Listen up, joggers: No matter how hard you’ve been pushing yourself, you’re nowhere close to running at 40 mph - the fastest speed at which a body can biologically move, according to scientists.
That’s the rate man’s muscle contraction speeds permit him to run, according to Wyoming University biomechanics expert Dr. Matthew Bundle, as reported in The Telegraph.
At 40 mph, a runner would sprint across the finish line in a 100-meter race in 6.67 seconds - which is how long it took Olympic gold medalist Usain Bolt to reach the 60-meter mark, says The Telegraph. Bolt was clocked at nearly 28 mph in the 100-meter sprint, which sounds impressive until you consider that lions run at 50 mph when in pursuit of prey and a cheetah’s speed approaches 70 mph.
It was thought that a human being’s primary hindrance to speed was that the limbs can only sustain a certain amount of force as they hit the ground. But new research says it’s actually the contraction of the muscles that dictates speed.
The Wyoming University researchers employed a high-speed treadmill that was capable of reaching speeds higher than 40 mph and could record exact measurements of the forces applied to its surface when someone ran on it. The subjects performed at high speeds in a variety of gaits.
Because the force generated by hopping on one leg at top speed was roughly 1.5 to 2 times greater than forward running at top speed, the researchers concluded that muscle speed, not ground force, is the determining factor in reaching our maximum speed.
Peter Weyand, Southern Methodist University physiologist and co-researcher, noted the view that speed is limited by the force with which limbs could strike the running surface is reasonable.
“However, our new data clearly shows that this is not the case,” he told The Telegraph. “Despite how large the running forces can be, we found that the limbs are capable of applying much greater ground forces than those present during top-speed forward running.”
(via NY Daily News)
Though you might feel a strong inkling toward loading up on sugary snacks during final exams or those last few hours of work, that might be a bad idea. Binging on sugar for as little as six weeks can actually make you dumber. Researchers at UCLA have found that a diet high in sugar can disrupt the memory and learning functions of the brain, while omega-3 fatty acids can actually counteract said disruption.
High-fructose corn syrup, in particular, creates problems. The liquid is six times sweeter than cane sugar and, as you’ve probably heard, commonly added to soft drinks and processed foods. The average American actually consumes more than 40 pounds of this stuff every year.
“We’re not talking about naturally occurring fructose in fruits, which also contain important antioxidants,” explained Gomez-Pinilla, who is also a member of UCLA’s Brain Research Institute and Brain Injury Research Center. “We’re concerned about high-fructose corn syrup that is added to manufactured food products as a sweetener and preservative.”
The researchers set a number of rats up on a sugar-high diet, and set aside another bunch on a sugar free diet. After six weeks, they asked said rats to do a little maze. They had done it well six weeks prior, but the sugar-fed rats had trouble after that time period.
“The second group of rats navigated the maze much faster than the rats that did not receive omega-3 fatty acids,” Gomez-Pinilla said. “The DHA-deprived animals were slower, and their brains showed a decline in synaptic activity. Their brain cells had trouble signaling each other, disrupting the rats’ ability to think clearly and recall the route they’d learned six weeks earlier.”
A closer look found that insulin had lost some of its power to influence the brain, which in turn disrupted the memory and learning functions of the brain.
Long story short, might not hurt to skip that Snickers.
Researchers from Harvard School of Public Health have found that greater consumption of sugar-sweetened beverages (SSBs) is linked with a greater genetic susceptibility to high body mass index (BMI) and increased risk of obesity. The study reinforces the view that environmental and genetic factors may act together to shape obesity risk.
The study appears Sept. 21 in an advance online edition of the New England Journal of Medicine.
“Our study for the first time provides reproducible evidence from three prospective cohorts to show genetic and dietary factors — sugar-sweetened beverages — may mutually influence their effects on body weight and obesity risk. The findings may motivate further research on interactions between genomic variation and environmental factors regarding human health,” said Lu Qi, assistant professor in the Department of Nutrition at HSPH and senior author of the study.
