Nutrition in the Prevention and Treatment of Abdominal Obesity

By Ronald Ross Watson

Nutrition in the Prevention and Treatment of Abdominal Obesity focuses on the important roles that exercise, dietary changes, and foods play in promoting as well as reducing visceral fat. Nutritionists, dieticians, and healthcare providers seeking to address the abdominal obesity epidemic will use this comprehensive resource as a tool in their long-term goal of preventing chronic diseases, especially heart, vascular, and diabetic diseases.

Experts from a broad range of disciplines are involved in dealing with the consequences of excessive abdominal fat: cardiology, diabetes research, studies of lipids, endocrinology and metabolism, nutrition, obesity, and exercise physiology. They have contributed chapters that define a range of dietary approaches to reducing risk and associated chronic diseases. They begin by defining visceral obesity and its major outcomes; they also discuss the importance and the challenges of dietary approaches to reduce abdominal obesity, as compared to clinical approaches, with major costs and risks.

• Offers detailed, well-documented reviews outlining the various dietary approaches to visceral obesity with their benefits and failures
• Includes chapters on types of foods, exercise, and supplements in reducing obesity and its chronic clinical companions, especially diabetes and cardiovascular disease
• Helps nutritionists, dieticians, and healthcare providers approach patients in making decision about nutritional therapies and clinical treatments for abdominal obesity, from an evidence-based perspective

• Language: English
• Publisher: Academic Press
• Release date: Feb 26, 2014
• ISBN: 9780124079342

Book preview

Italy.

Section 1: Epidemiology and Clinical Management of Visceral Obesity

Part 1: Epidemiology and Pathophysiology of Abdominal Obesity

Outline

Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones

Work and Abdominal Obesity Risk

Effects of Dietary Patterns and Physical Activity on the Establishment of Abdominal Obesity in Adolescents

Lifestyle Factors Affecting Abdominal Obesity in Children and Adolescents Risks and Benefits

Female Cancer Survivorship and Obesity

Evaluation of Visceral Fat in Massive Obesity

Beyond Nutrition Is There Any Role for Physical Activity in Nonalcoholic Fatty Liver Disease Therapy?

Abdominal Fat and African-Americans Incidence and Relationship to Disease

Chapter 1

Diet and Irritable Bowel Syndrome, with a Focus on Appetite-Regulating Gut Hormones

Magdy El-Salhya, c, Doris Gundersenb, Jan Gunnar Hatlebakkc and Trygve Hauskenc,    aSection for Gastroenterology, Department of Medicine, Stord Helse-Fonna Hospital, Norway, bDepartment of Research, Helse-Fonna, Haugesund, Norway, cSection for Gastroenterology, Institute of Medicine, University of Bergen, Norway

Abstract

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder with a prevalence of 5–20% and an incidence of 200/100,000. It is not known to be associated with the development of serious disease or with increased mortality, but it does considerably reduce the quality of life for patients and is an economic burden to society. Diet plays an important role in triggering the symptoms of IBS, especially the intake of foods that are rich in fermentable oligo-, di-, and monosaccharides, and polyols (FODMAPs), by influencing the dominance of Clostridium spp. in the intestinal flora and inducing abnormalities in gut endocrine cells. Dietary guidance aimed at establishing healthy eating habits by avoiding foods rich in FODMAPs and insoluble fiber and adjusting food composition has been found to reduce symptoms and improve the quality of life in IBS patients. Endocrine cells that produce several anorexigenic hormones in the gut are depleted in IBS patients, but the impact of this on appetite and body mass index in IBS patients is not known. Further studies are urgently needed to clarify this issue.

Keywords

Appetite

Cholecystokinin

Diet

Enteroglucagon

Irritable bowel syndrome

Ghrelin

Motility

Peptide YY

Visceral hypersensitivity

Introduction

Irritable bowel syndrome (IBS) is a common chronic gastrointestinal disorder with a prevalence of 5–20% and a reported incidence of 200 cases per 100,000 in the adult population [1–9]. IBS patients are often young and predominantly female, and IBS is associated with abnormal gastrointestinal motility and visceral hypersensitivity [2,6,10–25]. Patients with IBS complain of abdominal pain or discomfort, altered bowel habits, and bloating and/or abdominal distension [1]. The severity of symptoms varies from tolerable to severe, with some patients suffering from daily symptoms while others report intermittent symptoms at intervals of weeks or months [1].

