How Physician Obesity Specialists Use Drugs to Treat Obesity

Specialist physicians may have prescribing habits that are different from nonspecialist physicians. Little is known about the prescribing habits of physicians specializing in the treatment of obesity. An anonymous survey was given to the physician members of the American Society of Bariatric Physicians (ASBP). There was a 35% response rate (266 physicians) to the questionnaire that was represented nationally. Almost all prescribed medications and all of them recommended phentermine. The average maximal dose of phentermine was above that approved in the package insert, and these physicians disagreed with the National Institutes of Health (NIH) Obesity Treatment Guidelines. Phendimetrazine, metformin, and phentermine plus l ‐5‐hydroxytryptophan (5‐HTP) with carbidopa were all used more frequently than either orlistat or sibutramine. The combination of sibutramine and orlistat as well as 5‐HTP/carbidopa were prescribed by 14 and 20%, respectively. As 5‐HTP‐carbidopa was a combination not previously reported for the treatment of obesity, a retrospective chart review was performed in a single obesity practice, which may not be representative. Twenty‐two subjects had a 16% weight loss with phentermine over 6 months and an additional 1% weight loss with the addition of 5‐HTP/carbidopa for an additional 6 months. One subject who started on 5‐HTP/carbidopa alone lost 24.4% of initial body weight over 6 months. This questionnaire revealed that 20% of the obesity specialists responding to the survey used phentermine plus of 5‐HTP/carbidopa, an unreported combination. A controlled, randomized, clinical trial to evaluate the safety and efficacy of this combination in treating obesity should be considered.     

Obesity as a Disease: The Obesity Society 2018 Position Statement

The emerging obesity epidemic and accompanying health consequences led The Obesity Society (TOS) in 2008 to publish a position paper defining obesity as a disease. Since then, new information has emerged on the underlying mechanisms leading to excess adiposity and the associated structural, cardiometabolic, and functional disturbances. This report presents the updated TOS 2018 position statement on obesity as a noncommunicable chronic disease.     

Redrawing the US Obesity Landscape: Bias-Corrected Estimates of State-Specific Adult Obesity Prevalence

Background

State-level estimates from the Centers for Disease Control and Prevention (CDC) underestimate the obesity epidemic because they use self-reported height and weight. We describe a novel bias-correction method and produce corrected state-level estimates of obesity and severe obesity.

Methods

Using non-parametric statistical matching, we adjusted self-reported data from the Behavioral Risk Factor Surveillance System (BRFSS) 2013 (n = 386,795) using measured data from the National Health and Nutrition Examination Survey (NHANES) (n = 16,924). We validated our national estimates against NHANES and estimated bias-corrected state-specific prevalence of obesity (BMI≥30) and severe obesity (BMI≥35). We compared these results with previous adjustment methods.

Results

Compared to NHANES, self-reported BRFSS data underestimated national prevalence of obesity by 16% (28.67% vs 34.01%), and severe obesity by 23% (11.03% vs 14.26%). Our method was not significantly different from NHANES for obesity or severe obesity, while previous methods underestimated both. Only four states had a corrected obesity prevalence below 30%, with four exceeding 40%–in contrast, most states were below 30% in CDC maps.

Conclusions

Twelve million adults with obesity (including 6.7 million with severe obesity) were misclassified by CDC state-level estimates. Previous bias-correction methods also resulted in underestimates. Accurate state-level estimates are necessary to plan for resources to address the obesity epidemic.     

