|Year : 2016 | Volume
| Issue : 2 | Page : 81-87
Obesity associated noncommunicable disease burden
Jyoti Bala Banjare, Supriya Bhalerao
Obesity Research Laboratory, Interactive Research School for Health Affairs, Bharati Vidyapeeth Deemed University, Pune, Maharashtra, India
|Date of Web Publication||14-Apr-2016|
Interactive Research School for Health Affairs, Bharati Vidyapeeth Deemed University, Pune - 411 043, Maharashtra
Source of Support: None, Conflict of Interest: None
World is facing rapid transition in health sector for under nutrition and over nutrition. Obesity is a challenging epidemic and increased Body Mass Index (BMI) influences on almost all body systems leading to development of non-communicable diseases. Chronic but slow growing non-infectious pathology of body organization give upsurge onset of non-communicable disorders. Obesity related Non-communicable diseases (NCDs) leads to millions of deaths all around the world, rapidly becoming economic burden worldwide. Pathophysiology and extend of obesity is responsible for ill effects of health. In obesity Low grade Inflammation and antioxidant disproportion plays vital role in development of NCDs. Effective health education, professional counselling from public health authorities, free health care, and social insurance can be effective in controlling growing non communicable disease globally. The present analysis attempts to study association of obesity with different NCDs in terms of prevalence and underlying mechanisms.
Keywords: Body mass index, leptin, metabolic syndrome, waist circumference
|How to cite this article:|
Banjare JB, Bhalerao S. Obesity associated noncommunicable disease burden. Int J Health Allied Sci 2016;5:81-7
| Introduction|| |
Noncommunicable diseases (NCDs) are the leading causes of death globally, killing more people each year than all other causes combined. As the impact of NCDs increases, annual NCD deaths are projected to continue to rise worldwide. Of the 57 million global deaths in 2008, 36 million (~63%) deaths were due to NCDs, principally cardiovascular diseases (CVDs), diabetes, cancers, and chronic respiratory diseases [Table 1]. NCD deaths are projected to increase by 15% globally between 2010 and 2020 with the greatest increase in Africa, the Eastern Mediterranean, and South-East Asia, where they will increase by over 20%. The global status report on NCDs is the first worldwide report covering epidemiology, risk factors, and preventive strategies for NCDs. Among various risk factors responsible for the development of NCDs as per this report, obesity has been considered as a major risk factor. In all, 5% of NCDs are strongly associated with obesity and overweight.
As per the World Health Organization (WHO), 3.2 million deaths are due to physical inactivity. The unhealthy lifestyle, diet, sedentary lifestyle, dysfunction of lipid and glucose, raised body weight incline toward development of NCDs. With the transition in global economy, the distribution of body mass index (BMI) is shifting upward in many populations leading to an increasing proportion of obese people. This situation is putting more and more people to the risk of NCDs and up rise of death rate [Table 1]. It is, therefore, become imperative to study the magnitude of the obesity-related health issues and also the pathological linkages between obesity and the various disease conditions. In the present review, we provide an update on the association of obesity with various NCDs.
| Methodology|| |
The study was done in retrospective way. Various databases were searched using terms “Obesity” and “NCD.” The search included all hits up from January 2000 to May 2014. All studies indicating association between obesity and NCDs were included in the review. Further, to explore association between obesity and an individual disease under the category of NCDs, separate search using terms “Obesity” and “the name of the specific condition” was carried out.
| Results|| |
All database collected from reference shown in [Figure 1]. Leptin resistance [Figure 2] causing low-grade inflammation and oxidative stress were found to be greatly involved in the development of obesity-linked NCD. Obesity highly tends to metabolic syndrome (n = 15) along with other NCD's alone and shortening life span. The four major NCD linked to higher BMI is leading cause of death around the globe.
|Figure 2: Circulatory leptin from adipocytes in obesity and advent of noncommunicable disease|
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Obesity and metabolic syndrome
Metabolic syndrome is defined as the abnormalities in biochemical process which hints to health conditions such as high blood pressure, abnormal cholesterol, and high storage of excess fat leading to health risks such as diabetes and CVD. Central obesity is a key feature of this syndrome, reflecting the fact that the syndrome's prevalence is driven by the strong relationship between waist circumference and increasing adiposity.