Although IBS is not known to be associated with the development of serious disease or increased mortality, it does considerably reduce the patients quality of life by an amount comparable to that reported for patients with inflammatory bowel disease, diabetes, congestive heart failure, renal insufficiency, and hepatic cirrhosis [1,6,26–31]. In addition to the morbidity caused by IBS, this disorder represents an economic burden to society [1]. Although most IBS patients ignore their symptoms and regard them as a normal part of everyday life, they generate a substantial workload in both primary and secondary health care [32,33]. It has been reported that IBS patients are responsible for 12–14% of primary health-care visits and constitute 28% of referrals to gastroenterologists [34–43]. Added to this are the costs associated with diagnostic tests, medication, hospitalization, and the reduced productivity of IBS patients [36,41,42].

IBS diagnosis is based mainly on symptom assessment since there are no biochemical, radiological, or morphological diagnostic tests for the condition. The Rome criteria III are widely accepted and applied for the diagnosis of IBS [44]. Patients are subdivided further on the basis of differences in the predominant bowel pattern into diarrhea predominant (IBS-D), constipation predominant (IBS-C), or a mixture of both diarrhea and constipation (IBS-M). These three subtypes have a similar prevalence [34,45–49]. Although several biomarkers for the diagnosis of IBS have been considered, the only reproducible test is gut transit measured by radioisotope markers, and this test has a limited availability [50]. Duodenal chromogranin A cell density has been proposed as a good marker for the diagnosis of IBS, with high sensitivity and specificity, but needs to be confirmed in a large cohort of IBS patients [51]. Postinfectious IBS is a subset of IBS that occurs in a considerable number of patients and is defined as a sudden onset of IBS symptoms following gastroenteritis in individuals who have not previously had any gastrointestinal complaints [52]. However, postinfectious IBS has also been reported following nongastrointestinal infections such as respiratory, urinary tract, and skin infections [53]. It is reported that 6–17% of IBS patients believe that their symptoms began with an infective illness, and 7–31% of patients who suffer an acute episode of infectious gastroenteritis go on to develop postinfectious IBS despite clearance of the inciting pathogen [54–56].

There are both nonpharmacological and pharmacological options for the treatment of IBS. The nonpharmacological approach comprises the provision of information, reassurance, dietary guidance, regular exercise, probiotic intake, gut-directed hypnotherapy, cognitive therapy, acupuncture, and herbal therapy. Pharmacological treatment depends upon the symptoms and mainly includes antidiarrheal drugs, prokinetics, laxatives, antispasmodics, antidepressants, antianxiety drugs, and antibiotics [1].

Diet Intake in Irritable Bowel Syndrome Patients

IBS patients tend to avoid certain food items that they associate with onset of their symptoms such as milk and dairy products, wheat products, caffeine, certain meat, cabbage, onion, peas/beans, hot spices, fried food, and smoked food products [57,58]. It has been reported that 62% of IBS patients limit or exclude food items from their daily intake, with 12% of them making such drastic changes to their diet that long-term nutritional deficiencies are possible [59]. Despite such food avoidance, the dietary composition of IBS patients does not differ from the background population in terms of energy, carbohydrate, protein, and fat intake [60–66]. A common belief among IBS patients is that lactose is the main cause of their symptoms; they consequently reduce their intake of milk and dairy products, which in turn results in a low daily intake of calcium, vitamin B2, and phosphorus [59,63,65,67].

IBS patients have a lower consumption of food items known to be rich in fermentable oligo-, di-, and monosaccharides, and polyols (i.e. FODMAPs) such as buns, couscous, millet, pasta, spaghetti, rice, and some vegetables (e.g. raw broccoli, cabbage, garlic, green beans, leeks, mushrooms, onion, peppers, and tomatoes) [63]. However, they have a higher consumption of other FODMAP-rich vegetables such as grapes, mango, melon, peaches, pears, peas, and plums [63].