Okara,Soybean Residue,Prevents Obesity in a Diet-Induced Murine Obesity Model

We examined the effect of okara on the prevention of obesity in mice. A modified AIN-76 diet with a high fat content (14.1% of crude fat) was used as a basal diet. Male ICR mice were fed ad libitum with the basal diet or a dried okara-supplemented basal diet (10, 20, or 40%) for 10 weeks. The okara intake dose-dependently suppressed the development of body weight and epididymal white adipose tissue (EWAT), and prevented an increase of plasma lipids, including total cholesterol, LDL cholesterol, and non-esterified fatty acid. The okara intake also prevented steatosis in the liver. Real-time RT-PCR revealed that the okara intake induced down-regulation of the fatty acid synthetase gene and up-regulation of the cholesterol 7 alpha-hydroxylase (CYP7A1) gene in the liver. We also found that the okara intake caused a marked reduction in the expression of leptin and TNF-alpha genes in EWAT. Our results suggest that okara is beneficial in preventing obesity.     

The Yellow Mouse Obesity Syndrome and Mechanisms of Agouti-Induced Obesity

The yellow mouse obesity syndrome is due to dominant mutations at the Agouti locus, which is characterized by obesity, hyperinsulinemia, insulin resistance, hyperglycemia, hyperleptinemia, increased linear growth, and yellow coat color. This syndrome is caused by ectopic expression of Agouti in multiple tissues. Mechanisms of Agouti action in obesity seem to involve, at least in part, competitive melanocortin antagonism. Both central and peripheral effects have been implicated in Agouti-induced obesity. An Agouti-Related Protein (AGRP) has been described recently. It has been shown to be expressed in mice hypothalamus and to act similarly to agouti as a potent antagonist to central melanocortin receptor MC4-R, suggesting that AGRP is an endogenous MC4-R ligand. Mice lacking MC4-R become hyperphagic and develop obesity, implying that agouti may lead to obesity by interfering with MC4-R signaling in the brain and consequently regulating food intake. Furthermore, food intake is inhibited by intracerebro-ventricular injection of a potent melanocortin agonist and was reversed by administration of an MC4-R antagonist. The direct cellular actions of Agouti include stimulation of fatty acid and triglyceride synthesis via a Ca²⁺-dependent mechanism. Agouti and insulin act in an additive manner to increase lipogenesis. This additive effect of agouti and insulin is demonstrated by the necessity of insulin in eliciting weight gain in transgenic mice expressing agouti specifically in adipose tissue. This suggests that agouti expression in adipose tissue combined with hyperinsulinemia may lead to increased adiposity. The roles of melanocortin receptors or agouti-specific receptor(s) in agouti regulation of adipocyte metabolism and other peripheral effects remain to be determined. In conclusion, both central and peripheral actions of agouti contribute to the yellow mouse obesity syndrome and this action is mediated at least in part by antagonism with melanocortin receptors and/or regulation of intracellular calcium.     

Perceived Weight Discrimination and Obesity

Weight discrimination is prevalent in American society. Although associated consistently with psychological and economic outcomes, less is known about whether weight discrimination is associated with longitudinal changes in obesity. The objectives of this research are (1) to test whether weight discrimination is associated with risk of becoming obese (Body Mass Index≥30; BMI) by follow-up among those not obese at baseline, and (2) to test whether weight discrimination is associated with risk of remaining obese at follow-up among those already obese at baseline. Participants were drawn from the Health and Retirement Study, a nationally representative longitudinal survey of community-dwelling US residents. A total of 6,157 participants (58.6% female) completed the discrimination measure and had weight and height available from the 2006 and 2010 assessments. Participants who experienced weight discrimination were approximately 2.5 times more likely to become obese by follow-up (OR = 2.54, 95% CI = 1.58–4.08) and participants who were obese at baseline were three times more likely to remain obese at follow up (OR = 3.20, 95% CI = 2.06–4.97) than those who had not experienced such discrimination. These effects held when controlling for demographic factors (age, sex, ethnicity, education) and when baseline BMI was included as a covariate. These effects were also specific to weight discrimination; other forms of discrimination (e.g., sex, race) were unrelated to risk of obesity at follow-up. The present research demonstrates that, in addition to poorer mental health outcomes, weight discrimination has implications for obesity. Rather than motivating individuals to lose weight, weight discrimination increases risk for obesity.     

