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Www.bmj
1
18

Focal neurological deficits after trauma

A 38 year old woman developed headache (without neck pain) and weakness of her left upper and lower limbs after a concussive head trauma with scalp lacerations in a motor vehicle crash. On examination (more than 4.5 hours after the trauma), she was conscious, alert, and in cardiac sinus rhythm. There was no carotid bruit. She scored 7 points on the National Institute of Health stroke scale (maximum possible score 42). Positive neurological findings included mild blunting of the left nasolabial fold; left hemiparesis, with extensor muscles being weaker (3/5) than flexors in the left upper limb (4+/5), flexors being weaker (4 to 4+/5) than extensors in the left lower limb (4+ to 5/5), and distal more than proximal weakness in the left arm and leg. She also had brisk deep tendon reflexes in the limbs on the left side; a left extensor plantar response; left hemianopia; and left hemisensory (including the face) hypoaesthesia for pain, cold, and touch. Eyelid ptosis or paresis of extraocular movements were not present, and pupillary size and light reaction were normal.  
bmj.com
almost 5 years ago
Www.bmj
1
18

Multiple enlarging nodules on the lower limb

A 99 year old white woman presented with a 12 month history of nodules and plaques on her left shin. They had been slowly increasing in size and bled intermittently. She denied any history of trauma to her leg and had been systemically well. She reported having high blood pressure and that she had previously had “skin problems” affecting her lower left leg that required surgery. Her only regular drug was bendroflumethiazide, and she had no known drug allergies. She was a non-smoker and drank minimal alcohol. She lived in a ground floor flat and used a walking stick. On review of her medical notes, it was discovered that two areas of squamous cell carcinoma were excised from her left shin 10 years earlier.  
bmj.com
almost 5 years ago
1
0
94

Why do we use compression bandages on patients with leg ulcers?

I know that compression bandages are used in patients with venous leg ulceration, but would this not increase the risk of reducing blood supply and therefore the risk of further ulceration?  
Sally Ralton
about 7 years ago
5
0
93

why bipolar limb lead 3 in ecg is placed on left leg instead of right one?

while we are recording ecg ,then we place bipolar limb lead 3 on left leg why it is?  
diya shona
over 6 years ago
Foo20151013 2023 2njk5o?1444774020
4
1327

LWW: Case Of The Month - April 2013

This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.  
Lippincott Williams & Wilkins
almost 7 years ago
Foo20151013 2023 1eqve0g?1444774030
1
90