The Role of Diet in the Development of IBS Symptoms

Food Allergy or Intolerance

There is no convincing evidence for an allergic response to, or an intolerance for, any specific foodstuff in IBS [1,68–73]. In absence of a typical immunoglobulin E (IgE) reaction, another antibody class (IgG) has been suggested to be implicated in food-related allergies in IBS [74,75]. However, this suggestion is controversial, probably because the tests used are not sufficiently sensitive or specific [65,68,73,75–83]. Nevertheless, food allergy mediated by mucosal mechanisms may occur in patients with atopic and postinfectious IBS [1,55,84].

The triggering of IBS symptoms by the ingestion of wheat products is thought to be caused by the sugar polymers, fructans and galactans [85,86],. The occurrence of nonceliac gluten sensitivity in IBS patients is widely debated [87]. The existence of nonceliac gluten intolerance was advocated following a randomized, double-blind, placebo-controlled rechallenge trial [88]. It has been suggested that IBS patients with wheat intolerance who possess genotypes associated with celiac disease (HLA DQ2 or DR3) but do not have typical serological markers or changes in small intestine histology exhibit other immunologic evidence of gluten reactivity and respond to a gluten-free diet [89]. The role of gluten intolerance in IBS remains to be clarified. Celiac disease and IBS have overlapping clinical presentations, resulting in some patients with celiac disease being mistakenly diagnosed as having IBS [90,91]. The number of patients with celiac disease among those with IBS is reported to vary between 0.04% and 4.7% [92–102].

Poorly Absorbed Carbohydrates and Fibers

FODMAPs are short-chain carbohydrates that are poorly absorbed, and a significant portion of these ingested carbohydrates enter the distal small bowel and colon [103]. These sugars include fructose, lactose, sugar alcohols (sorbitol, maltitol, mannitol, xylitol, and isomalt), fructans, and galactans. Fructose and lactose are present in apples, pears, watermelon, honey, fruit juices, dried fruits, and milk and milk products. Polyols are used in low-calorie food products. Galactans and fructans are present in wheat, rye, artichokes, asparagus, broccoli and Brussels sprouts, cabbage, garlic, leeks, onions, legumes, lentils, and soy [90,91,104].

FODMAPs increase the osmotic pressure within the large intestine and provide a substrate for bacteria fermentation, leading to gas production and distension of the large intestine. An increase in the intraluminal pressure can stimulate the release of serotonin and substance P into the interstitial fluid. Serotonin activates the submucosal sensory branch of the enteric nervous system (ENS), which conveys the sensation to the central nervous system (CNS), probably causing abdominal pain and discomfort [105–107]. Furthermore, serotonin controls gastrointestinal motility and chloride secretion via interneurons and motor neurons, which may result in motility and secretion disturbances [105–107]. Although increasing dietary fiber intake is still recommended for patients with IBS, especially those with IBS-C, clinical practice shows that this increases abdominal pain, bloating, and distension [108]. However, it has been shown that soluble fiber intake is effective in improving overall IBS symptoms and has fewer side effects than insoluble fiber [44–46,109–111].

The fermentation of FODMAPs and insoluble fiber to produce gas and intraluminal distention depends upon the composition of the intestinal flora. A dominance of Clostridium spp. in the intestinal flora over beneficial bacteria such as Lactobacillus and Bifidobacterium spp., which do not produce gas upon fermenting carbohydrates, would worsen the IBS symptoms [1]. On the other hand, consuming foods supplemented with probiotics that contain these latter bacteria would increase tolerance to both FODMAPs and fiber [1].

Abnormalities in the Endocrine System of the Gut in Irritable Bowel Syndrome

The Endocrine System of the Gut

The field of endocrinology originated in 1902 following the discovery of secretin by Bayliss and Starling [112,113]. Despite the dominance of the concept of nervism in controlling the gut function, which was introduced by Pavlov in the nineteenth century, it has now been established that the gut is an endocrine organ that controls its own function [114]. This was possible due to the development of novel techniques for the isolation, purification, and measurement of a large number of recently discovered gut hormones [115]. It is currently believed that the gut is controlled by a complicated integrated mechanism that includes both endocrine and nervous components, which interact with each other [1]. This regulatory system—which lies within the gut and communicates with the CNS—is called the neuroendocrine system (NES) of the gut [1,107].