In the past three decades, consumption of SSBs has increased dramatically worldwide. Although widespread evidence supports a link between SSBs, obesity and chronic diseases such as diabetes, there has been little research on whether environmental factors, such as drinking sugary beverages, influence genetic predisposition to obesity. The research was based on data from three large cohorts, 121,700 women in the Nurses’ Health Study, 51,529 men in the Health Professionals Follow-up Study and 25,000 in the Women’s Genome Health Study. All of the participants had completed food-frequency questionnaires detailing their food and drink consumption over time.
The researchers analyzed data from 6,934 women from NHS, 4,423 men from HPFS, and 21,740 women from WGHS who were of European ancestry and for whom genotype data based on genome-wide association studies were available. Participants were divided into four groups according to how many sugary drinks they consumed: less than one serving of SSB per month, between 1-4 servings per month, between 2-6 servings per week, and one or more servings per day. To represent the overall genetic predisposition, a genetic predisposition score was calculated on the basis of the 32 single-nucleotide polymorphisms known to be associated with BMI (weight in kilograms divided by the square of the height in meters).
The results showed that the genetic effects on BMI and obesity risk among those who drank one or more SSBs per day were about twice as large as those who consumed less than one serving per month. The findings suggest that regular consumption of sugary beverages may amplify the genetic risk of obesity. In addition, individuals with greater genetic predisposition to obesity appear to be more susceptible to harmful effects of SSBs on BMI. “SSBs are one of the driving forces behind the obesity epidemic,” says Frank Hu, professor of nutrition and epidemiology at HSPH and a coauthor of this study. “The implication of our study is that the genetic effects of obesity can be offset by healthier food and beverage choices.”
(via Science Daily)
The human brain evolved to seek out foods high in fat and sugar. But a preference that started out as a survival mechanism has, in our age of plenty, become a self-destructive compulsion.
It is well known that bad diets can trigger obesity and diabetes. There is growing evidence that they trigger Alzheimer’s disease too, and some researchers now see it as just another form of diabetes.
If correct, this has enormous, and grave, implications. The world already faces an epidemic of diabetes. The prospect of a parallel epidemic of Alzheimer’s is truly frightening, in terms of human suffering and monetary cost.
This outcome will not be easily averted. Few people need to be told that too much high-fat, high-sugar food is a health hazard. And yet sales of fast food remain healthy (or should that be hefty?). Part of the reason is “future discounting”, another evolved feature of the human brain that makes us value short-term rewards over long-term risks.
What can be done? One option is to call in the lawyers. Some moderately successful attempts have already been made to sue food companies for their role in creating the obesity epidemic. If a causal link between fatty, sugary food and Alzheimer’s can be established, it is highly likely that more lawsuits will follow. Such actions have their place, but this is a laborious and expensive way to enact change.
Nor do the policy levers at our disposal appear promising. Public awareness campaigns have been of limited use in reversing the tide of obesity. Will the added threat of dementia prove harder to ignore? “Sin taxes” on unhealthy foods may work - Denmark and a handful of other countries are experimenting with them - but it is not yet clear whether they make any real difference. What’s more, they raise questions about personal responsibility and nanny-statism.
We may be left with only the option of medically blocking either the craving for fast food, or its consequences. That has its own complications, and sidesteps the problem rather than addressing it. But the human brain also evolved to find ingenious solutions to intractable problems. It may yet come to its own rescue.
(via New Scientist)
People can be obese but metabolically healthy and fit, with no greater risk of developing or dying from cardiovascular disease or cancer than normal weight people, according to the largest study ever to have investigated this seeming paradox.
The findings show there is a subset of obese people who are metabolically healthy — they don’t suffer from conditions such as insulin resistance, diabetes and high cholesterol or blood pressure — and who have a higher level of fitness, as measured by how well the heart and lungs perform, than other obese people. Being obese does not seem to have a detrimental effect on their health, and doctors should bear this in mind when considering what, if any, interventions are required, say the researchers.
