Sunday, November 30, 2008

Monday's WOD

AMRAP (as many rounds as possible) in 20 minutes of:
  • 5 sit-ups
  • 10 push-up
  • 15 squats

Over the course of the next couple weeks, we will concentrate on establishing the basic movements inherent to CrossFit and incorporating them into the WODs with growing complexity. Consistency before intensity will ensure future success and is the key to injury prevention.

Wednesday, November 26, 2008

Happy Thanksgiving!

If you are wondering how to survive all the temptation this Thanksgiving, check out this post from Mark's Daily Apple:

Great job on Helen today; the pics will be up shortly.

Tuesday, November 25, 2008

Great Job!

A big thanks to Millie (hope I spelled that right) and Kim; hope you had fun. Looks like we'll be hitting "Helen" on Wednesday. Take a look at the video for a demonstration of the WOD.

Sunday, November 23, 2008

Your Four Energy Systems and How to Train Them

Good info from

It reflects CrossFit's methodology of affecting all three metabolic pathways via one workout.

Your Four Energy Systems and How to Train Them

By John P. Hussman, Ph.D.

A good fitness program will train each of your energy systems. There are four of them. Don't give up on me here. This section is short, but important.

If you really want to understand how exercise produces changes in your body, it helps to know a little bit of biology. It will help you to understand exactly what you are trying to achieve in your workouts.

Whatever you eat and however you exercise, your body ultimately gets its energy from a little molecule called ATP (adenosine tri phosphate). It gets that name because it has three "phosphate groups" in it. Picture a little 3-leaf clover. When you pop one of those phosphate groups off, ATP gives off energy like a little Chinese firecracker, and is converted to ADP (adenosine di phosphate). The body then turns the ADP back into ATP, using fat or sugar (little chains of glucose called "glycogen") for the energy needed to put that third phosphate group back on.

Again, there are four ways that the body gets the energy to put that phosphate group back on, and they vary by speed, and by whether they burn oxygen or not. Remember - your objective is to train each system.

1) Explosive Force - The ATP-CP System

By far the fastest way to get that third phosphate group is to grab it off of a molecule called "creatine phosphate" or CP. When you are doing very explosive exercise for 10-30 seconds, such as an all-out sprint, the burst of energy is delivered by the ATP-CP system. Fast, doesn't require oxygen, but extremely limited to short periods of explosive force.

ADP + Creatine phosphate (CP) ==> ATP + Creatine

You train this system by including short wind sprints and relatively “low volume, high weight” resistance sets (4-7 repetitions of lifting and lowering a weight) into your program. You can support it nutritionally with by taking a creatine supplement with a small amount of apple juice or other sugar to assist transport into the cells.

2) Sugar Burning - Step 1 (Anaerobic Glycolysis)

The next fastest method of getting energy is to turn a sugar molecule into lactic acid. This doesn't require oxygen either. This system is effective for vigorous exercise of between 1-3 minutes in duration. When the intensity of the exercise requires more energy than what can be burned with the oxygen you are breathing, your body starts "partially" burning glucose “anaerobically” (without oxygen). This is the system you want to be using during "wind sprints". This is a system that has to be trained in order to get fast results, but again, this system can be used only for a limited period. As lactic acid builds up in your muscles, you start to feel them "burn". If you go beyond a few minutes of this, the acidity of the muscle tissue increases and the muscles start to have difficulty generating meaningful amounts of energy.

ADP + glucose ==> ATP + pyruvic acid (which converts to lactate if not burned with oxygen)

You train this system by including somewhat longer (1-3 minute) wind sprints and mid-range resistance training (8-12 repetitions) into your program. Since that work is also the basis of much of your muscle gain, you support it nutritionally with post-exercise protein, especially sources including the amino acid leucine, such as whey protein, and supplements including glutamine, vitamin C, and plenty of water.

3) Sugar Burning - Step 2 (Aerobic Glycolysis)

This is the next system, and for all practical purposes is the one you use most often when exercising. Once glucose has been converted to lactate anaerobically (without oxygen), the body then burns the lactate using oxygen to create even more ATP.

ADP + lactate + oxygen ==> ATP + water + carbon dioxide

You train this system by including sustained aerobic activity (20-40 minutes depending on intensity) into your program. You support it nutritionally by taking in some form of carbohydrate within 45-60 minutes after your workout. If you're targeting muscle gain more than fat loss, that post-workout meal is the only one that should generally include “high glycemic” carbs like bread, bagels, sugars, etc., since those carbohydrates will be used preferentially by the muscles at that time to rebuild glycogen.

