Subsequent Weight Gain Research Articles

Olanzapine-Induced Hyperglycemia in Anorexia Nervosa

Back to table of contents Previous article Next article Letters to the EditorFull AccessOlanzapine-Induced Hyperglycemia in Anorexia NervosaDAISUKE YASUHARA M.D.TOSHIHIRO NAKAHARA M.D., Ph.D.TOSHIRO HARADA M.D.AKIO INUI M.D., Ph.D.,DAISUKE YASUHARA M.D.Search for more papers by this authorTOSHIHIRO NAKAHARA M.D., Ph.D.Search for more papers by this authorTOSHIRO HARADA M.D.Search for more papers by this authorAKIO INUI M.D., Ph.D.Search for more papers by this author,Published Online:1 Mar 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To The Editor: Recent studies on anorexia nervosa have suggested that the atypical antipsychotic agent olanzapine has favorable effects on agitation, repetitive thinking about becoming obese, and subsequent weight gain (1 , 2) . Although hyperglycemia is a serious adverse effect of olanzapine (3) , the incidence varies from less than 1% to 10%, and to the best of our knowledge, there have been no previous reports of this effect in patients with anorexia nervosa. We present a case report of a patient with anorexia nervosa with olanzapine-induced hyperglycemia. A 27-year-old Japanese woman with a 2-year history of anorexia nervosa (restricting type) and no personal or family history of diabetes mellitus or other metabolic or mental disorders was admitted to our hospital with agitation, general fatigue, and fear of obesity. Laboratory results revealed aspartate aminotransferase of 39 IU/l and alanine aminotransferase of 61 IU/l; results of other laboratory examinations (e.g., antiglutamic acid decarboxylase antibodies) were normal. During the first week of hospitalization (body mass index: 14.1 kg/m 2 , mean value of daily energy intake: 1,043 kcal/day), we performed a corrected (1.75g-glucose/kg) oral glucose tolerance test, which showed impaired glucose tolerance (4.3 mmol/l at baseline, peak value of 9.2 mmol/l at 60 minutes, 8.6 mmol/l at 120 minutes) by World Health Organization criteria (4), with delayed insulin secretion (34.6 pmol/l at baseline, peak value of 198 pmol/l at 120 minutes). Thereafter, we prescribed olanzapine 5 mg/day to reduce agitation and fear of obesity; we also started a multidisciplinary treatment program (4). The patient’s agitation improved, and we performed another oral glucose tolerance test during the third week (body mass index: 14.2 kg/m 2 , energy intake: 1,157 kcal/day). Results showed diabetes mellitus (4.2 mmol/l at baseline, peak value of 12.2 mmol/l at 120 minutes) with exaggerated insulin secretion (30.8 pmol/L at baseline, peak value of 1,210 pmol/L at 60 minutes). However, symptoms of diabetes (e.g., excessive thirst or urination) were absent. The patient’s fear of obesity gradually decreased, and olanzapine therapy at 5 mg/day was carefully continued with monitoring of diabetic symptoms, weekly fasting blood glucose levels, and monthly oral glucose tolerance test examinations (3). The lack of symptoms of diabetes and weekly fasting blood glucose levels (range 4.2 to 4.8 mmol/l) remained stable over 10 weeks. Although the patient showed impaired glucose tolerance during the seventh week (body mass index: 15.2 kg/m 2 , energy intake: 1,600 kcal/day), the oral glucose tolerance test results returned to normal at the time of her discharge (body mass index: 18.3 kg/m 2 , energy intake: 1,800 kcal/day). The underlying mechanism of olanzapine-induced hyperglycemia remains unclear (3 , 5 , 6) . Theories regarding this mechanism include the induction of insulin resistance via 5-HT 1A antagonism or impaired insulin-signaling cascade, increased food intake via H 1 antagonism, impaired pancreatic beta cell function, induction of glucogenesis via a decrease in glycogen synthase (5) , increase in glycogen phosphorylase, and upregulation of cocaine and amphetamine regulated transcripts (6) . Exacerbating glucose tolerance with exaggerated insulin secretion was evident on the second oral glucose tolerance test despite no marked differences in fasting plasma glucose levels, body mass index, and energy intake compared with the first oral glucose tolerance test. These findings suggest that glucose intolerance might have been induced by olanzapine via insulin resistance (3 , 5 , 6) . Moreover, hyperglycemia improved after weight restoration despite continuous use of olanzapine, which indicates that undernutrition itself might be a risk factor for olanzapine-induced hyperglycemia, particularly in patients with anorexia nervosa. Clinicians treating acute patients with anorexia nervosa should carefully monitor glucose metabolism, especially in patients being treated with olanzapine. Sakuragaoka, Kagoshima City, JapanSupported by a research grant from the Japanese Ministry of Health, Labor, and Welfare. The authors report no competing interests.Reprints are not available; however, Letters to the Editor can be downloaded at http://ajp.psychiatryonline.org.