“It is well known that obesity is linked to a large number of chronic disease such as cardiovascular problems and cancer. However, there appears to be a sub-set of obese people who seem to be protected from obesity-related metabolic complications,” said the first author of the study, Dr Francisco Ortega (PhD). “They may have greater cardio-respiratory fitness than other obese individuals, but, until now, it was not known the extent to which these metabolically healthy but obese people are at lower risk of diseases or premature death.”
Dr Ortega is currently a research associate affiliated to the Department of Physical Activity and Sport, University of Granada (Spain), and at the Department of Biosciences and Nutrition, Karolinska Institutet (Stockholm, Sweden); but the project and investigation took place at the University of South Carolina (Columbia, USA) under the direction of Professor Steven Blair, who is responsible for the long-running “Aerobics Center Longitudinal Study” (ACLS) which provided the 43,265 participants for this current analysis.
The participants were recruited to the ACLS between 1979 and 2003. They completed a detailed questionnaire, including information on their medical and lifestyle history, and they had a physical examination that included a treadmill test to assess cardio-respiratory fitness and measurements of height, weight, waist circumference, and their percentage of body fat. Body fat percentage (BF%) was measured either by calculating the amount of water displaced when the person was completely submerged (the method that is considered the most accurate), or by taking the sum of seven skin fold measures (when folds of skin are pinched between measurement callipers). Blood pressure, cholesterol and fasting glucose levels were also measured. The study participants were followed until they died or until the end of 2003.
Dr Ortega and his colleagues found that 46% of the obese participants were metabolically healthy. After adjusting for several confounding factors, including fitness, the metabolically healthy but obese people had a 38% lower risk of death from any cause than their metabolically unhealthy obese peers, while no significant difference was seen between the metabolically healthy but obese and the metabolically healthy, normal weight participants. The risk of developing or dying from cardiovascular disease or cancer was reduced by between 30-50% for the metabolically healthy but obese people, and there were no significant differences observed between them and the metabolically healthy, normal weight participants.
“Our study suggests that metabolically healthy but obese people have a better fitness level than the rest of obese individuals. Based on the data that our group and others have collected over years, we believe that getting more exercise broadly and positively influences major body systems and organs and consequently contributes to make someone metabolically healthier, including obese people. In our study, we measure fitness, which is largely influenced by exercise,” said Dr Ortega.
“There are two major findings derived from our study. Firstly, a better cardio-respiratory fitness level should be considered from now on as a characteristic of this subset of metabolically healthy obese people. Secondly, once fitness is accounted for, our study shows for the first time that metabolically healthy but obese individuals have similar prognosis as metabolically healthy normal-weight individuals, and a better prognosis than their obese peers with an abnormal metabolic profile.”
The researchers say their findings have important clinical implications. “Our data suggest that accurate BF% and fitness assessment can contribute to properly define a subset of obese individuals who do not have an elevated risk of CVD [cardiovascular disease] or cancer,” they write.
Dr Ortega added: “Physician should take into consideration that not all obese people have the same prognosis. Physician could assess fitness, fatness and metabolic markers to do a better estimation of the risk of cardiovascular disease and cancer of obese patients. Our data support the idea that interventions might be more urgently needed in metabolically unhealthy and unfit obese people, since they are at a higher risk. This research highlights once again the important role of physical fitness as a health marker.”
A second study, which analysed data from over 64,000 patients on the Swedish Coronary Angiography and Angioplasty registry, has provided further evidence for a phenomenon known as the “obesity paradox,” whereby once someone has developed heart disease, they have a reduced risk of dying if they are overweight or obese, while underweight and normal weight patients have an increased risk.
The researchers looked at 64,436 patients who had developed acute coronary syndromes (ACS) such as unstable angina and myocardial infarction (heart attacks) and who underwent coronary angiography (a specialised x-ray test to discover detailed information about the condition of a patient’s coronary arteries) between May 2005 and December 2008.
