Rhabdomyolysis is caused by severe injury to muscle cells.  The condition is serious, and can lead to kidney failure if not properly treated.  Basically, muscle cells break down and release byproducts in the bloodstream.  One particular protein, myoglobin, is especially hard on the kidneys.  Rhabdomyolysis usually occurs when your average couch-potato decides to head to the gym for the first time in months, pushes his-or herself to the brink of exhaustion, and doesn’t drink enough water.

So today’s NYT story that said twenty-four athletes from McMinnville High School in Oregon were diagnosed at their local hospital with rhabdomyolysis caught my attention.  The players began complaining about symptoms — which typically include sore/swollen muscles and dark urine –  a few days after an intense preseason workout.

Was the summer layoff to blame?  Did the players report to camp out of shape, force their way through an intense workout, and not stay properly hydrated?  Maybe.  But doctors aren’t ruling out the possibility that supplements may have been involved.  Some of the student-athletes reported they regularly consumed  a protein shake, but weren’t sure exactly what was in it.

Creatine is a popular supplement among high school and college power athletes.  The supplement works by  increasing water retention in the body, which makes the muscle fibers larger.  But if the water pressure inside the cells is high enough, it’s possible the increased stress could potentially break down the cells themselves.  In fact, there have been a few case studies showing that taking creatine supplements, especially in high doses, may trigger rhabdomyolysis.

Granted, there are a number of compounding factors at play.  And we don’t even know if creatine was in the protein shake or not.  But it certainly makes you wonder when you see a wave of rhabdomyolysis occur in otherwise healthy young athletes.

So I’ll keep my eyes peeled for the results of the lab reports, which should surface in the coming days.

photo via Flickr @rdesai

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Exercising people are happy people.

Nonsense. Ever see someone’s face at mile 20 of a marathon? Do they look happy to you?

OK, maybe people aren’t happy while exercising, but evidence shows they’re better off, in general, after the fact. Physical activity has a positive effect on mood, and is considered a valid treatment strategy to battle anxiety disorders and even depression. Although most explanations are somewhat wishy-washy, researchers believe that hedonistic value of exercise is important in mental health. Exercise simply makes us feel good about ourselves. And this is not only true in humans, but in animals, as well. Rats and mice that are given free access to a running wheel will use it, and lab rodents typically won’t do anything that doesn’t provide them some sort of pleasure.

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It’s 6am and my alarm clock is buzzing, but I don’t hear it. I don’t even move. But the incessant noise wakes my wife, and her gentle nudges (read: elbows) and soft whispers (read: expletives) eventually convince me to get out of bed. Read more…

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My inbox flooded with links to the report released by NIH (and evangelized by TIME) stating that lifestyle interventions (diet, physical activity, mental exercises, etc.) may not be that effective in preventing Alzheimer’s Disease.

Before I mount my full counterattack, I need to carefully read through the studies the meta-analysis cites.  Still, a quick glance at the exclusion criteria of the meta-analysis reveals the authors limited their review to studies using patients over the age of fifty.  So really, these results imply that lifestyle modifications may not prevent, delay, or treat Alzheimer’s Disease if you start these changes later in life.

My second point is that all lifestyle modifications are not created equal.  Scientific evidence in animal studies suggests that of all interventions, aerobic exercise is our best chance of staving off cognitive decline.  In fact, this meta-analysis also found some correlation between exercise and preserving or improving cognitive ability.

There’s a good article in The Economist that discusses the failures of the drug industry to find a solution to treating Alzheimer’s Disease.  One particular quote resonates with my feelings on the NIH report:

Another fundamental problem is that, whatever is causing the damage, treatment is starting too late. By the time someone presents behavioural symptoms, such as forgetfulness, his brain is already in a significant state of disrepair. Even a “cure” is unlikely to restore lost function.

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We’ve all heard the mantra: keep LDL levels – the “bad” cholesterol – down, and the “good” HDL cholesterol up. But thanks in part to the ubiquity of statins, such as Lipitor, which allow us to simply pop a pill to limit LDL production in the body, we’ve recently adopted tunnel vision when thinking about managing cholesterol. LDL levels are all we seem to care about now, as we strive for lower and lower numbers at each visit to the doctor’s office.

However, I think we’re missing the bigger picture by focusing solely on LDL. First, it’s made us reliant on medication to solve a problem that can many times be addressed with changes in diet and exercise regimes. Once someone starts Lipitor treatment, they’ll be taking it for life, and if LDL levels don’t quite get as low as they should, it’s all too easy to solve the problem by increasing the dose. When patients first begin Lipitor treatment, physicians typically prescribe the lowest possible amount, 10mg. However, dosing can go as high as 80mg, which begs the question: Do higher doses of the drug really improve outcomes?

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A few months ago, a story ran in Wired Magazine that described a noticeable shift in the scientific method, and attributed the change to our ability to produce and store large amounts of data.
Historically, the scientific method was built around a testable theory.  But in the 21st century, theories were becoming obsolete; the data simply spoke for itself.

Data from our bodies is no exception — physiologic data can now be accessed as a real-time data stream thanks to personal health monitors. But does the vast amount of data we get from our bodies make us any healthier? Do we need to collect data 24-hours a day in order to learn something interesting about our health? Is it even feasible to wear these sensors all day, every day?