Olanzapine-Induced Hyperglycemia in Anorexia Nervosa

Back to table of contents Previous article Next article Letters to the EditorFull AccessOlanzapine-Induced Hyperglycemia in Anorexia NervosaDAISUKE YASUHARA M.D.TOSHIHIRO NAKAHARA M.D., Ph.D.TOSHIRO HARADA M.D.AKIO INUI M.D., Ph.D.,DAISUKE YASUHARA M.D.Search for more papers by this authorTOSHIHIRO NAKAHARA M.D., Ph.D.Search for more papers by this authorTOSHIRO HARADA M.D.Search for more papers by this authorAKIO INUI M.D., Ph.D.Search for more papers by this author,Published Online:1 Mar 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To The Editor: Recent studies on anorexia nervosa have suggested that the atypical antipsychotic agent olanzapine has favorable effects on agitation, repetitive thinking about becoming obese, and subsequent weight gain (1 , 2) . Although hyperglycemia is a serious adverse effect of olanzapine (3) , the incidence varies from less than 1% to 10%, and to the best of our knowledge, there have been no previous reports of this effect in patients with anorexia nervosa. We present a case report of a patient with anorexia nervosa with olanzapine-induced hyperglycemia. A 27-year-old Japanese woman with a 2-year history of anorexia nervosa (restricting type) and no personal or family history of diabetes mellitus or other metabolic or mental disorders was admitted to our hospital with agitation, general fatigue, and fear of obesity. Laboratory results revealed aspartate aminotransferase of 39 IU/l and alanine aminotransferase of 61 IU/l; results of other laboratory examinations (e.g., antiglutamic acid decarboxylase antibodies) were normal. During the first week of hospitalization (body mass index: 14.1 kg/m 2 , mean value of daily energy intake: 1,043 kcal/day), we performed a corrected (1.75g-glucose/kg) oral glucose tolerance test, which showed impaired glucose tolerance (4.3 mmol/l at baseline, peak value of 9.2 mmol/l at 60 minutes, 8.6 mmol/l at 120 minutes) by World Health Organization criteria (4), with delayed insulin secretion (34.6 pmol/l at baseline, peak value of 198 pmol/l at 120 minutes). Thereafter, we prescribed olanzapine 5 mg/day to reduce agitation and fear of obesity; we also started a multidisciplinary treatment program (4). The patient’s agitation improved, and we performed another oral glucose tolerance test during the third week (body mass index: 14.2 kg/m 2 , energy intake: 1,157 kcal/day). Results showed diabetes mellitus (4.2 mmol/l at baseline, peak value of 12.2 mmol/l at 120 minutes) with exaggerated insulin secretion (30.8 pmol/L at baseline, peak value of 1,210 pmol/L at 60 minutes). However, symptoms of diabetes (e.g., excessive thirst or urination) were absent. The patient’s fear of obesity gradually decreased, and olanzapine therapy at 5 mg/day was carefully continued with monitoring of diabetic symptoms, weekly fasting blood glucose levels, and monthly oral glucose tolerance test examinations (3). The lack of symptoms of diabetes and weekly fasting blood glucose levels (range 4.2 to 4.8 mmol/l) remained stable over 10 weeks. Although the patient showed impaired glucose tolerance during the seventh week (body mass index: 15.2 kg/m 2 , energy intake: 1,600 kcal/day), the oral glucose tolerance test results returned to normal at the time of her discharge (body mass index: 18.3 kg/m 2 , energy intake: 1,800 kcal/day). The underlying mechanism of olanzapine-induced hyperglycemia remains unclear (3 , 5 , 6) . Theories regarding this mechanism include the induction of insulin resistance via 5-HT 1A antagonism or impaired insulin-signaling cascade, increased food intake via H 1 antagonism, impaired pancreatic beta cell function, induction of glucogenesis via a decrease in glycogen synthase (5) , increase in glycogen phosphorylase, and upregulation of cocaine and amphetamine regulated transcripts (6) . Exacerbating glucose tolerance with exaggerated insulin secretion was evident on the second oral glucose tolerance test despite no marked differences in fasting plasma glucose levels, body mass index, and energy intake compared with the first oral glucose tolerance test. These findings suggest that glucose intolerance might have been induced by olanzapine via insulin resistance (3 , 5 , 6) . Moreover, hyperglycemia improved after weight restoration despite continuous use of olanzapine, which indicates that undernutrition itself might be a risk factor for olanzapine-induced hyperglycemia, particularly in patients with anorexia nervosa. Clinicians treating acute patients with anorexia nervosa should carefully monitor glucose metabolism, especially in patients being treated with olanzapine. Sakuragaoka, Kagoshima City, JapanSupported by a research grant from the Japanese Ministry of Health, Labor, and Welfare. The authors report no competing interests.Reprints are not available; however, Letters to the Editor can be downloaded at http://ajp.psychiatryonline.org.