4) Fat Burning (Aerobic Lipolysis)

This is by far the slowest system. It is, in fact, too slow to contribute extensively to energy production during exercise (if you ever deplete your glycogen stores so much that the body has to rely on fat burning for its energy, your muscle movement slows down dramatically). In order to mobilize fat, a "triglyceride" has to be broken down into fatty acids, bound to proteins, and other time-consuming feats. The good news is that fat metabolism is the main way that your glycogen stores are replenished after exercise.

Fat + oxygen + ADP ==> ATP + water + carbon dioxide

Though some trainers suggest long, slow aerobic workouts to burn fat, that's a very inefficient approach and can also compromise muscle gains. You train the lypolytic system best by working glycogen-depleting exercises like resistance training and wind sprints into your program (which give you an “afterburn” as you rebuild ATP through fat burning), working out in the morning on an empty stomach (in any case, definitely avoid sugary or high-glycemic carbs before workouts – insulin blocks fat burning), waiting about 30-60 minutes after the workout before having much carbohydrate, and by maintaining a nutrition plan of small meals that aren't large enough or glycemic enough to spike your blood sugar. You can also have a cup of caffeinated coffee (no cream or sugar) before workouts if it doesn't irritate your stomach – the caffeine triggers release of fatty acids into the bloodstream and will improve your endurance.

Thursday, November 20, 2008

Gary Taubes responds to question regarding GCBC

Below is from the blog of Michael Eades, M.D.

It is a list of common questions posed to Gary Taubes, author of Good Calories, Bad Calories.

17. November 2008, 12:35
A couple of weeks ago I posted that Gary Taubes had agree to answer questions from readers of this blog. Over a hundred readers sent in questions through the comment section. Many of these questions were actually multiple questions, so Gary ended up with probably 200+ questions to deal with.

I’ve gone through and compiled a list of the most common questions and presented them to Gary. Here are the questions followed by his responses.

The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?

The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.

What is your opinion on leptin in the grand scheme of obesity and fat storage?

I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.

Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.

In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:

“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.

“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “

A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet? And why it seems more difficult to lose on low-carb with increasing age?

I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.

Several people asked for a comment on any important studies that you may have left out of GCBC.

The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.

When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.

It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.

What you think of a Slow Burn type of exercise and low-carb dieting? Do you still stand by your notion that exercise doesn’t help people lose weight?

I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.

As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.

Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?

I am not.

What kind of response have you gotten from the medical/scientific community about GCBC?

In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.

Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.

When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.

So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.

What’s next? Another book?

What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.

How about a blog?

As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.

Many wrote that GCBC had changed their lives. Can you think of a book that has changed your life?

Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.

What do you know about Dr. Simeon’s HCG protocol?

Mostly nothing.

What led you to the idea that saturated fat doesn’t cause heart disease?

It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.

The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.

Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?

It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.

I tried to come up with a selection of questions that represented the majority of questions asked. I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time. So, I’m sorry if any specific question went unanswered, and I hope you understand. Thanks to everyone for the terrific response.

Wednesday, November 19, 2008

Weight Lifting Shoes

When doing Olympic lifts, you have to generate your force through your heels and they have to be in solid contact with the ground. CrossFit Santa Cruz Central had a link to this video, which illustrates the value of using weight lifting shoes. There are many different brands of weightlifting shoes out there and I don't endorse one over the other but I do own a pair and have found them beneficial.

Other good options when doing lifts is to be barefoot or in socks or Vibram Five Fingers. All ensure you have good contact with the ground and can generate explosive force and all are better options than running shoes.

Tuesday, November 18, 2008

Fish Oil

Great post from on fish oil.

Omega3 fish oil plays a vital role in our diet, not only for building the structure of nerves, supporting brain messengers and building the brain itself, but also for fat loss and muscle maintenance.

Omega3 fish oil consists of long-chain fatty acids EPA (Eicosapentanoic acid) and DHA (docosohexanoic acid).

I believe we should all be supplementing with Omega3’s, for one reason; it’s deficient in our foods. Back in the day, nearly every animal would feed on grass and plant based foods, keeping their Omega3’s nice and high. Now days though, the majority of animal products we purchase have been grain fed (cheaper for farmers) and this un-fortunately has a negative effect on the animals fatty acid profile, the Omega6 increases, and the Omega3’s decrease. So what once was a ratio of 2:1 - 3:1 Omega6 to Omega3, it is now a ratio of 20:1 – 30:1.

