Short-chain fatty acids and medium-chain fatty acids are primarily absorbed through the portal vein during lipid digestion, while long-chain fatty acids are packed into chylomicrons and enter lymphatic capillaries, and enter the blood first at the subclavian vein.
The short-chain fatty acid butyrate is particularly important for colon health because it is the primary energy source for colonic cells and has anti-carcinogenic as well as anti-inflammatory properties that are important for keeping colon cells healthy. Butyrate inhibits the growth and proliferation of tumor cell lines in vitro, induces differentiation of tumor cells, producing a phenotype similar to that of the normal mature cell, and induces apoptosis or programmed cell death of human colorectal cancer cells. Butyrate inhibits angiogenesis by inactivating Sp1 transcription factor activity and downregulating VEGF gene expression.
Fruits help with our bowel movement. Do not eat over ripe fruits and when detoxing or during the first 3 weeks of your weight loss program.
Most fruits should be eaten during the day. And beware of food combining. It is best to eat fruits 30minutes after a meal. Pineapple enzymes help breakdown fat in meat. And fiber in fruits encapsulates the fat and sugar out of the body.
Fruit is loaded with sugar, in particular fructose and sorbitol (a sugar alcohol), and both of those nutrients can cause gas and bloating. It’s also full of fiber—which, in addition to keeping your belly flat in the long term by moving your GI tract along, can be hard to digest and create gas as a result.
Snack on raspberries, strawberries or blueberries at the same time. The berries’ high water content will counteract cherries’ belly-ballooning properties. Or chase a snack with bloat-banishing detox water. Fruits like lemons and blueberries reduce bloating, and the extra liquid will aid fiber digestion.
Summary: Researchers have identified a genetic link between a diverse array of health disorders and sleep problems.
Source: Mass General.
A team of American and British scientists have for the first time discovered genetic connections between sleep disturbance and a range of medical disorders including obesity.
Lead author Jacqueline Lane, PhD, postdoctoral fellow at Massachusetts General Hospital (MGH), and joint senior authors Richa Saxena, PhD, assistant professor of Anæsthesia at MGH and Harvard Medical School, and Martin K Rutter, MD, FRCP, senior lecturer in Cardiometabolic Medicine from The University of Manchester, publish their groundbreaking research in Nature Genetics today.
The study looked at the biological controllers of sleep duration, insomnia and excessive daytime sleepiness and how they linked to the health and life histories of more than 112,000 people taking part in the world-leading UK Biobank study. Study participants reported their sleep duration, the degree of insomnia and daytime sleepiness, and then had their genes mapped. Other information about them, such as their weight and any diseases they suffered from, was also collected.
The researchers identified for the first time areas of the genome that are associated with sleep disturbance – including insomnia and excessive daytime sleepiness – and also discovered novel genetic links with several medical conditions, including restless legs syndrome, schizophrenia and obesity. The strongest genetic association for insomnia symptoms fell within a gene previously linked to restless legs syndrome – a nervous system disorder affecting around 1 in 20 people that leads to a strong urge to move one’s legs, which is often worse at night. Other gene regions were important for insomnia, but selectively in either men or women.
The team also identified genetic links between longer sleep duration and schizophrenia risk and between increased levels of excessive daytime sleepiness and measures of obesity (body mass index and waist circumference). The research also suggested that insomnia has shared underlying biology with major depression and abnormal glucose metabolism.
Funded by the U.S. National Institutes of Health and The University of Manchester’s Research Innovation Fund, the study marks a major advance in understanding the biology of sleep.
One in four British adults are obese, according to the U.N. Food and Agriculture Organization, prompting fears that the U.K. has become the “fat man of Europe.” And at any one time, about 280,000 people are being treated for schizophrenia by the National Health Service. Individuals with schizophrenia have a 1 in 10 chance of dying by their own hand within ten years of diagnosis.