Obesity and Smoking Habits

A large-scale survey of steel workers in South Wales has shown a considerable difference between the body weights of smokers and of non-smokers. The difference increases with age so that men over 40 years who have never smoked are on average 13 lb (5·9 kg) heavier than smokers. Even so, smokers are about 15 lb (6·8 kg) heavier than the weight standard considered desirable by the Metropolitan Life Insurance Company, while non-smokers are nearly 30 lb (13·6 kg) heavier.About 20% of the men are attempting to give up the smoking habit. Ex-smokers who have given up smoking for more than eight years approach the body weight of men of the same age who have never smoked.Many reports have been published on the health consequences of smoking and of obesity. Because smoking and obesity are inversely related studies of the interrelation of these two health hazards and of their relative importance are needed.     

Obesity and cortisol status.

The fact, that obesity is a prominent feature of hypercortisolism (Cushing's syndrome) has stimulated investigation on the possible existence of the reverse relationship, namely that hypercortisolism is a feature of obesity. We have reviewed half a century of literature on this question, and have found out the following: (1) Hypercortisolism can exist in two forms: systemic hypercortisolism, in which there is an overall bodily excess of cortisol, and tissue, or intracellular, hypercortisolism, in which there is increased intracellular concentration of cortisol without an overall bodily excess. (2) There are two parameters of systemic hypercortisolism: CPR and plasma cortisol concentration. Proper evaluation of the first parameter requires correction for the active metabolic mass, which is best performed by expressing CPR per gram of urinary creatinine. The second parameter can be confounded by the marked moment-to-moment fluctuations in plasma cortisol concentrations due to cortisol's episodic secretion. Proper evaluation requires measuring the 24-hour mean concentration. Of these two parameters of systemic cortisol status, the plasma concentration is the more critical and accurate. (3) Corrected CPR is normal in obese individuals, and 24-hour mean plasma cortisol concentrations are slightly but definitely subnormal. This combination of findings indicates diminished stimulability of the hypothalamic-pituitary-adrenal (HPA) axis, which normally regulates bodily cortisol status. This deduction is supported by empirical studies on HPA reactivity. (4) Tissue hypercortisolism, due to increased intracellular activity of 11beta-HSD-1, which catalyzes reduction of cortisone to cortisol, has been reported in obese mice and humans. The findings of various studies are not consistent, and whether the enzymatic overactivity is a cause or a result of obesity is still unclear.     

Ambulatory Management of Childhood Obesity

Objective: Childhood obesity is one of the most challenging issues facing healthcare providers today. The aims of this study were to describe the ambulatory management of childhood obesity by pediatricians (PDs) and family physicians (FPs) and to evaluate knowledge of and adherence to published recommendations. Research Methods and Procedures: A 42‐item, self‐administered questionnaire was mailed to 1207 randomly selected primary care physicians (PDs = 700, FPs = 507) between September 2001 and January 2002. Results: Of 339 (28%) responses, 287 were eligible (PDs = 213, FPs = 74). Most respondents were in group or solo practice (87%) in a suburban or urban, non‐inner city location (67%). The average age was 48 years (range = 31 to 85 years), and the mean years in practice was 17 (range = 1 to 55 years). Nineteen percent of physicians were aware of national recommendations. Three percent of physicians reported adherence to all recommendations. Knowledge of recommendations was not associated with a greater likelihood of adherence. However, physicians who were aware of recommendations were more likely to have positive attitudes about personal counseling ability (odds ratio = 2.4, confidence interval = 1.3 to 4.4) and the overall efficacy of obesity counseling (odds ratio = 4.3, confidence interval = 1.7 to 10.8). Poor patient motivation, patient noncompliance, and treatment futility were perceived as the most frequently encountered barriers to obesity treatment. Discussion: Most physicians are not aware of or adherent to national recommendations regarding childhood obesity. Awareness of recommendations was associated with more positive attitudes about personal counseling ability and the effectiveness of obesity counseling in general.     

