Author + information
- Norbert Stefan, MD∗ (, )
- Andreas Fritsche, MD and
- Hans-Ulrich Häring, MD
- ↵∗Department of Internal Medicine IV, University of Tübingen, Otfried-Müller-Strasse 10, 72076 Tübingen, Germany
Recently, much interest has been given to the novel concept of metabolically healthy obesity (MHO). It could help to direct the limited resources that are available for prevention of metabolic diseases to the people at highest risk (1). Mørkedal et al. (2) now showed that individuals with MHO are not at increased risk of acute myocardial infarction (AMI) compared with normal-weight, metabolically healthy subjects. In contrast, they have an increased incidence of heart failure (HF) (2). Lavie et al. (3) convincingly discussed mechanisms, explaining why obesity itself, and not necessarily only metabolic abnormalities such as hypertension, dyslipidemia, hyperglycemia, and subclinical inflammation, has an impact on the development of HF. Most recently, a meta-analysis questioned the concept of MHO for its relevance for cardiovascular events (4). The study of Mørkedal et al. now can show that it is necessary to separate the predictive effects of MHO on AMI and HF when it comes to the prediction of cardiovascular disease.
The study by Mørkedal et al. (2) cannot provide mechanisms explaining the lower risk of AMI in those with MHO compared with subjects with metabolically unhealthy obesity. We could show that MHO is associated with a moderately reduced visceral fat mass, but, more importantly, with a largely reduced liver fat content (5). We also provided evidence that genetic variability in the adiponectin receptor 1 gene determines the prevalence of MHO and that MHO correlates with lower levels of the liver-secreted glycoprotein fetuin-A (5). Particularly lower production of this proinflammatory hepatokine, which affects glucose and lipid metabolism and induces subclinical inflammation (6,7), may explain the lower risk of AMI in MHO.
Regarding preventive strategies in MHO, Mørkedal et al. (2) refer to a small study indicating that lifestyle intervention may decrease insulin sensitivity and thus be harmful for people with this condition (8). However, we could show in a larger study that visceral fat mass decreased and insulin sensitivity remained high during a lifestyle intervention in subjects with MHO (9).
The concept of MHO has gained much interest in the scientific community. However, because of its complex nature and the not fully understood mechanisms involved in the causes and consequences of MHO, it is very important to carefully deal with this popular concept when it comes to the prediction and prevention of metabolic diseases.
- American College of Cardiology Foundation
- Mørkedal B.,
- Vatten L.J.,
- Romundstad P.R.,
- Laugsand L.E.,
- Janszky I.
- Lavie C.J.,
- Milani R.V.,
- Ventura H.O.