The gut NES is a local regulatory system that controls the primary gut functions (i.e. the digestion and absorption of nutrients) by regulating gut motility, secretion, absorption, microcirculation, local immune defense, and cell proliferation [1,107]. Moreover, to optimize the digestion and absorption processes, the gut NES regulates appetite and the secretion of many gut hormones in order to reduce food intake and limit meal size [115].

The NES of the gut consists of two parts: (1) endocrine cells that are spread between the epithelial cells of the mucosa facing the gut lumen; and (2) peptidergic and serotonergic as well as nitric oxide-containing nerves of the ENS in the gut wall. The NES of the gut comprises a large number of bioactive messengers that act via endocrine, paracrine, or neuroendocrine pathways, or by synaptic signaling. The different components of this system interact and are integrated both with each other and with the afferent and efferent nerve fibers of the CNS [1]. The gut intraluminal content of carbohydrates, proteins, or fat triggers the release of different signaling substance of the NES of the gut (Fig. 1.1) [1,107].

Figure 1.1  Schematic drawing of triggering the release of different gut hormones by the intraluminal of nutrient content. Depending upon the intraluminal content of proteins, carbohydrates, or fat, a particular gut hormone is released into the interstitial fluid, where it may act via endocrine/paracrine action or as a neurotransmitters/neuromodulators on the neurons in the enteric nervous system. CCK, cholecystokinin; GIP, gastric inhibitory polypeptide; NPY, neuropeptide Y; PP, pancreatic polypeptide; PYY, peptide YY.

Abnormalities in Gut Endocrine Cells in Patients with Irritable Bowel Syndrome

There seems to be a general depletion of gut endocrine cells in patients with sporadic IBS [51,116,117]. Several abnormalities in the density of gut endocrine cells have been described in both sporadic and postinfectious IBS patients (Tables 1.1 and 1.2) [55,118–132]. It is noteworthy that the abnormalities observed are structural and not merely changes in hormone concentration. Changes in hormone levels reflect hormone synthesis and release in response to a physiologic condition, while structural changes represent a longstanding condition with long-term consequences. The abnormalities listed in Table 1.1 may explain the abnormal gastrointestinal secretion, motility, and visceral hypersensitivity seen in patients with IBS.

Table 1.1

Abnormalities in Gut Endocrine Cells in Patients with Sporadic Irritable Bowel Syndrome

IBS-C, irritable bowel syndrome, constipation predominant; IBS-D, irritable bowel syndrome, diarrhea predominant.

Table 1.2

Abnormalities in the Gut Endocrine Cell Densities in Patients with Postinfectious Irritable Bowel Syndrome

Irritable Bowel Syndrome and Appetite-Regulating Gut Hormones

Appetite regulation is complex and involves a large number of peptide hormones, several of which are gut hormones [115]. Many gut hormones act on the hypothalamic centers of appetite control [115]. The arcuate nucleus (ARC), which acts as the center for integrating neurological and blood-borne signals, lies in the median eminence. This region lacks a complete blood-brain barrier and is thus susceptible to factors circulating in the blood [133–135]. Similarly, the brainstem is proximal to other regions with an incomplete blood-brain barrier, allowing it to receive blood-borne signals [115,135]. The intake of palatable foods (hedonic feeding) is controlled by the brain reward system in the midbrain, which is modulated by blood-borne signals [135].

The function of five hormones known to be involved in appetite regulation are altered in the gut of IBS patients: ghrelin, cholecystokinin (CCK), peptide YY (PYY), enteroglucagon (oxyntomodulin), and serotonin. Ghrelin is an orexigenic hormone, while CCK, PYY, enteroglucagon, and serotonin are anorexigenic hormones.