According to the WHO, the likelihood of developing Type 2 diabetes rises steeply with increasing body fatness. Approximately, 85% of people with diabetes can be classified as Type 2, and of these 90% are obese or overweight (WHO). India, China, and the US are the three countries with the highest number of adults with diabetes. This increase in the prevalence of Type 2 diabetes is closely linked to the upsurge in obesity. Furthermore, approximately 197 million people worldwide have impaired glucose tolerance, most commonly because of obesity and the associated metabolic syndrome. This number is expected to increase to 420 million by 2025. The relationship between obesity and diabetes is of such interdependent that a new term “diabesity” has been coined. Both insulin resistance and defective insulin secretion appear very prematurely in obese patients, and both worsen similarly toward diabetes.
Obesity (especially visceral fat) is often escorted by increased risk of developing fatal and nonfatal CVD, including coronary artery disease, stroke, peripheral arterial disease, cardiomyopathy, and congestive heart failure., Along with abdominal adiposity, cardiovascular complications are also connected to increased levels of several adipokines (leptin, resistin, chemerin, vaspin, visfatin, and omentin). Both waist circumference and waist-hip ratio have been reported to be significant predictors of CVD and coronary heart disease. It has been examined that in older age, adiposity and adipocytes (adiponectin and leptin) links with the incident of stroke. High level of leptin is known to damage endothelial and vascular smooth muscle cells.
Weight, weight gain, and obesity account for approximately 20% of all cancer cases [Table 2]. Fat tissue produces excess amounts of estrogen, which is associated with the risk of cancers. Obese people often have increased levels of insulin and insulin-like growth factor-1 in their blood, which may promote the development of certain tumors. Fat cells may also have direct and indirect effects on other tumor growth regulators, including mammalian target of rapamycin and AMP-activated protein kinase. Obese people often have chronic low-level or “sub-acute” inflammation, which is associated with increased cancer risk. Other possible mechanisms include altered immune responses, effects on the nuclear factor kappa beta, and oxidative stress.
Increased body weight has been shown to be associated with increased death rates for all cancers combined and for cancers at multiple specific sites. A projection of the future health and economic burden of obesity in 2030 estimated that continuation of existing trends in obesity will lead to about 500,000 additional cases of cancer in the United States by 2030. This analysis also found that if every adult reduces their BMI by 1%, which would be equivalent to a weight loss of roughly 1 kg (or 2.2 lbs) for an adult of average weight, this would prevent the increase in the number of cancer cases and actually result in the avoidance of about 100,000 new cases of cancer.
Impaired wound healing
Obese individuals frequently face wound complications including skin wound infection, dehiscence, hematoma and seroma formation, pressure ulcers, and venous ulcers. In particular, a higher rate of surgical site infection occurs in obese patients. In surgical wounds, the increased tension on the wound edges frequently seen in obese patients also contributes to nonhealing of wounds. The difficulty or inability of obese individuals to reposition them further increases the risk of pressure-related injuries. The friction caused by skin-on-skin contact invites ulceration. Together, these factors predispose obese individuals to the development of impaired wound healing.
The association of obesity with venous thrombosis becomes stronger as the BMI increases. Morbidly obese (i.e. those with BMI over 40 kg/m 2) are at an even higher risk than those with BMI 30–40 kg/m 2. Obese patients were found to be 2.5 times as likely to have deep vein thrombosis (DVT) and 2.2 times as likely to have pulmonary embolism. Obesity raised the risk of DVT and pulmonary embolism in men and women alike. However, the risk was a bit higher for obese women.
