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Okay this is going to be controversial!Misconception: MSG or Ajinamoto (brand name) is bad for healthI have talked to many of my friends and asked them what is wrong in MSG that they do not want it to be added in their food, well nobody actually had an answer and most of them said they believed it because someone asked them not to use, as it bad for health.What is MSG?Monosodium Glutamate is the sodium salt of glutamic acid which is one of the most abundant naturally-occurring non-essential amino acids.Glutamate is found naturally in tomatoes, Parmesan cheese, potatoes, mushrooms, and other vegetables, meat, dairy products and fruits. The glutamate in MSG is chemically indistinguishable from glutamate present in food proteins. Our bodies ultimately metabolize both sources of glutamate in the same wayWhat is it used for?Monosodium glutamate is used as a flavor enhancer and food additive to deliver the fifth taste called umami which means savory in japanese. This flavor is similar to taste from meat soups and stewsIs it Dangerous to use MSG as a food additive?It is not dangerous. International and national bodies governing food additives currently consider MSG safe for human consumption as a flavor enhancer. The USFDA and fssai the premier regulatory body in USA and India repectively, considers MSG to be “generally recognized as safe”, the only requirement is those products need to have a label “added MSG”So what is the story behind the misconception?It all started in 1968 when Dr Ho Man Kwok wrote a letter to the New England Journal of Medicine musing about the possible causes of a syndrome he experienced whenever he ate at Chinese restaurants in the US. He had informed that the reason for these symptoms might be the wine used for cooking or the soy sauce or the MSG added to the food. Later it was called the ‘Chinese Restaurant Syndrome’which can cause, headache, nausea and other discomfort after having a Chinese meal.His suggestion went viral, spawning a huge number of scientific studies, books exposing ‘the truth’ about MSG, anti-MSG cookbooks, and even prompting Chinese restaurants to advertise that they didn’t use MSG in their cooking.Were any tests or experiments conducted to prove that MSG is not dangerous?Yes! the USFDA after receiving many reports of the Chinese syndrome with the help of an independent scientific group Federation of American Societies for Experimental Biology (FASEB) to examined the safety of MSG in the 1990′s.FASEB’s report concluded that MSG is safe. The FASEB report identified some short-term, transient, and generally mild symptoms, such as headache, numbness, flushing, tingling, palpitations, and drowsiness that may occur in some sensitive individuals who consume 3 grams or more of MSG without food. However, a typical serving of a food with added MSG contains less than 0.5 grams of MSG. Consuming more than 3 grams of MSG without food at one time is unlikely.One of the reasons to not use MSG products is 80% of processed foods use MSG as an additive and so here the villain is processed foods and not MSG.Well go enjoy your Chinese food without MSG stuck in your mind and remember anything too much is not good for health and that’s the key!!!EDIT 1: Since many of them of have asked for citations, i am adding a few links below for more information on this topic,Questions and Answers on Monosodium glutamate (MSG) - This is from the USFDAhttp://www.fssai.gov.in/Portals/0/Pdf/Order_Nestle.pdf - go to this file and read page 4, point B1 which clearly states that one of the reasons Maggi was banned was because the labeling said “No added MSG” when there was MSG in it. The offence is misleading as the rules of both FDI and fssai veheently states that if a food product contains MSG then the product label should support the fact “added MSG”http://www.fssai.gov.in/Portals/0/Pdf/Order_MSG_31_03_2016.pdf - Clarification on MSG as a flavor enhancer. Kt is also called Falvor enhancer 621. This clearly states that presently there is no analytical method to determine if MSG was added during manufacturing or occurred in the natural form.Monosodium glutamate (MSG): Is it harmful? - This is an excerpt from the famous Mayo clinic. Here it clearly explains the MSG symptom complex a set of sysmptoms shown a very less number of people after ingesting MSG.Cancer and MSG: Busting the Myth busting the myths of relation between MSG and Cancer

