2005.53367.x

Many studies have demonstrated a negative relationship between increased body mass index (BMI) and income. This relationship is most obvious in jobs that require interpersonal skills, often with a great deal of social interaction. The salary disparity between normal-BMI and high-BMI employees gets worse as the workers get older. Overall, being overweight or obese minimizes the chance of obtaining gainful employment. Health economists attribute this salary-weight association to consumers and employers disliking obese workers.

The wage-weight discussion expands not only to the actual salary workers bring home, but weight affects social success, too. Moving up or down the social hierarchy and accumulating social advantages is correlated to weight. A recent epidemiological study reported that downwardly mobile people were more likely to be overweight or obese than socially stable individuals of high socioeconomic status. The likelihood of being overweight or obese also increased with the accumulation of social disadvantages. This maintains the cycle of poor social status, increased weight, poor health, and decreased employment opportunities.

A recent health economics study calculates the overall economic burden attributable to overweight and obesity, if currently overweight adolescents become obese adults. The study examined the predicted population of working-age adults in the United States from 2020 to 2050. Based on current trends, that population will suffer from 161 million life-years complicated by obesity, diabetes, or heart disease. There will be 1.5 million life-years lost. These conditions will cost society $254 billion. Most of the expense is due to lost productivity either from early death or disease morbidity. Only $46 billion is related to direct medical expenses. Applying currently available treatments to obesity-related diseases would only decrease the life-years lost to 1.1 million, but would increase medical costs by $7 billion.

Most Americans spend most of their day at work. If society is losing money and resources because of overweight and obesity, it seems obvious that employers would want to address the issue and improve worker productivity. But, workplace interventions to promote proper nutrition and physical activity have little benefit in improving weight status. Most successful participants in workplace interventions already have a healthy or near-healthy BMI.

America is losing its reputation as a productive, prosperous country. If not to improve the physical health of the population, Americans should get fit and lose weight to improve the economic and fiscal health of this great nation.

References

Lemon SC, Zapka J, Li W, Estabrook B, Magner R, Rosal MC. Perceptions of worksite support and employee obesity, activity, and diet. American journal of health behavior 2009;33(3):299-308.

Anderson, L., Quinn, T., Glanz, K., Ramirez, G., Kahwati, L., Johnson, D., Buchanan, L., Archer, W., Chattopadhyay, S., & Kalra, G. (2009). The Effectiveness of Worksite Nutrition and Physical Activity Interventions for Controlling Employee Overweight and ObesityA Systematic Review American Journal of Preventive Medicine, 37 (4), 340-357 DOI: 10.1016/j.amepre.2009.07.003

Lightwood, J., Bibbins-Domingo, K., Coxson, P., Wang, Y., Williams, L., & Goldman, L. (2009). Forecasting the Future Economic Burden of Current Adolescent Overweight: An Estimate of the Coronary Heart Disease Policy Model American Journal of Public Health, 99 (12), 2230-2237 DOI: 10.2105/AJPH.2008.152595

Han, E., Norton, E., & Stearns, S. (2009). Weight and wages: fat versus lean paychecks Health Economics, 18 (5), 535-548 DOI: 10.1002/hec.1386

Clarke, P., O’Malley, P., Johnston, L., & Schulenberg, J. (2008). Social disparities in BMI trajectories across adulthood by gender, race/ethnicity and lifetime socio-economic position: 1986-2004 International Journal of Epidemiology, 38 (2), 499-509 DOI: 10.1093/ije/dyn214

Heraclides, A., & Brunner, E. (2009). Social mobility and social accumulation across the life-course in relation to adult overweight and obesity: The Whitehall II study Journal of Epidemiology & Community Health DOI: 10.1136/jech.2009.087692

Researching and developing new drugs based on genetics is costly and time consuming. Reinvesting time and money in older drugs to improve the effectiveness and safety may produce more “bang for the buck” in the move towards personalized medicine. Research is increasingly focused on learning why existing drugs work better in some people than others. Genetic markers are offering clues to why patients respond well, or not, to cancer protocols, cardiovascular drugs, psychiatric medications, and kidney disease treatments, to name a few. Someday, perhaps drug companies will move away from continuously developing newer, costlier agents and focus on using the old drugs for new tricks.

Many new drugs come to market with accompanying diagnostic and genetic tests to establish safety and efficacy goals, but these are costly analyses. Simple tests, though, such as blood tests or cheek swabs, may be useful in determining if a patient will respond well to a commonly prescribed medication. These fast, relatively inexpensive tests could improve the overall cost-effectiveness of drug therapy.

The complex diseases that plague society are not the result of one gene or event, but, rather, a dynamic combination of factors. By evaluating individual genomes and studying the relationship to environmental factors, clinicians will learn how to identify susceptible groups of people and tailor disease prevention strategies and optimize treatment protocols. Physicians and pharmacists will be able to determine which patients will respond well to chemotherapy regimens, who will experience adverse drug reactions from a cholesterol drug, and who will have worsening asthma from an inhaled medication.

The advent of personalized medicine and the departure from the current one-size-fits-all health care model requires a paradigm shift for patients and providers. New standards will emerge for the management of genetic information and education will be paramount for clinicians and patients. There are still more questions than answers regarding personalized medicine and tailoring therapy to each individual, but, hopefully, personalized medicine will be a large piece of the future health care puzzle, allowing more preventive medicine and evidence-based treatment selection.

References

Abrahams, E., Ginsburg, G., & Silver, M. (2005). The Personalized Medicine Coalition American Journal of PharmacoGenomics, 5 (6), 345-355 DOI: 10.2165/00129785-200505060-00002

Dean, C. (2009). Personalized Medicine: Boon or Budget-Buster? Annals of Pharmacotherapy, 43 (5), 958-962 DOI: 10.1345/aph.1L563

Leeder, J., & Spielberg, S. (2009). Personalized Medicine: Reality and Reality Checks Annals of Pharmacotherapy, 43 (5), 963-966 DOI: 10.1345/aph.1M065

Tan DS, Thomas GV, Garrett MD, et al. Biomarker-Driven Early Clinical Trials in Oncology: A Paradigm Shift in Drug Development. Cancer J. September/October 2009;15(5):406-420.

Rovin, B., McKinley, A., & Birmingham, D. (2009). Can We Personalize Treatment for Kidney Diseases? Clinical Journal of the American Society of Nephrology, 4 (10), 1670-1676 DOI: 10.2215/CJN.04140609

Wiechec, E., & Hansen, L. (2009). The effect of genetic variability on drug response in conventional breast cancer treatment European Journal of Pharmacology, 625 (1-3), 122-130 DOI: 10.1016/j.ejphar.2009.08.045

Campbell, D., & Levitt, P. (2008). Future of individualized psychiatric treatment Pharmacogenomics, 9 (5), 493-495 DOI: 10.2217/14622416.9.5.493