Thursday, 31 August 2017
Wednesday, 30 August 2017
Tuesday, 29 August 2017
Monday, 28 August 2017
Our gut feeling rarely lets us down, although we know very little about how it happens. As science discovers more about the connection between the gut and brain, the role of the little-known and rare enterochromaffin (EC) cells becomes central to our understanding of how the brain and gut communicate. We have all felt butterflies or that wrenching feeling in our stomach when we are anxious, and we also know that long term anxiety and depression often leads to various disorders of the gastrointestinal (GI) tract. We have known for some time about that our mental state can affect the gut, and what we are discovering now with the help of modern research is how gut health affects the brain and general well-being. These days, it seems that what has been missing from this cyclic relationship is our understanding of EC cell functions.
Basic features of the gut-brain axis
To fully appreciate the role of EC cells, we have to delve into some basic underlying concepts and facts. Our gut has more neurons than our spine or peripheral nervous system—that is why it is also known as the second brain. These neurons have various functions, like controlling gut motility, protecting against irritants (through increased motility or vomiting), and many other still to be understood functionalities. These gut neurons mostly work independently from the brain, but when required, they send information and get feedback from the brain, thus functioning as a closed loop often called the gut-brain axis.
EC cells play a vital part in the gut-brain axis. These cells have receptors that are always listening to various activities in the gut and sending feedback to the brain and other neurons of the gut through chemical messengers or hormones. Although EC cells have functional similarities to glands, they are spread all over the digestive tract, and they form about one percent of the gut epithelium. Although one percent may sound small, EC cells secrete more than 30 kinds of hormones and neurotransmitters (this number will likely increase as more are identified). In fact, they secrete more than 90% of the body’s serotonin, a neurotransmitter well-known for its role in various mental states, including mental disorders like depression and anxiety.
Now, it is well understood that the communication between the brain and gut is double-sided, forming a loop. Thus, mental distress causes gut disorders, and gut disorders may influence mental states. Moreover, EC cells have a critical role in this entire axis.
Brain and GI disorders
Stress is known not only to cause GI disorders, but it also makes the symptoms worse. Stress and psychological factors change the movement of the GI tract, worsen inflammatory processes, and even increase susceptibility to various infections. In all of these processes, EC cells play a crucial role. The release of serotonin from EC cells is the key mechanism for controlling the motility of the gut. They can be stimulated due to local irritation, as well as through nerve supply, especially the vagus nerve. Therefore psychological therapy has a special place in treating functional GI diseases, along with pharmaceutical therapy. EC cells are highly sensitive to the effect various chemical compounds like detergents and spices. They have been demonstrated to even have olfactory receptors—yes, the same receptors that are present in our nose.
Gut and brain disorders
Although the effect of mental stress on GI function has been known for ages, in recent times there has been increased interest in better understanding the influence of gut health on the brain. This became particularly important after research demonstrated that EC cells not only have an indirect influence on nerves through serotonin, they also seem to have direct links with neurons. Thus, EC cells appear to be directly connected to the brain. This means that changes in the gut are transmitted to the brain in milliseconds, and not in seconds or minutes as previously thought.
This fact gains further importance, considering that the vagus nerve (the main nerve connecting the brain and GI) has more afferent fibers (those sending a signal to the brain) than efferent fibers (those sending a signal from the brain to organs). These afferent fibers cause feelings like nausea when you eat the wrong kind of food. The role of these vagal signals from the GI to the brain and their relationship with other aspects of health are being investigated, like arousal, fatigue, and poor regulation of body temperature, and may become the target of future therapies.
Treatment strategies targeting the gut-brain axis
Many drugs for mental distress like depression have been used effectively to treat gut disorders. Inflammatory bowel syndrome (IBS) is one of the most prevalent of such disorders. Some researchers even call it a “mental disorder of the gut”. Selective serotonin uptake inhibitors (SSRIs) have shown increasingly important roles in the management of this disorder. SSRIs help to control overactive EC cells. The role of SSRIs is not limited to the treatment of IBS. Their role is being studied in various functional diseases of the GI, in controlling nausea, diarrhoea, constipation, vomiting, and many other disorders.
