Health risks associated with overweight and obesity
Abstract
Overweight and obesity cause or exacerbate a large number of health problems, both independently and in association with other diseases, and are among the most significant contributors to ill health (1–4). The intra-abdominal visceral deposition of adipose tissue, which characterizes upper body – central – obesity (assessed by waist circumference and/or waist : hip ratio) is a major contributor to the development of hypertension, elevated plasma insulin concentrations and insulin resistance, hyperglycaemia and hyperlipidaemia (metabolic syndrome). The concept of the metabolic syndrome refers to the phenomenon of risk-factor clustering – a collection of metabolic traits occurring in the same individual with the clustering presumably reflecting a unifying underlying pathophysiology that requires a holistic approach to their management (5–7). Many of the health risks associated with increasing body weight begin to appear in children and young people. Of great concern is the increasing prevalence of type 2 diabetes and associated medical complications in childhood (8–10). This early onset needs to be reflected by active management and research priorities to reduce the consequential health and economic burdens (11). Evidence from twin, adoption and family studies unequivocally indicates that inherited factors play a major role in the determination of inter-individual differences in fat mass. The identification of genetic variants influencing human fat mass is critical to obesity research. In general, mutations have been found in those rare children with extreme obesity and clear evidence for monogenic inheritance. Genetic studies in the more common forms of obesity have yet to have the same tangible success that has been seen with monogenic subtypes. Nevertheless, progress has been made in the identification of certain chromosomal loci containing genes conferring susceptibility to obesity. Body weight is determined by an interaction between genetic, environmental and psychosocial factors acting through the physiological regulation of energy intake and expenditure. Similarly, genetic, environmental and physiological factors are likely to determine the associated health risks. The genetic influences appear to operate through susceptibility genes, which may be expressed more frequently in certain ethnic groups (12). Such genes increase the risk of developing a characteristic but they are not essential for its expression or, by themselves, sufficient to explain the development of a disease. The differences in genetic susceptibility within a population are likely to determine those who are more likely to become obese and/or develop associated medical complications in any given set of environmental circumstances. Implicit to the susceptible gene hypothesis is the role of environmental factors that unmask latent tendencies to develop obesity and health risks. A challenge for the future will be to identify the genetic and environmental contributions to weight gain, the intra-abdominal distribution of fat (central obesity) and also to health problems, paying attention to those at particular risk, including certain ethnic groups, susceptible families and the socially deprived. A further challenge will be to discover whether these factors operate through weight gain, independently or in combination. Obesity is characterized by elevated fasting plasma insulin and an exaggerated insulin response to an oral glucose load: a positive correlation is observed between increasing central obesity and measures of insulin resistance. Post-hepatic insulin delivery is increased in central obesity leading to more marked peripheral insulin concentrations that, in turn, lead to peripheral insulin resistance. In both men and women, the lipolytic response to noradrenaline is more marked in abdominal than gluteal or femoral adipose tissue. Cortisol may also contribute to this enhanced lipolysis by further inhibiting the anti-lipolytic effect of insulin. Increased production of a fat-cell-specific protein called resistin by abdominal subcutaneous and omental adipose tissue is associated with decreased cellular insulin sensitivity. By contrast, there is an inverse relationship between adiponectin (an adipocyte-specific secretory protein) and adiposity and insulin sensitivity, with type 2 diabetes being characterized by low levels of adiponectin. Adiponectin is similar in structure to tumour necrosis factor-alpha (TNF-α), which paradoxically appears to be increased in abdominal adipose tissue. Increases in pro-inflammatory cytokines [interleukin 6, resistin, TNF-α and C-reactive protein (CRP)] reflect overproduction by the expanded adipose tissue mass (13,14). All of these factors contribute to the exaggerated release of free fatty acids (FFAs) from abdominal adipocytes into the portal system. FFAs have a deleterious effect on insulin uptake by the liver and contribute to the increased hepatic gluconeogenesis and hepatic glucose release observed
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In overweight women with type 2 diabetes, supplementation with 1.8 g/d EPA and DHA for 8 weeks did not affect IL-6, TNF-alpha, SAA, or adiponectin.
“¼ IL-6, TNF-a, SAA, adiponectin”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [630]
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- Authors
- Kopelman, P.
- Affiliations
- University of East Anglia (GB)
- Corresponding author
- Kopelman, P.
- Venue
- Obesity Reviews
- Publisher
- Wiley
- Published
- 2007-02-19
- Volume
- 8
- Issue
- s1
- Pages
- 13-17
- ISSN
- 1467-7881 (ISSN-L)
- 1467-789X
- OpenAlex
- W1979146329
- Semantic Scholar
- 3dbf3ff97e7b28751b6bd13b4dbde108b9191a27
- Cited by
- 731
- References
- 23
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 14 · 2023: 13 · 2022: 63 · 2021: 54 · 2020: 49 · 2019: 52 · 2018: 50 · 2017: 63 · 2016: 49 · 2015: 51 · 2014: 43 · 2013: 67 · 2012: 44
- FWCI
- 23.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Obesity Reviews (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity, overweight, abdominal obesity, visceral adipose tissue, metabolic syndrome, type 2 diabetes in children, genetic susceptibility to obesity, monogenic obesity, genetic and environmental factors, energy balance, ethnic differences in obesity, health risks of obesity, waist circumference, waist-to-hip ratio, insulin resistance, hypertension, hyperlipidemia, hyperglycemia, twin and adoption studies
- MeSH terms
- Diet, Heart, Heart Failure, Humans, Insulin Resistance, Metabolism, Obesity, Risk Factors, Sleep Apnea Syndromes, Biomarkers, Weight Gain, Weight Loss, Exercise, Cytokines, Overweight
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