I am embarking on a new self-tracking experiment to answer these questions (and possibly a few others). For 30 days, I will be using devices such as the Zeo personal sleep coach, the Philips DirectLife activity monitor, the Mio Motiva wristband on-demand heart rate monitor, and the Nike+ sportband. The goal of this study is not to pit one device against another; rather, I want to focus on what the data tells me, and how I can best use it to stay healthy.

I’ll get a blog post up here at least once a week, all the while working on a longer story about the journey that will be released at the end of the month.

Stay tuned. It should be a fun ride…

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from: well.blogs.nytimes.com

The afternoon of Day 1 of the Health 2.0 Conference was highlighted by the session, “The Patient is In”.  First up, a video that documented the experiences of a group of people that recently started using patient health tools, such as online health journals that track diet or exercise, support sites for quitting smoking, or home blood test kits.

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I think many of us assume that if  experts say that Vitamin C can boost the immune system, then grabbing a 500mg bottle at your local health nutrition store must be a good idea.  I know I’ve been guilty of this mindset.  But it turns out that if you exercise, taking antioxidant vitamins might not be in your best interest.  There was a good summary by Derek Lowe at ‘In The Pipeline’ about a new PNAS paper that argues against popping vitamins while engaged in an exercise routine.  The study found that the experimental group that took a combination of Vitamin C and Vitamin E actually lost some of the inherent benefits of exercise, such as changes in insulin sensitivity and formation of natural antioxidants.

My only criticism of the study is that Vitamin C is capable of regenerating Vitamin E, so I wonder whether this phenomenon will carry through for all supplemental antioxidants, or if it’s limited to the particular vitamins used in this study.

I see a recurring theme in the articles that pique my interest these days, and I can’t help but wonder, yet again, if this is another example of the differences of nutrients that exist in nature, and those made in a lab?  Should we be getting our vitamins from foods instead of supplemental pills?

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Making a choice that leads to better health is not always easy.  Otherwise, we would have many more ex-smokers and far fewer holiday pounds to shed.  We would have no need for nicotine gum and patches, or Weight Watcher’s meetings.  So if it’s that difficult, why bother?  For years, physicians have told the American public that reducing your calorie intake, eating a diet low in salt/sugar/saturated fat, and exercising 3-5 days per week will reduce your risk for heart disease and diabetes.  Now, new information has shown that the benefits of a healthy lifestyle are even more far reaching than initially thought — diet and exercise can affect our minds.

About 5-8% of people over the age of 65, and nearly 50% of people in their 80′s, show signs of dementia.  As the baby-boomer generation increases the population of the 55-64 age group in the U.S. from 29 to 40 million by 2014 , and their life expectancy continues to rise, the number of people affected by dementia is poised to increase as well.  Recent studies have shown that regular exercise may prove to be a potent mediator of dementia and Alzheimer’s Disease.  In one study, those who exercised 3 or more days per week had a 32% risk reduction in developing dementia compared to those who exercised less.  Exercise has also been linked in similar studies to moderate cognitive improvements in adults who are at risk for Alzheimer’s Disease, as well as a lower occurrence of vascular dementia.

Recent pre-clinical results have shown that diet is also tied to brain health.  A 2002 study revealed that rats fed a diet high in saturated fat and refined sugar for 2 years exhibited changes in both gene expression in the brain, as well as performance on a memory task (finding its way through a water maze).  This fast-food type diet decreased the levels of brain-derived neurotrophic factor (BDNF), which is a versatile molecule that mediates brain cell formation, function, and survival.  Both BDNF gene expression (mRNA) and BDNF protein production in the hippocampus, an area crucial for short-term memory, were significantly reduced in the animals fed the high-fat and refined sugar diet, compared to those on a low-fat, complex carbohydrate diet.  Although the experiment lasted for 2 years, and the greatest effects were seen at the end of the experiment, changes in gene expression were seen in as little as 6 months after the rats began downing cheeseburgers.  Even more striking, the rats had a significant deficit in the water maze memory task after only 3 months on the high fat/sugar diet, which shows that the “McDiet” led to a change in behavior in the mice.

Nevertheless, the research presented here had limitations.  The studies that looked at the effects of exercise on dementia were conducted in relatively small, non-diverse human populations and were not completely controlled against other “good health” factors that tend to occur when people exercise.  For example, exercisers are much more likely to do other healthy things, such as eating right, quitting smoking, getting quality sleep, or maintaining target weight.  The fast-food diet study was well controlled to show that decreased BDNF was not related to hypertension, atherosclerosis, obesity, and changes in activity level — but the results must be taken at face value since it was conducted in rodents, not humans.

So what does all of this mean?  The idea of eating right and getting more exercise is nothing new.  We’ve known for years that changing our health behaviors can stave off heart disease, and potentially let us live longer.  The studies mentioned here really highlight the positive-feedback nature of our actions — behavior changes (diet and exercise) cause physiological and molecular changes in the body, which in turn alter another behavior (memory).  This relationship tells us that our behavior choices no longer only determine life or death, but they also can impact our quality of life.  It’s true that the results don’t make a direct link between diet/exercise and brain health, but rather, a loose correlation between the two that requires further study.  But in my mind, it doesn’t really matter what keeps the brain healthy — my point isn’t that diet and exercise are the end-all cure for disease, but rather, that they are an extremely important part of an overall healthy lifestyle that will allow us to make the most of our golden years.

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