So if you are able to purchase grass fed beef, chicken (including eggs), lamb and fish, you’re onto a good thing, but keep in mind one more thing! Because if you place that meat on heat, most of the Omega3’s will die, so you’ll want to eat it raw to savour all those Omega3’s! Do we do that? No.. that’s why we ALL need to supplement.

Although there are thousands of articles, research papers and information out there about how good Omega3’s are, I still don’t believe enough people have decided to jump on the Omega3 supplementation bandwagon to dramatically start improving their health and body composition goals.

I feel somewhat inclined to just copy and paste parts of articles and research papers which discuss the benefits of taking Omega3 fish oil, but I thought to make this article less than 1000 pages, I would put some benefits in dot points!

enhances heart health by maintaining elasticity of cardio tissue
helps the heart beat in a strong and healthy way
ensures efficient heart function so that this key organ will last longer
increases lean body mass
increases metabolism by up to 400Kcal/day
reduced inflammation within muscle and connective tissue
improves fat burning
important for cell membrane structure and essential for proper brain function
improves insulin efficiency
prevents excessive muscle breakdown
increases brain health
improves nervous system function
contains antioxidants and their benefits

I would like to explain how increasing the Omega3 fish oils in our diets assists with muscle growth and maintenance.

Remembering the structure of fish-oil I mentioned above, research has shown that EPA is a powerful anti-catabolic and therefore prevents excessive muscle protein breakdown. This is pretty impressive because EPA, so far, is the only nutrient that has shown in research to block the molecular pathway that results in excessive muscle breakdown, even when on a calorie restricted diet.

Ok, so now that you all want to start taking Omega3’s, just hold on for a moment longer before you go out and make a random purchase on a product which has Omega3’s in it.

Omega3 fish oil initially is what you should buy and consume. There are products out there which have Omega3, Omega6 and Omega9 combined, these products are pretty useless to the majority of people out there who eat a balanced diet and who will consume enough Omega6 and Omega9 fatty acids anyway.

Omega6 is a fatty acid your body cannot create, however is found in food sources often consumed such as; nuts, eggs, meat and dairy, and Omega9’s are high in foods such as; nuts, olive oil and meat. So the only fat you need in these certain products are Omega3’s, the rest you already have an abundance of and too much of any fat can be harmful to the body.

Moving onto Cod liver Oil (CLO), which contains EPA and DHA but in typically smaller amounts than that of pure fish oil, it also contains naturally-occurring vitamin A & D which is an added bonus and helpful to those who don’t see much sun, such as those of you who work in the office and don’t get outdoors much. So if you decide to take CLO, I would recommend including pure Omega3 fish oil to your diet as well, just because the Omega3 ratio in CLO is significantly lower to that of pure fish oil.

Flaxseeds… A lot of people will turn to flaxseeds/flaxseed oil to obtain their Omega3’s, although flaxseeds contain a fairly high amount of Omega3’s, you need to be aware that the Omega3’s found in flaxseeds, and the Omega3 found in fish oil are different (not bad, just different). For Omega3’s to be used efficiently in the body we need the fats EPA and DHA, flaxseeds don’t contain EPA and DHA but contain the fatty acid ALA which our bodies will attempt to convert to EPA and DHA. This is a very hard process and is usually very inefficient as well, therefore our bodies will only end up getting a small percentage of EPA and DHA from the original flaxseed oil, generally less than 3% EPA and/or 1.5% DHA, so in other words, to obtain the same amount of omega3’s in 1tbs of fish oil, you would need to consume so much flaxseed oil it would make you physically sick.

So this leads me to fish oil, I would recommend consuming no less than 15-20g of Omega3 fish oil everyday, or 1tsp (5 x 1g capsules) per 20kg of lean body weight. The options available to consume Omega3 fish oil include capsules and liquid form. Good quality brands of Fish Oil include Carlson’s ( and Nordic Naturals (

Friday, November 14, 2008

Metcon circuits....some research

Acute physiological responses to different circuit training protocols.

Courtesy of Conditioning Research:

Here is a new bit of research that looks at this type of training. It compared circuit weight training with combined circuit training (weight training and treadmill run). The Combined Circuit Training wins......