Craving for sweet carbohydrate and fat‐rich foods – possible triggers and impact on nutritional intake

Summary This paper presents a review of the literature pertaining to the measurement and prevalence of, and triggers for, cravings for sweet carbohydrate and fat‐rich foods, and considers the impact of such cravings on nutrient intake. Difficulties in defining the construct and measurement of food cravings are discussed, and recent progress highlighted in the measurement arena by the development of two psychometric instruments that appear to have good validity and reliability. With regards to triggers for cravings for sweet carbohydrate and fat‐rich foods, most studies have focused on negative mood state. While it is likely that a variety of food‐related cues may influence cravings (e.g. the smell, sight, taste, and mouth‐feel or texture of food, as well as thoughts of and images of food), this is an area that has received relatively little attention in the scientific literature. Similarly, there is a lack of information about the impact of cravings on nutrient intake. Preliminary data indicate that, at least for older people, cravers’ nutrient intake meets or exceeds the recommended daily amounts for most nutrients. However, energy intake is higher among cravers compared with non‐cravers, and a greater proportion of their energy comes from carbohydrates, especially sugars. This may have an adverse effect on subsequent weight gain. Indeed, these preliminary data found cravers to have a higher body mass index than non‐cravers.

Food insecurity and subsequent weight gain in women

Cross-sectional data indicate that a relationship between household food insecurity and overweight exists among women in the USA. Cross-sectional data cannot determine if food insecurity leads to overweight as some have hypothesised. The purpose of the present study was to examine the relationship of food insecurity with subsequent weight gain in women using data from the Panel Study of Income Dynamics (PSID). Panel data from the 1999 and 2001 PSID, a nationally representative sample of households, were analysed using multivariate regression procedures. Average weight gain among all women (n = 5595) was 1.1 kg on average over the two years. There were no significant differences in the percentages of women who gained a clinically significant amount (2.3 kg) by food insecurity status. Overweight women who were on a weight-gain trajectory during the 2-year period gained less if they were food-insecure. This relationship was not observed among healthy-weight or obese women. Overall, food insecurity does not appear to be strongly associated with subsequent weight gain in women.

Musculoskeletal Fitness and Weight Gain in Canada

Obesity is a growing health issue in Canada, and identifying the determinants of weight gain is important for the development of appropriate prevention strategies. To quantify the association between musculoskeletal fitness (MSF) and subsequent weight gain and development of obesity. The sample included 606 participants (20-69 yr; 291 men, 315 women) from the Physical Activity Longitudinal Study (PALS), a follow-up of participants from the 1981 Canadian Fitness Survey. Standardized assessments of height, weight, MSF (push-ups, sit-ups, grip strength, and trunk flexibility), and cardiorespiratory fitness were made at baseline (1981). Follow-up data on self-reported height and weight and body mass index (BMI) were collected by survey in 2002-2004. Logistic regression was used to predict obesity and weight gain of > or = 10 kg between 1981 and 2002-2004. During the 20-yr follow-up, the prevalence of obesity (BMI > or = 30 kg.m(-2)) increased from 3.1 to 15.2%, reflecting a mean weight gain of 7.4 kg (men: 6.7 kg; women: 8.1 kg). Further, independent of age, sex, baseline BMI, physical activity, cardiorespiratory fitness, smoking, alcohol consumption, and income, low MSF was associated with significantly higher odds of having gained at least 10 kg during follow-up (OR: 1.78, 95% CI: 1.14-2.79). The results indicate that MSF is a significant predictor of weight gain during a 20-yr period. Promoting participation in activities that enhance MSF may be beneficial in attenuating age-related weight gain and in preventing obesity among Canadians.