The Effects of Overfeeding on Spontaneous Physical Activity in Obesity Prone and Obesity Resistant Humans

Despite living in an environment that promotes weight gain in many individuals, some individuals maintain a thin phenotype while self‐reporting expending little or no effort to control their weight. When compared with obesity prone (OP) individuals, we wondered if obesity resistant (OR) individuals would have higher levels of spontaneous physical activity (SPA) or respond to short‐term overfeeding by increasing their level of SPA in a manner that could potentially limit future weight gain. SPA was measured in 55 subjects (23 OP and 32 OR) using a novel physical activity monitoring system (PAMS) that measured body position and movement while subjects were awake for 6 days, either in a controlled eucaloric condition or during 3 days of overfeeding (1.4× basal energy) and for the subsequent 3 days (ad libitum recovery period). Pedometers were also used before and during use of the PAMS to provide an independent measure of SPA. SPA was quantified by the PAMS as fraction of recording time spent lying, sitting, or in an upright posture. Accelerometry, measured while subjects were in an upright posture, was used to categorize time spent in different levels of movement (standing, walking slowly, quickly, etc.). There were no differences in SPA between groups when examined across all study periods (P > 0.05). However, 3 days following overfeeding, OP subjects significantly decreased the amount of time they spent walking (?2.0% of time, P = 0.03), whereas OR subjects maintained their walking (+0.2%, P > 0.05). The principle findings of this study are that increased levels of SPA either during eucaloric feeding or following short term overfeeding likely do not significantly contribute to obesity resistance although a decrease in SPA following overfeeding may contribute to future weight gain in individuals prone to obesity.     

Familial Aggregation of Morbid Obesity

Recent studies have shown major gene effects for obesity in randomly ascertained families. To investigate the familial aggregation of a specific subset of obesity, which is particularly prone to medical complications, families with morbid obesity were studied. This condition occurs in 1%-2%of the population and is defined as 45.5 kg (100 pounds) or more over ideal weight. First-degree relatives of 221 morbidly obese probands (1560 adults) were identified, and height and weight (current and greatest) were obtained from each family member. Morbid obesity occurred in the family members of the probands 8 times more often than in the general population. Of the morbidly obese probands, 48% had one or more first-degree relatives who were also morbidly obese compared to a 6% population estimate. By the ages of 20–24, 12% of the morbidly obese probands were already 45.5 kg or more overweight, and 45% were 22.7 kg (50 pounds) or more overweight. There was little difference in the prevalence of familial morbid obesity by the gender of the probands: 47% of the male probands and 48% of the female probands had another morbidly obese relative, while 67% and 53% of the early onset (before age 25) male and female probands, respectively, had one or more first-degree relatives who were also morbidly obese. In addition to the extreme degree of familial aggregation, the prevalence of morbid obesity in parent-offspring sets was calculated within the morbidly obese families. Morbidly obese families who have one or two morbidly obese parents have a 2.6 times increased risk (p<0.002) of having one or more morbidly obese adult offspring, compared to families who have neither parent morbidly obese. Evidence for trimodality of the body mass index distribution was found for each gender (p = 0.0006 for male relatives and p = 0.075 for female relatives). The strong familial aggregation of morbid obesity indicates the need for further understanding of the genetic determinants of this extreme clinical disorder and how environmental factors affect the genetic expression of the trait. (OBESITY RESEARCH 1993;1:261–270)     

