Improving Weight Loss By Intermittent Use Of Very Low Energy Diet: The TANGO Diet Trial (Temporary Phases Of Accelerated Weight Loss For Noticeably Greater Outcomes)
Funder
National Health and Medical Research Council
Funding Amount
$660,736.00
Summary
Very low energy diet (VLED) is being increasingly used for the treatment of obesity, but the resultant weight loss is usually transient, partly because it induces powerful adaptive responses that inhibit weight loss and promote regain. We have shown that 'taking a break from dieting' for 2 weeks reduces these adaptive responses. In this project we will thus test whether weight loss outcomes with VLED can be improved via intermittent use, where periods on the VLED are alternated with 'breaks'.
Optimising Benefits And Minimising Potential Harms Of Obesity Treatments
Funder
National Health and Medical Research Council
Funding Amount
$707,370.00
Summary
This work aims to find safe and more effective obesity treatments for the over 2.1 billion people worldwide with overweight or obesity. Severely energy restricted diets are currently the most effective dietary obesity treatment, but these are underutilized due to concerns about potential harms. This work will investigate using severe diets intermittently rather than continuously, as a means of enhancing their benefits of long-term weight/fat loss while also reducing potential harmful effects.
Effects Of Fast Versus Slow Weight Loss On Fat, Muscle And Bone In Postmenopausal Women
Funder
National Health and Medical Research Council
Funding Amount
$316,450.00
Summary
Very low energy diets (VLED) are increasingly used to treat obesity. Of concern is the fact that VLED induce adaptive responses that can inhibit loss of, and promote regain of, abdominal fat while decreasing lean body mass, muscle strength and bone density. This project will therefore determine whether VLEDs could have negative effects on body composition that increase the risk of metabolic disease, sarcopenia or osteoporosis, and if so, what mechanisms are involved.
This proposal is designed to test the protein leverage hypothesis (PLH) in humans: the idea that the level of food consumption in humans, like other animals, is adjusted to maintain a target protein intake. As the prevalence of overweight and obesity increases, with its attendant health problems, the need to identify which dietary components limit rather than exacerbate energy intake is imperative. According to the PLH, the consumption of a diet low in % protein and high in % fat and carbohydrat ....This proposal is designed to test the protein leverage hypothesis (PLH) in humans: the idea that the level of food consumption in humans, like other animals, is adjusted to maintain a target protein intake. As the prevalence of overweight and obesity increases, with its attendant health problems, the need to identify which dietary components limit rather than exacerbate energy intake is imperative. According to the PLH, the consumption of a diet low in % protein and high in % fat and carbohydrate, typical of many Western countries, inevitably requires the ingestion of additional energy to maintain protein intake constant, thus driving weight gain. Conversely, the consumption of a diet that is relatively high in % protein requires the ingestion of lower levels of energy, creating the potential for weight loss. Preliminary experimental and population-level nutritional survey data support the PLH, as does the finding that protein is more satiating than other macronutrients. If, as predicted, small changes in the proportion of protein in diets described in the current study are found to impact on total energy intake there will be significant implications for weight control strategies. Thus, if the PLH is confirmed, public health dietary recommendations and government policy settings for the food industry will need to change. Large-scale intervention studies aimed at demonstrating the longer term impact on body weight will also be required.Read moreRead less
Understanding The Mechanisms For Ameliorating/preventing Antipsychotic-induced Obesity In Early Life
Funder
National Health and Medical Research Council
Funding Amount
$576,496.00
Summary
There has been a sharp worldwide increase during the last decade in antipsychotic prescriptions (mostly “off-label”) to paediatric patients. One important issue is that antipsychotic drugs were developed for adult patients and normally have serious side-effects. This project will not only reveal the mechanisms of antipsychotic-induced obesity side-effects in youth, but will also explore intervention strategies for preventing antipsychotic-induced weight gain/obesity in paediatric patients.
Studies Of The Effects Of Asymmetric Hearing Loss On The Brain
Funder
National Health and Medical Research Council
Funding Amount
$920,076.00
Summary
Hearing loss impairs the normal development and maintenance of auditory pathways. Irreversible pathologies persist when hearing is not restored in a timely manner. While cochlear implantation is the accepted treatment for profound sensorineural hearing loss, there is significant variability in outcomes. Some of this variability is linked to the degree of hearing asymmetry. Thus, we propose to study brain changes in the auditory system that accompany asymmetric hearing impairment.