Weight cycling of athletes and subsequent weight gain in middleage

Weight cycling of athletes and subsequent weight gain in middleage

Weight and Depressive Symptoms in Older Adults: Direction of Influence?

. The purpose of this study was to clarify the direction of the relationship between changes in depressive symptoms and changes in weight in older adults. Methods. The sample included a prospective cohort of individuals aged 53-63 (n = 9,130) enrolled in the Health and Retirement Study. We used separate cross-lagged models for men and women in order to study the impact of weight change on subsequent increases in depressive symptoms 2 years later and vice versa. . Weight gain did not lead to increased depressive symptoms, and weight loss preceded increased depressive symptoms only in unadjusted models among men (odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.04-1.53). Increased depressive symptoms were not predictive of subsequent weight loss, but they were predictive of subsequent weight gain in unadjusted models only (men: OR = 1.24, 95% CI = 1.00-1.54; women: OR = 1.12, 95% CI = 1.00-1.26). In adjusted models, baseline depressive symptoms predicted both weight loss and weight gain among both men and women. Increase in functional limitations and medical conditions were significant predictors of both weight loss and weight gain. Baseline functional limitations also predicted increased depressive symptoms. Discussion. Based on our findings, it is apparent that researchers need to examine the pathways between changes in weight and increases in depressive symptoms in the context of functional limitations and medical comorbidity.

Age at Menarche: Influences of Prenatal and Postnatal Growth

The objective of this study was to determine the influence of birth weight and postnatal weight gain on age at menarche. This was a prospective cohort study where girls from the West Australian Pregnancy (Raine) Cohort Study were followed prospectively from fetal life (18 wk of pregnancy) to adolescence (12-14 yr). Age at menarche was the main outcome measure. Growth status at birth was judged by expected birth weight ratio (EBW; a ratio of observed infant's birth weight over median birth weight appropriate for maternal age, weight, height, parity, infant sex, and gestational age). Postnatal growth status was judged by body mass index (BMI). Both EBW (P = 0.020) and BMI in childhood (8 yr of age) (P < 0.001) were associated with age at menarche. Menarche occurred earlier in girls with lower EBW and higher BMI. We have demonstrated for the first time that both birth weight and weight gain in childhood are associated with age at menarche. Weight gain before birth and subsequent weight gain up to the age of 8 yr were found to have opposing influences on the timing of menarche. Lower EBW combined with higher BMI during childhood predicted early age at menarche, and this relationship existed across normal birth weight and BMI ranges.

Weight Gain Occurs After Onset of Bipolar Illness in Overweight Bipolar Patients

Bipolar patients appear to have a risk of weight gain and obesity higher than the general population. This has traditionally been attributed to medication and disease variables, but there have not been any studies that have investigated this directly. We examined 32 consecutive bipolar subjects and 32 matched controls for weight, BMI, fat content, and historic weight at age 18. Bipolar patients were heavier (193.1 +/- 55.6 vs. 165.6 +/- 37.8 lbs., P = 0.03), with greater BMI (30.3 +/- 8.8 vs. 24.3 +/- 4.0, P = 0.001), and higher fat content (33.3 +/- 9.9 vs. 19.1 +/- 9.9%, P < 0.0001) than psychiatrically well controls. A larger fraction of bipolar subjects were obese (BMI > 30, 50% vs. 9.7%, z = 3.88, P < 0.01). However, weight at age 18 was not statistically different (143.0 +/- 35.8 for bipolar subjects vs. 152.8 +/- 42.7 lbs., P = 0.3). This is the first controlled study examining weight gain in bipolar illness and the first demonstration that premorbid weight is in the normal range for bipolar subjects. Subsequent weight gain is probably related to illness and treatment variables.

