Wednesday, June 27, 2012

USA Today on JAMA "Metabolic Advantage" Intervention Study

A study was published in JAMA that addressed the effectiveness of a variety of diets for weight loss maintenance.  The question was:  we know that folks can demonstrate a reduction in metabolic rate after weight loss that makes it more likely for them to regain weight; which diet minimizes this effect?  The study wasn't large, but it was an intervention study and the technology utilized for measuring the results was relatively uncommon in these types of studies and significant.  The answer was clear:  carb restriction worked best.

I think the fact that this study was done might be attributable to Gary Taubes' work, as it appears to be designed to test the hypothesis he re-discoverd and advocated in his books, "Good Calories Bad Calories" and "Why We Get Fat" (available in my aStore, by the way).

When I see a study published like this one, I get excited.  This one will draw comments from all of my favorite carb restriction bloggers.  This one is a shot in the face of the "calorie is a calorie" reductionists (who are correct and all wrong; correct about the physics and incorrect in their linear application of it to a human body as if it was a bomb calorimeter).  There will be some interesting attempts from the "C is a C" crowd to explain this one away.  Squirming and hemming and hawing will ensue as they try to deal with a cognitive dissonance they will be unable to reconcile.

What was the study?
The research finds that dieters who were trying to maintain their weight loss burned significantly more calories eating a low-carb diet than they did eating a low-fat diet.  But some experts say these findings are very preliminary.  The study, funded by the National Institutes of Health, was designed to see if changing the type of diet people consumed helped with weight maintenance because dieters often regain lost weight.  So scientists had 21 obese participants, ages 18 to 40, lose 10% to 15% of their initial body weight (about 30 pounds). After their weight had stabilized, each participant followed one of three different diets for four weeks. Participants were fed food that was prepared for them by diet experts. The dieters were admitted to the hospital four times for medical and metabolic testing.

I love this "reporter speak":  Some experts say the results are very preliminary.

Can study results be "very preliminary?"  That phrase makes me chuckle as I remember a high school teacher who directed that I "completely eliminate redundancy" and then lined through the word "completely."  Point taken.

And if they are "very preliminary" what does that mean anyway?  Was it a well done study or not?  If it is, what sense do you make of the study, Mr. Expert?  Those would have been some of the good questions to ask, but ones not asked so much by the "newspaper blah blahs" I suppose.

Here's the link to the JAMA report:

So why do I feel so smug about the result?  Why would I indulge in the "I told you so" routine to those who represent what I think of as 40+ years of bad science?  Mainly because their work has hurt people.  They have advanced the low fat message like an item of religious faith in spite of the lack of science to support it, while claiming they were speaking with scientific authority.  They projected their strongly held beliefs, and pretended it was a fact.  In short, they did what all humans do, but they did what they did from positions of power and authority, and their discipline was unequal to their power to influence.  I'm not saying "They lied, people died."  I don't mean to imply they deliberately deceived anyone.  They deceived themselves and didn't have the discipline to just say "This is what I think but it's not proved yet."  What they did is something to be angry about.

You can safely predict there won't be too many from the "calorie is a calorie" crowd who say "well, I guess I was wrong about low carb, sorry."  Not too many will say "Gee, I guess that Taubes guy isn't a money grubbing buffoon after all."  None will apologize to Dr. Atkins or the Eades or Loren Cordain.  In other words, there will be very few who swallow their pride and admit this one is a direct contradiction of what they thought they knew.

Here's the "titular head" of the "calorie is a calorie" crowd, cited as an "expert", to whom we are supposed to pay attention:
George Bray, an obesity researcher at Pennington Biomedical Research Center in Baton Rouge who has also studied this topic and who wrote the accompanying editorial in JAMA, says that other studies "show that you can do well on any diet as long as you stick to it. Adherence is the major key for weight loss and maintenance. There is no magic in any diet."
This is the same guy that has said diets don't work due to the toxic food environment and there's really no hope short of pharmaceuticals.  He's also ignoring the fact that low fat diets are hard to stick to because of the resulting hunger.  And he's pretending not to notice all the research that shows exactly what this JAMA study shows - low fat dieters who lose weight commonly suffer a reduced rate of metabolic activity (this was a featured component of the recent NYT article which said, essentially, "there's no hope for long term weight loss because the body compensates for weight loss by reduced metabolic rate").  And this is also a guy from the camp that has said that we all need to just walk or move enough to  burn 50 kcal/day or so to use up the extra "energy" we all tend to consume - now after a study that shows a 300kcal/day metabolic advantage, all he has to say is (to be fair, all he's reported to have said) "diets are great, just follow one".  From my completely inconsequential perspective, Dr. Brey's long career and his significance as a researcher has been to advocate a linear relationship, uncomplicated by hormonal and individual variances, between food intake and energy expenditure and weight gain/loss.  So, I wouldn't expect him to be confused by the facts since what the facts of this study say are "you were wrong". 

Eric Westman, a Duke University researcher who has conducted several studies on the low-carb diet and is co-author of The New Atkins for a New You, says this study documents that the "lower the carbohydrates, the better the metabolic effects. People burn more calories if they eat fewer carbohydrates."
What he should have said was "I told you so."

Marion Nestle, a nutrition professor at New York University, says longer studies conducted among people in their own environments, not with such controlled meals, have shown "little difference in weight loss and maintenance between one kind of diet and another." More research is needed to show that interesting results like these are applicable in real life, she says.  "In the meantime, if you want to lose weight, eat less." (emphais mine)
Part of what she says is a BFO - no one study is compelling in science, and oh by the way, things are different in the real world than for those eating prepared foods during a controlled experiment.  Gee, thanks for the insight.  Thanks also for the smug advice at the end, too, Professor N, that provides us all the information we need to know about the obesity/health care crisis in the US.  Message from Professor N to anyone that is overweight - "You are fat because you are gluttonous and lazy, get off your butt and starve yourself.  Your bad character is wrecking our health care system, knock it off."  Does she think that repeating that message for another 30 years is going to work better than it has for the last 30 years?  These people are a joke except there's no punch line - there's a nation of sick people and much of the dietary confusion of the last 30 years could be blamed on folks like Professor N and Dr. Brey. 