Obesity and adiponectin after kidney transplantation

Obesity and hyperlipidaemia are found very frequently after kidney transplantation (Tx) and may represent independent risk factors for development of atherosclerosis and chronic allograft nephropathy. In a prospective metabolic study, we monitored, a total of 68 obese transplant patients [body mass index (BMI) > 30 kg/m2] with dyslipidaemia over a period of 24 months. We compared the findings of a new therapeutic regimen 1 year (start of the study) and 2 years after renal transplantation. Based on a Subjective Global Assessment Scoring Sheet, we started at the end of the first year with an individualized hypoenergic-hypolipidaemic diet (IHHD). Subsequently, after corticoid withdrawal, IHHD was supplemented regularly with statins (atorvastatin 10-20 mg/day)) and followed-up for 2 years. All patients were on a regimen of cyclosporin A or tacrolimus and mycophenolate mofetil. During the study period, there was a significant decrease in BMI (p < 0.025) and an increase of the adiponectin level (p < 0.01). Long-term therapy was associated with a significant decrease in serum leptin (p < 0.01) and lipid metabolism parameters (p < 0.01). Inulin clearance, mean systolic and diastolic blood pressure, proteinuria, lipoprotein(a) and apo-lipoprotein E isoforms did not differ significantly. Based on our results, we assume that obesity and hyperlipidaemia after renal transplantation can be treated effectively by modified immunosuppression (corticosteroid withdrawal), statins and long-term diet (IHHD). The increased level of adiponectin may be a marker of reducing atherosclerotic and chronic allograft nephropathy processes.     

Obesity and low back pain

Obesity and low back pain (LBP) are common health problems among patients attending Primary Health Care (PHC) in general practice at the United Arab Emirates (UAE). The objective of this study was to determine whether obesity is associated with low back pain. A cross-sectional face-to-face interview questionnaire survey was conducted. The questionnaire was a modified version of the Roland-Morris Scale for evaluating back disability. The interviews were conducted in Arabic by qualified nurses. A multi-stage stratified sample 1,103 UAE national aged 25-65 years, who attended PHC clinics for any reason, were invited to participate but only 802 subjects were eligible to be included for the statistical analysis. The data were analyzed using univariate and multivariate statistical methods. Of the 802 subjects, 428 (53.4%) were males and 374 (46.6%) were females. The mean age of the males was 40.5 +/- 11.5 years and females was 38.2 +/- 10.5 years (p = 0.004). The mean BMI of the males was 26.4 +/- 7.4 and females was 27.8 +/- 5.6 (p = 0.002). The overall prevalence of LBP in the present study was 64.9% (95% confidence interval, 61.0-68.8) and respectively, 56.1% in males and 73.8% in females. The results revealed that there was association between BMI and some socio-demographic variables with the respect of with low back pain. Back pain had more influence on the life style habits on females than in males. Stepwise multiple regression analysis showed that only age (p < 0.0001), educational level (p = 0.001), gender (p = 0.002), place of living (p = 0.019), BMI (p < 0.0001), and housing condition (p = 0.02) had significant effect on the presence of LBP in patients. The present study showed that obesity is moderately associated with low back pain.     

Meal Frequency and Childhood Obesity

Objective: Previous studies have demonstrated an inverse association between meal frequency and the prevalence of obesity in adulthood. The aim of this study was to assess the relationship between meal frequency and childhood obesity. Research Methods and Procedures: Stature and weight of 4370 German children ages 5 to 6 years were determined in six Bavarian (Germany) public health offices during the obligatory school entry health examination in 2001/2002. An extensive questionnaire on risk factors for obesity was answered by their parents. Obesity was defined according to sex‐ and age‐specific BMI cut‐off points proposed by the International Obesity Task Force. The main exposure was daily meal frequency. Results: The prevalence of obesity decreased by number of daily meals: three or fewer meals, 4.2% [95% confidence interval (CI), 2.8 to 6.1]; four meals, 2.8% (95% CI, 2.1 to 3.7); and 5 or more meals, 1.7% (95% CI, 1.2 to 2.4). These effects could not be explained by confounding due to a wide range of constitutional, sociodemographic, and lifestyle factors. The adjusted odds ratios for obesity were 0.73 (95% CI, 0.44 to 1.21) for four meals and 0.51 (95% CI, 0.29 to 0.89) for five or more meals. Additional analyses pointed to a higher energy intake in nibblers compared with gorgers. Discussion: A protective effect of an increased daily meal frequency on obesity in children was observed and appeared to be independent of other risk factors for childhood obesity. A modulation of the response of hormones such as insulin might be instrumental.     