LWW: Case Of The Month - May 2013

This month’s case is by Barbara J. Mroz, M.D. and Robin R. Preston, Ph.D., author of Lippincott’s Illustrated Reviews: .Physiology (ISBN: 9781451175677). For more information, or to purchase your copy, visit: http://tiny.cc/PrestonLIR, with 15% off using the discount code: MEDUCATION. The case below is followed by a choice of diagnostic tests. Select the one lettered selection that would be most helpful in diagnosing the patient’s condition. The Case A 54-year-old male 2 pack-per-day smoker presents to your office complaining of cough and shortness of breath (SOB). He reports chronic mild dyspnea on exertion with a daily cough productive of clear mucus. During the past week, his cough has increased in frequency and is now productive of frothy pink-tinged sputum; his dyspnea is worse and he is now short of breath sometimes even at rest. He has had difficulty breathing when lying flat in bed and has spent the past two nights sleeping upright in a recliner. On physical examination, he is a moderately obese male with a blood pressure of 180/80 mm Hg, pulse of 98, and respiratory rate of 22. His temperature is 98.6°F. He becomes winded from climbing onto the exam table. Auscultation of the lungs reveals bilateral wheezing and crackles in the lower posterior lung fields. There is pitting edema in the lower extremities extending up to the knees.  Question Which if the following tests would be most helpful in confirming the correct diagnosis? A. Spirometry B. Arterial blood gas C. Complete blood count D. B-type natriuretic peptide blood test E. Electrocardiogram Answer? The correct answer is B-type natriuretic peptide blood test. Uncomfortable breathing, or feeling short of breath, is a common medical complaint with multiple causes. When approaching a patient with dyspnea, it is helpful to remember that normal breathing requires both a respiratory system that facilitates gas exchange between blood and the atmosphere, and a cardiovascular system that transports O2 and CO¬2 between the lungs and tissues. Dysfunction in either system may cause dyspnea, and wheezing (or bronchospasm) may be present in both cardiac and pulmonary disease. In this patient, the presence of lower extremity edema and orthopnea (discomfort when lying flat) are both suggestive of congestive heart failure (CHF). Elevated blood pressure (systolic of 180) and a cough productive of frothy pink sputum may also be associated symptoms. While wheezing could also be caused by COPD (chronic obstructive pulmonary disease) in the setting of chronic tobacco use, the additional exam findings of lung crackles and edema plus systolic hypertension are all more consistent with CHF. What does the B-type natriuretic peptide blood test tell us? When the left ventricle (LV) fails to maintain cardiac output (CO) at levels required for adequate tissue perfusion, pathways are activated to increase renal fluid retention. A rising plasma volume increases LV preload and sustains CO via the Frank-Starling mechanism. Volume loading also stimulates cardiomyocytes to release atrial- (ANP) and B-type (BNP) natriuretic peptides. BNP has a longer half-life than ANP and provides a convenient marker for volume loading. Plasma BNP levels are measured using immunoassay; levels >100 pg/mL are suggestive of overload resulting in heart failure. How does heart failure cause dyspnea? Increasing venous pressure increases mean capillary hydrostatic pressure and promotes fluid filtration from the vasculature. Excess filtration from pulmonary capillaries causes fluid accumulation within the alveoli (pulmonary edema) and interferes with normal gas exchange, resulting in SOB. Physical signs and symptoms caused by high volume loading include: (1) Lung crackles, caused by fluid within alveoli (2) Orthopnea. Reclining increases pulmonary capillary hydrostatic pressure through gravitational effects, worsening dyspnea when lying flat. (3) Pitting dependent edema caused by filtration from systemic capillaries, an effect also influenced by position (causing edema in the lower legs as in our ambulatory patient or in dependent areas like the sacrum in a bedridden patient). What would an electrocardiogram show? Heart failure can result in LV hypertrophy and manifest as a left axis deviation on an electrocardiogram (ECG), but some patients in failure show a normal ECG. An ECG is not a useful diagnostic tool for dyspnea or CHF per se. Wouldn’t spirometry be more suitable for diagnosing the cause of dyspnea in a smoker? Simple spirometry will readily identify the presence of airflow limitation (obstruction) as a cause of dyspnea. It's a valuable test to perform in any smoker and can establish a diagnosis of chronic obstructive pulmonary disease (COPD) if abnormal. While this wheezing patient is an active smoker who could have airflow obstruction, the additional exam findings above point more to a diagnosis of CHF. What would an arterial blood gas show? An arterial blood gas measures arterial pH, PaCO¬2, and PaO2. While both CHF and COPD could cause derangements in the values measured, these abnormalities would not necessarily be diagnostic (e.g., a low PaO2 could be seen in both conditions, as could an elevated PaCO¬2). Would a complete blood count provide useful information? A complete blood count could prove useful if anemia is a suspected cause of dyspnea. Test result BNP was elevated (842 pg/mL), consistent with CHF. Diuretic treatment was initiated to help reduce volume overload and an afterload reducing agent was started to lower blood pressure and improve systolic function.  
Lippincott Williams & Wilkins
over 6 years ago
Foo20151013 2023 y4lule?1444774066
1
2591

Staying Active with Diabetes

Many know that engaging in regular physical activity and exercise will tremendously improve one’s health and overall well-being. This goes the same, if not tenfold, for individuals suffering with diabetes. However, before rushing in a high intensity or physically straining physical régime, consult with your diabetes care provider. Make sure to discuss your plans take note of any precautions that may be needed to be made prior or during these activities. It will be interesting to know that individuals with type 2 diabetes who do participate in some exercise (even at work) reduce their risk for heart disease. Remember that a physical examination that focuses on the signs and symptoms of diseases affecting the heart and blood vessels, eyes, feet, nervous system, and kidneys must be made in advance before any extensive work out plan takes into action. Any strenuous strength training or high-impact exercise is generally not recommended for people with uncontrolled diabetes. Such strain caused by these exercises can weaken blood vessels in the eyes of patients who suffer from the common diabetic complication known as retinopathy. High-impact exercise can also injure blood vessels in the feet. In fact, diabetes can contribute to foot problems in several ways: diabetic neuropathy; which is a nerve disorder that causes numbing and pain in the hands, legs and feet as well as damage to internal organs; also poor circulation to the feet is another problem that can be associated due to diabetes. Keeping this in mind it is imperative to keeping your feet healthy, investing in some great therapeutic footwear like these can be a great step in moving toward healthy feet! One thing is for sure, physical activity can increase the health in anyone’s life. Always make sure to take care of your body and take the extra precautions needed in order to maintain proper health.  
Camille Mitchell
over 6 years ago
Foo20151013 2023 1nuvntv?1444774080
2
799