Or you could skip the blame and just accept the pathetic low fat pseudo science of the last 30-40 years and get over it, which I will endeavor to do after this article is complete.

In ten years, the blah blahs at the newspapers, however, will be writing about this study and more that will follow as if the superiority of a carb restricted diet has always been a well known fact.

Here's a blurb for those wary of the sin of epidemiology (which is to say confusing correlation with causation):
The authors note a downside to the low-carb diet: It appears to raise some risk factors for heart disease.
This is the high fat bias on display.  The article author - a newspaper blah blah for sure - had to find something bad to say about a study which shows a stunning finding in favor of high fat diets.

So, what does the study say about how high fat diets will kill you faster than drinking 16.1 ounce sodas in New York City?  "Risk factors" is the epidiological language for "factors which correlate to disease that we would like to think we know are causative." 

But for actually predicting heart disease, for example, the best numbers available are either:
-Ratio of LDL to total cholesterol (what my insurance company uses to figure out how soon I'll die)
-Ratio of triglycerides to HDL

Interesting results for study participants:
*Serum leptin was highest with the low-fat diet (mean [95% CI], 14.9 [12.1-18.4] ng/mL), intermediate with the low–glycemic index diet (12.7 [10.3-15.6] ng/mL), and lowest with the very low-carbohydrate diet (11.2 [9.1-13.8] ng/mL; overall P < .001) (Table 3)
In other words, leptin levels are higher with a high carb/lowfat diet, which is known to result in increased hunger and decreased metabolic output - leptin resistance anyone?

*Regarding components of the metabolic syndrome, indexes of peripheral (P = .02) and hepatic (P = .03) insulin sensitivity were lowest with the low-fat diet. Comparing the low-fat, low–glycemic index, and very low-carbohydrate diets, serum HDL cholesterol (mean [95% CI], 40 [35-45] mg/dL; 45 [41-50] mg/dL; and 48 [44-53] mg/dL, respectively; overall P < .001), triglycerides (107 [87-131] mg/dL; 87 [71-106] mg/dL; and 66 [54-81] mg/dL, respectively; overall P < .001)
In other words, low carb is great for HDL and triglycerides (already known, so essentially these stats validate the test protocol)

*CRP tended to be higher with the very low-carbohydrate diet (median [95% CI], 0.78 [0.38-1.92] mg/L for low-fat diet; 0.76 [0.50-2.20] mg/L for low–glycemic index diet; and 0.87 [0.57-2.69] mg/L for very low-carbohydrate diet; P for trend by glycemic load = .05). Blood pressure did not differ among the 3 diets.
This is not a good indicator, but the significance of CRP compared to the other markers, which are more positive, is not known.

The study conclusion:
The results of our study challenge the notion that a calorie is a calorie from a metabolic perspective.

Hell yes they do!  Eat meat, vegetables, eggs, nuts and seeds, little fruit or starch, and no sugar/wheat.

(Minor edits June 27, 2012, 16.44)

A Clue About Insulin Sensitivity

In 1993, the New England Journal of Medicine Published a study demonstrating that highly unsaturated fatty acids (HUFA; e.g., arachidonate and docosahexaenoate [DHA]) in muscle membrane phospholipids are tightly correlated with insulin sensitivity [38].  Specifically, this means that the more of these HUGAs there are in the muscle membrane, the more insulin sensitive the muscle.  This observation subsequently has been corroborated and extended by multiple other studies.  For example the significant correlation between muscle HUFA and insulin sensitivity was shown to be specific to the phosphatidylcholine phospholipids which predominate on the outer layer of the muscle membrane [39].  This is interesting from the perspective that it implies a role for the background fatty acid composition of the membrane, per se, rather than the protein components inserted into it (like insulin receptors or glucose transporters).  In other words, figuratively speaking, what the 'fabric' of the wall itself is made of is very important for glucose transport - it's not just about the number of switches (i.e. receptors and transporters) inserted in the wall.

How these HUFAs get into muscle membranes is a very complex process involving both diet composition and metabolism of the various essential fats after they are eaten.  

The above is an excerpt from this very engaging book:

In all honesty I do not want to spend a bunch of time sorting out why the HUFAs get into cell membranes ... but I probably will.  

My guess is that where this is going is that inflammation is a contributor to insulin resistance by reducing either the contribution of HUFAs to cell membranes, or because in a high inflammation body (one in which the immune system is "on high alert" chronically) the HUFAs are oxidized too fast and thus lose their ability to serve as transport sites when commanded by the presence of insulin.  Or perhaps, a high insulin environment, in and of itself, damages the HUFAs. OR, as others have speculated, perhaps after some period of time of being stuffed full of sugars by the action of insulin, enough cell damage occurs that the cells develop a means to "defend themselves" from the sugar onslaught.  Or some combination of the above.  

In a way it does not matter.  If you are struggling to regain insulin sensitivity, you must eat a lot of fat, workout consistently, and probably practice fasting from time to time.  You must avoid fructose as much as possible.  And the fat you eat should include saturated fat, polyunsaturates from sources like nuts, and monounsaturates.  Lastly, you should ingest a balanced quantity of omega-3/6 fatty acids.

Eat meat, eggs, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.

Tuesday, June 26, 2012

Attia: Predicting Cardiac Risk

Doctors typically measure the following in a standard cholesterol test:
  • LDL-C – the concentration of LDL (“bad”) cholesterol in your blood
  • HDL-C – the concentration of HDL (“good”) cholesterol in your blood
  • TG – the level of triglycerides (“bad”) in your blood
Combining HDL-C and TG into a ratio (i.e., TG/HDL-C) is probably the single best predictor of cardiac risk you can derive from a standard cholesterol test.  The lower the ratio, the lower your chances of having an “adverse cardiac event,” as the medical community describes it (e.g., a heart attack). Despite what doctors tell you, LDL-C is pretty much useless for predicting your risk of heart disease. In fact, it’s not even part of the risk assessment for metabolic syndrome, which everyone agrees is the central link to heart disease (and virtually all other chronic diseases we’re afflicted with).
This guy's site is just a goldmine for detailed but digestible information, I highly recommend it.  Unlike me, he's willing to include photos and drawings with his posts which can be very helpful.  Like me, he's a student of the "carbohydrate hypothesis" as advocated by Gary Taubes most recently/commonly.  
This weekend, I gave my fourth presentation of a three hour brief I call "That Stuff Will Kill You".  The brief describes why a neolithic diet is toxic, how the paleolithic model might be useful to understand the pathology of the neolithic diet, and how one might best attempt to implement a diet based on the Paleolithic model.  I'm always amazed when folks stay for the 3rd hour, but also very gratified when they do.  I'm also very grateful to the audiences since each time I present, I become aware of how I might change the material to improve the impact on the audience.  
One thing I'm well aware of and grateful for - a big part of the reason these sessions are well received is that they are attended by CrossFitters.  As a group, it's difficult to imagine folks that are more eager to learn.

