Treatments to induce weight loss for the obese patient centre on the achievement of negative energy balance. This objective can theoretically be attained by interventions designed to achieve a reduction in energy intake and/or an increase in energy expenditure. Such ‘lifestyle interventions’ usually comprise one or more of the following strategies: dietary modification; behaviour change; increases in physical activity. These interventions are advocated as first treatment steps in algorithms recommended by current clinical obesity guidelines. Medication and surgical treatments are potentially available to those unable to implement ‘lifestyle interventions’ effectively by achieving losses of between 5 kg and 10 kg. It is accepted that the minimum of 5% weight loss is required to achieve clinically-meaningful benefits. Dietary treatments differ widely. Successful weight loss is most often associated with quantification of energy intake rather than macronutrient composition. Most dietary intervention studies secure a weight loss of between 5 kg and 10 kg after intervention for 6 months, with gradual weight regain at 1 year where weight changes are 3–4 kg below the starting weight. Some dietary interventions when evaluated at 2 and 4 years post intervention report the effects of weight maintenance rather than weight loss. Specific anti-obesity medications are effective adjuncts to weight loss, in most cases doubling the weight loss of those given dietary advice only. Greater physical activity alone increases energy expenditure by insufficient amounts to facilitate clinically-important weight losses, but is useful for weight maintenance. Weight losses of between half and three-quarters of excess body weight are seen at 10 years post intervention with bariatric surgery, making this arguably the most effective weight-loss treatment.

Following the discovery of TNF-α and leptin as secretory products of adipocytes in the early 1990s, subsequent obesity research focused on the new functional role of adipose tissue, as an active endocrine organ. Many more inflammatory peptides have been linked to adiposity, which ultimately characterised obesity as a state of low-grade systemic inflammation, or ‘metaflammation’ which may link obesity to its co-morbidities. The aim of the present review is to examine the effects of weight loss on inflammation in overweight and obese, but otherwise healthy, populations. Studies were broadly classified into four types (diet, physical activity, diet and physical activity combined, and surgical interventions) and discussed according to the method used to induce weight loss. All studies measured at least one obesity-related inflammatory marker (ORIM). The overall finding from the present review is that weight loss does improve inflammation in terms of both the inflammatory (C-reactive protein, TNF-α, IL-6 and leptin) and anti-inflammatory (adiponectin) ORIM. Within this, the greatest improvements in ORIM are observed in studies achieving a weight loss of at least 10 %. However, a number of methodological issues have been identified as potential limitations within the literature including the sex and age of subjects, sample size, study duration and the assessment of body composition. In conclusion, although a period of weight loss per se is capable of reversing the unfavourable inflammatory profile evident in the obese state, further studies are required to determine the time needed, in which a reduced weight is maintained, in order to benefit from improved inflammatory status long term.