To date, the same SSRIs that are used to treat mental health issues are being used to deal with GI problems. However, many clinical researchers are studying non-absorbable serotonergic agents for GI disturbances. Further studies are being done to target tryptophan hydroxylase, a precursor for the synthesis of serotonin.
The role of EC cells in gut functioning is being investigated in depth to better understand and treat disorders of the brain like dementia, Alzheimer’s disease, Parkinsonism, and autism. As we learn more about EC cells, we might be able to treat many medical illnesses more effectively.
Andrews, P.L.R., Sanger, G.J., 2002. Abdominal vagal afferent neurones: an important target for the treatment of gastrointestinal dysfunction. Curr. Opin. Pharmacol. 2, 650–656. doi:10.1016/S1471-4892(02)00227-8
Bellono, N.W., Bayrer, J.R., Leitch, D.B., Castro, J., Zhang, C., O’Donnell, T.A., Brierley, S.M., Ingraham, H.A., Julius, D., 2017. Enterochromaffin Cells Are Gut Chemosensors that Couple to Sensory Neural Pathways. Cell 170, 185–198.e16. doi:10.1016/j.cell.2017.05.034
Braun, T., Voland, P., Kunz, L., Prinz, C., Gratzl, M., 2007. Enterochromaffin Cells of the Human Gut: Sensors for Spices and Odorants. Gastroenterology 132, 1890–1901. doi:10.1053/j.gastro.2007.02.036
Dunlop, S.P., Jenkins, D., Neal, K.R., Spiller, R.C., 2003. Relative importance of enterochromaffin cell hyperplasia, anxiety, and depression in postinfectious IBS. Gastroenterology 125, 1651–1659. doi:10.1053/j.gastro.2003.09.028
Mawe, G.M., Hoffman, J.M., 2013. Serotonin signalling in the gut—functions, dysfunctions and therapeutic targets. Nat. Rev. Gastroenterol. Hepatol. 10, 473–486. doi:10.1038/nrgastro.2013.105Read More Here..
Saturday, 26 August 2017
Friday, 25 August 2017
People who consume more than one diet soda a day are nearly three times more likely to develop dementia or stroke. Surprisingly, no such association was found for sugared drinks. These are the latest findings from a study published in the journal Stroke on the 20th of April 2017.
This study comprised of more than 4000 participants enrolled in the Framingham Heart Study Offspring Cohort. Dietary intake of sugared drinks and artificially sweetened drinks were recorded at 3 different time points over 10 years. Participants were followed up for another 10 years and were observed for the development of stroke or dementia.
Interestingly, the association between artificial sweeteners and the risk of stroke or dementia were not influenced by potentially confounding factors, such as age, gender, smoking status, physical activity levels, and total calorie intake. Despite this, the researchers concluded that pre-existing diabetes or hypertension may be partially to blame for the correlation between artificial sweeteners and dementia. However, it is unclear if patients with these conditions could in fact be consuming more artificial sweeteners in an attempt to reduce sugar intake.
Nevertheless, the abovementioned study fuels emerging concerns that artificial sweeteners may not be the ‘safe alternative’ to sugar. As the first study to associate diet sodas to dementia, it underscores the potential harm that artificial sweeteners may have on the brain.
Moderate amounts of glucose are important for ensuring proper brain function. As the only source of energy for brain cells, glucose is responsible for powering neurons and for producing neurotransmitters that are vital for neuron to neuron signalling in the brain. Brain cells that support and maintain the neurons, such as astrocytes and microglia, also depend on glucose.
Neurons are exquisitely sensitive to drops in glucose levels. Epileptic syndromes have been ascribed to neurons that are deficient for a protein called glucose transporter type 1 (GLUT1), rendering brain cells unable to draw up glucose from the blood. Neurological conditions such as migraines, strokes, and traumatic brain injury all have a component of altered glucose metabolism in the brain.
On the other side of the coin, too much of a good thing is never a good idea. Excessive sugar intake induces a myriad of diseases, such as type 2 diabetes mellitus, metabolic syndrome, dental problems, and many others. According to the National Health and Nutrition Examination Survey from 2011–2014, half of all adults in the U.S. drank at least one sugary beverage a day.