Erythrocyte Membrane Phosphatidylserine Exposure in Obesity

It has been suggested that increased erythrocyte membrane phosphatidylserine (PS) exposure could contribute to hypercoagulability and hemorheological disturbances in obesity. The aim of our study was to evaluate PS exposure in obese patients and in a control group and to correlate this with hemorheological properties, i.e., erythrocyte aggregability (EA) and deformability, and to evaluate the effect of weight loss on these parameters. An anthropometric and analytical evaluation was performed at baseline and after 3 months on a diet (very low‐calorie diet for 4 weeks and low‐calorie diet for 2 months) on 49 severe or morbid obese patients (37 women, 12 men) and 55 healthy volunteers (39 women, 16 men). PS exposure on erythrocyte membrane was performed by flow cytometry. Erythrocyte aggregation was measured using the Myrenne MA₁ and the Sefam aggregometer. Erythrocyte deformability was determined in a stress diffractometer. Prothrombin fragment F1+2 (F1+2) was determined as a marker of the hypercoagulable state, and plasma malondialdehyde (MDA) as an indicator of oxidative stress. Obese patients had a higher EA index, higher PS exposure on erythrocyte membranes and higher levels of MDA and F1+2. The differences in erythrocyte aggregation and F1+2 between obese patients and the control group were maintained after adjusting for PS exposure. After 3 months of diet, a significant reduction in PS exposure on erythrocyte membrane was observed. Obese patients show increased PS exposure on erythrocyte membrane, with no effect on rheological properties. Increased PS exposure could contribute to hypercoagulability in these patients. Weight loss obtained with diet treatment reduces PS exposure on erythrocyte membrane.     

Obesity, metabolism, and hypertension

The relationship between obesity and hypertension is complex and poorly understood. A developing body of information suggests that metabolic factors related to the obese state are importantly involved. The pertinent observations include: (1) Diet influences sympathetic nervous system activity. Fasting suppresses, while carbohydrate and fat feeding stimulate, sympathetic activity. (2) Dietary-induced changes in sympathetic activity contribute to the changes in metabolic rate that accompany changes in dietary intake. (3) Insulin-mediated glucose metabolism in the hypothalamus provides a link between dietary intake and sympathetic nervous system activity. And (4) hyperinsulinemia, a consequence of insulin resistance in the obese, is associated with hypertension. These observations have suggested the following hypothesis. Hyperinsulinemia results in sympathetic stimulation which drives thermogenic mechanisms, thereby increasing metabolic rate. The net result is a restoration of energy balance at the expense of hyperinsulinemia and increased sympathetic activity. Hypertension is thus the unfortunate consequence of hyperinsulinemia, which increases renal sodium reabsorption, and sympathetic stimulation of the heart, kidney, and vasculature. The data on which this hypothesis is constructed are reviewed and the implications discussed.     

The Hypothalamic-Pituitary-Adrenal Axis in Obesity

The hypothalamic-pituitary-adrenal (HPA) axis normally maintains the concentration of Cortisol within a narrow range with a diurnal variation characterized by higher Cortisol concentrations in the morning and reduced levels in the evening. Excessive or deficient secretion of Cortisol is associated with pathologic changes. Obesity has been linked with age, sex and racial alterations in the functioning of the HP A axis which are reviewed. The possible relationship of altered HPA axis activity with the long-term complications of obesity are considered.     