The concept of entropy was introduced into the theory of thermodynamics by Rudolf Clausius in the 1850s. Clausius defined the entropy [math]S[/math] as a state function of a thermodynamic system, such that the infinitesimal change in the entropy of the system is given by[math]dS = \delta Q [/math][math][/math][math]/ T ~,\tag 1[/math]where [math]\delta Q[/math] is the infinitesimal amount of heat that the system either absorbs ([math]\delta Q > 0[/math]) or rejects ([math]\delta Q < 0[/math]), while [math]T[/math] is the system’s temperature.Making this definition exact would require me also to provide rigorous definitions of “thermodynamic system”, “state function”, “heat”, and “temperature”. If you haven’t studied the subject, I suggest consulting the first couple of chapters of H. B. Callen’s Thermodynamics and an Introduction to Thermostatistics, 2nd ed. (Wiley, 1985), or of any other good introductory textbook in thermodynamics.The reason why the definition of entropy based on eq. (1) is useful is that it allowed Clausius to formulate what we now call the “2nd law of thermodynamics”: that the world’s entropy tends towards a maximum. In a reversible process entropy is conserved. In an irreversible process the total entropy increases. A process which would cause total entropy to decrease (for instance, lukewarm water spontaneously separating itself into a layer of cold water and a layer of hot water) is forbidden.Clausius couldn’t prove that this law is always valid. Rather, he postulated it and then proceeded to show (based on the pioneering and until then neglected work of Sadi Carnot, in whose honor Clausius apparently chose the letter [math]S[/math] for the entropy) that a great variety of physical phenomena could be thereby explained.One of the major achievements of theoretical physics in the late 19th century was to show that the 2nd law of thermodynamics could be explained statistically. The point is that when we see a thermodynamic system (for instance, a gas in a closed container), we can’t in practice determine the microscopic details of what the molecules and atoms within it are doing. All we can do is measure a few macroscopic variables (such as volume, pressure, and temperature). These macroscopic variables define what we call the system’s macrostate. Each macrostate could correspond to many different possible physical configurations of the molecules and atoms in the system. Each of those possible configurations is called a microstate.Ludwig Boltzmann showed that Clausius’s definition of entropy in terms of heat and temperature could be substituted for a more fundamental definition in terms of the number of microstates compatible with a given macrostate:[math]S = k_B \ln \Omega~.\tag 2[/math]In eq. (2) —first written in this simple form not by Boltzmann himself but by Max Planck— [math]S[/math] is the entropy of a thermodynamic system that is in some given macrostate, [math]\Omega[/math] is the number of different microstates that are compatible with the macrostate (i.e., in how many ways you could re-arrange in the molecules and atoms without changing the macrostate), and [math]k_B[/math] is a universal constant (the “Boltzmann constant”). A modern theoretical physicist would prefer to work in units in which [math]k_B = 1[/math] (making [math]S[/math] dimensionless) but this requires measuring temperatures in a different scale to the one that experimentalists are used to.There are at least three key things to note about eq. (2). The first is that the entropy [math]S[/math] quantifies our ignorance of what the physical system is really doing. We know the macrostate (determined by macroscopic state variables like volume, pressure, and temperature, which we can easily measure). If the macrostate completely determined the actual physical state of the system, then a single microstate would be allowed, so that [math]\Omega = 1[/math] and therefore, by eq. (2), [math]S = 0[/math]. Thus, zero entropy corresponds to complete knowledge of the physical state. More entropy corresponds to more possible microstates, and therefore to greater ignorance.The second very important thing about eq. (2) is that it tells us the 2nd law of thermodynamics is a statistical result. If we assume that all of the possible microstates are equally likely, the probability of a macrostate is proportional to [math]\Omega[/math]. The natural logarithm [math]\ln[/math] is a monotonically increasing function, so a more probable state has greater [math]S[/math]. Therefore, when [math]S[/math] increases a system is going from a less probable to a more probable state. When systems are composed of a great many particles (which is true of a glass of water, and even truer of the observable Universe) it is overwhelmingly more likely for entropy to increase than to decrease. The 2nd law becomes, for all intents and purposes, a certainty.The third very important thing about eq. (2) is that is has the right form to reproduce a fundamental property of the entropy as originally introduced by Clausius: it is an extensive variable. This means that the entropy of two systems considered jointly is equal to the sum of the entropy of each of the system. Note that the number of microstates of the two systems considered together is the product of the number of microstates of each separately; or, if you prefer, that the probability of the combined system being in some macrostate is the product of the probabilities of the two separate macrostates. Thus, by a basic property of logarithms:[math]S_{\rm total} = k_B \ln \left( \Omega_1 \cdot \Omega_2 \right) = k_B \left( \ln \Omega_1 [/math][math][/math][math]+ \ln \Omega_2 \right) = S_1 [/math][math][/math][math]+ S_2~, \tag 3[/math]where [math]\Omega_1[/math] is the number of microstates of the first system and [math]S_1[/math] the corresponding entropy (while, of course, [math]\Omega_2[/math] is the number