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By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is a consultant for GlaxoSmithKline and is on the speaker's bureau of GlaxoSmithKline, 3M, Wyeth-Ayerst, Pfizer, Novartis, Bristol-Myers Squibb, AstraZeneca, Jones Pharma, and Boehringer Ingelheim.
Does Chocolate Make Acne Worse?
Currently prevailing scientific opinion denies any relationship between diet and acne: teenagers throughout the land rejoice over their freedom to eat as much pizza, popcorn, chocolate, and soda (the four food groups from age 14-20) as they wish. But the last word may not yet be in.
Acne is related to both androgen and insulin in a complex fashion. Probably the most commonly recognized syndrome of hyperinsulinemia and hyperandrogenism is PCOS (Polycystic Ovary Syndrome). The constellation of acne, oligomenorrhea, obesity, infertility, and hirsutism in women should lead to a search for PCOS. Since hyperinsulinemia and acne in PCOS are comorbid, the link between diet—which can lead to hyperinsulinemia—and acne becomes plausible.
Young adult subjects with acne (n = 54) were randomized to either a low-glycemic index diet (LGID) or a non-modified high carbohydrate diet (control) for 12 weeks. All acne medications were discontinued, but all participants in both groups used daily Cetaphil skin cleanser.
At the end of 12 weeks, acne lesion counts were significantly lower in the LGID compared to control. Similarly, insulin sensitivity had improved in the LGID group, but worsened in the control group. Finally, sex hormone binding globulin (SHBG) levels, which are responsible for how much free testosterone circulates, were reduced in the control group (producing more free testosterone, and greater proclivity to acne). Adrenal androgens were also lower in the LGID group. Smith RN, et al. J Am Acad Dermatol. 2007;57:247-256.
Psoriasis Goes More Than Skin Deep
It is increasingly recognized that some immune-mediated disorders have consequences much more far reaching than their primary tissue compartment pathology. For instance, we know that patients with rheumatoid arthritis have an increased risk of CV disease, pulmonary disease, and malignancy. A critical link between immune-mediated disease and atherosclerosis appears to be inflammation. Psoriasis has already signaled its ability to induce distant inflammation by its association with comorbid psoriatic arthritis.
Several population-based studies have found an increased risk of cardiovascular disease in persons with psoriasis. The UK's General Practice Research Database (n = 130,976) found a 3-fold increase in risk of MI for young adults with severe psoriasis. A Swedish study of hospitalized patients showed a greater mortality amongst psoriasis patients by 50% compared with expected.
There are several putative mechanisms for increased CV risk. Persons with psoriasis more commonly smoke, and are more commonly overweight and sedentary. Also, some of the therapeutic agents for psoriasis may increase CV risk. Finally, inflammatory markers associated with psoriasis may participate in the pathways of inflammation that lead to atherosclerosis. In the same way we have come to recognize that the presence of rheumatoid arthritis is worthy of being considered a "CV risk factor," clinicians may appreciate a newly identified association of psoriasis and CV disease. Kremers HM, et al. J Am Acad Dermatol. 2007;57:347-354.
Riding the Chromium Pendulum
Chromium at one time carried the moniker "Glucose Tolerance Factor" due to its critical role in glucose metabolism. In severe chromium deficiency states, diabetes not uncommonly ensues; severe chromium deficiency is, however, uncommon in the United States. Despite the uncertain role of chromium in persons of normal nutrition, sales of chromium indicate popularity amongst the general public: 6% of mineral supplement sales are attributable to chromium.
In an effort to provide clarification of the role of chromium supplements, Balk et al performed a systematic review of randomized controlled trials (n = 41 trials that met eligibility criteria). The discussion that follows pertains to diabetic or pre-diabetic subjects.
Although 11 of 14 studies found no effect or a statistically insignificant effect, the overall systematic review showed that chromium supplementation reduced A1c about 0.6%; there was also a modest favorable effect on fasting glucose: a reduction of about 18 mg%. There was some variability in response to chromium depending upon formulation. Chromium provided as brewers yeast had the greatest effect, followed by chromium picolinate, and lastly chromium chloride.
This systematic review finds favorable effects of chromium supplements. Because the studies which showed the most favorable impact were often of the least quality, the authors opine that this conclusion should not be viewed as definitive. Balk EM, et al. Diabetes Care. 2007;30:2154-2163.