Production Rates of Cortisol in Obesity

Objective: To determine the metabolic clearance rates (MCRs) and endogenous production rates (PRs) of cortisol (F) in grades 2 and 3 obese men (n = 9) and women (n = 6). Research Methods and Procedures: The MCRs and the endogenous PRs of cortisol (F) were determined in grades 2 and 3 obese men (n = 9) and women (n = 6) using the stable isotope dilution technique and mass spectrometry. Results: In obese women, endogenous PRs of F (0.6 ± 0.4 mg/h) were similar to those of nonobese women, but MCRs of F were higher in obese women (9 ± 4 L/h) compared with nonobese women (5 + 2 L/h; p < 0.05). The MCR of F was correlated with the ratio of excreted cortisone to F metabolites. Furthermore, obese women were characterized by an increased ratio of androsterone to etiocholanolone (p < 0.01). In obese men, the MCRs (11 ± 6 L/h) and the endogenous PRs of F (0.6 ± 0.3 mg/h) were both similar to those of nonobese men, but the MCR of F was directly correlated with the ratio of excreted cortisone to F metabolites (r = 0.7833, p = 0.012). Discussion: These data demonstrate sex‐specific differences in F metabolism in obesity. The rise in MCRs of F is more pronounced in obese women than in men. However, the increase in the MCR of F is moderate in both genders and exceeds the normal range only in a subgroup of obese individuals.     

The Road to Obesity or the Path to Prevention: Motorized Transportation and Obesity in China

Objective: Dependence on motorized forms of transportation may contribute to the worldwide obesity epidemic. Shifts in transportation patterns occurring in China provide an ideal opportunity to study the association between vehicle ownership and obesity. Our objective was to determine whether motorized forms of transportation promote obesity. Research Methods and Procedures: A multistage random‐cluster sampling process was used to select households from eight provinces in China. Data were included on household vehicle ownership and individual anthropometric and sociodemographic status. Cross‐sectional data (1997) from 4741 Chinese adults aged 20 to 55 years were used to explore the association between vehicle ownership and obesity. Cohort data (1989 to 1997) from 2485 adults aged 20 to 45 years in 1989 (59% follow‐up) were used to measure the impact of vehicle acquisition on the odds of becoming obese. Results: Our main outcome measure was current obesity status and the odds of becoming obese over an 8‐year period. In 1997, 84% of adults did not own motorized transportation. However, the odds of being obese were 80% higher (p < 0.05) for men and women in households who owned a motorized vehicle compared with those who did not own a vehicle. Fourteen percent of households acquired a motorized vehicle between 1989 and 1997. Compared with those whose vehicle ownership did not change, men who acquired a vehicle experienced a 1.8‐kg greater weight gain (p < 0.05) and had 2 to 1 odds of becoming obese. Discussion: Encouraging active forms of transportation may be one way to protect against obesity.     

Obesity and cardiovascular disease

Available evidence clearly indicates a rapid progression in the prevalence of obesity worldwide. As a consequence, there has also been a marked increase in the prevalence of type 2 diabetes all over the world and this chronic metabolic disease is now considered as a coronary heart disease risk equivalent. However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low density lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. This agglomeration of abnormalities has been referred to as the metabolic syndrome which can be identified by the presence of three of the five following variables: abdominal obesity, elevated triglyceride concentrations, low HDL-cholesterol levels, increased blood pressure and elevated fasting glucose. Post-mortem analyses of coronary arteries have indicated that obesity (associated with a high accumulation of abdominal fat measured at autopsy) was predictive of earlier and greater extent of large vessels atherosclerosis as well as increase of coronary fatty streaks. Metabolic syndrome linked to abdominal obesity is also predictive of recurrent coronary events both in post-myocardial infarction patients and among coronary artery disease men who underwent a revascularization procedures. It is suggested that until the epidemic progression of obesity is stopped and obesity prevented or at least properly managed, cardiologists will be confronted to an evolving contribution of risk factors where smoking, hypercholesterolemia and hypertension may be relatively less prevalent but at the expense of a much greater contribution of abdominal obesity and related features of the metabolic syndrome.