Rutter says, “This clinical science is an important step forwards in understanding the biological basis for these conditions; so it’s very exciting. Scientists have long observed a connection between sleep disorders and these conditions in epidemiological studies. But this is the first time these biological links have been identified at a molecular level.”
UK Biobank aims to improving the prevention, diagnosis and treatment of a wide range of serious and life-threatening illnesses. Lane says, “We’re particularly pleased to be able to use UK Biobank data in this way; it’s an amazing resource for scientists.”
Saxena adds, “It’s important to remember there is no molecular targeting available for conditions which affect sleep: all we really have are sedatives. So we hope that this research will enable scientists to develop new ways to intervene on a range of conditions in a much more fundamental way. We acknowledge these findings will need further study, but we believe this knowledge amounts to a key advance in our understanding of the biology behind sleep – a major influence on our health and behaviour.”
Funding: Funding provided by National Institutes of Health, University of Manchester Research Innovation Fund.
Source: Terri Ogan – Mass General
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Original Research: Abstract for “Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits” by Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter and Richa Saxena in Nature Genetics. Published online December 19 2016 doi:10.1038/ng.3749
Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits
Chronic sleep disturbances, associated with cardiometabolic diseases, psychiatric disorders and all-cause mortality, affect 25–30% of adults worldwide. Although environmental factors contribute substantially to self-reported habitual sleep duration and disruption, these traits are heritable and identification of the genes involved should improve understanding of sleep, mechanisms linking sleep to disease and development of new therapies. We report single- and multiple-trait genome-wide association analyses of self-reported sleep duration, insomnia symptoms and excessive daytime sleepiness in the UK Biobank (n = 112,586). We discover loci associated with insomnia symptoms (near MEIS1, TMEM132E, CYCL1 and TGFBI in females and WDR27 in males), excessive daytime sleepiness (near AR–OPHN1) and a composite sleep trait (near PATJ (INADL) and HCRTR2) and replicate a locus associated with sleep duration (at PAX8). We also observe genetic correlation between longer sleep duration and schizophrenia risk (rg = 0.29, P = 1.90 × 10−13) and between increased levels of excessive daytime sleepiness and increased measures for adiposity traits (body mass index (BMI): rg = 0.20, P = 3.12 × 10−9; waist circumference: rg = 0.20, P = 2.12 × 10−7).
“Genome-wide association analyses of sleep disturbance traits identify new loci and highlight shared genetics with neuropsychiatric and metabolic traits” by Jacqueline M Lane, Jingjing Liang, Irma Vlasac, Simon G Anderson, David A Bechtold, Jack Bowden, Richard Emsley, Shubhroz Gill, Max A Little, Annemarie I Luik, Andrew Loudon, Frank A J L Scheer, Shaun M Purcell, Simon D Kyle, Deborah A Lawlor, Xiaofeng Zhu, Susan Redline, David W Ray, Martin K Rutter and Richa Saxena in Nature Genetics. Published online December 19 2016 doi:10.1038/ng.3749
Summary: According to a new study, children of obese parents may face neurodevelopmental delays.
Children of obese parents may be at risk for developmental delays, according to a study by researchers at the National Institutes of Health. The investigators found that children of obese mothers were more likely to fail tests of fine motor skill–the ability to control movement of small muscles, such as those in the fingers and hands. Children of obese fathers were more likely to fail measures of social competence, and those born to extremely obese couples also were more likely to fail tests of problem solving ability.
The study, appearing in Pediatrics, was conducted by scientists at the NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
“The previous U.S. studies in this area have focused on the mothers’ pre- and post-pregnancy weight,” said the study’s first author, Edwina Yeung, Ph.D., an investigator in NICHD’s Division of Intramural Population Health Research. “Our study is one of the few that also includes information about fathers, and our results suggest that dad’s weight also has significant influence on child development.”
Dr. Yeung and her coauthors cited research indicating that about 1 in 5 pregnant women in the United States is overweight or obese.