Obesity Part 1 – Fat Kid in a Fat Society

Introduction to Obesity One of my favourite past-times is to sit in a bar, restaurant, café or coffee shop and people watch. I am sure many of you reading this also enjoying doing this too. People are fascinating and it is intriguing to observe: what they do; how they act; what they wear and what they look like. My family and I have always observed those around us and discussed interesting points about others that we have noticed. When I first came up to visit Birmingham University my family all sat in a coffee shop in the centre of Birmingham and noticed that on average the people walking past us looked much slimmer than what we were used to seeing back in south Wales. Now, when I go home it is more painfully obvious than ever that the people in my home region are much, much heavier than they should be and are noticeably bigger than they used to be even a short number of years ago. This change in the population around me is what first made me seriously think about obesity, as a major problem affecting the world today. Nowadays obesity is all around us! It is noticeable, it is spreading and it should worry us all. Not just for our own individual health but also for the health of our society. Obesity affects everything from the social dynamic of families, to relationships at school or work, to how much the NHS costs to run. Obesity is a massive problem and if we as a society don’t start getting to grips with it, then it will have huge implications for all of us! I am currently in my 5th year at medical school. While I have been here I have taken a keen interest in obesity. The physiology, the psychology, the anatomy, the statistics and the wider affects on society of obesity have all been covered in curriculum lectures and extra curriculum lectures. I have taken part in additional modules on these subjects and sort out many experts in this field while on hospital placements. Obesity is fascinating for some many reasons and I thought that it would be a great topic to write some blogs about and hopefully start some discussions. Warning For my first blog on the topic of obesity I quickly want to write a bit about myself and my battle with weight. Everyone’s favourite topic is themselves, but I like to think that’s not why I have written this and I hope it doesn’t come across as a narcissistic ramble. I don’t intend to try and make myself come off well or suggest that I have all the answers (because I know very well that I don’t) and I hope it doesn’t come across like that. I want to write a bit of an autobiography because I wish to demonstrate how easy it is to go from a chunky kid to a technically obese teenager to a relatively fat adult without really realising what was happening. Chunky Child to Fat adult While planning this blog I realised that my Meducation profile picture was taken when I was at my all time fattest. At the graduation ceremony at the end of my 3rd year at university after completing my intercalation I was over 19 stones. At 6 foot 2” this gave me a BMI of >33 which is clinically obese. I had a neck circumference of >18”, a chest circumference of 48”, a waist of >40”, a seat of >52” and a thigh circumference of >28” per leg. Why do I know all of these rather obscure measurements? Partly because I am quite obsessive but mainly because I had to go to buy a tailor made suit because I could no longer buy a suit from a shop that I could fit into and still be able to move in. The only options left to me where massive black tent-suits or to go to a tailors. After the graduation I sat down at my computer (whilst eating a block of cheese) and compared my face from the graduation photos to pictures I had taken at the start of university and the difference in shape and size was amazingly obvious. I had got fat! I realised that if I had a patient who was my age and looked like me with my measurements then I would tell him to lose weight for the good of his health. So, I decided that finally enough was enough and I that I should do something about it. Before I describe how I got on with the weight management I will quickly tell the back story of how I came to be this size. I have always been a big guy. I come from a big family. I have big bones. I had “puppy fat”. I was surrounded by people who ate too much, ate rubbish and were over weight themselves, so I didn’t always feel that there was anything wrong with carrying a bit of tub around the middle. When I went to comprehensive school at age 12 I had a 36” waist. I thought I carried the weight quite well because I was always tall and had big ribs I could sort of hide the soft belly. Soon after arriving at the new school I had put on more weight and for the first time in my life I started to get bullied for being fat! And I didn’t like it. It made me really self-aware and knocked my confidence. Luckily, we started being taught rugby in PE lessons and I soon found that being bigger, heavier and stronger than everyone else was a massive advantage. I soon got my own back on the bullies… there is nowhere to hide on a rugby field! This helped me gain my confidence and I realised that the only way to stop the bullying was to confront the bullies and to remake myself in such a way as that they