Monday, June 25, 2012

BBC News - What caused the obesity crisis in the West?

Contrary to popular belief, we as a race have not become greedier or less active in recent years. But one thing that has changed is the food we eat, and, more specifically, the sheer amount of sugar we ingest.
"Genetically, human beings haven't changed, but our environment, our access to cheap food has," says Professor Jimmy Bell, obesity specialist at Imperial College, London.
"We're being bombarded every day by the food industry to consume more and more food.
"It's a war between our bodies and the demands our body makes, and the accessibility that modern society gives us with food. And as a scientist I feel really depressed, because we are losing the war against obesity."

First off, did you laugh as I did at his goofy lament about being a "scientist" that's depressed?  I think I know what he was trying to say, but do you have to be a scientist to notice the negative reinforcing cycle of human suffering that results from the obesity epidemic?  And if you knew that someone caused that spiral, or accelerated it, by using strongly held belief dressed up like science and backed by the power of the government, would you feel (scientist or not) angry about it?

I have, but I don't now.  I think eventually the government will get it right about the science - it's getting to the point that even the government hasn't any more wiggle room - but right now, all that matters is improving my ability to help others sort this mis-information mess out. 

The reference to genetics is noteworthy, as it shows the paleolithic model, as a framework for the problem of human nutrition, is gaining a wider influence.

As to the reference about the food companies bombarding us to make us eat more food - OK, if that's how you want to see it, but I also see folks who desperately want the food companies to make low fat food, low cal foods, very tasty and cheap foods, foods that are "whole grain", and foods that have vitamins/minerals and other supposedly healhy characteristics - in other words, the food industry is doing what it should, which is providing the consumer with what the consumer will pay for.  If consumers hadn't been lied to about the role of fat and sugar in their diets, much of the food industry leverage to see cheap, processed low fat nastiness would not exist.

The same, big, nasty, souless food industry (spare me the drama please) is also going to be the one that figures out how to provide the market with inexpensive (relatively) grass fed animals on a large scale.  They will give us what we want, for the sake of their profits, which will pay their employees, who will pay their taxes and FICA, and the big souless machine will have done far more to benefit us than the equally soulless but unaccountable to anyone USDA.  The difference in these two large, soulless bureacracies (USDA and the food industry giants) is that one will cease to exist when it no longer supplies what the customer wants at a price the customer will pay, whereas the USDA will continue to do whatever the heck it does no matter how badly it does it.

Fructose is easily converted to fat in the body, and scientists have found that it also suppresses the action of a vital hormone called leptin.
"Leptin goes from your fat cells to your brain and tells your brain you've had enough, you don't need to eat that second piece of cheesecake," says Dr Robert Lustig, an endocrinologist.
He says when the liver is overloaded with sugars, leptin simply stops working, and as a result the body doesn't know when it's full.
Fructose isn't just "easily converted into fat" in the body, that is what happens to fructose in the body, period.  The problem with that is that above a certain dosage level, fructose so "buggers up" (sorry, BBC article, just had to us their colloquialism) the liver's capacity to do its myriad metabolic chores that it can't keep the rest of the machine running "unbuggered."  So, you get fatty liver, insulin resistance, and metabolic syndrome along with you HFCS laden gatorade, coke and dr. pepper.

HFCS, or sucrose (nearly the same thing) is, by the way, a silly thing to put in a sports drink - the body that's depleted of glycogen and glucose from high intensity exercise does NOT need fructose to get back up to speed quickly - it needs glucose.  Glucose was what made the original gatorade such a game changer - but it didn't taste good.  So, the gatorade folks did what all of us ignorant consumers demanded - made gatorade more tasty by making their drink less effective.  If I needed a gatorade like sports drink for rapid replenishment of glucose/glycogen, I'd get the zero cal sports drink and add a calculated amount (determined via experimentation) of pure glucose from cane syrup.  But if you or your kid just needs to rehydrate and maintain electrolytes post-workout, give them salty foods, a potassium supplement and regular food - the body will replenish the glycogen within 24 hours.  And if you are working out to assist in recovery of metabolic health and body composition - please skip the high carb post workout drinks/shakes. 

Another cut from the article:
Overnight, low-fat products arrived on the shelves. Low-fat yoghurts, spreads, desserts and biscuits. All with the fat taken out, and largely replaced with sugar.
The public embraced the new products, believing them to be healthier. But the more sugar we ate, the more we wanted.
By the time anyone began to ask if it was a good thing to replace fat with sugar, it was too late - but it was a decision with huge implications for the obesity crisis.
"If fat's the cause, that's a good thing to do," says Dr Lustig. "If sugar's the cause, that's a disastrous thing to do, and I think over the last 30 years we've answered that question."
Well, yes we have.

Having included a bit from the "calorie is a calorie" crowd, the fructose gang, and the sugar haters more generally, the author also includes a bit from the "palatability" crowd, who think that foods laden with sugar, fat and salt have a unique power to make us want to eat more and more.  My problem with this crowd is pretty simple - their statement of the problem does not help very much (eliminate sugar salt and fat from the diet?  Good luck living like that for 50 years), but to the extent that it works, I still don't know how they think they can say it is the three foods together that causes the problem, vice just the sugar.  In other words, getting a client off of sugars/starches works for most of them.  What then is the point of making a big speculative fuss about the supposed evils of fat-sugar-salt together?  Further, I eat all the salt and fat that I want, and I've never had better appetite control - and it's a good thing I do, too, since I lose a bunch of salt daily in the heat of the South - 99 degrees today here in Memphis.  In short, the "food pallatability" crowd doesn't impress me.

