Context Obesity is a chronic disease that is difficult to manage without holistic therapy. The therapeutic armamentarium for obesity primarily consists of four forms of therapy: lifestyle modification (i.e., diet and exercise), cognitive behavioral therapy, pharmacotherapy, and bariatric surgery. Evidence acquisition Evidence was consolidated from randomized controlled trials, observational studies, and meta-analyses. Evidence synthesis After two years, lifestyle interventions can facilitate weight loss that equates to ~5%. Even though lifestyle interventions are plagued by weight regain, they can have substantial effects on type 2 diabetes and cardiovascular disease risk. Although 10-year percent excess weight loss can surpass 50% after bariatric surgery, weight regain is likely. To mitigate weight regain, instituting a multifactorial maintenance program is imperative. Such a program can integrate diet, exercise, and pharmacotherapy. Moreover, behavioral therapy can complement a maintenance program well. Conclusions Obesity is best managed by a multidisciplinary clinical team that integrates diet, exercise, and pharmacotherapy. Bariatric surgery is needed to manage T2D and obesity in select patients.

The etiology of anemia appears to be iron-related and precipitated by the female sex. Scant iron supplementation is likely causative. However, anemia of chronic inflammation cannot be discounted as being somewhat causal. Subsequently, the aggregate may have had a synergistic influence.

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Summary Aims Metformin is a commonly prescribed anti‐hyperglycaemic pharmacological agent, and it remains a staple in the management of type II diabetes. In addition to metformin's glucose lowering effects, research has indicated that metformin inhibits glycation‐mediated and oxidative modification of lipoprotein residues. The purpose was to discuss the effects of metformin as it relates to high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) modification. Materials and methods The purpose was to conduct a narrative and pragmatic review on the effects of metformin as it pertains to HDL and LDL modification. Results High‐density lipoprotein (HDL) concentration is a quantitative measure and therefore does not provide insight into its function, which is a qualitative property. Dysfunctional HDLs are unable to carry out functions normally associated with HDL because they can be modified by glycating agents. Metformin may counteract HDL dysfunction by abating HDL modification. Reductions in HDL modification may improve reverse cholesterol transport ability and thus possibly diminish cardiovascular risk. Similarly, metformin‐mediated attenuations in LDL modification may reduce their atherogenic potency. Conclusion Metformin may partially ameliorate HDL dysfunction and reduce LDL modification by inhibiting alpha‐dicarbonyl‐mediated modification of apolipoprotein residues; consequently, the results are salient because cardiovascular disease incidence may be reduced given that reverse cholesterol transport activity predicts risk, and modified LDL are proatherogenic.