University City of Sao Paulo, Sao Paulo, Brazil

AIM: The purpose of present study was to compare the acute physiological responses to a circuit weight training with the responses to a combined circuit training (weight training and treadmill run). METHODS: The sample consisted of 25 individuals at an average state of training, 10 men and 15 female, between 18 and 35 year old. There were selected 60 second sets of resistance exercises to the circuit weight training (CWT). Whereas in the combined circuit training (CCT), the subjects spent 30 seconds on the same resistance exercises and 30 seconds running on the treadmill. The rest intervals between the sets lasted 15 seconds. The analysis of variance (ANOVA) with 5% significance level was utilized to the statistical analysis of the results. RESULTS: Comparing circuit training protocols, it was noted that CCT elicits a higher relative and absolute VO(2) and energy expenditure values than CWT for both genders (P<0.05). Regarding inter-gender comparison, males showed higher absolute and relative VO(2) and absolute energy expenditure values for both CWT and CCT than females (P<0.05). Females showed a significant greater %VO(2max) value for both CWT and CCT. Due to the experimental conditions used to state both circuit training bouts (CWT and CCT), the VO(2) rate found was higher than the values reported by previous studies which used heavier weight lift.

CONCLUSION: CCT seems adequate to produce cardiovascular improvements and greater energy expenditure for both men and women, while CWT group classes are sufficient only for unfit women.

Thursday, November 13, 2008


A New York Times article on dynamic stretching; looks like they finally caught up with CrossFit's stretching methodology:

Stretching: The Truth

WHEN DUANE KNUDSON, a professor of kinesiology at California State University, Chico , looks around campus at athletes warming up before practice, he sees one dangerous mistake after another. “They’re stretching, touching their toes. . . . ” He sighs. “It’s discouraging.”

If you’re like most of us, you were taught the importance of warm-up exercises back in grade school, and you’ve likely continued with pretty much the same routine ever since. Science, however, has moved on. Researchers now believe that some of the more entrenched elements of many athletes’ warm-up regimens are not only a waste of time but actually bad for you. The old presumption that holding a stretch for 20 to 30 seconds — known as static stretching — primes muscles for a workout is dead wrong. It actually weakens them. In a recent study conducted at the University of Nevada, Las Vegas , athletes generated less force from their leg muscles after static stretching than they did after not stretching at all. Other studies have found that this stretching decreases muscle strength by as much as 30 percent. Also, stretching one leg’s muscles can reduce strength in the other leg as well, probably because the central nervous system rebels against the movements.

“There is a neuromuscular inhibitory response to static stretching,” says Malachy McHugh, the director of research at the Nicholas Institute of Sports Medicine and Athletic Trauma at Lenox Hill Hospital in New York City . The straining muscle becomes less responsive and stays weakened for up to 30 minutes after stretching, which is not how an athlete wants to begin a workout.

THE RIGHT WARM-UP should do two things: loosen muscles and tendons to increase the range of motion of various joints, and literally warm up the body. When you’re at rest, there’s less blood flow to muscles and tendons, and they stiffen. “You need to make tissues and tendons compliant before beginning exercise,” Knudson says.

A well-designed warm-up starts by increasing body heat and blood flow. Warm muscles and dilated blood vessels pull oxygen from the bloodstream more efficiently and use stored muscle fuel more effectively. They also withstand loads better. One significant if gruesome study found that the leg-muscle tissue of laboratory rabbits could be stretched farther before ripping if it had been electronically stimulated — that is, warmed up.

To raise the body’s temperature, a warm-up must begin with aerobic activity, usually light jogging. Most coaches and athletes have known this for years. That’s why tennis players run around the court four or five times before a match and marathoners stride in front of the starting line. But many athletes do this portion of their warm-up too intensely or too early. A 2002 study of collegiate volleyball players found that those who’d warmed up and then sat on the bench for 30 minutes had lower backs that were stiffer than they had been before the warm-up. And a number of recent studies have demonstrated that an overly vigorous aerobic warm-up simply makes you tired. Most experts advise starting your warm-up jog at about 40 percent of your maximum heart rate (a very easy pace) and progressing to about 60 percent. The aerobic warm-up should take only 5 to 10 minutes, with a 5-minute recovery. (Sprinters require longer warm-ups, because the loads exerted on their muscles are so extreme.) Then it’s time for the most important and unorthodox part of a proper warm-up regimen, the Spider-Man and its counterparts.

“TOWARDS THE end of my playing career, in about 2000, I started seeing some of the other guys out on the court doing these strange things before a match and thinking, What in the world is that?” says Mark Merklein, 36, once a highly ranked tennis player and now a national coach for the United States Tennis Association. The players were lunging, kicking and occasionally skittering, spider-like, along the sidelines. They were early adopters of a new approach to stretching.