Ghrelin is a 28-amino-acid peptide hormone that was first isolated from the stomach [124,136–138]. The major source of circulating ghrelin is endocrine cells of the oxyntic mucosa of the stomach, but small amounts are expressed in the small intestine, the large intestine, and the ARC of the hypothalamus [136–139]. Ghrelin has several functions, including regulating the release of somatotropin/growth hormone (GH) from the pituitary gland, where it acts synergistically with the GH-releasing hormone [136–139]. Moreover, ghrelin accelerates gastric and intestinal motility [140–153]. Ghrelin also increases appetite and feeding and plays a major role in energy metabolism [115,135]. Thus, both central and peripheral administration of ghrelin stimulates food intake and body weight gain [136]. Ghrelin is involved in meal initiation: ghrelin plasma levels rise during fasting and fall upon eating, and are inversely correlated with body weight. Moreover, basal ghrelin levels rise after weight loss [154–164]. As mentioned above, patients with IBS-D have a high density of ghrelin-producing cells, while in IBS-C the density of these cells is low (Fig. 1.2) [118]. However, the plasma ghrelin level in these patients does not appear to differ from that of healthy controls [118,119,165]. It has been postulated that the change in the number of ghrelin units (cells) is compensated by a change in synthesis and/or release of this hormone and that symptoms develop when there is fatigue in this compensation mechanism [118]. This change in ghrelin implies an increase in appetite and food intake in IBS-D, and a corresponding decrease in IBS-C.

Figure 1.2  Ghrelin-immunoreactive cells in the oxyntic mucosa of a healthy subject (A), a patient with irritable bowel syndrome, diarrhea predominant (B) and a patient with irritable bowel syndrome, constipation predominant (C).

In addition to the functions of CCK shown in Table 1.1, this hormone has an anorexigenic action [166–177]. There are two receptors for CCK: CCK-A and CCK-B (or CCK-1 and CCK-2, respectively) [178–182]. Both receptor subtypes are distributed throughout the CNS and gut, although CCK-A receptors predominate in the gut and CCK-B receptors predominate in the brain [178–182]. The density of duodenal CCK cells is reported to be reduced in sporadic IBS (Fig. 1.3) and increased in postinfectious IBS [120,121]. An increase in food intake in sporadic IBS and decreased food intake in postinfectious IBS is therefore to be expected.

Figure 1.3  Cholecystokinin-producing cells in the duodenum of a healthy subject (A) and a patient with irritable bowel syndrome (B).

PYY is released into the circulation following a meal in proportion to the calories ingested and the meal composition [183]. Infusion of PYY3-36 reduced food consumption during test meals, and obese subjects had a low PYY plasma level [184,185]. Circulating PYY3-36 binds to Y2 receptors on the presynaptic terminals of hypothalamic neuropeptide Y (NPY) and agouti-related protein (AgRP) neurons, and inactivation of these neurons is associated with the induction of anorexia [186]. PYY is a major regulator of the ileal brake in that it acts to inhibit further food intake once nutrients, and especially lipids, have reached the distal small intestine (ileum) [187–196]. The density of PYY cells is generally decreased in sporadic IBS (Table 1.1 and Fig. 1.4). However, whether this increases food intake and appetite in IBS patients remains to be established.

Figure 1.4  Peptide YY-immunoreactive cells in the colon of a healthy subject (A) and a patient with irritable bowel syndrome (B).

Enteroglucagon is released into the blood circulation following food ingestion in proportion to the amount of calories ingested [197,198]. It has some effect on incretin and reduces gastric motility and secretion [199–204]. However, enteroglucagon is considered to have only a modest anorexigenic effect [135]. Serotonin is also known to exert an anorexigenic effect [205]. The densities of enteroglucagon- and serotonin-producing cells are reduced in patients with IBS, which might have an impact on their food intake and appetite.

While several appetite-regulating gut hormones are altered in patients with IBS, body mass index (BMI) and appetite have not been studied in detail, and the few available data are controversial. Thus, while Simrén et al. reported that most of the 330 IBS patients they examined were normal or overweight, Kubo et al. found that low BMI was associated with IBS in the 367 patients they investigated [57,206]. It is noteworthy that several studies found that food intake in IBS patients did not differ from that of the normal control population [60–66]. It has yet to be determined whether IBS patients have increased appetite or whether the avoidance of eating because of worsening of symptoms upon eating prevents excessive food intake and therefore excessive weight gain. Further studies are needed to clarify this issue.