What is behind our seemingly innate attraction to sweetness? The concept of ‘sugar addiction’ has stemmed from observing binging, withdrawal, and craving-like behavior in rats that were exposed to sugar. The current theory holds that intermittent, excessive sugar consumption causes altered neurochemical transmissions (one of them being a large release of the neurotransmitter dopamine) in the nucleus accumbens, the brain’s feelgood center. These brain changes are strikingly similar to those that occur in response to addictive drugs.
Excess amounts of sugar may also predispose us to developing brain diseases. Another study, which also utilized the data from the Framingham Heart Study Offspring cohort, discovered that people who drank two sugary drinks a day had lower total brain volume, smaller hippocampal volumes (an area of the brain responsible for forming memories), and poorer memory.
Given mankind’s insatiable appetite for sugar, artificial sweeteners were introduced to help the masses limit their sugar intake. Also known as low calorie sweeteners, FDA-approved artificial sweeteners include aspartame, neotame, acesulfame-K, sucralose, and saccharin. Low calorie sweeteners can be up to 13,000 times sweeter than regular sugar but with a fraction of the calories.
In recent years, evidence has sprung up rebutting the perceived beneficial health effects of artificial sweeteners. A large systemic review of 37 studies on these sweeteners revealed that increased intake actually resulted in increased weight and waist circumference, as well as higher occurrences of type 2 diabetes, obesity, metabolic syndrome, hypertension, and heart disease.
Furthermore, artificial sweeteners and regular sugar act differently on the brain. Brain scans of people who sipped regular sugary drinks showed stronger activation of more regions involved in reward centers compared to those who sipped drinks with sweeteners. This means that artificial sweeteners may not be as satisfying as regular sugar, leaving a person craving for more sweet foods that ultimately leads to a higher total calorie intake.
All these factors are especially worrying when taking into consideration the estimated 1 in 4 children and 2 in 5 adults who consume low calorie sweeteners on a daily basis.
Does this mean that artificial sweeteners do more harm than good? The jury’s still out on that one, as artificial sweeteners are helpful in certain populations, like diabetics. Regardless, both sugar and artificial sweeteners are best consumed in moderation—whether or not artificial sweeteners confer health benefits remains to be elucidated.
Pase M.P. et al. Sugar and artificially sweetened beverages and the risks of incident stroke and dementia. Stroke. 2017;48:1139-1146. Doi: 10.1161/STROKEAHA.116.016027.
Mergenthaler, P., Lindauer, U., Dienel, G. A., Meisel, A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends in Neurosciences. 2013; 36(10):587–597. doi: 10.1016/j.tins.2013.07.001.
Rosinger A., Herrick K., Gahche J., Park S. Sugar-sweetened beverage consumption among US adults, 2011-2014. NCHS Data Brief. 2017 Jan;(270):1-8. PMID: 28135185
Avena, N. M., Rada, P., & Hoebel, B. G. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews. 2008; 32(1):20–39. doi: 10.1016/j.neubiorev.2007.04.019.
Pase M.P. et al. Sugary beverage intake and preclinical Alzheimer’s disease in the community. Alzheimers Dement. 2017 Mar 6. pii: S1552-5260(17)30050-X. doi: 10.1016/j.jalz.2017.01.024.
Bellisle F., Drewnowski A. Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 2007; 61:691–700; doi: 10.1038/sj.ejcn.1602649.
Meghan B. Azad et al. Non-nutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies. CMAJ July 17, 2017 189:E929-E939; doi: 10.1503/cmaj.161390.
Frank G.K. et al. Sucrose activates human taste pathways differently from artificial sweetener. Neuroimage. 2008 Feb 15;39(4):1559-69. doi: 10.1016/j.neuroimage.2007.10.061.
Sylvetsky AC, Jin Y, Clark EJ, Welsh JA, Rother KI, Talegawkar SA. Consumption of low-calorie sweeteners among children and adults in the United States. J Acad Nutr Diet. 2017. doi: 10.1016/j.jand.2016.11.004.Read More Here..
Confidence in your ability to remain active improves day-to-day life, study finds
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