While static stretching is still almost universally practiced among amateur athletes — watch your child’s soccer team next weekend — it doesn’t improve the muscles’ ability to perform with more power, physiologists now agree. “You may feel as if you’re able to stretch farther after holding a stretch for 30 seconds,” McHugh says, “so you think you’ve increased that muscle’s readiness.” But typically you’ve increased only your mental tolerance for the discomfort of the stretch. The muscle is actually weaker.

Stretching muscles while moving, on the other hand, a technique known as dynamic stretching or dynamic warm-ups, increases power, flexibility and range of motion. Muscles in motion don’t experience that insidious inhibitory response. They instead get what McHugh calls “an excitatory message” to perform.

Dynamic stretching is at its most effective when it’s relatively sports specific. “You need range-of-motion exercises that activate all of the joints and connective tissue that will be needed for the task ahead,” says Terrence Mahon, a coach with Team Running USA, home to the Olympic marathoners Ryan Hall and Deena Kastor. For runners, an ideal warm-up might include squats, lunges and “form drills” like kicking your buttocks with your heels. Athletes who need to move rapidly in different directions, like soccer, tennis or basketball players, should do dynamic stretches that involve many parts of the body. “Spider-Man” is a particularly good drill: drop onto all fours and crawl the width of the court, as if you were climbing a wall. (For other dynamic stretches, see the sidebar below.)

Even golfers, notoriously nonchalant about warming up (a recent survey of 304 recreational golfers found that two-thirds seldom or never bother), would benefit from exerting themselves a bit before teeing off. In one 2004 study, golfers who did dynamic warm- up exercises and practice swings increased their clubhead speed and were projected to have dropped their handicaps by seven strokes over seven weeks.

Controversy remains about the extent to which dynamic warm-ups prevent injury. But studies have been increasingly clear that static stretching alone before exercise does little or nothing to help. The largest study has been done on military recruits; results showed that an almost equal number of subjects developed lower-limb injuries (shin splints, stress fractures, etc.), regardless of whether they had performed static stretches before training sessions. A major study published earlier this year by the Centers for Disease Control, on the other hand, found that knee injuries were cut nearly in half among female collegiate soccer players who followed a warm-up program that included both dynamic warm-up exercises and static stretching. (For a sample routine, visit And in golf, new research by Andrea Fradkin, an assistant professor of exercise science at Bloomsburg University of Pennsylvania, suggests that those who warm up are nine times less likely to be injured.

“It was eye-opening,” says Fradkin, formerly a feckless golfer herself. “I used to not really warm up. I do now.”

You’re Getting Warmer: The Best Dynamic Stretches

These exercises- as taught by the United States Tennis Association’s player-development program – are good for many athletes, even golfers. Do them immediately after your aerobic warm-up and as soon as possible before your workout.

(for the hamstrings and gluteus muscles)
Kick one leg straight out in front of you, with your toes flexed toward the sky. Reach your opposite arm to the upturned toes. Drop the leg and repeat with the opposite limbs. Continue the sequence for at least six or seven repetitions.

(for the lower back, hip flexors and gluteus muscles)
Lie on your stomach, with your arms outstretched and your feet flexed so that only your toes are touching the ground. Kick your right foot toward your left arm, then kick your leftfoot toward your right arm. Since this is an advanced exercise, begin slowly, and repeat up to 12 times.

(for the shoulders, core muscles, and hamstrings)
Stand straight, with your legs together. Bend over until both hands are flat on the ground. “Walk” with your hands forward until your back is almost extended. Keeping your legs straight, inch your feet toward your hands, then walk your hands forward again. Repeat five or six times. G.R.

Wednesday, November 12, 2008

Beware the statin study....

If you haven't heard yet, the news media has been discussing a statin study and their pitch has been more people need to be taking statins even if they have normal cholesterol levels. Here is a link to MSNBC's article on the study:

Below is a post from Michael Eades, M.D. that helps shed some more light on the study and its findings.

Let’s first take a look at the reporting.

The lede from MSNBC:
People with low cholesterol and no big risk for heart disease dramatically lowered their chances of dying or having a heart attack if they took the cholesterol pill Crestor, a large study found.

The headline from Fox News:
Study: Cholesterol Drug Causes Risk of Heart Attack to Plummet

The New York Times headline and lede (on the front page, no less):
Cholesterol-Fighting Drugs Show Wider Benefit

A large new study suggests that millions more people could benefit from taking the cholesterol-lowering drugs known as statins, even if they have low cholesterol, because the drugs can significantly lower their risk of heart attacks, strokes and death.