Here's where my best efforts to understand the problem of the millions year old human genome in the age of annual mono crop dominated agriculture - eat meat, vegetables, eggs, nuts and seeds, little fruit or starch, no sugar/wheat. 

Thursday, June 21, 2012

Coaching For St. Jude

Folks, it's a big honor to be the presenter at this St. Jude Children's Research Hospital fund raiser at CrossFit 901.  If interested, click the link.  I'd be happy to see you there!

Use It Or Lose It


A contributing factor to the loss of muscle mass and strength with adult aging is the reduction in the number of functioning motor units (MUs). Recently, we reported that lifelong competitive runners (master runners = ∼66 yr) had greater numbers of MUs in a leg muscle (tibialis anterior) than age-matched recreationally active controls. This suggested that long-term exposure to high levels of physical activity may limit the loss of MU numbers with adult aging. However, it is unknown if this finding is the result of long-term activation of the specifically exercised motoneuron pool (i.e., tibialis anterior) or an overall systemic neuroprotective effect of high levels of physical activity.
Purpose: The purpose was to estimate the number of functioning MUs (MUNEs) in the biceps brachii (an upper body muscle not directly loaded by running) of nine young (27 ± 5 yr) and nine old (70 ± 5 yr) men and nine lifelong competitive master runners (67 ± 4 yr).
Methods: Decomposition-enhanced spike-triggered averaging was used to measure surface and intramuscular EMG signals during elbow flexion at 10% of maximum voluntary isometric contraction.
Results: Derived MUNEs were lower in the biceps brachii of runners (185 ± 69 MUs) and old men (133 ± 69 MUs) than the young (354 ± 113 MUs), but the old and master runners were similar.
Conclusions: Although there were no significant differences in MUNE between both older groups in the biceps brachii muscle, with the number of subjects tested here, we cannot eliminate the possibility of some whole-body neuroprotective effect. However, when compared with the remote biceps muscle, a greater influence on age-related spinal motoneuron survival was found in a chronically activated MN pool specific to the exercised muscle.

You already know that as you age you lose muscle, and you may know that an estimate is that you lose 6% per year of muscle unless you engage in strength training, which is estimated to slow the rate of muscle loss to 1%. 

As a side note, the fact that Louie Simmons is powerlifting in the neighborhood of 700 pounds in the deadlift, 800 pounds in the back squat, and 600 pounds in the bench press at age 60+ is ... well, I don't know what to say about that except that Louie is one incredible lifter.  I doubt he has any serious contenders for the title of "World's Strongest 60 Year Old."  Yes, I know powerlifters use funny lifting suits and they are not shy about their use of drugs which allow them to train harder, some of which are of questionable legality.  Still - that's a lot of hard work and determination and guts.

If I read this abstract right, the short version is that it appears you delay muscle loss for those muscle you put to work.  The authors hope there's a systemic benefit, but this test did not show that effect. 

In other words, common sense prevails - if you want to sustain your ability to move yourself around as you age, train all the functions of the body.  Run, jump, climb, push, pull, lift and press.  If you want to maintain the ability to generate power (speed and force), you must train with explosive elements (punching, kicking, throwing, oly lifting, jumping, sprinting).  This stuff isn't, as the old joke goes, rocket surgery.

Tuesday, June 19, 2012


Here's an interesting statement, in which correlation and causality are confounded:
A condition like high blood pressure is sneaky. You don’t feel it, and it generally doesn’t cause any outward signs or symptoms. Yet it silently damages blood vessels, the heart, kidneys, and other organs.
So let's think for a moment about causality - if folks with hypertension also are more likely to have blood vessel damage, does that mean it is caused by the high blood pressure?  Obviously, not.  There could be a third factor that's causing both.

So the authors move on:
High blood pressure — also known as hypertension — isn’t a disease. It is a sign that something is wrong in the body. In some people with hypertension, the culprit is a narrowing of the arteries supplying the kidneys (renal artery stenosis), or an overactive thyroid gland (hyperthyroidism) or adrenal glands (aldosteronism). When these are treated, blood pressure drops back to normal. More often, though, doctors find no underlying cause for high blood pressure. This condition is called essential hypertension.
So, in this analysis from the smart folks writing this magazine for Harvard, the fact that 80% of those with hypertension can reduce their BP back to normal by restricting carbs isn't even worth mentioning.  That is inexcusable.  It is not a secret, it's a treatment that requires no medication, and has as side effects the following:  proven superior results (by interventions studies up to one year) for weight loss, lipid profile improvement, reduction of gout, and reduction of NAFLD.  In short, there's absolutely no drawback to this treatment.   

Back to the causality v. correlation issue:
High blood pressure contributes to the development of stroke, heart attack, heart failure, and kidney disease. In the United States, it directly accounts for about 60,000 deaths a year and contributes to another 300,000.
This is statistical gymnastics - neat tricks but only as accurate as the assumptions of those doing the calculations.  The fundamental question - is high blood pressure a cause of or a correlate with the other diseases of civilization? - has not been answered to my knowledge aside from the fact that it seems to be a correlate.  The evidence of that is that the best intervention for controlling HBP is also the best intervention for treating the other correlates of HBP, which are also correlates of metabolic syndrome, all of which get worse when folks are sick enough to be diagnosed as "diabetic."  IOW - did those folks suffer from the HBP or did they suffer from the underlying problem - lack of glycemic control - for which HBP is only one of several correlates?

