Environmental contributions to autism: Explaining the rise in incidence of autistic spectrum disorders

The incidence of autism spectrum disorders, a heterogenous group of neurodevelopmental disorders is increasing. In response, there has been a concerted effort by researchers to identify environmental risk factors that explain the epidemiological changes seen with autism. Advanced parental age, maternal migrant status, maternal gestational stress, pregnancy and birth complications, maternal obesity and gestational diabetes, maternal vitamin D deficiency, use of antidepressants during gestation and exposure to organochlorine pesticides during pregnancy are all associated with an increased risk of autism. Folic acid use prior to pregnancy may reduce the risk of autism. Exposure to antenatal ultrasonography, maternal gestational cigarette and alcohol use do not appear to influence the risk of autism in offspring. There is little evidence that exposure to environmental toxins such as thimerosal, polybrominated diphenyl ethers and di-(2-ethylhexyl) phthalate in early childhood increases the risk of autism. Apart from birth complications, the current evidence suggests that the majority of environmental factors increasing the risk of autism occur in the antenatal period. Consistent with the rise in incidence in autism, some of these environmental factors are now more common in developed nations. Further research is required to determine how these environmental exposures translate to an increased risk of autism. Understanding how these exposures alter neurodevelopment in autistic children may inform both the aetiopathogenesis and the strategies for prevention of autism.

Parkinson's disease, nutrition, and surgery in context of critical care

Parkinson’s disease is a common neurodegenerative disorder with a higher risk of hospitalization than the general population. Therefore, there is a high likelihood of encountering a person with Parkinson’s disease in acute or critical care. Most people with Parkinson’s disease are over the age of 60 years and are likely to have other concurrent medical conditions. Parkinson’s disease is more likely to be the secondary diagnosis during hospital admission. The primary diagnosis may be due to other medical conditions or as a result of complications from Parkinson’s disease symptoms. Symptoms include motor symptoms, such as slowness of movement and tremor, and non-motor symptoms, such as depression, dysphagia, and constipation. There is a large degree of variation in the presence and degree of symptoms as well as in the rate of progression. There is a range of medications that can be used to manage the motor or non-motor symptoms, and side effects can occur. Improper administration of medications can result in deterioration of the patient’s condition and potentially a life-threatening condition called neuroleptic malignant-like syndrome. Nutrients and delayed gastric emptying may also interfere with intestinal absorption of levodopa, the primary medication used for motor symptom management. Rates of protein-energy malnutrition can be up to 15 % in people with Parkinson’s disease in the community, and this is likely to be higher in the acute or critical care setting. Nutrition-related care in this setting should utilize the Nutrition Care Process and take into account each individual’s Parkinson’s disease motor and non-motor symptoms, the severity of disease, limitations due to the disease, medical management regimen, and nutritional status when planning nutrition interventions. Special considerations may need to be taken into account in relation to meal and medication times and the administration of enteral feeding. Nutrition screening, assessment, and monitoring should occur during admission to minimize the effects of Parkinson's disease symptoms and to optimise nutrition-related outcomes.

Current practice in nutrition diagnosis and intervention for the management of Parkinson's disease in Australia and Canada

Aim To document current practice by dietitians in Australia and Canada in the nutrition management of Parkinson's disease. This will help identify priority areas for review and development of practice guidelines and direct future research. Methods Current practice in the phases of the Nutrition Care Plan was captured using an online survey distributed to Dietitians Association of Australia members and Practice-Based Evidence in Nutrition subscribers through their email newsletters. The results of the diagnosis, intervention and monitoring phases are presented here. Results Eighty-four dietitians responded. There was consistency in practice for nutrition issues that are encountered in other populations, such as malnutrition and constipation. There was more variation in practice in the nutrition issues that are more specific to Parkinson's disease, such as nutrition and meal interactions with medication. A lack of awareness of emerging treatments, such as deep brain stimulation surgery, appears to exist in the responding dietitians. Conclusions The variation in practice that was present for the nutrition issues specific to Parkinson's disease may reflect the lack of quality evidence and subsequently evidence-based guidelines in these areas. Work to provide background information about treatment options and to translate current evidence for the nutrition issues that are specific to Parkinson's disease into practice recommendations should be completed.

Long-term effect of childhood liver transplantation on body cell mass

Malnutrition is common in end-stage liver disease, but a correction after transplantation is expected. Body cell mass (BCM) assessment using total body potassium (TBK) measurements is considered the gold standard for assessing nutritional status. The aim of this study was to examine the BCM and, therefore, nutritional status of long-term survivors after childhood liver transplantation. © 2014 American Association for the Study of Liver Diseases.