The Wall Street Journal, usually a more measured source, effuses:
Cholesterol Drug Cuts Heart Risk in Healthy Patients
AstraZeneca PLC’s cholesterol drug Crestor sharply lowered risk of heart attacks among apparently healthy patients in a major study that challenges longstanding heart-disease prevention strategies. The findings could substantially broaden the market for statins, the world’s best-selling class of medicines.

I could go on, but you get the picture. I’m sure you’ve read all this in your own papers. But it’s not just the papers and media that are harping on this study - it s even the statinators themselves.

Here is the commentary from Steven Nissen, M.D., a Master Statinator if there ever was one:
The extent of reduction in death, heart attacks, and stroke is larger than we’ve seen in any trial I can remember. I don’t know how you get much bigger than that.

Says Dr. W. Douglas Weaver, president of the American College of Cardiology:
[The findings] really change what we are going to do in the future. This targets a patient group that normally would not be screened or treated to prevent cardiovascular disease.
And in a statement that I’m sure will prove true, Dr. Weaver follows up with:
This will become an important part of the armamentarium of the primary care doctor. I see this as being part of that panel of preventions that they will be applying in men over 50 and women over 60.

Dr. TIm Garder, president of the American Heart Association, opines without any evidence whatsoever that
This is likely to be a class effect, not a specific drug effect. This is a win for all statins, I would say.

The above is a sampling of the reporting and the blathering so far about the Jupiter study. The general impression that most people (and, sadly, most physicians) will take away is that statins will prevent heart disease even in those people who don’t have risk factors for heart disease. Any one of any sex at any age should queue up for a dose of statins to prevent heart disease.

That’s the reporting. Now for the data. What does the study actually show?

If you believe the data from this study (we’ll get to that later), it indicates that men over 50 and women over 60 with normal LDL-cholesterol levels AND elevated C-reactive protein levels who took the very expensive ($3.50 per day) statin drug rosuvastatin (Crestor) minimally reduced their risk of developing heart disease or dying of any cause as compared to those who took placebo.

That’s it, folks. And that’s only if you believe the data.

The study says nothing about men under 50 or women under 60. The study says nothing about other types of statin drugs reducing risk. And the study applies ONLY to those men over 50 and women over 60 who have fairly markedly elevated C-reactive protein levels. The study says nothing about anyone of an sex or any age who doesn’t have a markedly elevated C-reactive protein level.

So, what’s the big deal? Well, the big deal is that there is finally a study that shows some benefit to statin drugs in terms of decreasing all-cause mortality. And, as I’ve posted before, those studies are few and far between.

There is so much excitement on the part of the statinators of renown because their coffers will soon be filled to overflowing with fees from AstroZeneca (and other statin manufacturers that want to piggyback onto this study) for speaking gigs promoting Crestor. (Here is a post on the payola to doctors promoting anti-depressant drugs. Drug company income from anti-depressant drugs is a drop in the bucket compared to the income from statins, so you can only imagine how lucrative it is to be a speaking statinator.) There is considerable excitement at AstroZeneca and the other statin makers because the physicians who are non-critical thinkers and non-study readers (sadly, the vast majority) will commence giving statins to just about everyone who walks through their office doors.

It appears to be another modern medical triumph - everyone profits but the patients. Looks like Erasmus was way ahead of his time when he wrote about Jupiter way back in the 14th century.

Jupiter, not wanting man’s life to be wholly gloomy and grim, has bestowed far more passion than reason /you could reckon the ration as twenty-four to one.
Passion to reason in the ratio of 24 to 1. That equation certainly applies to the media covering this study and the statinators feeding them their info.

Let’s take a look at what the study really shows. But before we do, let’s psychoanalyze the people putting the study together. What do you think they wanted out of this study.
Typically a study starts with an hypothesis, say, zinc cures the common cold. The study then involves giving people suffering from colds zinc or a placebo to see what happens. The researchers then say that the data confirms the hypothesis or refutes it. It’s not good to go into a study with a predetermined idea of what you want. You just need an hypothesis. Your hypothesis could be that zinc has no effect on the common cold. You wouldn’t go into a study with the idea that we’re by God going to prove zinc cures the common cold. It just doesn’t work that way.

But what about the Jupiter study? Know what Jupiter stands for? It stands for Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin. Which translates to by God we’re going to prove that statins prevent something. We certainly know the mindsets of the people running this study.