Effect of Dietary Guidance

Dietary guidance should include information regarding the importance of regular meals and healthy eating habits, the avoidance of dietary FOODMAPs, and the insoluble fiber content of the dietary components and to avoid them. This guidance should also include helping patients to identify the food items that they do not tolerate well [63,66]. the provision of dietary guidance to IBS patients resulted in the consumption of a better diet with respect to vitamins and minerals. In addition, patients were made aware of FODMAP-rich food items so that these could be avoided or consumed in low quantities, ultimately resulting in reduced symptoms and an improved quality of life [63]. Patients also consumed more food items supplemented with Lactobacillus and Bifidobacterium spp. which in turn increased their tolerance to FOODMAPs [63].

Conclusion

IBS is a common gastrointestinal disorder. Although it does not develop into a serious disease or increase mortality, it does considerably reduce the quality of life of the patients and is an economic burden to society. Diet plays an important role in the development of IBS symptoms. IBS symptoms can be caused by the intake of FODMAP-rich foods, the dominance of Clostridium spp. in the intestinal flora, and abnormalities in gut endocrine cells. Guidance aimed at establishing healthy eating habits, the avoidance of FODMAP-rich food and insoluble fiber, and adjusting the dietary composition reduces symptoms and improves the quality of life in IBS patients. Several of the endocrine cells that produce anorexigenic gut hormones are depleted in IBS patients. However, the possible impact on appetite and BMI in IBS patients is unknown; further studies are therefore urgently needed to clarify this issue.

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Chapter 2

Work and Abdominal Obesity Risk

Maria Teresa Anselmo Olintoa, b, Raquel Canutoc, d and Anderson da Silva Garceza,    aPostgraduate Program in Collective Health, University of Vale do Rios dos Sinos, RS, Brazil, bDepartment of Nutrition, Federal University of Health Science of Porto Alegre, RS, Brazil, cDepartment of Nutrition, University of Vale do Rios dos Sinos, RS, Brazil, dDepartment of Nutrition, University of Caxias do Sul, RS, Brazil

Abstract

Scientific literature indicates that work characteristics are possible risk factors for abdominal obesity. The focus of this section is to describe the scientific evidence for associations between work characteristics and abdominal obesity. We describe how occupational position, job strain, physical activity at work, shift work, and unemployment are associated with an increased occurrence of abdominal obesity. Furthermore, we explore the influence of gender and socioeconomic characteristics on these associations. An examination of the causes of abdominal obesity with a focus on occupational health can improve our understanding of the multifactorial nature of this important public health problem.

Keywords

Abdominal obesity

Work

Shift work

Job strain

Occupational physical activity

Occupational status

Unemployment

Understanding the determinants of obesity is important for global public health and the global economy. The etiology of obesity is multifaceted, involving interactions between individuals and their social, cultural, and physical environments. Traditionally, the causes of general obesity (as well as abdominal obesity) have been linked to an imbalance between caloric intake and physical activity [1]. However, modern life has led to other changes in human behavior, such as those influenced by work and the workplace.

Therefore, several researchers have focused on occupational health to investigate the role of certain work characteristics as possible risk factors for abdominal obesity. In these studies, an increased prevalence of abdominal obesity has been associated with working position, job strain, physical activity at work, shift work, and unemployment. Thus, this section focuses on how such work characteristics influence the occurrence of abdominal obesity, with the aim of advancing our understanding of factors associated with abdominal obesity among workers.

Occupational Status

An individual’s occupation indicates certain levels of status and power, which reflect the material and symbolic capital related to the conditions at work. Occupation-based indicators may be related to health not only through issues such as differential accessibility to health care but also by reflecting social networks or psychosocial processes that are associated with health outcomes. Thus, several studies have investigated the relationship between employment grade and changes in cardiometabolic factors worldwide.

Two studies conducted in European countries (the United Kingdom and Norway) investigated the relationship between occupational status and waist circumference (WC) in both sexes: they concluded that participants at higher employment grades had smaller WCs [2,3]. A study in Portugal examined the gender-specific prevalence of variations in WC across occupational levels. Among women, there was an inverse correlation between occupation and abdominal obesity. However, abdominal obesity was not associated with occupation among men [4].

