Insufficient pregnancy weight gain associated with schizophrenia
Swedish researchers claim to have found a link between insufficient maternal weight gain during pregnancy and the development of schizophrenia spectrum disorders in children in later life. The authors used data from Swedish health and population registers to follow up 526 042 people born between1982 and 1989. The subjects were followed from the age of 13 years until the end of 2011. Gestational weight gain was calculated as the difference in maternal weight between the first antenatal visit and delivery. The group included 2910 people with non-affective psychoses at the end of the follow-up period, of whom 704 had narrowly defined schizophrenia. Extremely inadequate gestational weight gain was defined as less than 8 kg for mothers with normal baseline body mass index. Among the people with non-affective psychosis, 184 patients (6.32%) were found to have had mothers with extremely inadequate gestational weight gain, compared with 23 627 unaffected individuals (4.5%). Extremely inadequate gestational weight gain was associated with increased risk for non-affective psychoses in children in an analysis adjusted for other potential confounding factors and in sibling comparison models. The authors suggested that malnutrition could be a mediating factor, although other mechanisms could not be ruled out based on observational studies. They also noted that severely inadequate gestational weight gain may indicate an existing maternal medical condition. The study was published in JAMA Psychiatry.
New test for motor neuron disease biomarkers
Researchers from Flinders University have developed a new urine test which will help motor neuron disease (MND) patients to more accurately track the progression of their disease. At present, there are no validated pharmaco-dynamic biomarkers for MND or amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. The new test, developed in collaboration with the University of Miami, measures a key protein biomarker – 75ECD – found in the urine of patients with MND as the disease progresses. Regular accurate and affordable testing of symptoms could lead to improved treatment and better interventions, said Flinders University senior research fellow Dr Mary-Louise Rogers. “A standardised, easy-to-collect urine test could be used as a more accurate progression and prognostic biomarker in clinical trials. This will accelerate progress towards more rapid identification of improved treatments for MND and save time and money by faster exclusion of less effective or ineffective drugs. And in the future, it also could potentially be used to test people for early signs of pre-familial MND progression and used instead of patient questionnaires for regular testing of disease progress or drug suitability in existing MND cases.” The new test is set to be used in clinical trials. News of the test was published in Neurology.
Inflammatory disease trigger revealed
New medicines for the treatment of inflammatory diseases, such as psoriasis and multiple sclerosis, may result from a discovery made by researchers from the Walter and Eliza Hall Institute (WEHI) of Medical Research. As part of an international collaboration, WEHI scientists have found that a potent inflammatory molecule released by dying cells – interleukin 1-b (IL-1b) – triggers inflammation during necroptosis. Necroptosis is a recently described form of cell death linked to inflammatory disease, which is important for protecting humans against infection by sacrificing infected or diseased cells. Necroptosis can, however, become inappropriately or excessively activated, triggering damaging inflammation that leads to inflammatory disease. The findings suggest that targeting IL-1b could lead to suppression of inflammation associated with multiple inflammatory diseases, including multiple sclerosis, ischaemia-reperfusion injury, atherosclerosis, liver disease, pancreatitis, psoriasis, inflammatory bowel disease and infectious diseases. “Our research suggests that existing drugs that block IL-1b might be useful in treating these diseases,” said WEHI’s researcher Dr Lisa Lindqvist. “We are also exploring how IL-1b is signaled to be secreted during necroptosis, so that we can create new drugs to stop its release and reduce inflammation, to treat inflammatory diseases.” The research was published in Proceedings of the National Academy of Sciences.
Can back pain be a killer?
The 600 000 older Australians who suffer from back pain have a 13% increased risk of dying from any cause, University of Sydney researchers have found. Published in the European Journal of Pain, the study of 4390 Danish twins aged over 70 years old investigated whether spinal pain increased the rate of all-cause and disease-specific cardiovascular mortality. Low back pain is a major problem, ranked as the highest contributor to disability in the world. Nearly four million people in Australia suffer from low back pain and the total cost of treatment exceeds $1 billion a year. “Our study found that, compared to those without spinal pain (back and neck), a person with spinal pain has a 13% higher chance of dying every year. This is a significant finding as many people think that back pain is not life-threatening,” said senior author Associate Professor Paulo Ferreira, physiotherapy researcher from the University of Sydney’s Faculty of Health Sciences. “As this study was done in twins, the influence of shared genetic factors is unlikely because it was controlled for in our analysis. These findings warrant further investigation because while there is a clear link between back pain and mortality, we don’t know yet why this is so. Spinal pain may be part of a pattern of poor health and poor functional ability, which increases mortality risk in the older population,” he said. “Back pain should be recognised as an important comorbidity that is likely to affect people’s longevity and quality of life.” This study follows previous research that found that people with depression are 60%more likely to develop low back pain in their lifetime.
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