After a couple of critical reads of this paper (full text here), I can’t see a real problem with the data. But there are a few sort of fishy things going on with this study and three really fishy things. Before you read on, give a quick read through to a post I wrote a while back about relative risk so that you will be familiar with the kinds of statistics we’ll be talking about.

Although the relative risk numbers in this study appear to be correct, you’ve got to realize that these are small numbers we’re talking about. Out of almost 18,000 subjects there is a difference of not quite 50 deaths between the two groups during the years over which the study took place. Which means, of course, that neither subjects in the placebo group nor subjects in the Crestor group were at great risk of dying. There is a difference, but in these small numbers (as explained in the post linked above) it is almost meaningless.

You can really see the difference when you look at this graph taken from the study.

Notice the bottom two curves. Those are the all-cause deaths from the placebo and Crestor groups. As you can see, the two curves are pretty much superimposed upon one another. That’s what it looks like when very small numbers are involved. The authors had to use a different scale to make it look like there was a major difference as they did in the two divergent curves at the top of this chart.

Let’s look at the sort of fishy aspects of this study. First, the patient population is most unusual. How many subjects are there out there who have both normal LDL-cholesterol levels (defined as 130 mg/dl or below) AND elevated C-reactive protein levels. Not very many. Especially if you eliminate anyone with any history of inflammatory disorders, which the researchers did. Most people who have an inflammation arising from the metabolic syndrome, obesity or other common inflammatory disorders will have both elevated lipids AND elevated C-reactive protein levels. They are typically found together. The authors of this study had to use 1315 sites in 26 different countries to get the 17,802 subjects involved. Simple division tells us that there were an average of about 13 subjects per center. Not many. To paraphrase F. Scott Fitzgerald who said “the rich are different from you and me.” Well, these subjects are different from you and me. And what may work for them may not necessarily work for you and me.

Second, when you look at Table 1 showing the baseline characteristics of the participants, you can see that in virtually all respects the two groups of subjects look identical, which is as it should be in a randomized study. But closer evaluation indicates that there not identical in a couple of parameters. In the category Family history of premature CHD (coronary heart disease) we see that there are 51 more subjects with a family history of premature CHD in the placebo group than in the Crestor group. Since a family history of premature CHD is probably the strongest risk factor for developing premature CHD, do you think a few more of the subjects in the placebo group may have developed it? And maybe died as a result?

Third, looking at this same table and checking the very next category, Metabolic syndrome, we find that 71 more patients in the placebo group with metabolic syndrome than we do in the Crestor group. Since the metabolic syndrome is another strong risk factor for development of CHD, do you think some of that difference in deaths could have come from this disparity in the groups? As I say, not conclusive, but fishy.

The three real fishy things are more problematic. First, according to the paper
At the time the study was terminated, 75% of the participants were taking their study pills.
Which means, of course, that 25% weren’t taking their study pills. And we don’t really know how many of the deaths in the study group came from the 75% taking their meds or the 25% who weren’t because the data was evaluated using an intention-to-treat analysis.

The second fishy deal on this study is that both the placebo group and the Crestor group reported the same number of side effects. Say what? Crestor is a potent statin, known for causing side effects, and the group taking this drug reported no more side effects than those taking the placebo. That’s real fishy. When you look at the most common side effect of statin drugs - muscle pains - only 19 people out of 18,000 reported this symptom: 10 in the Crestor group and 9 in the placebo group. Something totally fishy is going on here.

Finally, the fishiest thing of all. They stopped the study right in the middle of it. When studies are done that might put people at risk by giving them potentially dangerous drugs, it is typical for an outside group to take a peek at the data at certain milestones to make sure the study medication isn’t killing people. When this data is evaluated, and it is found that subjects on the experimental medicine are dying at unacceptably high rates, the study is often halted. I’ve never seen a study halted because the placebo group was dying at higher rates. That really makes me wonder.

One of the negative findings in this study was that the group on Crestor developed diabetes during the trial at a significantly higher rate than did those on placebo. I suspect that the outside group checked the progress of the study, found that the subjects on Crestor were at the time of the evaluation showing better results than those on placebo, so the decision was made to stop the study while it was looking good. Had it gone on for the full term, the deaths could have evened out, way more people could have developed diabetes, or who knows what might have occurred had the study continued. So, the powers that be decided to quit while ahead.