Interesting study, but hopefully, upon review, you will see the baked in correlation v. causality issue here:
These researchers looked at the 1,007 men and women admitted to the hospital over a 10-month period for any potentially heart-related problem. These ranged from chest pain and fainting to heart attack, heart failure, atrial fibrillation, and pericarditis. In this group, 69% had been diagnosed with high blood pressure before being admitted to the hospital. Each person was followed for one year. At the end of that time, 17% of those with high blood pressure had died, compared with 9% of those with normal blood pressure. Rehospitalization for a cardiac problem followed the same pattern: 31% of those with high blood pressure, and 18% of those without (American Journal of Cardiology, published online, Aug. 24, 2011).
But, the smart folks writing this magazine want you to know there's hope:
But there is actually good news about high blood pressure: there is a lot a person can to do help keep it in check, and even prevent it from occurring in the first place.
How? The National Heart, Lung, and Blood Institute; the Centers for Disease Control and Prevention; and the American Heart Association offer these recommendations:
  • Achieve and maintain a healthy weight for your height.
  • Exercise regularly.
  • Eat a diet that is rich in fruits, vegetables, and whole grains.
  • Limit sodium intake to under 2,300 milligrams a day (one teaspoon of salt), and get plenty of potassium (at least 4,700 mg per day) from fruits and vegetables.
  • Drink alcohol in moderation, if at all.
  • Reduce stress.
  • Monitor your blood pressure regularly, and work with your doctor to keep it in a healthy range.
(sarcasm alert!)...and when all that doesn't work, keep on popping those pills.  It frankly wouldn't take all those big dollar, big brain, high credentialed organizations to give you this kind of nearly pointless, assinine advice.  I could have done that for a lot less than they have been paid over the years. (This ends the sarcasm alert)

In a follow up post, I'll throw out a bit of speculation about the "lies, damned lies, and statistics" aspect of the high blood pressure concern. 

Why You Love Fat

So let's take a hypothetical 5'6" 132 pound woman with 25% body fat set adrift in a life-boat with plenty of water and no food.  Her 33 pounds of adipose tissue is about 85% by weight triglyceride, so she has about 115,000 Calories of fat reserves.  She can also burn about half of her body protein content (10,000 kcal of her 20,000 total) before she dies.  Sitting quietly in the boat (i.e. no rowing) she'll start out burning about 2000 Calories per day.  This implies that she'd last about 62 days.

Kids, I don't recommend that you try this at home.

But I can't think of a better illustration of the role fat plays in the human genome.  It's the human grade A diesel, it's the stuff we're made to run on for the majority of human function.  We need glucose for the brain, and to fuel top end physical output and a few other body functions - and we can use glucose for a bunch of fuel options when needed.

The big takeaway?  If you over glucose yourself, the body converts the glucose to fat, but the process isn't healthy; it's an emergency reaction to a glucose toxicity problem.  If you eat too much fat, on the other hand, it's no big deal.  The body easily manages fat storage and liberation and you will run just fine.

Fat is your friend, your ally, and your best fuel once you get the carb intake under control.  Eat meat, eggs, vegetables, nuts and seeds, little fruit or starch, no sugar no wheat.

Monday, June 18, 2012

Entertainment Value

I read an interesting article in the Harvard Healthbeat magazine one day, and then subscribed to their email version.  Occasionally, they print something informative, mostly it's almost comedy in that they keep recommending dietary and fitness material that seems either non-scientific or just plain wrong.
But the entertainment value is there sometimes, so I still read. 

Here's a post that started to get my attention:
Exercise is more than just a good health habit; it’s also a specific and effective treatment for many knee and hip problems. Strength in the muscles around a damaged knee or hip can help support that joint by taking over some of its responsibilities. For example, your hips have to do less work to support your body weight if your quadriceps, gluteals, hamstrings, and abdominal muscles are stronger. A strong quadriceps can take over the shock-absorbing role usually played by the meniscus or cartilage in the knee.
So far so good, right?  I see this phenomenon every day - "My joints hurt so I'm not active" is the near universal refrain.  Folks, that is the E-ticket to more joint pain AND overall frailty and the daily increase in the limits of what you can do, how you will feel, and what you life experience can be.

The proper balance of strength in the muscles can hold the joint in the most functional and least painful position. With any knee or hip problem, the first muscles to lose strength are the largest antigravity muscles, the quadriceps and gluteals, so an exercise plan for any injury is likely to focus on these.
Muscles work in pairs — one contracts while the opposing one relaxes. For example, when you straighten your knee, your quadriceps on the front of your thigh contracts, and the hamstrings on the back relax. Imbalances in the function of paired muscles can cause joint problems and invite injury. 

Why would they reduce the magnificent complexity of the interaction between the hamstrings, glutes, quads and back to such drivel?  Here's a bet I'll never lose - try and pull your best deadlift or stand up under a big ole squat by relaxing your quads to let the hamstrings work, or vice versa.  My friends, it you did it, I would be impressed, you would have learned how to overcome all of your natural instincts.  

In short - the quads and hamstrings and back and glutes all play a critical role in the "straitening of your knee", which is really as much about opening the hip as it is the knee when you are applying force in the real world.  Try and kick a ball by "straightening your knee."  WEAK!  Now do it right and use the hips - POWER.

One does not really need to know anything about straightening one's knee - one needs to know how to lift an object from the ground, or to raise one's center of gravity, or to lift an object overhead, or how to use the strength gained from doing these movements when one needs to shovel, or saw or push an object, or climb a ladder or stairwell.  

In other words, if you have monster strong hamstrings but cannot safely lift your fallen parent from the ground, who cares about the hamstring strength?  Being able to use a let extension machine with a big weight translates to nothing, being able to squat, deadlift, and press translates to everything.  Or as Greg Glassman said, more or less, you can do any amount of leg curls, leg extensions, abduction, adduction, and calf raises - that's never going to give you a big squat.  If that's not self evident, you have some thinking and experimenting to do.  

On the good note, even Harvard is on to the idea of functional movements:
Open-chain exercises may be more effective for particular therapeutic goals such as increasing quadriceps strength after ACL injury. But over all, physical therapists are incorporating more closed-chain exercises into rehabilitation programs and recommending them for people with painful joints because these exercises involve more muscles and joints and help to create stability around a joint.

This is why the experiment in using man made machines to create fitness hasn't accomplished much.  It does allow people to do something without having to get help in relearning how to squat or deadlift, but it leaves a lot of fitness on the table when compared to functional movements.

The overarching point is that there's a lot of mis-information out there.  The learning starts by refusing to believe what these authorities say unless you can satisfactorily subject their claims to validation.  

More on the mis-information coming from the kinds of high fallutin' sources soon - but the takeaway today sports fans is if you want more work capacity for life, sport or combat - squat and deadlift.  If you want to move better, run jump climb throw kick and punch.  If you want your body to work well, forget the goofy isolation exercises and do the stuff your great great great ancestors did to feed themselves.  Don't worry about what muscles do what, just move and work.  