Association between Reduced Sleep and Weight Gain in Women

Physiologic studies suggest that sleep restriction has metabolic effects that predispose to weight gain. The authors investigated the association between self-reported usual sleep duration and subsequent weight gain in the Nurses' Health Study. The 68,183 women who reported habitual sleep duration in 1986 were followed for 16 years. In analyses adjusted for age and body mass index, women sleeping 5 hours or less gained 1.14 kg (95% confidence interval (CI): 0.49, 1.79) more than did those sleeping 7 hours over 16 years, and women sleeping 6 hours gained 0.71 kg (95% CI: 0.41, 1.00) more. The relative risks of a 15-kg weight gain were 1.32 (95% CI: 1.19, 1.47) and 1.12 (95% CI: 1.06, 1.19) for those sleeping 5 and 6 hours, respectively. The relative risks for incident obesity (body mass index: >30 kg/m(2)) were 1.15 (95% CI: 1.04, 1.26) and 1.06 (95% CI: 1.01, 1.11). These associations remained significant after inclusion of important covariates and were not affected by adjustment for physical activity or dietary consumption. These data suggest that short sleep duration is associated with a modest increase in future weight gain and incident obesity. Further research is needed to understand the mechanisms by which sleep duration may affect weight.

Growth, current size and the role of the 'reversal paradox' in the foetal origins of adult disease: an illustration using vector geometry

Numerous studies have reported inverse associations between birth weight and a range of diseases in later life. These have led to the development of the 'foetal origins of adult disease hypothesis'. However, many such studies have only been able to demonstrate a statistically significant association between birth weight and disease in later life by adjusting for current size. This has been interpreted as evidence that the impact of low birth weight on subsequent disease is somehow dependent on subsequent weight gain, and has led to a broadening of the hypothesis into the 'developmental origins of health and disease'. Unfortunately, much of the epidemiological evidence used for both of these interpretations is prone to a statistical artefact known as the 'reversal paradox'. The aim of this paper is to illustrate why, using vector geometry.

Does Maternal Control During Feeding Moderate Early Infant Weight Gain?

Our objective with this study was to examine whether observed maternal control during feeding at 6 months of age moderates the development of early infant weight gain during the first year of life. Sixty-nine women were observed feeding their 6-month-old infants during a standard meal. Mealtimes were coded for maternal use of controlling feeding behavior. All infants were weighed at birth and at 6 and 12 months of age, and weight gain was calculated from birth to 6 months and from 6 to 12 months. Weight scores and weight gain scores were standardized for prematurity, age, and gender. Infant weight gain between 6 and 12 months of age was predicted by an interaction between early infant weight gain (birth to 6 months) and observed maternal control during feeding at 6 months. When maternal control was moderate or low, there was a significant interaction with weight gain from birth to 6 months in the prediction of later infant weight gain from 6 to 12 months, such that infants who showed slow early weight gain accelerated in their subsequent weight gain, and those with greater early weight gain decelerated. Conversely, when maternal control was high, infant weight gain followed the opposite pattern. Maternal control of solid feeding can moderate infant weight gain.

Association of Initial Antipsychotic Response to Clozapine and Long-Term Weight Gain

The aim of this study was to test whether the initial antipsychotic response to clozapine is related to subsequent weight change. This study was an 8-year retrospective chart review of 96 hospitalized patients with schizophrenia. Data on monthly weight change, initial clinical response, age, gender, clozapine dose, and concomitant use of mood stabilizers and other antipsychotics were analyzed. Fifty-five (57.3%) of the patients received clozapine over the entire 8-year period; these subjects experienced an average weight gain of 11.7 kg (SD=1.6). Seventeen of these patients (30.9%) who had a significant initial clinical response (CGI improvement rating of 1 or 2 during the first 14 months) gained significantly more weight (13.8 kg [SD=8.4]) than did the 38 patients without a significant initial response (4.5 kg [SD=12.0]). Multiple linear regression analysis showed significant initial clinical response and lower baseline body mass index were associated with significantly more weight gain. The results show that initial antipsychotic response to clozapine is associated with subsequent long-term weight gain as measured over 8 years.