Obesity increases the risk of all “forms” of preeclampsia. Thus, the risk of severe and mild preeclampsia  and preeclampsia occurring in early and late gestation  are greater in obese and overweight women. Circulating leptin is increased in preeclampsia and correlates with maternal BMI. Since leptin is also produced by the placenta, the placenta is likely a major contributor to circulating concentrations of leptin during pregnancy. There is no consensus on the precise relationship between adiponectin concentrations and preeclampsia yet, as studies have reported higher as well as lower concentrations.
It is also evident that this relationship is not limited to obese and overweight women because increases in BMI in the normal range is also associated with an increased risk of preeclampsia. The fact that “fat mass is important” is supported by findings that weight loss reduces preeclampsia risk. Levels of placental growth factor (PGF), a member of the vascular endothelial growth factor family, are lower in preeclamptic women. Some studies have demonstrated that the levels of both sFlt-1 and PGF are lower in obese pregnant women.
Obstructive sleep apnea
There are several mechanisms proposed for the increased risk of obstructive sleep apnea (OSA) with obesity. These include reduced pharyngeal lumen size due to fatty tissue within the airway or in its lateral walls, decreased upper airway muscle protective force due to fatty deposits in the muscle, and reduced upper airway size secondary to mass effect of the large abdomen on the chest wall and tracheal traction. These mechanisms emphasize the great importance of fat accumulated in the abdomen and neck regions compared with the peripheral one. Conversely, OSA may itself predispose individuals to worsen obesity because of sleep deprivation, daytime long duration sleep, and disrupted metabolism.
Obesity-induced changes in central mechanisms regulating airway tone or ventilatory control stability may also be implicated. Leptin, for example, which is increased significantly in obesity, has important effects on regulation of chemo reflex function and hence breathing control. In a recent study of patients with OSA and BMI-matched control subjects, ghrelin levels were shown to be significantly higher in patients with OSA. However, some of the studies reported are on increased leptin levels in patients with OSA.
Obesity associated restricted lung mechanics induces series of biophysical effects in the lungs which are known to alter lung physiology, such as reduced lung volumes, increased small airway resistance, induce bronchodilator reversibility, induce peak flow variability, and enhance bronchial-hyperresponsiveness, which are conducive to the development of asthma. Weight has also demonstrated a dose-response association with asthma symptoms. In a retrospective study of 143 adults, demonstrated linear relationship between asthma severity and BMI. In another study  it was shown that with each 1 kg/m 2, the asthma severity score changes.
Depression and cognitive deficit
Recent data from the National Health and Nutrition Examination Survey estimates 17% of youths ages 2–19-year-old to be overweight compared to just 5% a few decades ago. Obesity is also been reported to have association with impaired cognitive function (including Alzheimer's disease [AD], Parkinson's, and Huntington's diseases, schizoaffective disorder, bipolar disorder, and major depressive disorder). Interestingly, higher levels of serum leptin appear to protect against cognitive decline in elderly individuals, suggesting leptin resistance as a causal pathway from obesity to cognitive impairment. According to recent studies, 40–60% of schizophrenia patients are overweight or obese.
Obesity is related to vascular diseases, and there is increasing evidence linking vascular risk factors to dementia and AD. Nevertheless, the association between obesity and the risk of dementia has not been extensively studied, and the few studies conducted so far have yielded somewhat conflicting results. Further, although vascular risk factors are interrelated and tend to cluster together, earlier studies have focused on a single risk factor alone.
Infertility and polycystic ovary syndrome are believed to be directly associated with obesity. Obesity, particularly abdominal, is responsible for most of the reproductive disorders in females. Increased adiposity is associated with several abnormalities of sex steroid metabolism and results in increased androgen production and suppression of sex hormone binding globulin. The abdominal fat in women is known to produce male hormones called androgens, which in turn prevent follicular maturation and contribute to anovulation. Leptin levels associated with obesity causes impaired testosterone and oestrogen level. When it comes to amenorrhea (lack of menstruation and ovulation), 45% of women are obese. Obesity contributes to anovulation and menstrual irregularities, reduced conception rate, and reduced response to fertility treatment. It also increases miscarriage and contributes to maternal and perinatal complications. In case of male infertility, obesity may cause androgen imbalance and erectile dysfunction.