Does Early Overnutrition Differentially Alter Hypothalamic Neuropeptides That Regulate Food Intake In The Rat
Funder
National Health and Medical Research Council
Funding Amount
$346,250.00
Summary
In Australia the incidence of obesity, in particular childhood obesity, is increasing dramatically, and the possible long term consequences of this are of great concern. The brain regulates appetite through a number of chemical transmitters such as neuropeptide Y (NPY) which is present in the brains of mammals and causes increased food intake. The effects of overeating from a young age on these brain transmitters has been largely ignored although this may impact on subsequent eating behaviour. I ....In Australia the incidence of obesity, in particular childhood obesity, is increasing dramatically, and the possible long term consequences of this are of great concern. The brain regulates appetite through a number of chemical transmitters such as neuropeptide Y (NPY) which is present in the brains of mammals and causes increased food intake. The effects of overeating from a young age on these brain transmitters has been largely ignored although this may impact on subsequent eating behaviour. In addition to NPY we will study other transmitters in the brain that have profound effects on appetite, some increasing, and others decreasing, food intake. These may form useful therapeutic targets for new drugs for obesity. Key targets we will study include melanocortins, glucagon-like peptide 1, urocortin, melanin concentrating hormone, agouti related peptide, and NPY. We will determine whether overnutrition from birth to weaning leads to changes in these appetite regulating neurotransmitters in the brain, and monitor the hormonal signals that impact on their activity. We will also determine whether early overnutrition exacerbates the subsequent responses to a high fat diet by comparison with rats made obese as adults. We will measure brain concentrations of the neurotransmitters, the amount released from the brain, and determine whether the feeding responses to injections of these agents is altered in obese animals. We have evidence that these transmitters interact in a co-ordinated fashion to affect feeding; this project will examine whether these interactions are maintained in the various types of obesity. Rats are commonly used for this type of study as the processes regulating feeding are very similar to those in humans and these agents cause similar effects in rats and humans. It is hoped that this information will provide new insight into the way brain adapts to overnutrition, and provide potential treatments for obesity and other feeding disorders.Read moreRead less
GENETIC PREDICTION OF FRACTURE IN A RISK-STRATIFIED POPULATION
Funder
National Health and Medical Research Council
Funding Amount
$363,000.00
Summary
Osteoporosis is a condition characterised by excessive bone loss and impaired bone quality, which ultimately results in fracture with minimal trauma. Osteoporosis affects 27% of women and 11% of men aged 60 years or above in the community, and costs Australia around $7 billion each year. Individuals with low bone mineral density (BMD) have a significantly higher risk of fracture than those with normal BMD. In the long-term (14-year) Dubbo Osteoporosis Epidemiology Study, more than half of indivi ....Osteoporosis is a condition characterised by excessive bone loss and impaired bone quality, which ultimately results in fracture with minimal trauma. Osteoporosis affects 27% of women and 11% of men aged 60 years or above in the community, and costs Australia around $7 billion each year. Individuals with low bone mineral density (BMD) have a significantly higher risk of fracture than those with normal BMD. In the long-term (14-year) Dubbo Osteoporosis Epidemiology Study, more than half of individuals with osteoporosis (e.g., low BMD) did not sustain a fracture, while approximately 60% of fracture cases had BMD above the high risk levels. Thus, BMD alone is not a good discriminant of fracture versus non-fracture cases. It is widely known that the liability to fracture is determined in part by genes. Previous studies, including from our group, have suggested a number of candidate genes that are associated with fracture risk. The fundamental issue that this study is concerned is that how and whether genetic markers could be used to facilitate case finding. It is proposed that common variations of certain genes are associated with fracture risk independent of BMD. That is, they can identify individuals at relatively high and low fracture risk after stratification for BMD. Hence, some markers may identify those individuals likely (and unlikely) to fracture even with low (osteoporotic) BMD. Similarly, some, possibly the same, markers may identify individuals at high risk of fracture despite relatively good (ie non-osteoporotic) BMD. It is further proposed that no single gene will achieve this outcome, but rather a small set of such gene polymorphisms will provide clinically useful risk information. This effect is entirely analogous to the use of clinical risk indicators (eg, age, weight, sex, family history, etc) to assess the risk of future fracture.Read moreRead less