Dr Oskar Angerås, consultant cardiologist and PhD student at the Sahlgrenska Academy, University of Gothenburg (Gothenburg, Sweden) who led the research, explained: “We found that patients who were underweight with a body mass index (BMI) of less than 18.5 kg/m2 had the greatest risk of dying. Their risk was double that of normal weight patients, who had a BMI of between 21 and 23.5 kg/m2. Compared to the group with lowest risk — those with a BMI of 26.5 to 28 kg/m2, they had three times the risk of death.”
The researchers found that the relation between BMI and mortality was U-shaped. “Those with the lowest risk of death were overweight and obese patients with BMIs ranging from 26.5 to about 35 kg/m2. The highest risk was found among underweight and morbidly obese patients, that is those with a BMI above 40 kg/m2,” said Dr Angerås.
It is well known that maintaining a healthy weight is one of the ways to avoid developing heart problems. However, the researchers say that advice to lose weight has been extended to overweight and obese patients who have already developed heart problems, despite limited scientific evidence that this helps. As a result of their findings, the authors write: “We believe that no evidence exists that proves weight reduction in itself has a positive prognostic value after ACSs. Actually some evidence suggests that weight loss after ACSs might in fact have a negative effect. We believe that given the current state of our knowledge, obesity paradox requires much more attention and deserves to be recognized in the guidelines.”
In an accompanying editorial on both papers, Stephan von Haehling, Oliver Hartmann and Stefan Anker conclude: “The available studies, together with previously published study data, permit the conclusion that weight loss in patients with chronic illness and a BMI <40 kg/m2 is always bad, and in fact not a single study exists to suggest that weight loss in chronic illness makes patients live longer. In this context, fat tissue has several beneficial effects, for example in its action as an endocrine organ, but also, nevertheless, as an aid in protecting against hip fracture. Obesity may carry benefit up to a certain degree, and it should be recognized that obesity is not necessarily associated with abnormal metabolic function.”
(via Science Daily)
What we do know from this study is a calorie is not just a calorie as far as body weight is concerned. And we doctors have to rethink our romance with high-carb, low-fat diets. Since they’ve become our diet of choice, Americans have become fatter and fatter. —Dr. Zorba Paster
Background: The health benefits of organic foods are unclear.
Purpose: To review evidence comparing the health effects of organic and conventional foods.
Data Sources: MEDLINE (January 1966 to May 2011), EMBASE, CAB Direct, Agricola, TOXNET, Cochrane Library (January 1966 to May 2009), and bibliographies of retrieved articles.
Study Selection: English-language reports of comparisons of organically and conventionally grown food or of populations consuming these foods.
Data Extraction: 2 independent investigators extracted data on methods, health outcomes, and nutrient and contaminant levels.
Data Synthesis: 17 studies in humans and 223 studies of nutrient and contaminant levels in foods met inclusion criteria. Only 3 of the human studies examined clinical outcomes, finding no significant differences between populations by food type for allergic outcomes (eczema, wheeze, atopic sensitization) or symptomatic Campylobacter infection. Two studies reported significantly lower urinary pesticide levels among children consuming organic versus conventional diets, but studies of biomarker and nutrient levels in serum, urine, breast milk, and semen in adults did not identify clinically meaningful differences. All estimates of differences in nutrient and contaminant levels in foods were highly heterogeneous except for the estimate for phosphorus; phosphorus levels were significantly higher than in conventional produce, although this difference is not clinically significant. The risk for contamination with detectable pesticide residues was lower among organic than conventional produce (risk difference, 30% [CI, −37% to −23%]), but differences in risk for exceeding maximum allowed limits were small. Escherichia coli contamination risk did not differ between organic and conventional produce. Bacterial contamination of retail chicken and pork was common but unrelated to farming method. However, the risk for isolating bacteria resistant to 3 or more antibiotics was higher in conventional than in organic chicken and pork (risk difference, 33% [CI, 21% to 45%]).
