1. Carlin, Brian MD
  2. Roitman, Jeffrey L. EdD

Article Content

Goldberg Y, Boaz M, Matas Z, Goldberg I, Shargorodsky M Clin Nutr. Published online first November 17, 2008; doi:10.1016/j.clnu.2008.10.001.


BACKGROUND & AIMS: Obesity is associated with increased arterial stiffness, an early marker of vascular wall damage. However, data on the long-term vascular impact of intentional weight loss are limited. The aim of the present study was to evaluate the effect of weight loss induced by nutritional and exercise intervention on arterial compliance, metabolic and inflammatory parameters in obese patients who participated in a weight reduction program.


METHODS: In an open label, prospective study, 37 obese subjects attended a 24 weeks nutritional and exercise interventional program. Arterial elasticity was evaluated using pulse-wave contour analysis (HDI CR-2000, Eagan, Minnesota) at baseline and at the end of the study. Fasting glucose, HbA1C, insulin, lipid profile, hs-CRP, fibrinogen were measured at baseline and after 6 months. Insulin resistance was assessed by homeostasis model assessment-insulin resistance (HOMA-IR).


RESULTS: BMI decreased from 36.1 +/- 7.4kg/m(2) at baseline to 32.8 +/- 7.4kg/m(2) after 6 months (p < 0.0001). Large artery elasticity index (LAEI) increased from 12.1 +/- 4.1 to 15.8 +/- 4.7ml/mmHgx10 during the study (p < 0.0001). Small artery elasticity index (SAEI) increased from 4.4 +/- 2.4 to 5.5 +/- 2.7ml/mmHgx100 (p < 0.0001). There was a significant improvement in fasting hyperglycemia, HbA1C and significant decrease in LDL-cholesterol, fibrinogen and C-reactive protein. Modest reduction in HOMA-IR was observed. The change in weight was positively associated with LAEI, SAEI, total cholesterol, insulin and HOMA-IR.


CONCLUSIONS: Moderate weight loss induced by nutritional and exercise intervention improved small and large artery elasticity. The increase in arterial elasticity was associated with improvement in glucose and lipids homeostasis as well as markers of inflammation.


Additional Recommended Reading: Dai J, Jones DP, Goldberg J, et al. Association between adherence to the Mediterranean diet and oxidative stress. Am J Clin Nutr. 2008;88(5):1364-1370.


Editor's Comment. This month I have selected 2 articles (with 2 supplemental articles) on what may be the single most common comorbid condition: obesity and overweight. Almost 70% of the population is either overweight or obese (body mass index >= 25.0). The article by Hajer et al may be a challenging read for many practitioners, but the substance of the article is important. In addition, clinicians may want to supplement their reading with an article by Lee and Pratley in JCRP (see citation above). These articles review information about adipose tissue and its role in metabolic dysfunction.


Fat cells were previously thought to be storage depots for energy. It is now clear that adipose tissue is not simply stored calories but rather functions in a much more active metabolic role. Many substances are produced and secreted by adipose tissue. These substances, called adipokines, influence immune function, metabolism, and insulin resistance. They are proinflammatory and are associated with endothelial dysfunction. Adipokines are produced by fat cells and production appears to be related to both the size of the cell and the distribution. Adipokines play a major role in almost all of the pathophysiology that underlies type 2 diabetes and atherosclerotic heart disease. Being obese (having excess adipose tissue) is, then, associated with this pathophysiological dysfunction.


Hajer et al (and Lee and Prately) discuss the details and pathophysiology of adipokines, adipose tissue, and obesity. They make it clear that increased adipose tissue means increased adipokine production and release with the accompanying pathophysiology. The link to both diet and exercise is also clear. Goldberg et al link exercise, diet, and specifically the Mediterranean diet pattern to decreased levels of weight and inflammatory markers.


The point of all this is to provide clinicians with the information that supports the interventions that we promote. With our obese/overweight patients there are many, important reasons to promote weight loss, a healthy dietary pattern, and regular exercise ("every day or almost every day"). This is the optimal lifestyle intervention for almost every chronic disease that our patients exhibit either as a primary diagnosis or as a comorbid condition. Supporting our interventions with real, hard research documenting their effectiveness is increasingly important. I believe it is incumbent on us as professionals not only to provide lifestyle interventions that are shown to be effective but also to give patients reasons that these are important to incorporate.


Modifying the condition (overweight) that causes much of the pathophysiology that accompanies coronary artery disease, type 2 diabetes, metabolic syndrome, and many other chronic conditions is an effective way to intervene in the pathophysiology of the condition. Losing weight helps accomplish this outcome (see the study above and others). Interestingly, exercise as well as adherence to the Mediterranean dietary pattern also decreases inflammatory markers. The arsenal that we have to battle chronic disease is full of lifestyle interventions that help patients address the core pathophysiology of the disease process. No drug does that nearly as effectively.