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At least 19 recordsLinked to original sources
PubMed1995

Rate of weight gain, weight fluctuation, and incidence of NIDDM.

The relationships of rate of weight gain and weight fluctuation to incidence of non-insulin-dependent diabetes mellitus (NIDDM) were examined in Pima Indians. The 1,458 subjects were participants in a prospective study with examinations approximately every 2 years. Rate of weight gain was defined as the slope of the regression line of weight with time for two or more consecutive examinations > or = 2 years apart and weight fluctuation as the root-mean-square departure from this line for four examinations. Among men, incidence of NIDDM was strongly and significantly related to rate of weight gain (e.g., age-adjusted incidence = 56.7/1,000 person-years in those with weight gain > or = 3 kg/year and 16.9/1,000 person-years for those losing weight [Ptrend < 0.01]). In women, weight gain was significantly related to diabetes incidence only in those who were not initially overweight (body mass index < 27.3 kg/m2). In contrast to the relationship with weight gain, weight fluctuation was not associated with incidence of diabetes in either sex. These findings suggest that weight control in overweight individuals may be a more effective strategy for prevention of NIDDM in men than in women, whereas prevention of obesity may prevent diabetes in both sexes. Concern about a diabetogenic effect of weight fluctuation should not deter weight-control efforts.

Adult↗
PubMed1980

Relationships between eating rate of sheep and live weight gain, weight and fill of the gastrointestinal tract.

Nine ewe and eight wether weanling lambs were fed a pelleted diet containing 60% roughage and 40% concentrate for 12 h/day. Feed consumption (FC) was measured during the first 30 and 60 min (FC-30, -60). Total daily consumption (FCT) was also measured. With these data, feed efficiency (FE), eating rate index (ERI = FC/BW.75) and propensity to eat (percentage FC/unit of time) were calculated. After the completion of these studies, the lambs were slaughtered and weights of the full gastrointestinal tract (GIT) organs, empty organs and wet digesta were obtained. Dry digesta in the organs were estimated from samples of oven-dried digesta. Respective values for males and females were: FE, 6.36 and 7.50 (P less than .01); average daily gain (ADG), 285 and 230 g (P less than .02); FC-30, 597 and 488 g (P less than .05), and FC-60, 706 and 583 g (P less than .05). Significant correlations were found only for females for FC-30 with FCT, ADG with FE and FC-60 with FE (P less than .05). Significant correlations of ERI-30 and ERI-60 with ADG and FE were also observed for the combined sex data. Correlations between eating rate terms and organ or digesta weights were significant only for some reticulorumen (RR) and abomasal parameters. When data from the GIT were correlated with animal performance (FC, ADG, FE), the highest correlations observed were generally for females. Correlations with organ or digesta weights tended to be highest for the small intestine (SI) and ADG; these were followed by values of about equal magnitude for RR organ or digesta weights and ADG or FE. The highest correlations were those between ADG and full organ weight of the SI for males (.86, P less than .01) and between ADG and wet digesta weights of the SI for females (.86, P less than .01). It is concluded that organ and (or) digesta weights of the SI are highly related to animal performance and may be as important as the RR in affecting voluntary feed consumption of pelleted diets.

Animal Feed↗
PubMed1995

The relationship of maternal attitude toward weight gain to weight gain during pregnancy and low birth weight.

OBJECTIVE: To evaluate the relationships between maternal attitude toward weight gain, actual weight gain, and infant birth weight. METHODS: Maternal attitude toward weight gain during pregnancy was assessed in 1000 women, using an 18-item questionnaire administered at a mean of 20 weeks' gestation. Composite scores were compared with pregnancy weight gain, maternal body mass index (BMI), and infant birth weight. RESULTS: In the total population, the attitude score was not significantly related to pregnancy weight gain (r = -0.05, P = .08) and was negatively associated with birth weight (r = -0.09, P < .004). Maternal body size as measured by BMI was strongly associated with both weight gain and birth weight. Obese women (BMI greater than 26.6) tended to have negative attitudes and had the lowest mean weight gain (10.2 kg), but had the heaviest babies (3400 g). Thin women (BMI less than 19.6) had significantly higher attitude scores and a higher mean weight gain (14.1 kg) than did obese women. A significantly larger proportion of thin women achieved recommended gains when compared with larger women, but had the lightest babies (3114 g). Within the group of thin women, after adjustment for smoking, race, and gestational age at delivery, attitude scores were not significantly associated with either weight gain or birth weight. CONCLUSION: Maternal attitude regarding weight gain is strongly influenced by pre-pregnancy body size; thin women tend to have positive attitudes and obese women tend to have negative attitudes about weight gain. Within BMI groups, a positive attitude does not predict appropriate weight gain or birth weight. These findings may explain in part why nutritional counseling programs tend to be associated with only minimal increases in birth weight.