In the study, authors reviewed data collected from the Upstate KIDS study, which originally sought to determine if fertility treatments could affect child development from birth through age 3. More than 5,000 women enrolled in the study roughly 4 months after giving birth in New York State (excluding New York City) between 2008 and 2010. To assess development, parents completed the Ages and Stages Questionnaire after performing a series of activities with their children. The test isn’t used to diagnose specific disabilities, but serves as a screen for potential problems, so that children can be referred for further testing.
Children in the study were tested at 4 months of age and retested 6 more times through age 3. When they enrolled, mothers also provided information on their health and weight–before and after pregnancy–and the weight of their partners.
Compared to children of normal weight mothers, children of obese mothers were nearly 70 percent more likely to have failed the test indicator on fine motor skill by age 3. Children of obese fathers were 75 percent more likely to fail the test’s personal-social domain–an indicator of how well they were able to relate to and interact with others by age 3. Children with two obese parents were nearly three times more likely to fail the test’s problem solving section by age 3.
It is not known why parental obesity might increase children’s risk for developmental delay. The authors note that animal studies indicate that obesity during pregnancy may promote inflammation, which could affect the fetal brain. Less information is available on the potential effects of paternal obesity on child development. The authors added that some studies have indicated that obesity could affect the expression of genes in sperm.
If the link between parental obesity and developmental delays is confirmed, the authors wrote, physicians may need to take parental weight into account when screening young children for delays and early interventional services.and each was interviewed for about two hours.
Funding: The study was funded by National Institutes of Health, NIH/Eunice Kennedy Shriver National Institute of Child Health and Human Development.
Source: Robert Bock – NIH/NICHD
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Parental Obesity and Early Childhood Development” by Edwina H. Yeung, Rajeshwari Sundaram, Akhgar Ghassabian, Yunlong Xie, and Germaine Buck Louis in Pediatrics. Published online January 2017 doi:10.1542/peds.2016-1459
Parental Obesity and Early Childhood Development
BACKGROUND: Previous studies identified associations between maternal obesity and childhood neurodevelopment, but few examined paternal obesity despite potentially distinct genetic/epigenetic effects related to developmental programming.
METHODS: Upstate KIDS (2008–2010) recruited mothers from New York State (excluding New York City) at ∼4 months postpartum. Parents completed the Ages and Stages Questionnaire (ASQ) when their children were 4, 8, 12, 18, 24, 30, and 36 months of age corrected for gestation. The ASQ is validated to screen for delays in 5 developmental domains (ie, fine motor, gross motor, communication, personal-social functioning, and problem-solving ability). Analyses included 3759 singletons and 1062 nonrelated twins with ≥1 ASQs returned. Adjusted odds ratios (aORs) and 95% confidence intervals were estimated by using generalized linear mixed models accounting for maternal covariates (ie, age, race, education, insurance, marital status, parity, and pregnancy smoking).
RESULTS: Compared with normal/underweight mothers (BMI <25), children of obese mothers (26% with BMI ≥30) had increased odds of failing the fine motor domain (aOR 1.67; confidence interval 1.12–2.47). The association remained after additional adjustment for paternal BMI (1.67; 1.11–2.52). Paternal obesity (29%) was associated with increased risk of failing the personal-social domain (1.75; 1.13–2.71), albeit attenuated after adjustment for maternal obesity (aOR 1.71; 1.08–2.70). Children whose parents both had BMI ≥35 were likely to additionally fail the problem-solving domain (2.93; 1.09–7.85).
CONCLUSIONS: Findings suggest that maternal and paternal obesity are each associated with specific delays in early childhood development, emphasizing the importance of family information when screening child development.
“Parental Obesity and Early Childhood Development” by Edwina H. Yeung, Rajeshwari Sundaram, Akhgar Ghassabian, Yunlong Xie, and Germaine Buck Louis in Pediatrics. Published online January 2017 doi:10.1542/peds.2016-1459