Association of Initial Antipsychotic Response to Clozapine and Long-Term Weight Gain

The aim of this study was to test whether the initial antipsychotic response to clozapine is related to subsequent weight change. This study was an 8-year retrospective chart review of 96 hospitalized patients with schizophrenia. Data on monthly weight change, initial clinical response, age, gender, clozapine dose, and concomitant use of mood stabilizers and other antipsychotics were analyzed. Fifty-five (57.3%) of the patients received clozapine over the entire 8-year period; these subjects experienced an average weight gain of 11.7 kg (SD=1.6). Seventeen of these patients (30.9%) who had a significant initial clinical response (CGI improvement rating of 1 or 2 during the first 14 months) gained significantly more weight (13.8 kg [SD=8.4]) than did the 38 patients without a significant initial response (4.5 kg [SD=12.0]). Multiple linear regression analysis showed significant initial clinical response and lower baseline body mass index were associated with significantly more weight gain. The results show that initial antipsychotic response to clozapine is associated with subsequent long-term weight gain as measured over 8 years.

Analysis of Recent Papers in Hypertension

Analysis of Recent Papers in Hypertension

Weight cycling of athletes and subsequent weight gain in middleage

To study the effects of repeated cycles of weight loss and regain as young adults on long-term weight development. A follow-up study with questionnaires in 1985, 1995 and 2001. Finland. A national cohort of 1838 male elite athletes who had represented Finland in major international sport competitions in 1920-1965, including 370 men engaged in sports in which weight-related performance classes are associated with weight cycling (boxers, weight lifters and wrestlers; further called as weight cyclers), and 834 matched control men with no athletic background. Weight change since the age of 20 years, body mass index (BMI) and prevalence of obesity and overweight. The weight cyclers gained 5.2 BMI units from age 20 years to their maximum mean weight, which was at age 58.7 years. Corresponding figures for the controls were 4.2 BMI units at 58.5 years and for other athletes 3.3 BMI units at age 62.5 years. The proportion of obese (BMI> or =30 kg/m(2)) subjects was greatest among the weight cyclers both in 1985 and 1995. In 2001, the weight cyclers were more often obese than other athletes, but did not differ from the controls. The odds ratio for the weight cyclers to be obese compared to other athletes in 1985 was 3.18 (95% confidence intervals 2.09-4.83), and compared to the controls 2.0 (1.35-2.96). The enhanced weight gain of the weight cyclers was not accounted for by present health habits (smoking, alcohol use, use of high-fat milk or physical activity) or weight at age 20 years. Repeated cycles of weight loss and regain appear to enhance subsequent weight gain and may predispose to obesity. Chronic dieting with weight cycling may be harmful for permanent weight control.

Psychological Workload and Weight Gain Among Women with and without Familial Obesity

High job demands and low job influence may be associated with subsequent weight gain. Predisposition to obesity may further modify such associations. The purpose of the study was to determine whether familial predisposition to obesity modified associations between psychological workload and 6-year weight changes among nurses. A total of 6404 Danish nurses 45 to 65 years old, who belonged to the workforce in both 1993 and 1999, answered a questionnaire on psychological workload, body weight, and familial obesity. Women were considered to be predisposed to obesity if they were overweight and had at least one obese parent. Parents' body shape was reported using pictograms. An increased psychological workload, reflected by high job demands and low influence in job, was associated with an increased body weight. This was particularly the case for nurses being predisposed to obesity, suggesting a synergy between familial obesity predisposition and the psychological workload environment. An interaction test among job demands, familial predisposition to obesity, and weight gain on adjusted data was made. The test showed p = 0.05. The adjusted interaction test among influence in job, familial predisposition to obesity, and weight gain showed p = 0.02. Predisposed nurses who were busy in their job gained 4.4 kg, whereas other nurses gained only 3.2 kg during the 6 years. Similarly, nurses predisposed to obesity with low influence in job had a higher body weight gain (5.4 vs. 3.2 kg) compared with other nurses. High psychological workload due to high job demands and low influence in job seems to predict weight gain in general and, in particular, among those nurses with a familial predisposition to obesity.

Predictors of weight gain in a Mediterranean cohort: the Seguimiento Universidad de Navarra Study