Black or African American↗
PubMed2004

Pharmacogenetics of antipsychotic-induced weight gain.

Weight gain appears to be a serious side effect encountered during treatment with many antipsychotic drugs. Although the propensities of inducing weight gain vary considerably between antipsychotics, weight gain is mostly observed in atypical antipsychotics, increasingly prescribed for a variety of psychiatric disorders. Beside the psychological consequences weight gain may influence patients' compliance and secondary medical comorbidities related to being overweight may arise, including diabetes, hypertonia, respiratory problems, and some types of cancer. Obesity research generally suggests that a complex system of neurotransmitters, neuropeptides, hormones and immune related factors interact in neural circuits involving at least the hypothalamus, the solitary tract and cortical structures to regulate energy homeostasis and body weight. Antipsychotics that have weight gain inducing properties may disrupt associated pathways at any of these levels, although it remains unclear what the mechanisms of action might be. Given the potential deleterious effects of weight gain, individual predictors of weight gain would be extremely helpful at the beginning of pharmacological treatment with atypical antipsychotics, allowing obesity to be avoided or for counteractive steps such as dietary restrictions to be taken in predisposed individuals. So far, only a few predictors to detect individuals at high risk have been reported and these have limited power. It is likely that genetic factors play a major role in determining individual response to antipsychotics as well as their side effect profile. In this article, we have reviewed literature related to antipsychotic-induced weight gain and have discussed the major issues, before updating the reader on current obesity research findings. Finally, we emphasize previous studies relating to the pharmacogenetics of antipsychotic-induced weight gain.

Animals↗
PubMed1988

Monoamine oxidase inhibitors and weight gain.

Weight gain associated with antidepressant therapy is a common problem that often results in noncompliance. Some authors suggest that monoamine oxidase inhibitors (MAOI) are less likely to produce weight gain than tricyclic antidepressants. This paper addresses the relative potential for weight gain with the MAOI. Assessing the potential for antidepressant-induced weight gain necessitates separating the weight changes associated with alterations in mood disorders from those due to drug-induced alterations in appetite control. The mechanisms of appetite control are reviewed briefly followed by proposed mechanisms by which the MAOI may alter this control. A literature review suggests that phenelzine is the MAOI most likely to induce weight gain; reports of isocarboxazid-induced weight gain are less common. There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug. The MAOI probably have different effects on the mechanisms of appetite control.

Humans↗
PubMed1995

Lithium and body weight gain.

Weight gain is an undesirable side-effect of long-term lithium administration which notably interferes with treatment compliance. The mechanisms of this weight gain remain unclear, making its management in patients difficult. In this paper, studies describing the features of this weight gain in patients and in rats treated with chronic lithium administration are reviewed. The effects of lithium on body weight differ between patients and rats in a number of ways, including the observation that excessive weight gain is observed in both male and female patients, but only in female rats. Nevertheless, an animal model of lithium-induced weight gain may be able to provide useful insights into some of the specific mechanisms involved, particularly those related to interactions with gonadal steroid function. We discuss the effects of lithium on the endocrine system, neurotransmitters, metabolism, electrolyte regulation, and feeding behavior, which might underlie lithium's effects on body weight. Finally, suggestions for the management of weight gain in the clinical setting are presented. These include, in the long term, dietary control and physical activity and, in the short term, choosing among several drugs that have been tested either in patients or in animal models of obesity. If weight gain still cannot be controlled and treatment compliance is at risk, the mood stabilizers carbamazepine or valproic acid might be substituted for lithium treatment.

Animals↗
PubMed2002

Differential activation of orexin neurons by antipsychotic drugs associated with weight gain.

Weight gain is one side effect of many antipsychotic drugs (APDs). A small number of lateral hypothalamic/perifornical area (LH/PFA) neurons express the orexins, peptides that are critically involved in body weight regulation and arousal. We examined the ability of APDs to activate orexin neurons, as reflected by induction of Fos. APDs with significant weight gain liability increased Fos expression in orexin neurons, but APDs with low or absent weight gain liability did not. The weight gain liability of APDs was correlated with the degree of Fos induction in orexin neurons of the lateral LH/PFA. In contrast, amphetamine, which causes weight loss, increased Fos expression in orexin neurons of the medial but not lateral LH/PFA. We compared the effects of amphetamine and clozapine, an APD with weight gain liability, on orexin neurons innervating the prefrontal cortex. Clozapine induced Fos in 75% of the orexin neurons that project to the cortex, but amphetamine induced Fos in less than a third of these cells. These data suggest that APD-induced weight gain is associated with activation of distinct orexin neurons and emphasize the presence of anatomically and functionally heterogeneous populations of orexin neurons.