Resting energy expenditure in children with inflammatory bowel disease

OBJECTIVES: There is controversy in the literature regarding the effect of inflammatory bowel disease (IBD) on resting energy expenditure (REE). In many cases this may have resulted from inappropriate adjustment of REE measurements to account for differences in body composition. This article considers how to appropriately adjust measurements of REE for differences in body composition between individuals with IBD. PATIENTS AND METHODS: Body composition, assessed via total body potassium to yield a measure of body cell mass (BCM), and REE measurements were performed in 41 children with Crohn disease and ulcerative colitis in the Royal Children's Hospital, Brisbane, Australia. Log-log regression was used to determine the power function to which BCM should be raised to appropriately adjust REE to account for differences in body composition between children. RESULTS: The appropriate value to "adjust" BCM was found to be 0.49, with a standard error of 0.10. CONCLUSIONS: Clearly, there is a need to adjust for differences in body composition, or at the very least body weight, in metabolic studies in children with IBD. We suggest that raising BCM to the power of 0.5 is both a numerically convenient and a statistically valid way of achieving this aim. Under circumstances in which the measurement of BCM is not available, raising body weight to the power of 0.5 remains appropriate. The important issue of whether REE is changed in cases of IBD can then be appropriately addressed. © 2007 Lippincott Williams & Wilkins, Inc.

Body composition and components of energy expenditure in children with end-stage liver disease

Background: Better understanding of body composition and energy metabolism in pediatric liver disease may provide a scientific basis for improved medical therapy aimed at achieving optimal nutrition, slowing progression to end-stage liver disease (ESLD), and improving the outcome of liver transplantation. Methods: Twenty-one children less than 2 years of age with ESLD awaiting liver transplantation and 15 healthy, aged-matched controls had body compartment analysis using a four compartment model (body cell mass, fat mass, extracellular water, and extracellular solids). Subjects also had measurements of resting energy expenditure (REE) and respiratory quotient (RQ) by indirect calorimetry. Nine patients and 15 control subjects also had measurements of total energy expenditure (TEE) using doubly labelled water. Results: Mean weights and heights were similar in the two groups. Compared with control subjects, children with ESLD had higher relative mean body cell mass (33 ± 2% vs 29 ± 1% of body weight, P < 0.05), but had similar fat mass, extracellular water, and extracellular solid compartments (18% vs 20%, 41% vs 38%, and 7% vs 13% of body weight respectively). Compared with control subjects, children with ESLD had 27% higher mean REE/body weight (0.285 ± 0.013 vs 0.218. ± 0.013 mJ/kg/24h, P < 0.001), 16% higher REE/unit cell mass (P < 0.05); and lower mean RQ (P < 0.05). Mean TEE of patients was 4.70 ± 0.49 mJ/24h vs 3.19 ± 0.76 in controls, (P < 0.01). Conclusions: In children, ESLD is a hypermetabolic state adversely affecting the relationship between metabolic and non-metabolic body compartments. There is increased metabolic activity within the body cell mass with excess lipid oxidation during fasting and at rest. These findings have implications for the design of appropriate nutritional therapy.

Energy expenditure and the body cell mass in cystic fibrosis

Poor nutritional status in patients with cystic fibrosis (CF) is associated with severe lung disease, and possible causative factors include inadequate intake, malabsorption, and increased energy requirements. Body cell mass (which can be quantified by measurement of total body potassium) provides an ideal standard for measurements of energy expenditure. The aim of this study was to compare resting energy expenditure (REE) in patients with CF with both predicted values and age-matched healthy children and to determine whether REE was related to either nutritional status or pulmonary function. REE was measured by indirect calorimetry and body cell mass by scanning with total body potassium in 30 patients with CF (12 male, mean age = 13.07 ± 0.55 y) and 18 healthy children (six male, mean age = 12.56 ± 1.25 y). Nutritional status was expressed as a percentage of predicted total body potassium. Lung function was measured in the CF group by spirometry and expressed as the percentage of predicted forced expiratory volume in 1 s. Mean REE was significantly increased in the patients with CF compared with healthy children (119.3 ± 3.1% predicted versus 103.6 ± 5% predicted, P < 0.001) and, using multiple regression techniques, REE for total body potassium was significantly increased in patients with CF (P = 0.0001). There was no relation between REE and nutritional status or pulmonary disease status in the CF group. In conclusion, REE is increased in children and adolescents with CF but is not directly related to nutritional status or pulmonary disease.