would be unable to bully me. I decided to take up rugby and to start getting fit. I joined a local club, starting playing regularly, joined a gym and was soon looking less tubby. Reflecting (good medical jargon, check) on my life now I can see that my PE teachers saved me. By getting me hooked on rugby they helped get me into many other sports and physical activity in general and without their initial support I think my life would have gone very differently. Rugby was my saviour and also later on a bit of a curse. As I grew up I got bigger and bigger but also sportier. I started putting muscle on my shoulders, chest and legs which I was convinced hid how fat I actually was. I developed a body shape that was large but solid. I was convinced that although I was still carrying lots of excess weight I no longer looked tubby-fat. When I was 14 my PE teachers introduced me to athletics. They soon realised that I was built for shot putt and discuss throwing and after some initial success at small school competitions I joined a club and took it up seriously. At this age I had a waist of about 38” but was doing about 3-4 hours of exercise almost everyday, what with rugby, running, gym, swimming and athletics – in and out of school. My weight had by now increased to roughly 15 stones and my BMI was over 30. I was physically fit and succeeding at sport but still carrying quite a lot of fat. I no longer thought of myself as fat but I knew that other people did. Between the ages of 14 and 18 I started to be picked for regional teams in rugby and for international athletic competitions for Wales. My sporting career was going very well but the downside of this was that I was doing sports that benefited from me being heavier. So the better I got the heavier I wanted to become. I got to the stage where I was eating almost every hour and doing my best to put on weight. At the time I thought that I was putting on muscle and being a huge, toned sports machine. It took me a while to realise that actually my muscles weren't getting any bigger but my waist was! By the time I had completed my A-levels I was for the first time over 18 stones and had a waste of nearly 40”. So, at this point I was doing everything that I had been told that would make me more adapted for my sport and I was succeeding but without noticing it I was actually putting on lots of useless excess weight that in the long term was not good for me! During my first year of university I gave up athletics and decided that I no longer needed to be as heavy for my sports. This decision combined with living away from home, cooking for myself and walking over an hour a day to and from Uni soon began to bear fruit. By the summer of my first year at Uni, aged 19, I had for the first time in my life managed to control my weight. When I came to Uni I was 18 stone. After that first year I was down to 14 stone – a weight I had not been since I was 14 years old! I had played rugby for the Medical school during my first year but as a 2nd row/back row substitute. These positions needed me to be fit and not necessarily all that heavy and this helped me lose the weight. During my second year I began to start as a 2nd row and was soon asked to help out in the front row. I enjoyed playing these positions and again realised that I was pretty good at it and that extra weight would make me even better. So between 2nd year and the end of 3rd year I had put on nearly 5 stone in weight and this put me back to where I started at my graduation at the end of 3rd year. The ironic and sad thing is about all this that the fatter, less “good looking” and unhealthier I became, the better I was adapted for the sports I had chosen. It had never occurred to me that being good at competitive sports might actually be bad for my health. The Change and life lessons learnt At the beginning of my 4th year I had realised that I was fatter than I should be and had started to pick up a number of niggly injuries from playing these tough, body destroying positions in rugby. I decided that I would start to take the rugby less seriously and aim to stay fit and healthy rather than be good at a competitive sport. With this new attitude to life I resolved to lose weight. Over the course of the year there were a number of ups and downs. I firstly went back to all the men’s health magazines that I had stock piled over the years and started to work out where I was going wrong with my health. After a little investigation it became apparent that going running and working out in the gym was not enough to become healthy. If you want to be slim and healthy then your diet is far more important than what physical activity you do. My diet used to be almost entirely based on red meat and carbs: steak, mince, bacon, rice and pasta. Over the year I changed my diet to involve far more vegetables, more fibre, more fruit, more salad and way less meat! The result was that by Christmas 2012 I was finally back below 18 stones. The diet had started to have benefits. Then came exams! By the end of exams in April 2013 I had gone back up 19 stones and a waist of >40”. I was still spending nearly 2 hours a day doing weights in the gym and running or cycling 3 times a week. Even with all this exercise and a new