Amphetamine↗
PubMed2004

[Psychotropics and weight gain].

Weight overload and obesity became these last years a major health problem. However gain weight is a frequent side effect of a large number of psychotropics. This article proposes to discuss this potential while reviewing various molecules. This reveals that the atypical antipsychotics are most likely to induce weight gain, in particular clozapine and olanzapine. The tricyclic antidepressants and mirtazapine come next, with the majority of the mood stabilizers. The old antipsychotics seem to involve less gain of weight. The SSRI make lose weight in the first weeks of treatment, but induce a moderate weight gain on the long term.

Adolescent↗
PubMed2005

Polymorphism of the adrenergic receptor alpha 2a -1291C>G genetic variation and clozapine-induced weight gain.

Weight gain, leading to further morbidity and poor treatment compliance, is a common consequence of treatment with clozapine. The substantial interindividual and interracial differences in drug-induced weight gain suggest that genetic factors may be important. Several studies showed that alpha-2, adrenoceptor may related to feeding behavior with rat or lipolytic activity of human adipocyte tissue, they are related to body weight change. In the study, we try to test the possible relation of clozapine-induced weight gain and adrenergic receptor alpha 2a -1291C>G genetic polymorphism in a long term follow up (14.0 +/- 6.2 months). Our results show the genotype GG (8.45 +/- 7.2 Kg) with higher mean body weight gain than genotype CC (2.79 +/- 6.1 Kg) (p = 0.023). The finding identify a genetic factor associated with clozapine-induced weight gain in schizophrenic patients.

Adult↗
PubMed2006

The influence of maternal socioeconomic and emotional factors on infant weight gain and weight faltering (failure to thrive): data from a prospective birth cohort.

AIMS: To study the influence of maternal socioeconomic and emotional factors on infant weight gain and weight faltering (failure to thrive) in the first year of life. METHODS: The Gateshead Millennium Baby Study is a population birth cohort in northeast England studied prospectively from birth, via parental questionnaires and a health check aged 13 months. Data were collected on maternal education, deprivation, eating attitudes, and depression, using the Edinburgh Post Natal Depression Scale (EPDS) at 3 months. Weight gain was assessed using change in weight SD score, conditional on birth weight (Thrive Index); weight faltering was defined as conditional weight gain below the 5th centile. RESULTS: Of 923 eligible infants born at term, 774 (84%) had both weight and questionnaire data. Replicating a previous finding, both the highest and the lowest levels of deprivation were associated with weight faltering; this was independent of the type of milk feeding. No relation was found with maternal educational status. Maternal eating restraint was unrelated to weight gain. Infants of mothers with high depression symptom scores (EPDS >12) had significantly slower weight gain and increased rates of weight faltering up to 4 months (relative risk 2.5), especially if they came from deprived families, but by 12 months they were no different from the remainder of the cohort. CONCLUSIONS: In this setting, social and maternal characteristics had little influence on infants' weight gain, apart from a strong, but transient effect of postnatal depression.

Child of Impaired Parents↗
PubMed1988

Antidepressants and weight gain.

Weight gain is an often reported, but incompletely understood, side effect of many antidepressant medications. We will discuss the literature with respect to the following issues: weight gain as a pharmacological effect of antidepressants or as an effect of recovery from depression; the incidence of antidepressant-induced weight gain and possible reasons for individual variability in its occurrence; possible mechanisms of antidepressant-induced weight gain; and options for clinical management. Further elucidation of these issues may contribute to our understanding of the neurobiology of affective disorders and appetitive mechanisms.

Antidepressive Agents↗
PubMed2003

Effects of carnitine and taurine on fatty acid metabolism and lipid accumulation in the liver of cats during weight gain and weight loss.