Growth hormone resistance and somatomedins in children with end-stage liver disease awaiting transplantation

Background: The success of orthotopic liver transplantation as treatment for end-stage liver disease has prompted investigation of strategies to maintain or improve nutrition and growth in children awaiting transplantation, because malnutrition is an adverse prognostic factor. The purpose of this study was to evaluate the effect of recombinant human growth hormone therapy on body composition and indices of liver function in patients awaiting transplant. Methods: The study was designed as a placebo- controlled, double-blind, crossover trial. Patients received 0.2 U/kg growth hormone, subcutaneously, or placebo daily for 28 days during two treatment periods, separated by a 2-week washout period. Ten patients (mean age, 3.06 ± 1.15 years; range, 0.51-11.65 years, five men), with extrahepatic biliary atresia (n = 8) or two with Alagille's syndrome (n = 2), with end-stage liver disease, completed the trial while awaiting orthotopic liver transplantation. Height, weight, total body potassium, total body fat, resting energy expenditure, respiratory quotient, hematologic and multiple biochemical profile, number of albumin infusions, insulin-like growth factor-1 and 1, growth hormone binding protein (GHBP), and insulin-like growth factor binding protein-1 (IGFBP-1) and insulin-like growth factor binding protein (IGFBP-3) were measured at the beginning and end of each treatment period. Results: Growth hormone treatment was associated with a significant decline in serum bilirubin (-34.6 ± 16.5 μmol/l vs. 18.2 ± 11.59 μmol/l; p < 0.02) but there was no significant effect on any anthropometric or body composition measurements, or on any biochemical or hematologic parameters. Conclusions: These children with end-stage liver disease displayed growth hormone resistance, particularly in relation to the somatomedin axis. Exogenous growth hormone administration may be of limited value in these patients

The Australian Nutrition Foundation - Improving the health of school canteens

School canteens represent Australia's largest take-away food outlet. With changes in lifestyles and family roles, canteens are used increasingly as a source of food for students. The nutritional quality of foods offered can have a significant impact on the nutritional status of students both now, and in the future. The Australian Nutrition Foundation has been developing its work in the field of school canteens over the past six years. Perhaps its most significant contribution to improving the health of canteens has been the development of the "Food Selection Guidelines for Children and Adolescents". These Guidelines are used to assess foods most suitable for sale in school canteens and for purchasing food in boarding schools. Products meeting the Guidelines are added to the ANF Registered Product List which school canteens and kitchens use as a type of "buying guide". This project has been successfully piloted in Queensland and this year has been expanded to a national campaign.

Cytomegalovirus infection after liver transplantation in children

Post-liver transplant cytomegalovirus (CMV) infection (seroconversion or virus isolation) and CMV disease (infection plus clinical signs and symptoms) were studied in relation to pretransplant recipient and donor serology, age, nutritional status and the effect of paediatric versus adult (reduced size) grafts. Of 70 children receiving 79 transplants, 26 (37%) had evidence of CMV infection, and eight (11.5%) had evidence of CMV disease, four of whom died. The primary infection rate (where the recipients were CMV negative) was 71% with mortality of 7% with most receiving a CMV-positive graft. The active secondary infection rate (reactivation or reinfection, where the recipients were CMV positive) was 60% with mortality of 12.5%. No significant differences in infection on disease rates were found comparing malnourished versus well-nourished patients, or between those who received whole or reduced-size grafts. The high prevalence of CMV infections supports the view that clinical signs alone are inadequate to direct investigations for CMV. Both primary and active secondary CMV infection can result in serious morbidity and mortality in children receiving liver transplants. These data do not support the strategy of providing immunoprophylaxis to seronegative recipients only, at least in paediatric liver transplantation.

Malnutrition in children with chronic liver disease accepted for liver transplantation : clinical profile and effect on outcome

The nutritional profiles of 37 children (aged 0.5-14.0 years) with chronic liver disease at the time of acceptance for orthotopic liver transplantation (OLTP) have been evaluated using clinical, biochemical and body composition methods. Nutritional progress while waiting for a donor has been related to outcome, whether transplanted or not. At the time of acceptance, most children were underweight (mean standard deviation (s.d.) weight = -1.4 ± 0.2) and stunted (mean s.d. height = - 2.2 ± 0.4), had low serum albumin (27/35) and had reduced body fat and depleted body cell mass (measured by total body potassium - mean % expected for age = 58 ± 5%, n = 15). Mean ad libitum nutrient intake was 63 ± 5% of recommended daily intake (RDI). Those who died while waiting (n = 8) had significantly lower mean initial s.d. weight compared with those transplanted. The overall actuarial 1 year survival of those who were transplanted (mean waiting time = 75 days) was 81% but those who were initially well nourished (s.d. weight >-1.0) had an actuarial 1 year survival of 100%. There were no significant differences in actuarial survival in relationship to age, type of transplant (whole liver or segmental), liver biochemistry or the presence or absence of ascites. Of the total group accepted for OLTP, whether transplanted or not, the overall 1 year survival for those who were relatively well nourished was 88% and for those undernourished (initial s.d. weight <-1.0) was 38% (P<0.003). Declining nutritional status during the waiting period also adversely affected outcome. We conclude that malnutrition and/or declining nutritional status is a major factor adversely affecting survival in children awaiting OLTP. In transplant units where waiting time is greater than 40 days, earlier referral, prioritization of cases and the use of adult donor livers may reduce this risk and efforts to maintain or improve nutritional status deserve further study.