Limitation: Studies were heterogeneous and limited in number, and publication bias may be present.
Conclusion: The published literature lacks strong evidence that organic foods are significantly more nutritious than conventional foods. Consumption of organic foods may reduce exposure to pesticide residues and antibiotic-resistant bacteria.
Primary Funding Source: None.
DICOM is a format used by medical devices to exchange images. DICAM stands for Digital Imaging and COmmunications in Medicine. Last week I had some pictures taken from my left knee. The CD with the different was delivered today. Unfortunately the installer / viewer is Microsoft Windows only.
[…] xmedcon, the GUI X Window System Medical Image Conversion Utility. It’s a basic X11 applications […]
Enzymes involved in breaking down fat can now be manipulated to work three times harder by turning on a molecular switch recently observed by chemists at the University of Copenhagen. Being able to control this chemical on/off button could have massive implications for curing diseases related to obesity including diabetes, cardio vascular disease, stroke and even skin problems like acne. But the implications may be wider.
The results suggest that the switch may be a common characteristic of many more enzymes. Since enzymes are miniscule worker-molecules that control a vast variety of functions in cells, if the switches are standard, it may well be one of the most important discoveries in enzymology.
“If many enzymes turn out to be switched on in the same way as the ones we’ve studied, this opens a door to understanding- and maybe curing, a wide range of diseases”, says professor Dimitrios Stamou.
Stamou heads a multidisciplinary team of scientists at the Nanoscience Center and Department of Chemistry at the University of Copenhagen who published their discovery in the prominent scientific journal “Journal of the American Chemical Society”.
The discovery of the enzymatic ignition key contradicts previous ideas of how cells control the function of enzymes such as the fat eating lipase used in the current study.
Researchers used to think that these enzymes work continuously at varying levels of efficiency. But in fact they are quite lazy. Very much like construction workers they work at a fixed efficiency for a given amount of time (working hours), and then they rest. And that’s good news for enzyme designers.
Tripping their newfound switch resulted in tripling the working hours of lipase enzymes, from 15 percent of the time to 45 percent by the Copenhagen team
In enzymes, function is decided by the shape of the molecule. So making them more efficient would have required a major reconstruction. In some cases so difficult that it is on the order of transforming a handsaw into a chainsaw, says the chemist, Assistant Professor Nikos Hatzakis, who was deeply involved in the scrutiny of the enzymes.
“Changing the fundamental shape of a tool is always difficult. Whether it’s saw or an enzyme. But working longer hours with the same tool is infinitely easier. What we’ve achieved, is to make enzymes work longer hours,” explains Hatzakis.
Observing that enzymes even have an on-off switch may sound easy, but first the Bio Nano- team had to devise a way to study individual enzyme molecules. These are so small, that there are trillions in just a drop of water. So measuring the work of only one enzyme could be compared to looking down from the moon to detect each time a carpenter in a building in Copenhagen swings his hammer.
To perform their studies the researchers chose a fat degrading lipase enzyme model system in collaboration with Danish industrial enzyme producer Novozymes.
They used ‘fat’ that would emit light each time the enzyme took a bite. This way they could monitor each and every catalytic cycle or single movement of work. To ensure realism the enzymes were placed on an artificial cell wall. An “in vivo like membrane system,” says Stamou.
“Natural enzymes live in cells. Looking at them in a non native environment, would tell us as much as looking at a carpenter working in outer space wearing a space suit would tell us about builders,” explains Dimitrios Stamou and concludes:
“Now that we have understood how to switch enzymes on and off we could use this knowledge in the future both for curing diseases but also to design novel enzymes for industrial applications.”