OBJECTIVE: To determine the effects of carnitine (Ca) or taurine (Ta) supplementation on prevention of lipid accumulation in the liver of cats. ANIMALS: 24 adult cats. PROCEDURE: Cats were fed a weight-gaining diet sufficient in n-6 polyunsaturated fatty acids (PUFAs), low in long-chain n-3 PUFAs (n-3 LPUFA), and containing corn gluten for 20 weeks. Cats gained at least 30% in body weight and were assigned to 4 weight-reduction diets (6 cats/diet) for 7 to 10 weeks (control diet, control plus Ca, control plus Ta, and control plus Ca and Ta). RESULTS: Hepatic lipids accumulated significantly during weight gain and weight loss but were not altered by Ca orTa after weight loss. Carnitine significantly increased n-3 and n-6 LPUFAs in hepatic triglycerides, decreased incorporation of 13C palmitate into very-low-density lipoprotein and hepatic triglycerides, and increased plasma ketone bodies. Carnitine also significantly increased weight loss but without altering the fat to lean body mass ratio. Taurine did not significantly affect any variables. Diets low in n-3 LPUFAs predisposed cats to hepatic lipidosis during weight gain, which was further exacerbated during weight loss. Mitochondrial numbers decreased during weight gain and weight loss but were not affected by treatment. Carnitine improved fatty acid oxidation and glucose utilization during weight loss without correcting hepatic lipidosis. CONCLUSIONS AND CLINICAL RELEVANCE: The primary mechanism leading to hepatic lipidosis in cats appears to be decreased fatty acid oxidation. Carnitine may improve fatty acid oxidation but will not ameliorate hepatic lipidosis in cats fed a diet low in n-3 fatty acids.

Animals↗
PubMed1981

Prediction of food intakes, weight gains, organ weights, and tumor size in tumor-bearing rats by the four-parameter mathematical model for physiological responses.

Groups of male weanling rats bearing the transplantable Novikoff ascites hepatoma were fed diets containing graded levels of protein. The food intakes and weight gains were recorded daily. Seven days after inoculation of the rats with the tumor (6 days in Experiment 2), the rats were sacrificed, their organs were weighed, and the tumor and ascites fluid volumes were determined. These results were analyzed by the four-parameter mathematical model for physiological responses. It was found that tumor-bearing rats eat and gain weight at the same rates as control rats fed identical diets, implying that this rapidly growing tumor does not interfere with the normal food intake and growth control mechanisms and that food intakes and weight gains are predictable by the four-parameter model. Organ growth was regulated in both normal and tumor-bearing rats but some actual organ weights in tumor-bearing rats were smaller than in control rats due to the presence of the tumor. However, other organs (spleen, lung, kidneys, and small intestine) of the tumor-bearing rats showed significant differences (p less than 0.01, Student's t test) from control rats. It was also possible to predict the growth of the tumor on the basis of the casein content of the diet.

Animals↗
PubMed2003

Comorbidity of schizophrenia and galactosemia: effective clozapine treatment with weight gain.

Weight gain with atypical antipsychotics such as clozapine has been hypothesized to have a multifactorial genesis. Beside changes in neurotransmitter systems caused by antipsychotic-induced receptor blockade, hormonal changes and other neuroleptic side-effects (sedation, reduced activity, reduced basal metabolic rate, dry mouth) are also discussed. Our unique case report of a patient with comorbid galactosemia and schizophrenia is an interesting example of weight gain being a positive side-effect of clozapine, not necessarily associated with increased appetite and higher caloric intake.

Adult↗
PubMed2000

Relation of weight gain and weight loss on subsequent diabetes risk in overweight adults.

STUDY OBJECTIVE: To determine whether long term weight gain and weight loss are associated with subsequent risk of type 2 diabetes in overweight, non-diabetic adults. DESIGN: Prospective cohort. Baseline overweight was defined as BMI>/=27.3 for women and BMI>/=27. 8 for men. Annual weight change (kg/year) over 10 years was calculated using measured weight at subjects' baseline and first follow up examinations. In the 10 years after measurement of weight change, incident cases of diabetes were ascertained by self report, hospital discharge records, and death certificates. SETTING: Community. PARTICIPANTS: 1929 overweight, non-diabetic adults. MAIN RESULTS: Incident diabetes was ascertained in 251 subjects. Age adjusted cumulative incidence increased from 9.6% for BMI<29 to 26. 2% for BMI>/=37. Annual weight change over 10 years was higher in subjects who become diabetic compared with those who did not for all BMI<35. Relative to overweight people with stable weight, each kg of weight gained annually over 10 years was associated with a 49% increase in risk of developing diabetes in the subsequent 10 years. Each kg of weight lost annually over 10 years was associated with a 33% lower risk of diabetes in the subsequent 10 years. CONCLUSIONS: Weight gain was associated with substantially increased risk of diabetes among overweight adults, and even modest weight loss was associated with significantly reduced diabetes risk. Minor weight reductions may have major beneficial effects on subsequent diabetes risk in overweight adults at high risk of developing diabetes.

Adult↗