of microstates of the second system and [math]S_2[/math] the corresponding entropy).Willard Gibbs, the great American mathematical physicist, introduced the concept of “statistical ensemble“ in his book Elementary Principles of Statistical Mechanics, published in 1902. Gibbs’s treatment is more general than Boltzmann’s, because it allows the various microstates of an ensemble to have different probabilities. For such a generalized ensemble, Gibbs showed that the entropy could be expressed as[math]\displaystyle S = - k_B \sum_i p_i \ln p_i [/math][math][/math][math]~, \tag 4[/math]where the sum is over all of the possible microstates, each with probability [math]p_i[/math]. Note that if we are certain of the microstate (say, [math]p_0 = 1[/math] and [math]p_i = 0[/math] for [math]i > 0[/math]) then [math]S = 0[/math], since [math]\lim_{x \to 0^+} x \ln x = 0[/math]. The more evenly distributed the probabilities [math]p_i[/math] are, the greater the entropy [math]S[/math] will be.The term “entropy” is used in other contexts, notably information theory. But there’s an important difference in how the concept is used in the two disciplines: in thermodynamics the entropy measures variability that we don’t care about: how much you could re-arrange the microscopic componentes without changing the macrostate that we actually deal with and control in the lab. In information theory, on the other hand, entropy measures variability that we do care about, because it’s the vehicle for conveying information to someone else: it quantifies one’s ignorance before decoding the actual message contained in a given source.There’s a famous and amusing story about this. Information theory was developed by Claude Shannon in the 1940s. In quantifying the maximum amount of information encodable in some source, Shannon arrived at a formula of the same form as eq. (4). Shannon asked the eminent mathematician and theoretical physicist John von Neumann what to call that quantity. According to one version of the story, von Neumann replied that Shannon should call it “entropy”, for two reasons:In the first place, a mathematical development very much like yours already exists in Boltzmann's statistical mechanics, and in the second place, no one understands entropy very well, so in any discussion you will be in a position of advantage.See: History of entropy.

Disclaimer: this is a sad story.I finished med school at 26. At 28, I was a first year surgical resident covering the ICU. An 18-year-old kid was in a car accident. He was a passenger in a car that got t-boned (that’s when a car crashes into the side of another car making a T… like the bone in a T-bone steak). I was 28, he was 10 years younger.Because he was in the passenger seat he absorbed the brunt of the force on the right side of his body. His right leg was broken in multiple places, his pelvis was shattered, and he sustained major head trauma.I “met” him after surgery, but he never met me. He was in a medically induced coma in a traction bed. I was in charge of the ICU during the day. There were pins coming out of his leg and spine, but he still looked 18. He was muscular (looked like he played sports), it’s probably what helped him survive the wreck.He had a lot of brain swelling, even though they had already removed part of his skull to decompress the pressure on his brain. In an effort to keep his brain swelling as low as possible, they wanted him kept in a deep coma, and it required very high doses of a drug called propofol (the drug that famously killed Michael Jackson).It should be noted that medically induced comas are scary for family to see, but they are done to help protect the patient.In passing, by this point, I had met the family. They were distraught.Three days after the accident, I noticed his urine had turned black. Black urine is called myoglobinuria, and it’s a sign of muscle breakdown. Why? It made no sense. He was lying in bed. If it was from the accident, it would have appeared in the first 24 hours after the accident. Why was this happening now? At the same time, his blood pressure started to drop. Plus, blood tests showed the acid in his system was rising, and this is a sign of the body shutting down.We treated the symptoms the best we could, but we didn’t know the cause. He didn’t have any obvious infection. He had a young and healthy heart. Throughout this all, we (the doctors) debated if we should lower his propofol because it can have a side effect of lowering blood pressure, which was another new problem. The neurosurgeon wanted him kept as deep as possible because he wanted to protect his brain, while also maintaining good blood pressure so that the brain would have good blood flow. We kept the propofol going but gave him other medications to raise his blood pressure.Nothing we did stopped the acid from rising in his blood to critical levels. No matter what we gave him, his blood pressure got worse, and the level of acid in his blood continued to rise.Within less than 24 hours they were trying to set up emergency dialysis to offset the acid levels. It was getting late. Logistically arranging it was taking a number of phone calls, and while that