In conclusion, this study investigated the importance of the timing of protein intake after each exercise bout over 12 weeks of resistance training on morphological and strength characteristics of skeletal muscle in elderly individuals. Based on the findings in the present study it appears that the timing of protein intake after strength training bouts can be important for protein synthesis and hypertrophy of skeletal muscle in elderly individuals, and that this appears not to be related to the hyperinsulinaemia in response to the intake of a protein-carbohydrate supplement. The present findings support the hypothesis that early intake of protein after resistance exercise enhances total muscle mass as well as hypertrophy of single muscle fibres in elderly humans. — Timing of postexercise protein intake is important for muscle hypertrophy with resistance training in elderly humans | The Journal of Physiology
The researchers concluded that muscle metabolism after exercise can be manipulated via dietary means. In terms of the most beneficial timing of protein intake, immediate postexercise consumption appears to be best. Furthermore, leucine may play an especially important role in stimulating muscle growth in the postactivity recovery period. —Muscle-Building Effect of Protein Beverages for Athletes Investigated | Science Daily
For generations medical orthodoxy has maintained that the appendix is useless, warranting attention only for its tendency to become painfully inflamed and requiring swift removal. But now the reputation of this cul-de-sac in the human gut has been rehabilitated by a theory from a team of immunologists .
The US scientists found that the appendix acted as a “good safe house” for bacteria essential for healthy digestion, in effect re-booting the digestive system after the host has contracted diseases such as amoebic dysentery or cholera, which kill off helpful germs and purge the gut.
This function has been made obsolete by modern, industrialised society; populations are now so dense that people pick up essential bacteria from each other, allowing gut organisms to regrow without help from the appendix, the researchers said.
But in earlier centuries, when vast tracts of land were more sparsely populated and whole regions could be wiped out by an epidemic of cholera, the appendix provided survivors with a vital individual stockpile of suitable bacteria.
“The function of the appendix seems related to the massive amount of bacteria that populates the human digestive system,” said Bill Parker, a professor of surgery and one of the scientists responsible for establishing its status as a useful organ. “The location of the appendix, just below the normal one-way flow of food and germs in the large intestine, helps support the theory.”
Other studies had shown that, in less-developed countries where the appendix may still be useful, the rate of appendicitis was lower than in the US, he said.
The theory, developed by a team from Duke University Medical School, North Carolina, and published in the Journal of Theoretical Biology, has sent ripples through the scientific community. It “seems by far the most likely” explanation for the function of the appendix and “makes evolutionary sense”, said Douglas Theobald, a professor of biochemistry at Brandeis University in Boston.
“I’ll bet we’ll eventually find the same sort of thing with the tonsils,” said Gary Huffnagle, a professor of internal medicine and microbiology at the University of Michigan.
The appendix is a worm-like tube between two and four inches long protruding from the start of the large intestine. Doctors routinely remove it should it become infected and inflamed – a burst appendix can cause peritonitis, which can kill.
In the UK, one in six people will have their appendix out at some point in their lives, although appendicitis is most common between the ages of eight and 14. NHS surgeons perform about 39,000 appendectomies a year.
And other ‘spare parts’
Men have nipples and mammary tissue which can be stimulated to produce milk. They can also get breast cancer.
Early humans had an extra row of molars to help with the vast quantity of vegetation they had to chew .
The remains of a tail lost long before man began to walk upright six million years ago.
Humans have 12 ribs but about eight per cent of people have an extra pair, as do chimps and gorillas.
(via The Independant)
Skeptical? That’s what the report in the Canadian Medical Association Journal said— smoking may be beneficial to long-distance runners. Yet the report wasn’t condoning smoking for long-distance runners or any other athlete as much as it was showing how easy it is for scientists and the media that reports on science to cherry pick data to prove pretty much anything.
Last winter the Canadian Medical Association Journal published a fascinating article by Ken Myers discussing the (as-yet unexamined) benefits of cigarette smoking on endurance running performance.
Ken is a friend and elite distance runner (we used to literally run with the same crowd while I was doing my undergrad in Calgary) so I was very excited and a bit confused when I saw his article. Could smoking really be beneficial for distance runners like myself?