Obesity increases the amount of cholesterol in bile, which can cause stone formation. It has been reported that the women with a BMI > 32 kg/m 2 may be as much as 3 times as likely to develop gallstones as those with a BMI of 24 or 25 kg/m 2. The risk may be 7 times higher in women with a BMI above 45 kg/m 2 than in those with normal BMI.
Obesity is also a risk factor for increased risk of gallstone-related complications and cholecystectomy in children and adolescents. Obese adolescents with cholelithiasis had higher BMI and abdominal circumference measurements when compared with adolescents without cholelithiasis.
Nonalcoholic fatty liver syndrome
Fatty liver disorders are common among the asymptomatic obese, and the incidence of this disorder in liver biopsy specimens of obese individuals range between 60% and 100% of the cases. Concerning the more severe nonalcoholic fatty liver syndrome types, various studies have implicated high levels of obesity in these disorders. Visceral fat is known to drain directly into the portal system, exposing the liver to large amounts of free fatty acids that may be oxidized or synthesized to triglycerides and either stored (steatosis) or secreted into the circulation.
Among the upper gastrointestinal diseases, obesity is an established risk factor for reflux esophagitis. Hiatal hernia has been identified in almost 40% of morbidly obese patients  especially among men. Improvement in gastroesophageal reflux disease (GERD) has been reported on weight loss, and there are several reports suggesting a decrease in GERD symptoms after bariatric surgery. In all, obesity is a strong risk factor for reflux gastritis and hiatal hernia, even in the presence of other factors.
Obesity implications for the musculoskeletal system include both degenerative and inflammatory conditions, with the greatest burden resulting from osteoarthritis (OA). A study reported that subjects with a BMI > 30 kg/m 2 were 6.8 times more likely to develop knee OA than normal-weight controls. A recent meta-analysis reported that the pooled odds ratio for developing OA was 2.63 (95% confidence interval; 2.28–3.05) for obese subjects compared to normal-weight controls.
OA affects all aspects of life through pain and limitation of mobility. Rheumatic arthritis was also seen highly related to obesity and prevalence of co-morbidities. For early prediction of the disease, body measurement is recommended.
A recent combined follow-up analysis has shown that high- and low-BMI inclined analysis of 57 international prospective studies found that BMI is a strong predictor of mortality among adults. Overall, moderate obesity (BMI 30–35 kg/m 2) was found to reduce life expectancy by an average of 3 years, whereas morbid obesity (BMI 40–50 kg/kg/m 2) reduces life expectancy by 8–10 years.
A number of other studies have estimated the impact of obesity on life expectancy within the UK, based on routinely available data. Two of the studies estimated that around 9% of all deaths were attributable to excess adiposity.,
In addition, a large, recently published study in the US by Finkelstein et al., modeled life expectancy using routine data. This showed a modest association between excess weight and life expectancy for those with BMI 25–35 kg/m 2; for those with BMI > 35 kg/m 2, excess weight was associated with a significant reduction in life expectancy.
| Conclusion|| |
This extensive review suggests that obesity is associated with all major NCDs although the strength of association might be different. The major pathological events seen in obesity such as chronic low-grade inflammation due to increased leptin levels and oxidative stress are primarily responsible for the development of these diseases. The insufficiency of important organ systems such as venous due to increase fat mass in obesity also contributes to the NCDs.
Policy makers and government organizations must prioritize cure and prevention for prevalence of NCDs. The (WHO)-Food and Agriculture Organization have discussed about reducing the levels of salt in foods, limiting unsuitable marketing of unhealthy foods and nonalcoholic beverages to take necessary action against weight gain, and prevent associated disorders. Balanced diet and physical activity will play a significant role on reducing the affliction of disease worldwide.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]
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