Evaluation of growth and changes in body composition following neonatal diagnosis of cystic fibrosis

Early deficits in nutritional status that might require specific treatment and early response to nutritional therapy were studied longitudinally in 25 infants with cystic fibrosis (CF) diagnosed by neonatal screening, using anthropometric and research body composition methodology, and evaluation of pancreatic function. At the time of confirmed diagnosis (mean 5.4 weeks), body mass, length, total body fat (TBF), and total body potassium (TBK) were all significantly reduced. Following diagnosis and commencement of therapy there was a normalization of weight, length, and TBK by 6-12 months of age, indicating catch-up growth. But in some individuals the response was incomplete, and as a group, mean total body fat remained significantly lower than normal at 1 year of age. Seven of 25 (28%) were pancreatic sufficient at diagnosis, and all but one had evidence of declining pancreatic function requiring the institution of pancreatic enzyme therapy during the next 1-9 months. The median age of commencement of enzyme therapy was 10 weeks (range 5 weeks to 11 months). These longitudinal assessments emphasize the dynamic changes occurring in absorptive function, body composition, and nutritional status following neonatal diagnosis of cystic fibrosis and may reflect previously described abnormalities of energy metabolism in this age group. Abnormal body composition is evident in most CF infants following diagnosis by neonatal screening but pancreatic damage may still be evolving. We suggest that early active nutritional therapy and surveillance for changes in pancreatic function are warranted in CF infants diagnosed by neonatal screening.

Survival, growth and quality of life in children after orthotopic liver transplantation: A 5 year experience

The aims of this study were to investigate outcome and to evaluate areas of potential ongoing concern after orthotopic liver transplantation (OLT) in children. Actuarial survival in relation to age and degree of undernutrition at the time of OLT was evaluated in 53 children (age 0.58-14.2 years) undergoing OLT for endstage liver disease. Follow-up studies of growth and quality of life were undertaken in those with a minimum follow-up period of 12 months (n = 26). The overall 3 year actuarial survival was 70%. Survival rates did not differ between age groups (actuarial 2 year survival for ages <1, 1-5 and >5 years were 70, 70 and 69% respectively) but did differ according to nutritional status at OLT (actuarial 2 year survival for children with Z scores for weight <-1 was 57%, >-1 was 95%; P = 0.004). Significant catch-up weight gain was observed by 18 months post-transplant, while height improved less rapidly. Quality of life (assessed by Vineland Adaptive Behaviour Scales incorporating socialization, daily living skills, communication and motor skills) was good (mean composite score 91 ± 19). All school-aged children except one were attending normal school. Two children had mild to moderate intellectual handicap related to post-operative intracerebral complications. Satisfactory long-term survival can be achieved after OLT in children regardless of age but the importance of pre-operative nutrition is emphasized. Survivors have an excellent chance of a good quality of life and of satisfactory catch-up weight gain and growth.

Body composition studies in cystic fibrosis and myelomeningocele

One of the major considerations of improving the management of many chronic diseases has been the realisation of the importance of nutrition, and, in children, the maintenance of normal growth. Cystic Fibrosis (CF) and Myelomeningocele (MMC) are two such disease states in which nutritional status has a significant effect on morbidity.

Total body potassium in cystic fibrosis

To further evaluate the nature of malnutrition, define at-risk groups, and confirm the efficacy of nutritional supplementation on body composition in cystic fibrosis (CF), we have conducted longitudinal and cross-sectional studies of total body potassium (TBK) in 161 unselected CF subjects aged 1 month to 17 years. TBK was determined by measurement of40K in a whole body counter, reflecting body cell mass (BCM), the vital work-performing and growing cellular component of the body. Compared with normal TBK data for age and sex from pooled measurements of 1,629 healthy children aged 1 week to 17 years, CF infants (n = 12) diagnosed by newborn screening were depleted in TBK at diagnosis and showed catch-up with therapy by 1 year; CF children aged 2-17 years (n = 140) showed a tendency for inadequate accretion of TBK (and thus BCM) with increasing age, although the normal correlation between TBK and weight and height was maintained in the majority suggesting a pattern of nutritional stunting of growth; and malnourished CF children (n = 9) showed significant catchup in TBK with long-term nutritional rehabilitation (85-98% of TBK predicted for weight and height). These studies suggest that potentially serious, but possibly correctable deficits, in the growth of the body cell mass as measured by TBK occur commonly in CF. These deficits may be established very early in life and if not corrected lead to progressive nutritional growth retardation with increasing age. © 1989 Raven Press, Ltd., New York.