But, let’s assume I’m taking this study at its absolute worst. Let’s look at it in the best light possible. If we do, we find that a small group of unusual patients - those with low LDL-cholesterol AND high C-reactive protein - may slightly decrease their risk for all-cause mortality by taking a drug that costs them almost $1,300 per year and slightly increases their risk for developing diabetes. That’s the best spin possible given the data from this study. Compare that to the spin the media is giving it.

Tuesday, November 11, 2008

The History of Veterans Day

World War I – known at the time as “The Great War” - officially ended when the Treaty of Versailles was signed on June 28, 1919, in the Palace of Versailles outside the town of Versailles, France. However, fighting ceased seven months earlier when an armistice, or temporary cessation of hostilities, between the Allied nations and Germany went into effect on the eleventh hour of the eleventh day of the eleventh month. For that reason, November 11, 1918, is generally regarded as the end of “the war to end all wars.”

In November 1919, President Wilson proclaimed November 11 as the first commemoration of Armistice Day with the following words: "To us in America, the reflections of Armistice Day will be filled with solemn pride in the heroism of those
who died in the country’s service and with gratitude for the victory, both because of the thing from which it has freed us and because of the opportunity it has given America to show her sympathy with peace and justice in the councils of the nations…"

The original concept for the celebration was for a day observed with parades and public meetings and a brief suspension of business beginning at 11 a.m.

The United States Congress officially recognized the end of World War I when it passed a concurrent resolution on June 4, 1926.An Act (52 Stat. 351; 5 U. S. Code, Sec. 87a) approved May 13, 1938, made the 11th of November in each year a legal holiday - - a day to be dedicated to the cause of world peace and to be thereafter celebrated and known as "Armistice Day."
Armistice Day was primarily a day set aside to honor veterans of World War I, but in 1954, after World War II had required the greatest mobilization of soldiers, sailors, Marines and airmen in the Nation’s history; after American forces had fought aggression in Korea, the 83rd Congress, at the urging of the veterans service organizations, amended the Act of 1938 by striking out the word "Armistice" and inserting in its place the word "Veterans." With the approval of this legislation (Public Law 380) on June 1, 1954, November 11th became a day to honor American veterans of all wars.

Later that same year, on October 8th, President Dwight D. Eisenhower issued the first "Veterans Day Proclamation" which stated: "In order to insure proper and widespread observance of this anniversary, all veterans, all veterans' organizations, and the entire citizenry will wish to join hands in the common purpose. Toward this end, I am designating the Administrator of Veterans' Affairs as Chairman of a Veterans Day National Committee, which shall include such other persons as the Chairman may select, and which will coordinate at the national level necessary planning for the observance. I am also requesting the heads of all departments and agencies of the Executive branch of the Government to assist the National Committee in every way possible." (Click here for the full text of the proclamation.)

On that same day, the President sent a letter to the Honorable Harvey V. Higley, Administrator of Veterans' Affairs (VA), designating him as Chairman of the Veterans Day National Committee. (Click here for the text of President Eisenhower’s letter.)

In 1958, the White House advised VA's General Counsel that the 1954 designation of the VA Administrator as Chairman of the Veterans Day National Committee applied to all subsequent VA Administrators. Since March 1989 when VA was elevated to a cabinet level department, the Secretary of Veterans Affairs has served as the committee's chairman.

The Uniforms Holiday Bill (Public Law 90-363 (82 Stat. 250)) was signed on June 28, 1968, and was intended to insure three-day weekends for Federal employees by celebrating four national holidays on Mondays: Washington's Birthday, Memorial Day, Veterans Day, and Columbus Day. It was thought that these extended weekends would encourage travel, recreational and cultural activities and stimulate greater industrial and commercial production. Many states did not agree with this decision and continued to celebrate the holidays on their original dates.

The first Veterans Day under the new law was observed with much confusion on October 25, 1971. It was quite apparent that the commemoration of this day was a matter of historic and patriotic significance to a great number of our citizens, and so on September 20th, 1975, President Gerald R. Ford signed Public Law 94-97 (89 Stat. 479), which returned the annual observance of Veterans Day to its original date of November 11, beginning in 1978. This action supported the desires of the overwhelming majority of state legislatures, all major veterans service organizations and the American people.

Veterans Day continues to be observed on November 11, regardless of what day of the week on which it falls. The restoration of the observance of Veterans Day to November 11 not only preserves the historical significance of the date, but helps focus attention on the important purpose of Veterans Day: A celebration to honor America's veterans for their patriotism, love of country, and willingness to serve and sacrifice for the common good.