Adult fat content: reinterpreting and modelling the Benn Index and related sex differences

Background: In women, the height exponent, p, of the Benn Index, (body mass)/height^p, is typically lower than in men, body masses are more weakly correlated with height and fat masses tend to be higher. In both sexes fat masses correlate only weakly with height. Changes in fat mass are typically accompanied by changes in fat-free mass.

Aims: To integrate these facts, together with other published findings relating to fat content and to explain why p is lower in women.

Methods: Data and statistics are taken from the literature. The differences in p are explored by Monte Carlo and algebraic modelling. Mean transverse areas of the body (MTAs), calculated as (body mass)/height, are related to height.

Results and conclusions: The body can be modelled as consisting of a component, M₁, varying roughly with the cube of height and another, M₂, varying little with height. The low correlation between total body mass and height is due both to M₂ and to data scatter. The low p values in women relate especially to M₂. Relationships amongst height, fatness, MTAs and girths of body parts generally conform to this interpretation. Questions are raised as to how health risks are best related to fat mass.     

Adiposity, inflammation and hyperglycaemia in rural and urban Indian men: Coronary Risk of Insulin Sensitivity in Indian Subjects (CRISIS) Study

Aims/hypothesis The aim of this study was to investigate whether the higher prevalence of insulin resistance and glucose intolerance in urban compared with rural Indian men is related to their higher adiposity (percentage body fat) and the associated inflammatory state. Methods We studied 149 rural, 142 urban slum and 150 urban middle-class male residents (age 30–50 years), who were selected by stratified random sampling. We measured body fat (bioimpedance), waist circumference, glucose tolerance (75 g OGTT), insulin resistance [homeostasis model assessment (HOMA-IR)], beta cell function (insulinogenic index) and inflammatory markers (total leucocyte count, IL-6, TNF-α and C-reactive protein). Results Adiposity, waist circumference, HOMA-IR, insulinogenic index and both fasting and 120 min plasma glucose concentrations increased progressively from rural through to urban slum and urban middle-class men. Inflammatory markers were higher in urban than in rural men. Adiposity was strongly related to HOMA-IR (r = 0.57, p < 0.001) and to insulinogenic index and glycaemic parameters (r = 0.25, p < 0.001 for both). Adiposity explained approximately two thirds of the difference in HOMA-IR between the urban middle-class men and the rural and slum residents, but its contribution to the difference in insulinogenic index and 120 min plasma glucose concentration was not significant. Inclusion of C-reactive protein, IL-6 and total leucocyte count in the models did not further explain these results, nor did the inclusion of waist circumference. There was a significant residual difference after these adjustments. Conclusions/interpretation Adiposity is a major contributor to the difference in insulin resistance between rural and urban Indian men; there was no additional contribution from inflammation or central obesity. Other unmeasured factors also seem to contribute to the metabolic differences between rural and urban men.     

Dairy shows different associations with abdominal and BMI-defined overweight: Cross-sectional analyses exploring a variety of dairy products

Background and aims

Previous studies have suggested weight–regulatory properties for several dairy nutrients, but population-based studies on dairy and body weight are inconclusive. We explored cross–sectional associations between dairy consumption and indicators of overweight.

Custom made Ilizarov ring fixator for fracture care in morbidly obese patients

Background  Fracture care in obese patients is becoming an everyday problem because the prevalence of obesity in European countries has tripled since the last 20 years. Patients and method  With the use of a custom made Ilizarov ring fixator with a ring diameter of 300 to 340 mm, fracture stabilization in three morbidly obese patients was performed. The patients’ body mass index (BMI) ranged from 59 to 89. There were one proximal tibia fracture and two pilon fractures. The tibia fracture was stabilized with a 340-mm frame and the pilon fractures were stabilized by primary ankle arthrodesis with 300-mm frames. Primary ankle arthrodesis was performed because polyneuropathy and Charcot arthropathy were present in one patient and in the other patient because time from injury to referral was too long for reconstruction. Results  All patients were able to fully weight bear. Frame removal after fracture correction and consolidation was performed only in the patient with the tibial fracture (patient BMI 89). The other patients died during the treatment because of decompensated comorbidities. Conclusion  The Ilizarov technique is a good fixation modality for stabilizing fractures of the lower limb in morbidly obese patients. Associated medical comorbidities are the limitations of successful fracture care. Financial Disclaimer: The authors have received nothing of value.     

