New Hampshire Health News Digest

Dietary Sugar and Mental Illness: A Surprising Link | Psychology Today Dietary Sugar and Mental Illness: A Surprising Link Sugar and Mental Illness: A Surprising Link Published on July 23, 2009 Noted British psychiatric researcher Malcolm Peet has conducted a provocative cross-cultural analysis of the relationship between diet and mental illness. His primary finding may surprise you: a strong link between high sugar consumption and the risk of both depression and schizophrenia. In fact, there are two potential mechanisms through which refined sugar intake could exert a toxic effect on mental health. First, sugar actually suppresses activity of a key growth hormone in the brain called BDNF. This hormone promotes the health and maintenance of neurons in the brain, and it plays a vital role in memory function by triggering the growth of new connections between neurons. BDNF levels are critically low in both depression and schizophrenia, which explains why both syndromes often lead to shri

Protein behind overeating identified -Health/Science-The Times of India WASHINGTON: Researchers, for the first time, have demonstrated in mice that a protein called brain-derived neurotrophic factor (BDNF) is critical in managing satiety, and is the main cause behind obesity and overeating. The study, led by Maribel Rios, PhD, and assistant professor of neuroscience at the Sackler School of Graduate Biomedical Sciences at Tufts University School of Medicine in Boston and colleagues, revealed that it is the lack of BDNF that is responsible for triggering overeating and obesity. Researchers showed that the mice in which the BDNF gene was deleted in two of the primary appetite-regulating regions of the brain ate more and became significantly heavier than their counterparts. "Prior to this study, we knew that the global lack of BDNF and/or its receptor during development leads to overeating and obesity in young mice. However, it remained unclear and controversial whether BDNF mediate

Working Out Your Brain | GNIF Brain Blogger In nature’s original design plan, the brain was the leader for coordinating our physical activities: the “motor high-command.” It comes as little surprise then, that exercise strengthens the brain’s interconnections, and rejuvenates the mind. The chemical link between the mind and body is best exemplified by the brain derived neurotrophic growth factor (BDNF), a protein found in our brain which helps brain cells to stay healthy, sprout new connections, and develop plasticity (the ability to form new connections between cells). Previous experiments have shown that short-term and long-term exercise both lead to a release of BDNF from various parts of our brain, more so from the cortex, basal forebrain and hippocampus, which are areas considered vital for learning, higher thinking, and memory. A new study, published in Medicine & Science in Sports & Exercise, the official journal of the American College of Sports Medicine, actually conf

HDLighthouse.org Conclusion Exercise is a simple and widely practised behavior that activates molecular and cellular cascades that support and maintain brain plasticity. It induces expression of genes associated with plasticity, such as that encoding BDNF, and in addition promotes brain vascularization, neurogenesis, functional changes in neuronal structure and neuronal resistance to injury. Significantly, these effects occur in the hippocampus, a brain region central to learning and memory. BDNF availability could be crucial for these mechanisms. Exercise-driven increases in the level of hippocampal BDNF are controlled by neuronal activity, neurotransmitters and interactions with peripheral factors that include estrogen, corticosterone and possibly IGF-1. The peripheral influence illustrates how exercise can relate overall body status to brain function. Exercise recruits use-dependent plasticity mechanisms that prepare the brain to encode meaningful information from the environment an

Exercise: a behavioral intervention to enhance bra...[Trends Neurosci. 2002] - PubMed Result Exercise: a behavioral intervention to enhance brain health and plasticity. Cotman CW, Berchtold NC. Institute for Brain Aging and Dementia, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697-4540, USA. cwcotman@uci.edu Extensive research on humans suggests that exercise could have benefits for overall health and cognitive function, particularly in later life. Recent studies using animal models have been directed towards understanding the neurobiological bases of these benefits. It is now clear that voluntary exercise can increase levels of brain-derived neurotrophic factor (BDNF) and other growth factors, stimulate neurogenesis, increase resistance to brain insult and improve learning and mental performance. Recently, high-density oligonucleotide microarray analysis has demonstrated that, in addition to increasing levels of BDNF, exercise mobilizes gene express

Nutrition and schizophrenia: beyond omega-3 fatty ...[Prostaglandins Leukot Essent Fatty Acids. 2004] - PubMed Result Nutrition and schizophrenia: beyond omega-3 fatty acids. Peet M. Swallownest Court Hospital, Aughton Road, Sheffield S26 4th, UK. malcolmpeet@Yahoo.com There are now five placebo-controlled trials of EPA in the treatment in schizophrenia, and four of these have given positive or partly positive findings. A cross-national ecological analysis of international variations in outcome of schizophrenia in relation to national dietary practices, showed that high consumption of sugar and of saturated fat is associated with a worse long-term outcome of schizophrenia. It is known that a high sugar, high fat diet leads to reduced brain expression of brain-derived neurotrophic factor (BDNF) which is responsible for maintaining the outgrowth of dendrites. Low brain BDNF levels also lead to insulin resistance which occurs in schizophrenia and is associated with diseases of the metabol