was going on, I had a gut feeling there was a chance he wouldn’t make it through the night.The attending covering the ICU went home (that’s the head of the ICU). It was just me. I called her and let her know of my concerns. She agreed I should call the family.It was the first time I had done this. I was 28. He was 18, but I just knew his parents needed to come in to say goodbye.Soon after I got off the phone, my premonition became a reality. His heart rate became erratic. Soon after that his heart stopped. We called a code and initiated advanced cardiac life support (chest compressions). It was futile.A few minutes after the time of death was called his parents walked into the intensive care unit. I was gutted. As they entered, I looked them in the eye shaking my head and his mother knew right away. “I’m sorry, he didn’t make it.”They said their goodbyes.I couldn’t. I couldn’t figure out why someone so young with the heart of a bull would have such a profound circulatory collapse. It didn’t make sense. I started to review the medications he was on, and all the literature related to those medications. There had to be something.It took me many weeks (six weeks of research starting that night and ultimately writing a paper), but I found it. There it was.Propofol was a pretty new drug at the time, only out for 10 or 15 years. At first it was only used to put people to sleep for surgery because it had a rapid induction (that’s fancy doctor speak for it worked fast). Because it kept the intracranial pressure low (ICP), neurosurgeons loved the drug and started to run it for the duration of their cases. The lightbulb moment was a case in the neurosurgery literature of a patient with unexplained acidosis and myoglobinuria during a 15 hour surgery that seemed to resolve after the propofol infusion was stopped. As I dug deeper, I came across an article in The Lancet (one of the oldest and most prestigious medical journals) from a pediatric neurosurgery intensive care unit that was using propofol for long-term sedation. They reported a number of cases (more than a dozen) of kids developing unexplained acidosis and signs of muscle breakdown in children in medically induced comas using propofol, with half progressing to death. They coined a term in that article called “propofol infusion syndrome.” Could this be why he died?In searching for the mechanism to explain “propofol infusion syndrome”, I found a basic science article that talked about how propofol was metabolized. It is broken down into a number of molecules, but one of the intermediary molecules can be toxic to cells and how they break down energy necessary to function. With higher levels of infusion this toxic metabolite builds up to toxic levels, with the most metabolically active cells showing signs first - the heart and skeletal muscles. As the skeletal muscles break down, they release myoglobin, and it releases in the urine. As the heart muscle gets weakened, the blood pressure drops, and the heart gives out, resulting in cardiovascular collapse.Propofol poisoned this young man.But here’s where my research took a sickening turn. I uncovered a letter to the editor in an obscure journal written by the chief medical officer of AstraZeneca (the makers of Propofol), an anesthesiologist by training, denying the existence of the so-called “propofol infusion syndrome.” I was enraged. I checked a bottle. I noted the package insert for propofol did not include any dosage limits. I get it, no limits, more drug sales, but slowly, in small numbers, the case was being built, and kids were dying.Determined to do something about it, I wrote a paper on it. It was a case report and review of the literature.I made sure to include the letter to the editor he wrote in my research article, juxtaposed with all the research available to date, demonstrating that high doses of propofol given over extended periods of time (particularly in children) can lead to death.Shortly after my paper was published, I was happy to see that the latest AstraZeneca package insert included a dosing limit which also included a lower limit for children and the warning that one of the side effects of prolonged administration includes metabolic acidosis and myoglobinuria. The inserts now said, in the event of those developments, propofol should be stopped immediately, and an alternative sedation regimen should be instituted. Though they didn’t mention “propofol infusion syndrome” by name, I knew my article reached this drug company.I will never forget that case. This young man’s life was tragically cut short. I’d like to think his death, while tragic, was a medical mystery that needed to be solved.I called the article “Too Much of a Good Thing” because propofol can be a good drug…[1][1][1][1]Footnotes[1] Too Much of a Good Thing? Tracing the History of the... : Journal of Trauma and Acute Care Surgery[1] Too Much of a Good Thing? Tracing the History of the... : Journal of Trauma and Acute Care Surgery[1] Too Much of a Good Thing? Tracing the History of the... : Journal of Trauma and Acute Care Surgery[1] Too Much of a Good Thing? Tracing the History of the... : Journal of Trauma and Acute Care Surgery