Clinical Briefs

By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.

What Things are Making us Gain Weight?

Source: Mozaffarian D, et al. N Engl J Med 2011;364:2392-2404.

Since two-thirds of americans are overweight or obese, most of us should probably be trying to better understand why. Perhaps the observation that the daily number of calories per capita continues to increase, while daily energy expenditure dwindles, is enough to satisfy the casual observer. Or is the character of caloric intake — such as high glycemic index carbohydrate vs low — a critical factor? As yet, despite simple answers (just reduce calories), there are few simple solutions (folks cannot/will not adhere to calorie-based dietary restrictions).

Might it help to identify commonplace "culprit" foods — that is, dietary components associated most often with weight gain, rather that just total calorie counts?

Based on follow-up of healthy U.S. adults during observational periods lasting as long as 20 years (n = 120,877), Mozaffarian et al determined that several commonplace dietary and lifestyle factors were associated with weight gain. For instance, over a 4-year interval, for every additional daily serving of potato chips, there was a 1.69 lb weight gain. Sugar-sweetened beverages were next on the list of items associated with weight gain. Perhaps, not surprisingly, physical activity, fruits, grains, nuts, and vegetables were inversely associated with weight.

Despite widespread public awareness of the health consequences of being overweight and obesity, most are not able — using currently advised methods — to reverse the trend for weight gain. Whether targeting elimination of specific dietary components (e.g., sugar-sweetened beverages) and/or the augmentation of selected favorable components (e.g., nuts, grains, fruits) will prove to be effective remains to be determined.

The Ipswich Touch Test for Diabetic Peripheral Neuropathy

Source: Rayman G, et al. Diabetes Care 2011;34:1517-1518.

Type 2 diabetes (DM2) remains the #1 cause of atraumatic limb amputation in the United States. The primary cause of foot ulcers that progress to limb loss is diabetic neuropathy, which decreases sensory awareness of tissue trauma, allowing destruction to progress without warning signs that would otherwise stimulate seeking care for injuries or infections. Albeit consistently recommended by consensus guidelines, routine examination of the feet remains markedly suboptimal by both clinicians and patients alike. Although monofilament and tuning fork testing are highly effective in identifying the presence of diabetic neuropathy, they also remain underutilized.

The Ipswich Touch Test (named after the United Kingdom Hospital in which it was developed) is performed by "lightly touching/resting the tip of the index finger for 1-2 seconds on the tips of the first, third, and fifth toes and the dorsum of the hallux." The presence of neuropathy is defined by this method as having two or more of the eight sites (four sites on each foot) being insensate.

The gold-standard for identification of diabetic neuropathy in this trial was vibration perception threshold as determined by a neurothesiometer. Both monofilament and the Ipswich Touch Test were highly sensitive and had strong positive-predictive value for the presence of neuropathy. When the Ipswich Touch Test was compared with monofilament testing, there was near-perfect agreement. As discussed by the authors, perhaps the lack of requirement for specialized measurement tools will prompt clinicians to be more consistently proactive in seeking to define diabetic neuropathy in the feet.

Disease-Modifying Antirheumatic Drugs and Risk for Developing Diabetes

Source: Solomon DH, et al. JAMA 2011;305:2525-2531.

Prior to the advent of disease-modifying antirheumatic drugs (DMARDs), the possibilities for remission of disorders like rheumatoid arthritis (RA) and severe psoriasis (PSOR) were remote. Along with the welcome dramatic clinical improvements seen with DMARDs, concerns about adverse effects — such as adversities associated with either the consequences of their immunomodulatory activity or direct toxic effects — require a high level of vigilance. Recently, however, there has been recognition that biologic DMARDs such as TNF inhibitors or hydroxychloroquine, when used in RA or PSOR, might be associated with a lesser risk of diabetes.

Solomon et al performed a retrospective study of RA/PSOR patients who began treatment with a DMARD (n = 121,280) in the United States and Canada. Compared with nonbiologic DMARDs (examples include sulfasalazine, leflunomide, cyclosporine, and others), use of biologic DMARDs was associated with a 23%-46% lesser risk of new-onset diabetes. Because cardiovascular (CV) risk is magnified in persons with RA, treatment choices may be influenced by consideration of agents less likely to further augment CV risk through induction of diabetes.