Obesity: The worldwide epidemic

James, Philip

doi:10.1016/j.clindermatol.2004.01.010

Cited by 387 publications

(204 citation statements)

References 14 publications

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“…Due to the global epidemic of obesity, there is also a large increase in the prevalence of type 2 diabetes mellitus (22). It has been estimated that every 1 kg increase in weight is associated with a 9% relative increase in prevalence of diabetes (23), whereas weight loss appears to be a more dominant predictor of reduced diabetes incidence than changes in diet or activity level (24).…”

Section: Discussionmentioning

confidence: 99%

Oxidative DNA damage and obesity in type 2 diabetes mellitus

Al-Aubaidy

Jelinek²

2011

European Journal of Endocrinology

153

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Objective: This study illustrates the relationship between oxidative DNA damage and obesity in patients with prediabetes and type 2 diabetes compared with controls. Design and methods: Participants attended the School of Community Health, Diabetes Screening Clinic, Charles Sturt University, Australia, between February 2006 and June 2008. A total of 162 participants (35 type 2 diabetic patients; eight prediabetic subjects; and 119 age-, gender-, and weight-matched controls) were investigated. All patients were selected on clinical grounds. Results: Serum 8-hydroxy 2 0 -deoxy-guanosine (8-OHdG) level was significantly greater in the prediabetic subjects (671.3G140 pg/ml) compared with controls (210.1G166 pg/ml; P!0.01). The diabetic group (1979.6G1209 pg/ml) had the highest level of 8-OHdG. There was a significant increase in serum 8-OHdG in obese subjects (848.5G103 pg/ml; P!0.001) and overweight subjects (724G102 pg/ml; PZ0.005) compared with the lean subjects (196.5G327 pg/ml). Conclusion: Our results indicate that serum 8-OHdG is increased already in prediabetes suggesting oxidative DNA damage to be present with minor elevation of blood glucose levels (BGLs). The statistically significant positive correlation between serum 8-OHdG and body mass index in the diabetic group indicates that obesity has an additive effect to increased BGL contributing to oxidative DNA damage. European Journal of Endocrinology 164 899-904

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Section: Discussionmentioning

confidence: 99%

Oxidative DNA damage and obesity in type 2 diabetes mellitus

Al-Aubaidy

Jelinek²

2011

European Journal of Endocrinology

153

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“…These figures are likely to increase further as the rate of childhood obesity is increasing [32]. In parts of Africa, the prevalence of obesity is as low as 5% [29]. …”

Section: Lifestyle Factors and Development Of Colorectal Cancermentioning

confidence: 99%

“…The obesity epidemic is not restricted to industrialized societies; this increase is often faster in developing countries than in the developed world [29]. The proportion of people classified as overweight or obese is high.…”

Section: Lifestyle Factors and Development Of Colorectal Cancermentioning

confidence: 99%

Colon Cancer: A Civilization Disorder

Watson¹,

Collins²

2011

Dig Dis

229

152

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Colorectal cancer arises in individuals with acquired or inherited genetic predisposition who are exposed to a range of risk factors. Many of these risk factors are associated with affluent Western societies. More than 95% of colorectal cancers are sporadic, arising in individuals without a significant hereditary risk. Geographic variation in the incidence of colorectal cancer is considerable with a higher incidence observed in the West. Environmental factors contribute substantially to this variation. A number of these risk factors are associated with a Western lifestyle and could be considered a product of ‘civilization’. Recently, smoking has been recognized as a risk factor. Energy consumption also influences colorectal cancer risk, with obesity increasing risk and exercise reducing risk. However, the strongest contribution to environmental risk for colorectal cancer is dietary. Consumption of fat, alcohol and red meat is associated with an increased risk. Fresh fruit and vegetables and dietary fibre may be protective. Much has been learnt recently about the molecular pathogenesis of colorectal cancer. Colorectal cancer always arises in the context of genomic instability. There is inactivation of the tumour suppressor genes adenomatous polyposis coli, p53, transforming growth factor-β, activation of oncogene pathways including K-ras, and activation of the cyclooxygenase-2, epidermal growth factor receptor and vascular endothelial growth factor pathways. The mechanisms by which some environmental factors modify the mutation risk in these pathways have been described.

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“…Obesity, defined as body mass index (BMI, calculated as weight in kilograms/height in meters squared) >30 and overweight (BMI ≥25) are major public health problems in the USA [1], Europe [2], and elsewhere in the world. The US National Health and Nutrition Examination Survey (NHANES) from 2001–2002 estimates that 66% of adults are either overweight or obese, 31% were obese, and 5% were extremely obese (BMI ≥40) [3].…”

Section: Introductionmentioning

confidence: 99%

Surgery for Obesity: Panacea or Pandora’s Box?

2006

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Background: Given the increasing prevalence of obesity, healthcare providers should be cognizant of various non-operative (diet, exercise, behavior therapy, and medications) and operative obesity treatments. This review critically evaluates these treatments, especially bariatric surgeries. Methods: Medline analyses using a combination of the following terms: obesity, bariatric surgery, and outcomes were performed with particular emphasis on prospective studies and randomized trials. Results: Non-operative treatments result in modest sustained weight loss (5–8%) at one year. Surgery is recommended for those with BMI >40 or >35 with comorbidities. Laparoscopic adjustable gastric banding, a restrictive procedure, causes 35–54% excess weight loss (EWL) at 1 year. Malabsorptive procedures (biliopancreatic diversions with and without duodenal switch) induce 72–77% EWL but are only performed at few centers. Roux-en-Y gastric bypass, acting through a combination of restriction and malabsorption, results in 69% EWL at 1 year and 49% at 14 years. Each procedure is associated with unique anatomic and nutritional complications. Overall, operative treatment improves comorbidities and may improve all-cause mortality. Conclusions: Surgery is an effective long-term treatment for selected obese patients who have failed other treatments. Further research is needed on prospective comparisons of procedures, evaluation of long-term outcomes, especially between centers and increasingly unrealistic patient expectations.

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Obesity: The worldwide epidemic

Cited by 387 publications

References 14 publications

Oxidative DNA damage and obesity in type 2 diabetes mellitus

Oxidative DNA damage and obesity in type 2 diabetes mellitus

Colon Cancer: A Civilization Disorder

Surgery for Obesity: Panacea or Pandora’s Box?

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