self- awareness of my size, a terrible diet over the 3 week exam period had meant that I gained a lot of fat. After exams I went travelling in China for 3 weeks. While I was there I ate only local food and lots of coffee. Did not each lunch and was walking around exploring for over 6 hours a day. When I got back I was 17.5 stone, about 106kg. My waist had shrunk back down to 36” and I could fit into clothes I had not worn in years. This sudden weight loss was not explained by traveller’s diarrhoea or any increased activity above normal. What made me lose weight was eating a fairly healthy diet and eating far less calories than I normally would. I know this sounds like common sense but I had always read and believed that if you exercised enough then you could lose weight without having to decrease your calorie intake too much. I have always hated the sensation of being hungry and have always eaten regular to avoid this awful gnawing sensation. I had almost become hunger-phobic, always eating when given the opportunity just in case I might feel hungry later and not because I actually needed to eat. The time in China made me realise that actually I don’t NEED to eat that regularly and I don’t NEED to eat that much. I can survive perfectly ably without regular sustenance and have more than enough fat stores to live my life fully without needing to each too much. My eating had just become a habit, a WANT and completely unnecessary. After being home for a month I have had some ups and downs trying to put my new plans into action. Not eating works really easily in a foreign country, where it’s hot, you are busy and you don’t have a house full of food or relatives that want to feed you. I have managed to maintain my weight around 17.5 stones and kept my waist within 36” trousers. I am counting that as a success so far. The plan from now on is to get my weight down to under 16.5 stones because I believe that as this weight I will not be carrying too much excess weight and my BMI will be as close to “not obese” as it is likely to get without going on a starvation diet. I intend to achieve this goal by maintain my level of physical activity – at least 6 hours of gym work a week, 2 cardio sessions, tennis, squash, cycling, swimming and golf as the whim takes me. BUT MORE IMPORTANTLY, I intend to survive off far fewer calories with a diet based on bran flakes, salad, fruit, nuts, chicken and milk. I am hoping that this very simple plan will work! Conclusion Writing this short(-ish) autobiography was quite cathartic and I would really recommend it for other people who are trying to remake themselves. Its helped me put my thoughts in order. Over the years I wanted to lose weight because I wanted to look better. This desire has now matured into a drive to be not just slimmer but healthier; I no longer want to be slimmer just for the looks but also to reduce the pressure on my joints, to reduce the pressure on my cardiovascular system, to reduce my risks of being fat when I am older, to hopefully reduce the risk of dying prematurely and to some extent to make life cheaper – eating loads of meat to prevent hunger is expensive! I hope this blog has been mildly interesting, but also informative of just how easy it is for even a health conscious, sporty individual to become fat in our society. I also wanted to document how difficult it is to lose weight and maintain that new lower weight for any prolonged length of time. At some point I would like to do a blog on the best methods for weight loss but that may have to wait until I have found what works for me and if I do actually manage to achieve my goals. Would be a bit hypercritical to write such a blog while still having a BMI yo-yoing around 32 I feel! Thought for the day 1 - Gaining wait is easy, becoming fat is easy, losing fat is also technically easy! The hard part is developing AND then maintaining a healthy mental attitude towards your weight. The human body has evolved to survive starvation. We are almost perfectly made to build up high density fat stores just in case next year’s crops fail and we have to go a few months on broth. I will say it again – We are designed to survive hard conditions! The problem with the modern world and with modern society is that we no longer have to fight to survive. For the first time in human history food is no longer scarce… it is in fact incredibly abundant and cheap (http://www.youtube.com/watch?v=-Z74og9HbTM). It is no surprise that when a human body is allowed to eat want and how much it craves and then do as little activity as possible, that it puts on fat very quickly. This has to be one of the major ironies of our age – When the human race has evolved society enough that we no longer need to have fat stores in case of disaster, that we are now the fattest humans have ever been! 2 – The best bit of advice I was ever given is this: “Diets ALWAYS fail! No matter what the diet or how determined you are, if you diet then within 2 years you will be the same weight or heavier than you are now. The only way to a healthy body is through a healthy LIFESTYLE CHANGE! You have to make changes that you are prepared to keep for a long time.”  
jacob matthews
over 6 years ago
Foo20151013 2023 e2a8vo?1444774258
7
294