High consumption of sugar-sweetened drinks has been associated with weight gain and obesity in the United States. This trend may also be affecting populations with different eating patterns who increasingly are adopting typical US dietary patterns. We assessed whether the consumption of sweetened drinks and other food items increased the likelihood of weight gain in a Mediterranean population. This was a prospective cohort analysis of 7194 men and women with a mean age of 41 y who were followed-up for a median of 28.5 mo with mailed questionnaires. Dietary exposure was assessed with a previously validated semiquantitative food-frequency questionnaire. During follow-up, we observed that 49.5% of the participants increased their weight (x weight gain: 0.64 kg; 95% CI: 0.55, 0.73 kg). In the participants who had gained > or =3 kg in the 5 y before baseline, the adjusted odds ratio of subsequent weight gain for the fifth quintile compared with the first quintile of sugar-sweetened soft drink consumption was 1.6 (95% CI: 1.2, 2.1; P for trend = 0.02). This association was absent in the participants who had not gained weight in the 5-y period before baseline. The consumption of hamburgers, pizza, and sausages (as a proxy for fast-food consumption) was also independently associated with weight gain (adjusted odds ratio for the fifth compared with the first quintile = 1.2; 95% CI: 1.0, 1.4; P for trend = 0.05). We also found a significant, but weaker, association between weight gain and both red meat and sweetened fruit juice consumption. In a Mediterranean cohort, particularly in the participants who had already gained weight, an increased consumption of sugar-sweetened soft drinks and of hamburgers, pizza, and sausages was associated with a higher risk of additional subsequent weight gain.

Work stress, weight gain and weight loss: evidence for bidirectional effects of job strain on body mass index in the Whitehall II study

Previous research has focused on overall associations between work stress and body mass index (BMI) ignoring the possibility that stress may cause some people to eat less and lose weight and others to eat more. Using longitudinal data, we studied whether work stress induced weight loss in lean individuals and weight gain in overweight individuals. Prospective cohort study. A total of 7965 British civil servants (5547 men and 2418 women) aged 35-55 at study entry (The Whitehall II study). Work stress, indicated by the job strain model and measured as job control, job demands and job strain, was assessed at baseline and BMI at baseline and at 5-year follow-up. In men, the effect of job strain on weight gain and weight loss was dependent on baseline BMI (P</=0.03). In the leanest quintile (BMI<22 kg/m(2)) at baseline, high job strain and low job control were associated with weight loss by follow-up, whereas among those in the highest BMI quintile (>27 kg/m(2)), these stress indicators were associated with subsequent weight gain. No corresponding interaction was seen among women. Inconsistent findings reported by previous studies of stress and BMI have generally been interpreted to indicate the absence of an association. In light of our results, the possibility of differential effects of work stress should also be taken into account.

.BETA.2- and .BETA.3-Adrenoceptor Polymorphisms Relate to Subsequent Weight Gain and Blood Pressure Elevation in Obese Normotensive Individuals

High blood pressure (BP) is a major determinant of cardiovascular events in obesity. The beta2- and beta3-adrenoceptor polymorphisms are associated with obesity and hypertension. In the present study, we examine the relationships of beta2- and beta3-adrenoceptor polymorphisms with further weight gain-induced BP elevation in obese subjects. Changes in BP, body weight, total body fat-mass, waist-to-hip ratio, plasma norepinephrine (NE) and leptin levels, and beta2(Arg16Gly)- and beta3(Trp64Arg)-adrenoceptor polymorphisms were measured periodically over a 5-year period in 55 entry obese (body mass index [BMI]> or =25.0 kg/m(2)) normotensive (BP<140/90 mmHg) men. BP elevation and weight gain were defined as > or =10% increases from entry levels over 5 years in mean BP or BMI. Obese subjects with weight gain, BP elevation or weight gain-induced BP elevation had higher frequencies of the Gly16 allele of Arg16GIy and Arg64 allele of Trp64Arg. Subjects carrying the Gly16 or Arg64 alleles had significantly greater total fat-mass and waist-to-hip ratio at entry and over a 5-year period compared to the subjects who did not carry these polymorphisms. Subjects carrying the Gly16 allele had similar levels of plasma NE, higher levels of plasma leptin and a lower slope of the regression lines between plasma leptin and NE levels. Those carrying the Arg64 allele had higher plasma NE levels at entry and over a 5-year period compared to the subjects without the Arg64 allele, but plasma leptin levels and slopes were similar. The findings demonstrate that the Arg64 allele of the beta3-adrenoceptor polymorphisms relates to weight gain-induced BP elevation accompanying high plasma NE (heightened sympathetic activity) in obese men. The Gly16 allele of the beta2-adrenoceptor polymorphisms links to weight gain-induced BP elevation associated with leptin resistance. beta2- and beta3-adrenoceptor polymorphisms could predict the future BP elevation and further weight gain-induced BP elevation in originally obese subjects.