If you can't sort this out on your own, consult a CrossFit coach, who can teach you the fundamentals of human movement, which you can then apply to barbells or tree limbs.  

Friday, June 15, 2012

Hyperlipid: Insulin and the Rewards of Overfeeding

The link below will take you to the blog of "Peter of Hyperlipid".  His blogline is telling:
"You need to get calories from somewhere, should it be from carbohydrate or fat?"
The reason this is the question is that protein almost never makes up more than 40% of kcal, and you have to work pretty darned hard to get that much of your kcal from protein.  There are two reasons for that.  One - high protein foods are generally even higher fat (at least, they are if they are of good quality), and two, no one sits around gnawing protein.  It's work, it's high in satiety, and frankly people who have that impulse just get busy and do something else instead.  If you have video of yourself depressed and compulsively eating high quality protein, by all means send it to me, I'll reconsider the above summary of what I consider the facts to be. 
In other words, do your best but you won't get fat eating meat, eggs, bacon, or fish.  If you get 600 kcal/day on protein, you'll be in the range of world class powerlifters for protein intake.  
Peter's blog can be hard to read.  He likes sarcasm and he likes to be subtle.  He's not a big fan of mercy as regards those whom he thinks are using substandard science or logic.
This particular article references the brouhaha that took place last year between blogger and researcher Stephen Guyanet, of Whole Health Source, and science writer Gary Taubes, when Gary confronted Stephen at the Ancestral Health Symposium.  That confrontation brought to a head two competing theories of why carbs make people fat, and why carb restriction makes it easier for fat people to get leaner and more healthy; and why it does so faster than simple calorie restriction.
So what's the study he uses to make his point - that fat regulation is regulated by insulin more than by leptin and the notional "adipostat" that is conjected to be dis-regulated by highly palatable foods (salt, sugar and fat laden foods) - ?  In this case, it is a study in which young healthy "blokes" are overfed to the tune of 2000kcal/day.
That's a lot.  That's enough to theoretically force a weight gain of a pound every two days. Most "blokes" supposedly run on 2700kcal/day, so bumping them up to 4700 kcal means they were eating almost as much as Morgan Spurlock was (of Super Size Me fame or infamy).  Turns out, they were eating a bunch of high carb junk to get the extra kcal, just as Morgan did.  Would you be surprised to find that in the case of these subjects, overeating by 2000 kcal/day of mostly processed carbs made them fat and sick, just like it did for Morgan?  Nope, me either.
As Peter puts the next part:
Now, all you have to do is to go and ask any cutting edge, state of the art obesity researcher and you can be told that hyperinsulinaemia is a consequence of obesity, not a cause, and that carbohydrates are the worlds greatest slimming aid because insulin is a satiety hormone and, oh, did I fall asleep there?????? Sorry.
So what stats does Peter use to prove that it's not fat accumulation that causes excess insulin, but instead the excess intake which causes high insulin which commands storage of fat (and of excess blood sugar as fat)?  Here's the summary:
If insulin resistance is the result of increasing fat mass, then insulin levels should increase as the subjects - lean healthy blokes - gain fat.  However, that's not what happens.  The insulin rates fall as the rate of fat gain falls.  That's a weird one too - if kcal is still excess, why does the rate of fat gain stall?
The chaps gained, from Table 3, 1kg of fat mass in the first week and only 0.5kg of fat in the second week... Oh, I guess this must be because the subjects either (a) sneaked off to the gym in the second week or (b) flushed their Snicker Bars down the loo in the second week, without passing them through their gastro intestinal tract first (good idea!) or (c) got bored with Snickers and stopped finding them rewarding. And of course they disconnected their Actiheart monitors at the gym.
Otherwise how you can eat 2000kcal over your energy expenditure, equivalent to nearly 200g of fat gain per day, and gain a kilo of fat in the first week, then continue to eat an excess 2000kcal/d for a second week and only gain half a kilo of fat? Calories in, calories out, you know the rules. Hmmm, in the second week there are 14,000 excess calories-in, 5,000 stored, very interesting.
We all know the obese lie about calories. It seems probable that so too must experimental subjects, in direct proportion to the duration of their over eating! Now we know. Bit of a milestone paper this one.

Uh, well, let's hope you are not allergic to sarcasm.  But as he explains, what this study shows is exactly what the body should do, which is: become increasingly insulin resistant as the massive over-feeding continues, to protect the cells from damage which results when tissues are "over-stuffed".  The result is hyperglycemia, as the ability of insulin to shunt excess sugar into cells is blunted via "cellular self defense" aka insulin resistance.
Depending upon the individual predilections of the overfed, some may have had fat cells that remains insulin sensitive long after others lost all insulin sensitivity (that would be the endomorphs, folks, whereas the ectomorphs would lose insulin sensitivity the fastest, since they are quite obviously not lipophillic).  Once the insulin resistance progresses far enough, the liver will begin to store the fat that cannot be stuffed into other tissues - intra-abdominal obesity will increase.  With enough fructose, non-alcoholic fatty liver disease will manifest itself, which will accelerate the insulin resistance.
In short - Peter's brilliant analysis has taken an otherwise just plain weird experiment and shown how it provides the predicted result if viewed through the lens of the carbohydrate/insulin hypothesis.  
Eat meat, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.

Thursday, June 14, 2012

Low Carb Beats Low Cal For Health - Again



Effective diabetic management requires reasonable weight control. Previous studies from our laboratory have shown the beneficial effects of a low-carbohydrate ketogenic diet (LCKD) in patients with type 2 diabetes after its long term administration. Furthermore, it favorably alters the cardiac risk factors even in hyperlipidemic obese subjects. These studies have indicated that, in addition to decreasing body weight and improving glycemia, LCKD can be effective in decreasing antidiabetic medication dosage. Similar to the LCKD, the conventional low-calorie, high nutritional value diet is also used for weight loss. The purpose of this study was to understand the beneficial effects of LCKD compared with the low-calorie diet (LCD) in improving glycemia.