Circulating adiponectin represents a biomarker of the association between adiposity and bone mineral density

An association exists between adiposity, insulin resistance, and osteoporosis; however, the mechanism of this relationship remains enigmatic. We aimed to determine whether the insulin resistance index (HOMA-IR), serum adiponectin, or leptin levels are associated with bone mineral density (BMD). A cross-sectional, observational study was designed. Eighty-four postmenopausal ambulant women [52.5 (50.0–58.0) years; body mass index (BMI): 29.4 (25.9–33.8) kg/m²] referred for osteoporosis screening were enrolled. Anthropometric measures, fasting serum adiponectin and leptin levels, and the HOMA-IR were determined. The relationships between these variables and lumbar, hip, and forearm BMD measured by dual-energy X-ray absorptiometry (DXA) were analyzed. Considering all 84 participants, the HOMA-IR index was 1.82 (1.17–2.86), serum adiponectin was 13.25 (10.49–16.88) μg/ml, and serum leptin was 19.26 (14.94–24.90) ng/ml. BMI, waist circumference, and leptin positively correlated with hip and lumbar BMD, whereas adiponectin negatively correlated. Multivariate analysis confirmed an inverse relation between serum adiponectin level and femoral neck and lumbar BMD measurements. In total hip and forearm areas, there was no independent association of adipocytokines with BMD measurements. Instead, waist circumference was independently associated with BMD measurements. In conclusion, adiponectin may represent a biomarker in the relationship between visceral fat mass and BMD. However, this association is probably confounded by the specific body composition parameters (i.e., waist circumference, BMI) in postmenopausal women.     

Control of puberty in farmed fish

Puberty comprises the transition from an immature juvenile to a mature adult state of the reproductive system, i.e. the individual becomes capable of reproducing sexually for the first time, which implies functional competence of the brain–pituitary–gonad (BPG) axis. Early puberty is a major problem in many farmed fish species due to negative effects on growth performance, flesh composition, external appearance, behaviour, health, welfare and survival, as well as possible genetic impact on wild populations. Late puberty can also be a problem for broodstock management in some species, while some species completely fail to enter puberty under farming conditions. Age and size at puberty varies between and within species and strains, and are modulated by genetic and environmental factors. Puberty onset is controlled by activation of the BPG axis, and a range of internal and external factors are hypothesised to stimulate and/or modulate this activation such as growth, adiposity, feed intake, photoperiod, temperature and social factors. For example, there is a positive correlation between rapid growth and early puberty in fish. Age at puberty can be controlled by selective breeding or control of photoperiod, feeding or temperature. Monosex stocks can exploit sex dimorphic growth patterns and sterility can be achieved by triploidisation. However, all these techniques have limitations under commercial farming conditions. Further knowledge is needed on both basic and applied aspects of puberty control to refine existing methods and to develop new methods that are efficient in terms of production and acceptable in terms of fish welfare and sustainability.     

Sexual Dimorphism in Body Fat Distribution and Risk for Cardiovascular Diseases

The prevalence of obesity has dramatically increased over the past decade along with the cardiovascular and other health risks it encompasses. Adipose tissue, which is distributed in the abdominal viscera, carries a greater risk for cardiovascular disorders than adipose tissue subcutaneously. There is a sex difference in the regional fat distribution. Women have more subcutaneous fat, whereas men have more visceral fat. Therefore, obesity-related metabolic disorders are much lower in premenopausal women than men. Peripheral metabolic signals like leptin and insulin are involved in the food intake, body weight, body fat distribution, and cardiovascular disease. Key areas in the brain, including the hypothalamus, integrates these peripheral adiposity signals to maintain overall adiposity levels, and these brain regions are directly influenced by sex hormones. Therefore, differences in cardiovascular disease may be under the influence of sex hormones either directly in the brain or through their influence of body fat distribution. The role of estrogen in mediating body fat distribution and cardiovascular disease is the focus of this review.     