Monkey See, Monkey Do.

So you're sitting in a bus when you see a baby smile sunnily and gurgle at his mother. Your automatic response? You smile too. You're jogging in the park, when you see a guy trip over his shoelaces and fall while running. Your knee jerk reaction? You wince. Even though you're completely fine and unscathed yourself. Or, to give a more dramatic example; you're watching Titanic for the umpteenth time and as you witness Jack and Rose's final moments together, you automatically reach for a tissue and wipe your tears in whole hearted sympathy ( and maybe blow your nose loudly, if you're an unattractive crier like yours truly). And here the question arises- why? Why do we experience the above mentioned responses to situations that have nothing to do with us directly? As mere passive observers, what makes us respond at gut level to someone else's happiness or pain, delight or excitement, disgust or fear? In other words, where is this instinctive response to other people's feelings and actions that we call empathy coming from? Science believes it may have discovered the answer- mirror neurons. In the early 1990s, a group of scientists (I won't bore you with the details of who, when and where) were performing experiments on a bunch of macaque monkeys, using electrodes attached to their brains. Quite by accident, it was discovered that when the monkey saw a scientist holding up a peanut, it fired off the same motor neurons in its brain that would fire when the monkey held up a peanut itself. And that wasn't all. Interestingly, they also found that these motor neurons were very specific in their actions. A mirror neuron that fired when the monkey grasped a peanut would also fire only when the experimenter grasped a peanut, while a neuron that fired when the monkey put a peanut in its mouth would also fire only when the experimenter put a peanut in his own mouth. These motor neurons came to be dubbed as 'mirror neurons'. It was a small leap from monkeys to humans. And with the discovery of a similar, if not identical mirror neuron system in humans, the studies, hypotheses and theories continue to build. The strange thing is that mirror neurons seem specially designed to respond to actions with clear goals- whether these actions reach us through sight, sound, smell etc, it doesn't matter. A quick example- the same mirror neurons will fire when we hop on one leg, see someone hopping, hear someone hopping or hear or read the word 'hop'. But they will NOT respond to meaningless gestures, random or pointless sounds etc. Instead they may well be understanding the intentions behind the related action. This has led to a very important hypothesis- the 'action understanding' ability of mirror neurons. Before the discovery of mirror neurons, scientists believed our ability to understand each other, to interpret and respond to another's feeling or actions was the result of a logical thought process and deduction. However, if this 'action understanding' hypothesis is proved right, then it would mean that we respond to each other by feeling, instead of thinking. For instance, if someone smiles at you, it automatically fires up your mirror neurons for smiling. They 'understand the action' and induce the same sensation within you that is associated with smiling. You don't have to think about what the other person intends by this gesture. Your smile flows thoughtlessly and effortlessly in return. Which brings us to yet another important curve- if mirror neurons are helping us to decode facial expressions and actions, then it stands to reason that those gifted people who are better at such complex social interpretations must be having a more active mirror neuron system.(Imagine your mom's strained smile coupled with the glint in her eye after you've just thrown a temper tantrum in front of a roomful of people...it promises dire retribution my friends. Trust me.) Then does this mean that people suffering from disorders such as autism (where social interactions are difficult) have a dysfunctional or less than perfect mirror neuron system in some way? Some scientists believe it to be so. They call it the 'broken mirror hypothesis', where they claim that malfunctioning mirror neurons may be responsible for an autistic individual's inability to understand the intention behind other people's gestures or expressions. Such people may be able to correctly identify an emotion on someone's face, but they wouldn't understand it's significance. From observing other people, they don't know what it feels like to be sad, angry, surprised or scared. However, the jury is still out on this one folks. The broken mirror hypothesis has been questioned by others who are still skeptical about the very existence of these wonder neurons, or just how it is that these neurons alone suffered such a developmental hit when the rest of the autistic brain is working just dandy? Other scientists argue that while mirror neurons may help your brain to understand a concept, they may not necessarily ENCODE that concept. For instance, babies understand the meaning behind many actions without having the motor ability to perform them. If this is true, then an autistic person's mirror neurons are perfectly fine...they were just never responsible for his lack of empathy in the first place. Slightly confused? Curious to find out more about these wunderkinds of the human brain? Join the club. Whether you're an passionate believer in these little fellas with their seemingly magical properties or still skeptical, let me add to your growing interest with one parting shot- since imitation appears to be the primary function of mirror neurons, they might well be partly responsible for our cultural evolution! How, you ask? Well, since culture is passed down from one generation to another through sharing, observation followed by imitation, these neurons are at the forefront of our lifelong learning from those around us. Research has found that mirror neurons kick in at birth, with infants just a few minutes old sticking their tongues out at adults doing the same thing. So do these mirror neurons embody our humanity? Are they responsible for our ability to put ourselves in another person's shoes, to empathize and communicate our fellow human beings? That has yet to be determined. But after decades of research, one thing is for sure-these strange cells haven't yet ceased to amaze and we definitely haven't seen the last of them. To quote Alice in Wonderland, the tale keeps getting "curiouser and curiouser"!  
Huda Qadir
almost 6 years ago
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