Three hundred and sixty-three overweight and obese participants were recruited from the Al-Shaab Clinic for a 24-wk diet intervention trial; 102 of them had type 2 diabetes. The participants were advised to choose LCD or LDKD, depending on their preference. Body weight, body mass index, changes in waist circumference, blood glucose level, changes in hemoglobin and glycosylated hemoglobin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, uric acid, urea and creatinine were determined before and at 4, 8, 12, 16, 20, and 24 wk after the administration of the LCD or LCKD. The initial dose of some antidiabetic medications was decreased to half and some were discontinued at the beginning of the dietary program in the LCKD group. Dietary counseling and further medication adjustment were done on a biweekly basis.


The LCD and LCKD had beneficial effects on all the parameters examined. Interestingly, these changes were more significant in subjects who were on the LCKD as compared with those on the LCD. Changes in the level of creatinine were not statistically significant.


This study shows the beneficial effects of a ketogenic diet over the conventional LCD in obese diabetic subjects. The ketogenic diet appears to improve glycemic control. Therefore, diabetic patients on a ketogenic diet should be under strict medical supervision because the LCKD can significantly lower blood glucose levels.

This is a study to give considerable weight to.  It included a relatively large number of subjects, it was an intervention study, and the duration was 24 weeks.  The population included 102 diabetics.

Would that I could get access to the rest of the study, I would love to see the changes in uric acid (the cause of gout when the blood levels are too high).

Wednesday, June 13, 2012

Move, It Makes You Smarter

... but there is another, easy-to-achieve, scientifically proven way to make yourself smarter. Go for a walk or a swim. For more than a decade, neuroscientists and physiologists have been gathering evidence of the beneficial relationship between exercise and brainpower. But the newest findings make it clear that this isn't just a relationship; it is the relationship. Using sophisticated technologies to examine the workings of individual neurons - and the makeup of brain matter itself - scientists in just the past few months have discovered that exercise appears to build a brain that resists physical shrinkage and enhance cognitive flexibility. Exercise, the latest neuroscience suggests, does more to bolster thinking than thinking does.

Whatever the activity, though, an emerging message from the most recent science is that exercise needn't be exhausting to be effective for the brain. When a group of 120 older men and women were assigned to walking or stretching programs for a major 2011 study, the walkers wound up with larger hippocampi after a year. Meanwhile, the stretchers lost volume to normal atrophy. The walkers also displayed higher levels of B.D.N.F. in their bloodstreams than the stretching group and performed better on cognitive tests.

Gretchen Reynolds writes the Phys Ed column for The Times's Well blog. Her book, ''The First 20 Minutes,'' about the science of exercise, will be published this month. Editor: Ilena Silverman

Tuesday, June 12, 2012

Why You Love To Run; It's Humanity's Best Thing

I find this sort of analysis fascinating:
But how did we get this way? After all, our brainy, tool-using ancestors could have just sneaked up on prey animals and brought them down with a spear or arrow. Why did evolution shape us as great distance runners?
The answer, argue Lieberman and Bramble, is that snares, nets, and really effective projectile weapons, such as the bow and arrow, were probably invented by Homo sapiens—modern humans. There's no evidence that early Stone Age hunters had weapons much better than sharp sticks. Such armaments would have required them to kill prey animals at close quarters, where they would have been at high risk of getting fatally gored, bitten, or kicked. Thus, they probably obtained meat mainly via "persistence hunting"—chasing an antelope, for instance, until it was nearly keeling over with heat exhaustion—and scavenging. The latter was very much a running game: When distant, circling vultures tipped them off about a lion kill, they had to get there before hyenas, which strip everything edible from carcasses. And they typically could only outrace hyenas in the hot sun. As a result, they carved out a new carnivore niche: the hot-day meat chaser.
Intriguingly, existing hunter-gatherers still sometimes resort to persistence hunting in hot weather. That's because the nutritional payoffs can greatly exceed the energy costs of running down meat for us fleet-footed types. In fact, our ancestors' meat-rich diets probably contributed to the evolution of modern human traits, such as small guts, small teeth, and big brains.

The other thing humans do well is locate something by sound - only owls can do this better than humans. Bats and dolphins use sonar, not quite the same as just hearing and finding.

At any rate, my fellow hot day meat chasers, if you love to take off and run, now you know why - it's why you are here.

Sunday, June 10, 2012

CrossFit for Hope

Janet and I completed Hope in the hot DC sun yesterday with a crew of CrossFit monsters.  Doing the workout with CrossFit hero Nicole Carroll, and CrossFit Games worthy Neil Maddux, and many other delightful CrossFitters, made for a day to remember.

As incredible was to be welcomed into the warmth of the CrossFit HQ staff at the parties and meals that preceded and followed the event.  The staff looked tired but satisfied - as they should be after flying to Copenhagen, then Kenya, and then the west coast, and now to DC for Hope.  This is a group that is purpose driven and paying the price for it as well as reaping the rewards.  I am grateful to be associated with CrossFit.

There's no CrossFitter that won't feel proud to support St. Jude's children!!

The relatively dry heat and 2PM sun was an eye opener.  We were both able to keep the perspective though - we could choose at any moment to let up and stop the suffering.  The children supported at St Jude Children's Research Hospital cannot make the pain go away so easily.  I walked away from the arena, slowly, with 164 reps and six blisters/tears on my hands - and the humility of knowing I could have done more reps.  There's pride and humility in getting to the point where resolve meets pain and fatigue.

The children that St. Jude treats can't stop the illness, but we can help them and we can help St Jude fund the research that might stop these diseases - and others.

Here's a profile of a young lady who beat cancer, lost a leg in the fight, and is as charming and strong and powerful as any 13 year old you will ever meet.  Janet and I dined with her last night and she taught me the ending to the story of "Fire of the Gods" (who knew that Hercules saved Prometheus? I didn't, but Kate did, and I'm pretty sure she doesn't have a blog about that myth).  That was after she did more reps in Hope most of us competitors did.  Kate is testimony that how the cards are played matters far more than what cards one receives.  If you meet her, she will look you in the eye, listen intently and respond with strength, pride, passion and precision!  You will benefit from humility and inspiration as you speak with her.