The gender-specific association between occupational status and abdominal obesity is more evident among Asian workers. Two studies conducted in Japan and China reported higher levels of abdominal obesity among management-level males compared with other male workers. In contrast, a higher waist-hip ratio (WHR) was recorded in female laborers compared with female engineers [5,6]. Similarly, a Cameroon study found that, in men only, the risk of abdominal obesity was significantly higher for those at high compared with low occupational levels [7].

Therefore, the influence of occupational status on the occurrence of abdominal adiposity is gender dependent. Women with higher status positions are protected from abdominal obesity; men in the same positions are at an increased risk.

In addition to gender, abdominal obesity may be influenced by social position, which is represented by three characteristics: occupational status, education, and income. Occupational status is both a consequence of educational level and a determinant of income level. In investigations of the influence of social position on health outcomes, these three characteristics should be considered simultaneously. Accordingly, we conducted a brief review of the scientific literature (from the last 5 years) concerning studies of the relationships among education, income, and obesity in men and women.

We retrieved 21 studies that examined the relationship between educational status and abdominal obesity. Of the 19 studies with male participants, nine found a positive association between educational status and abdominal obesity [6,8–15], whereas seven demonstrated a negative association [16–22]. However, 15 of 21 studies found higher rates of abdominal obesity among women with lower educational status [9,10,13,14,17–27], and the other five found no association between these two factors in women.

Nine articles regarding the relationship between income and abdominal obesity were retrieved. Of these, five studies reported that income level was positively associated with abdominal obesity in men [6,9,10,12,21]. In women, income was negatively associated with income, according to seven studies [6,9,10,12,21,22,28].

These data provide strong evidence for an association between low social status (income, education, and occupational status) and abdominal obesity in women. Moreover, abdominal obesity is linked to higher social positions in men, although this finding is more controversial than the results for women.

The consequences of social inequality have been more conclusively established for women than for men. However, the link between occupational status (i.e. social position) and abdominal obesity is partly mediated by individual behavioral characteristics (dietary habits, leisure time physical activity, smoking, and physiologic stress). This link is also strongly related to work characteristics, such as job strain and physical activity at work.

Job Strain

Employees throughout the world are currently facing immense challenges, such as an increasingly fast-paced business environment and growing demands for increased productivity [29]. Since 2000, many companies located in industrialized countries have been attempting to dynamically outrun other firms in the global economic race by introducing various managerial innovations, such as just-in-time production and total quality management. As a result, we can expect profound changes in the amount of work stress experienced by employees.

The impact of job stress on health outcome has been studied since the publication of Karasek’s model in 1981. According to this model, a combination of a heavy workload (defined as high job demands) and low job control may be experienced by an individual as job strain. Four different types of psychological work experiences were generated by combining high or low job demands with high or low job control (decision latitude). These experiences were divided into four job categories: high-strain jobs, low-strain jobs, active jobs, and passive jobs. Thus, individuals with high job demands and low job control may have an increased risk of mental job strain, which can eventually lead to fatigue, depression, sleeping difficulties, burnout, substance abuse, or other physical ailments. Active jobs with both high demands and high levels of control are considered to be stimulating jobs with fewer negative psychological effects or health risks. Passive jobs, in contrast, do not allow individuals to use their skills; such occupations may lead to psychological strain and diseases [30].

Stress at work is linked to coronary heart disease, according to retrospective and prospective studies, as well as meta-analyses [16,31,32]. Stress may contribute to coronary heart disease via psychological effects on behavior and metabolism; these metabolic changes could directly increase abdominal adiposity. Furthermore, abdominal obesity is an important component of metabolic syndrome [33] and a risk factor for vascular diseases [34,35]. Therefore, several studies have found that work stress is linked to the development of abdominal obesity.

Most studies that investigated this relationship measured work stress using Karasek’s Job Strain Questionnaire; they provided evidence that job strain is an independent risk factor for abdominal obesity [36,37]. Major life events and periods of acute stress appear to play a greater role in the onset of general obesity for men than for women, as has been previously reported [38]. Nonetheless, an association between perceived stress and abdominal obesity is present in both sexes [39,40].