Here are Ken’s arguments:
- Serum hemoglobin is related to endurance running performance. Smoking is known to enhance serum hemoglobin levels and (added bonus), alcohol may further enhance this beneficial adaptation.
- Lung volume also correlates with running performance, and training increases lung volume. Guess what else increases lung volume? Smoking.
- Running is a weight-bearing sport, and therefore lighter distance runners are typically faster runners. Smoking is associated with reduced body weight, especially in individuals with chronic obstructive pulmonary disease (these folks require so much energy just to breath that they often lose weight).
In the discussion, Ken goes on to point out that:
Cigarette smoking has been shown to increase serum hemoglobin, increase total lung capacity and stimulate weight loss, factors that all contribute to enhanced performance in endurance sports. Despite this scientific evidence, the prevalence of smoking in elite athletes is actually many times lower than in the general population. The reasons for this are unclear; however, there has been little to no effort made on the part of national governing bodies to encourage smoking among athletes.
Ken Myers isn’t accusing scientists of outright being deceitful, just that they should be careful in how they interpret data. And also to the media, who like to pull even crazier conclusions out of scientific papers without even checking to see if it makes any sense.
Mithridates VI or Mithradates VI, also known as Mithridates the Great, was the King of Pontus in Asia Minor 120 BC to 63 BC.
The ambitious Mithridates engaged Rome three times in three seperate Mithridatic Wars, fighting against the great Roman generals Sulla, Lucullus,and Pompey the Great, proving to be one of their most competent adversaries.
He is also said to have been guarding himself against poisons from an early age by taking increasing sub-lethal doses of poison until he felt he could tolerate lethal doses. This experimenting later produced a universal antidote, his Antidotum Mithridaticum, which consisted of several ingredients.
It is rumored that when Mithridates was finally defeated by Pompey in the Third Mithridatic War, he attempted suicide by poison but failed due to his accumulated immunity to the poison and was forced to make one of his servants kill him by sword.
The Antidotum Mithridaticum was used for the next 1900 years under the name theriac.
While more exercise is always recommended, engaging in 150 minutes of moderate-intensity leisure activity is better than doing nothing at all and can lower the risk of heart disease by 14 percent compared to people who are inactive, according to a new study.
It also showed that there was a significant outcome for women, who showed stronger results than men.
Increased levels of physical activity led to even lower risk of coronary heart disease (CHD), with a higher percentage for those who exceed two and a half hours per week.
“The overall findings of the study corroborate federal guidelines - even a little bit of exercise is good, but more is better - 150 minutes of exercise per week is beneficial, 300 minutes per week will give even more benefits,” said Jacob Sattelmair, ScD, of the Department of Epidemiology at the Harvard School of Public Health.
In a meta-analysis, Sattelmair and his colleagues examined more than 3,000 studies of physical activity and heart disease, and included 33 of them in their analysis. Among those, nine looked at how much exercise people were actually doing.
“Early studies broke people into groups such as active and sedentary. More recent studies have begun to assess the actual amount of physical activity people are getting and how that relates to their risk of heart disease,” said Sattelmair.
The study appears in Circulation, journal of the American Heart Association.
(via Yahoo! Lifestyle)
Like other parts of the body, brain cells begin to eat themselves as a last-ditch source of energy to ward off starvation, a study found.
The body responds by producing fatty acids, which turn up the hunger signal in the brain and increase our impulse to eat.
Researchers from the Albert Einstein College of Medicine at Yeshiva University in New York said the findings could lead to new scientifically proven weight loss treatments. Tests on mice found that stopping the brain cells from eating themselves – a process known as autophagy – prevented levels of hunger from rising in response to starvation.
The chemical change in their brains caused the mice to become lighter and slimmer after a period of fasting, the researchers reported in the journal Cell Metabolism.
(via The Telegraph)