Gonadal effects on food intake and adiposity: a metabolic hypothesis.

Ovarian and testicular steroids have important effects on body weight and composition in rats. Estradiol and testosterone decrease adiposity, while progesterone increases carcass fat content. These hormone-induced changes in body weight and composition are accompanied by changes in food intake and voluntary exercise, suggesting that the hormones induce behavioral changes which alter body weight and adiposity. However, several lines of evidence indicate that these behavioral changes are neither necessary nor sufficient to produce the hormone-induced body weight shifts. Rather, peripheral metabolic effects of gonadal steroids may be of primary importance in the control of fat disposition. Steroid effects on triglyceride clearance from circulation, along with changes in hepatic synthesis, may in turn alter the availability of triglycerides as an oxidizable fuel, contributing to the changes in food intake. From this perspective, estradiol- and progesterone-induced changes in food intake are viewed as consequences, rather than causes, of changes in fat metabolism. It is suggested that during naturally-occurring reproductive states gonadal steroids interact with other hormones, such as prolactin, to partition available triglycerides among tissues which oxidize, excrete or store long-chain fatty acids (e.g., striated muscle, mammary gland, or adipose tissue, respectively).     

Leptin does not reduce body fat content but augments cold defense abilities in thermoneutrally reared rat pups

 A previous study showed that recombinant leptin markedly affects the body fat content and thermoregulatory energy expenditure of lean (+/+ and +/fa) suckling-age rats, and we wanted to find out whether leptin in doses that halved body fat of cold-reared lean pups had any effect in thermoneutrally reared lean pups. When +/+ pups were artificially reared from 4 to 16 days of age at thermoneutrality and treated as before with leptin from day 7, their total metabolic rate throughout the treatment period was only 4% higher than that of the control littermates and their final body fat content only 4% lower (both P>0.05). We conclude from comparisons of the results in +/+ pups at cold and thermoneutral conditions that leptin does not stimulate, but rather disinhibits, sympathetically mediated thermoregulatory thermogenesis. Received: 26 February 1997 / Received after revision: 14 July 1997 / Accepted: 17 July 1997     

Transgenerational effects of prenatal exposure to the Dutch famine on neonatal adiposity and health in later life

Objective  Maternal undernutrition during gestation is associated with increased metabolic and cardiovascular disease in the offspring. We investigated whether these effects may persist in subsequent generations.
Design  Historical cohort study.
Setting  Interview during a clinic or home visit or by telephone.
Population  Men and women born in the Wilhelmina Gasthuis in Amsterdam between November 1943 and February 1947.
Methods  We interviewed cohort members (F1) born around the time of the 1944–45 Dutch famine, who were exposed or unexposed to famine in utero , about their offspring (F2).
Main outcome measures  Birthweight, birth length, ponderal index and health in later life (as reported by F1) of the offspring (F2) of 855 participating cohort members, according to F1 famine exposure in utero .
Results  F1 famine exposure in utero did not affect F2 ( n = 1496) birthweight, but, among the offspring of famine-exposed F1 women, F2 birth length was decreased (−0.6 cm, P adjusted for F2 gender and birth order = 0.01) and F2 ponderal index was increased (+1.2 kg/m³, P adjusted for F2 gender and birth order = 0.001). The association remained unaltered after adjusting for possible confounders. The offspring of F1 women who were exposed to famine in utero also had poor health 1.8 (95% CI 1.1–2.7) times more frequently in later life (due to miscellaneous causes) than that of F1 unexposed women.
Conclusions  We did not find transgenerational effects of prenatal exposure to famine on birthweight nor on cardiovascular and metabolic disease rates. F1 famine exposure in utero was, however, associated with increased F2 neonatal adiposity and poor health in later life. Our findings may imply that the increase in chronic disease after famine exposure in utero is not limited to the F1 generation but persists in the F2 generation.