Workload stress is a potential determinant of central adiposity that deserves considerable attention. One explanation for the association between workload stress and central adiposity is that the waist-hip circumference ratio and the abdominal sagittal diameter are estimations of body fat centralization that are highly dependent on endocrine status. The central accumulation of fat is a consequence of long-term activation of the hypothalamic-pituitary-adrenal (HPA) axis due to stress. Cortisol, other steroid hormones, and growth are involved in this process. Cortisol activates lipoprotein lipase (LPL), the gatekeeper of lipid accumulation in adipocytes. Furthermore, in the presence of insulin, cortisol inhibits the lipid mobilization system. Because these events are mediated by central glucocorticoid receptors, which are present at a higher density in intra-abdominal visceral fat than in other depots, cortisol activity and the consequent accumulation of fat are accentuated in this adipose tissue [41,42].

Additionally, stress affects the behavior of workers. Almost 50% of the members of a representative sample from the USA who were concerned about the amount of stress in their lives coped by engaging in unhealthy behaviors, such eating to relieve stress [43]. Stress affects eating in a bidirectional fashion: a subset of stressed individuals (approximately 30%) decrease their food intake and lose weight during or after stress, whereas most stressed individuals increase their food intake [44] and exhibit an intensified preference for higher-fat, energy-dense foods [43,45]. Stress has also been shown to reduce leisure time physical activity [46], again potentially favoring a positive energy balance.

Another unhealthy behavior with a high prevalence among workers under stress is smoking [47]. Population-based studies have demonstrated that smokers have a larger WC and WHR than former smokers and never smokers; WHR is positively associated with the number of cigarettes smoked per day [48]. Studies of workers who smoke have demonstrated the same association [36]. For example, in a cross-sectional study in Great Britain, Kwok found that cigarette smoking, particularly smoking >20 cigarettes per day, was associated with a larger WC and WHR [49].

Occupational Physical Activity

In recent decades, occupational physical activity levels have been broadly affected by changes in society and in the economy. These changes have been accompanied by a substantial decrease in physically active occupations and an increase in sedentary activities [50,51]. Furthermore, changes in the workplace such as computerization and mechanization may cause workers to be more vulnerable to weight gain; daily occupation-related energy expenditure has exhibited a decreasing trend [50,52]. Thus, occupational physical activity plays an important role in total energy expenditure, i.e. occupation-related physical activity has a significant impact on daily caloric expenditure [50,53].

Because occupational physical activity is an important factor in daily energy expenditure, physically active occupations may help protect against abdominal obesity. Correspondingly, studies have shown an inverse association between the activity level of an occupation and abdominal obesity: workers in high-activity occupations have a reduced risk of abdominal obesity compared with workers in low-activity or sedentary occupations [5,54–60].

Steeves et al. showed that the association between occupational physical activity and abdominal obesity was independent of leisure time, transportation, and domestic activity levels and sociodemographic factors among citizens of the USA [54]. In addition, Chu and Moy showed that occupational physical activity was more strongly associated with abdominal obesity than were household, transportation, and leisure time physical activities among middle-aged adults in a middle-income country [56]. These findings indicate that occupational physical activity level is linked to central adiposity and has an impact on the risk of abdominal obesity that is independent of other types of physical activity.

The association between occupational physical activity and abdominal obesity is also dependent on socioeconomic status (education and income). Individuals with a lower socioeconomic position are more likely to hold jobs with a higher level of occupational physical activity, whereas individuals with a higher socioeconomic position engage in more leisure time physical activity [55,61]. Interestingly, socioeconomic status has a significant impact on the tendency for individuals with higher levels of occupational physical activity to engage in less leisure time activity: subjects from lower socioeconomic levels were less active during leisure time compared with those from higher socioeconomic levels, even after controlling for occupational physical activity [62,63]. Furthermore, occupational and leisure time physical activities may affect each other: most people who classified their jobs as active reported being sedentary in their leisure time [64–66].

In summary, technological and economic factors contribute to low energy expenditures in people’s daily routines, including decreases in physical activity levels at work. However, occupational physical activity has been demonstrated to be a protective factor against abdominal obesity: high-activity