I am grateful for the weekend, grateful to have been in the company of these inspiring people, and grateful to have been with Janet all weekend.  We had a blast!

I hope to post some video of us at work on the National Mall, to silence the throngs of skeptics who don't think we really did it!

Thank you to those who have donated, and who make other charitable choices aside from supporting St. Jude.  If you would like to add to CrossFit's 1.7+ million dollar projected fundraising total, click here:

Institute For Justice, My Hero

Peter Attia's cogent summary follows at the link below.  If you read it, you will wonder how it is possible.

After being diagnosed with diabetes, and nearly dying of its complications, Steve did his own research and learned that the high-carb/low-fat diet his doctors recommended may not have been the “best” choice for him.  He adopted a low-carb “Paleo” diet and lost about 80 pounds, freed himself of his medications, normalized his blood glucose, and claims to feel healthier than ever.  Like many of us who have experienced the virtues of carbohydrate restriction, he believes a well-formulated low-carb diet is the simplest, cheapest, and most effective way to treat diabetes.
Of course, as you know, this goes against the conventional wisdom promoted by most licensed dietitians and physicians who advocate a high-carb/low-fat diet and, if necessary, medication to lower blood glucose.
In December 2011, Steve started a Dear Abby-style advice column on his blog to answer reader questions.  In January 2012, the North Carolina Board of Dietetics/Nutrition informed Steve that he could not give readers personal advice on diet, whether for free or for compensation, because doing so constituted the unlicensed, and thus criminal, practice of dietetics.
The State Board also told Steve that his private emails and telephone calls with friends and readers were illegal.   Violating the North Carolina licensing law can lead to fines, court orders to be silent, and even jail.

Saturday, June 9, 2012

CrossFit for Hope

We hope to be on the national mall today performing CrossFit for Hope and enjoying the incredible day.  Supporting St Jude Children's Hospital in this way makes me feel very proud to be a CrossFitter.

Goal for CrossFit:  Raise one day's operating expenses for the Hospital, $1.7 million dollars.

Go check the website for more information:

And if you have not, please sponsor me for $10 or more, from this link:

And for those that already donated, thank you!!

Friday, June 8, 2012

How The Inuit Lived Carb Free


Background. The question whether even-chain fatty acids can be converted into glucose has a long-standing tradition in biochemistry. Since the glyoxylate shunt is absent from mammals, the question has been considered to be solved. It is of particular relevance for understanding the metabolic state of natives of the arctic regions due to the very high fat content of their traditional diet only containing negligible amounts of carbohydrates.

Methods & Results. Using an in silico approach, we discovered several hitherto unknown routes in human metabolism that allow the conversion of even-chain fatty acids into carbohydrates in humans. These pathways proceed via ketogenesis over the intermediate of acetone and produce the gluconeogenic precursor pyruvate. While these pathways can make a contribution to glucose production during times of limited carbohydrate supply, we found that their capacity might be limited due to a high demand in reducing equivalents in acetone degradation. Considering the traditional diet of natives of the arctic regions, the detected pathways are not only important in order to improve carbohydrate supply, but moreover reduce the amount of protein that needs to be used for gluconeogenesis.

Conclusion. In summary, our study sheds new light on our understanding of the metabolic state of natives from the arctic regions on their traditional diet. Moreover, they provide an avenue for new analyses that can reveal how humans have adapted metabolically to a practically carbohydrate-free diet.

The takeaway is - when someone tries to tell us that we have to eat a certain amount of carbs per day to feed the brain, they are either lying or ignorant.  The body can make the glucose the brain needs by several alternate methods.  What you must eat is protein and fat.

Thursday, June 7, 2012

Guessing and Advising

In 1972, when the National Institutes of Health introduced the National High Blood Pressure Education Program to help prevent hypertension, no meaningful experiments had yet been done. The best evidence on the connection between salt and hypertension came from two pieces of research. One was the observation that populations that ate little salt had virtually no hypertension. But those populations didn’t eat a lot of things — sugar, for instance — and any one of those could have been the causal factor. The second was a strain of “salt-sensitive” rats that reliably developed hypertension on a high-salt diet. The catch was that “high salt” to these rats was 60 times more than what the average American consumes.
Still, the program was founded to help prevent hypertension, and prevention programs require preventive measures to recommend. Eating less salt seemed to be the only available option at the time, short of losing weight. Although researchers quietly acknowledged that the data were “inconclusive and contradictory” or “inconsistent and contradictory” — two quotes from the cardiologist Jeremiah Stamler, a leading proponent of the eat-less-salt campaign, in 1967 and 1981 — publicly, the link between salt and blood pressure was upgraded from hypothesis to fact.
In the years since, the N.I.H. has spent enormous sums of money on studies to test the hypothesis, and those studies have singularly failed to make the evidence any more conclusive. Instead, the organizations advocating salt restriction today — the U.S.D.A., the Institute of Medicine, the C.D.C. and the N.I.H. — all essentially rely on the results from a 30-day trial of salt, the 2001 DASH-Sodium study. It suggested that eating significantly less salt would modestly lower blood pressure; it said nothing about whether this would reduce hypertension, prevent heart disease or lengthen life.

So who pays for the damage if the government says "eating less salt with help you live longer", but in fact, eating less salt raises the liklihood that you perish early? 

You do. 

Which is why the government should constrain itself from offering dietary advice until the science is rock solid, confirmed by interventions studies, and well publicized and critiqued. 

Wednesday, June 6, 2012

Ioannidis - "Full Disclosure. We Don't Know Much."

We could solve much of the wrongness problem, Ioannidis says, if the world simply stopped expecting scientists to be right. That’s because being wrong in science is fine, and even necessary—as long as scientists recognize that they blew it, report their mistake openly instead of disguising it as a success, and then move on to the next thing, until they come up with the very occasional genuine breakthrough. But as long as careers remain contingent on producing a stream of research that’s dressed up to seem more right than it is, scientists will keep delivering exactly that.
“Science is a noble endeavor, but it’s also a low-yield endeavor,” he says. “I’m not sure that more than a very small percentage of medical research is ever likely to lead to major improvements in clinical outcomes and quality of life. We should be very comfortable with that fact.”

For anyone wanting to puzzle apart the confusion about science and health, this article is a must read.