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry There is substantial evidence that schizophrenia is associated with abnormalities of phospholipid metabolism and cell membrane PUFA levels (Peet, 2002). Two studies have shown that levels of PUFA in the normal daily diet correlate with the severity of schizophrenia symptoms. Mellor et al (1996) showed significant negative correlations between dietary intake of omega-3 fatty acids and symptoms of schizophrenia and of tardive dyskinesia. In a separate study, Stokes (2003) found that total PUFA in the normal daily diet correlated negatively with severity of schizophrenia symptoms and that this was independent of the dietary intake of other nutrients. In summary, people with schizophrenia consume the type of diet that is known to promote diseases of the metabolic syndrome (i.e. high in saturated fat, low in fibre, with a high glycaemic load). Furthermore, there is emerging e

ScienceDirect - Neuroscience : A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning Abstract We have investigated a potential mechanism by which a diet, similar in composition to the typical diet of most industrialized western societies rich in saturated fat and refined sugar (HFS), can influence brain structure and function via regulation of neurotrophins. We show that animals that learn a spatial memory task faster have more brain-derived neurotrophic factor (BDNF) mRNA and protein in the hippocampus. Two months on the HFS diet were sufficient to reduce hippocampal level of BDNF and spatial learning performance. Consequent to the action of BDNF on synaptic function, downstream effectors for the action of BDNF on synaptic plasticity were reduced proportionally to BDNF levels, in the hippocampus of rats maintained on the HFS diet between 2 and 24 months. In particular, animals maintained on the HFS diet showed a decreas

Diet, diabetes and schizophrenia: review and hypothesis -- Peet 184 (47): s102 -- The British Journal of Psychiatry However, evidence of a significant association between diet and the outcome and severity of schizophrenia raises the possibility that both diabetes and schizophrenia share a common pathology which is influenced by lifestyle factors such as diet and exercise. One physiological factor that could partly explain the link between diabetes, schizophrenia and diet is brain-derived neurotrophic factor (BDNF). This protein is required to maintain dendrites (Gorski et al, 2003), and its expression in the prefrontal cortex shows a significant increase during young adulthood at a time when the frontal cortex matures both structurally and functionally (Webster et al, 2002). The peak requirement for BDNF to preserve dendritic outgrowth thus occurs at the time of life when schizophrenia has its peak age of onset. Apart from influences on neuronal architecture, BDNF is also a neurotrans

BDNF - Depression BDNF - Depression Decreased serum brain-derived neurotrophic factor levels in major depressed patients. Recent findings with animal models have suggested a possible role for brain-derived neurotrophic factor (BDNF) in depression. We have therefore hypothesized that depression could be characterized by low levels of serum BDNF. Major depressed patients (15F+15M) diagnosed according to DSM-IV criteria and healthy controls (15F+15M) participated in the study. Serum BDNF was assayed with the ELISA method and the severity of depression was evaluated with Montgomery-Asberg-Depression Rating Scale (MADRS). BDNF levels were significantly lower in patients than in controls: 22.6+/-3 and 26.5+/-7 ng/ml (t-test=2.7; d.f.=58; P<0.01). They were negatively correlated to the MADRS scores (r=-0.55; P<0.02). Female patients were more depressed and released less BDNF than men. Analysis of covariance (MADRS and gender as independent variable vs. BDNF as dependent variable) indica

Entrez PubMed Brain-derived neurotrophic factor (BDNF) is one of a family of neurotrophic factors that participates in neuronal transmission, modulation and plasticity. Previous studies using animals have demonstrated that acute and chronic exercise leads to increases in BDNF in various brain regions. PURPOSE:: To determine the effects of acute exercise on serum BDNF levels in humans, and to determine the relationship between exercise intensity and BDNF responses. Additionally, the relationship between changes in BDNF and cognitive function was examined. METHODS:: Fifteen subjects (25.4 +/- 1.01 yr; 11 male, 4 female) performed a graded exercise test (GXT) for the determination of V O2max and ventilatory threshold (VTh) on a cycle ergometer. On separate days, two subsequent 30-min endurance rides were performed at 20% below the VTh (VTh - 20) and at 10% above the VTh (VTh + 10). Serum BDNF and cognitive function were determined before and after the GXT and endurance rides with an enzym

Entrez PubMed High impact running improves learning. Winter B, Breitenstein C, Mooren FC, Voelker K, Fobker M, Lechtermann A, Krueger K, Fromme A, Korsukewitz C, Floel A, Knecht S. Department of Neurology, University of Muenster, Muenster, Germany. bwinter@uni-muenster.de Regular physical exercise improves cognitive functions and lowers the risk for age-related cognitive decline. Since little is known about the nature and the timing of the underlying mechanisms, we probed whether exercise also has immediate beneficial effects on cognition. Learning performance was assessed directly after high impact anaerobic sprints, low impact aerobic running, or a period of rest in 27 healthy subjects in a randomized cross-over design. Dependent variables comprised learning speed as well as immediate (1 week) and long-term (>8 months) overall success in acquiring a novel vocabulary. Peripheral levels of brain-derived neurotrophic factor (BDNF) and catecholamines (dopamine, epinephrine, norepineph