Low Carb Diets Killing Swedish Ladies Like You Read About

Denise Minger hits another home run in regards to this study, which ominously concluded that women who followed "low carb, high protein" diets were at a "significant" risk of increased cardiovascular disease.  Note, this study wasn't an intervention study, and therefore should be taken for what non-intervention studies are worth as regards their ability to tell us what causes what.  Which is to say, it was a  cool math game, not much more.  That said, Denise pulls some "fun" correlations from the "study':

Lo and behold, the researchers help us answer that very question. In a table too unwieldy to capture in a screenshot, they list the incidence rate ratios (age-adjusted) for all cardiovascular disease diagnoses, based on a variety of characteristics unrelated to food:

• Being a current smoker (versus no smoking history): 2.78 — a 178% risk increase
• Having a body mass index in the “obese” range (versus in the normal range): 2.48 — a 148% risk increase
• Having a body mass index in the “underweight” range (versus the normal range):2.17 — a 117% risk increase
• Having a hypertension diagnosis (versus no hypertension): 2.50 — a 150% risk increase
• Having the highest self-rated level of physical activity (versus the lowest): 0.37 — a 63% risk decrease
• Having over 13 years of education (versus 10 or less): 0.45 — a 55% risk decrease
• Being over 170 cm in height (67 inches, or 5’7″) (versus being 160 cm/63 inches or under): 0.77 — a 23% risk decrease

Compared with things like going to school for a few extra years and not being vertically challenged, the risk associated with the “low carb, high protein” diet score is minuscule!

But frankly, it hardly matters anyway. All these numbers are based on a single survey from 1991 – ’92, with absolutely no follow-up questionnaires to see if the women’s diets or lifestyles changed afterwards. This whole study rests on the assumption that 44,000 women not only accurately reported their yearly food intake in the early ’90s, but that they kept eating, exercising, and weighing the same for the next 16 years. (Or conversely, that whatever they ate in 1991 singlehandedly determined the fate of their health for the rest of their lives.)

To sum it all up…

1. This study is observational—meaning it tells us nothing about cause and effect.
2. This study relies on one food frequency questionnaire that the women filled out upon enrollment in the Women’s Lifestyle and Health Cohort. We have no idea what they were eating during the next 16 years.
3. Women reported their food intake during the early ’90s, when low-fat diets were the gold standard for healthy eating. The most health-conscious women were likely to be eating the most carbohydrate at that time.
4. Food frequency questionnaires are all sorts of terrible and don’t let anyone ever tell you otherwise.
5. The study’s “diet score” design assumes that all low-carbohydrate diets are necessarily high in protein—resulting in a point-assigning system that doesn’t always identify true low carbers.
6. The women with the lowest carbohydrate intake in this study were still eating up to 123 grams of it a day (an amount that’s probably wildly underestimated, to boot)—meaning they weren’t actually eating a low-carbohydrate diet.
7. The true increase in cardiovascular disease risk from scoring high on the “low carb, high protein” scale is pretty minor—and pales in comparison to other lifestyle variables.

That’s it! 

http://rawfoodsos.com/2012/07/01/bad-science-strikes-again/#more-2329   
I really enjoy Denise's sense of humor, and if you are a food science geek like me, I highly recommend you read the entire post.

Here's another digestion of the study.  The author makes a bunch of good points, just one of which has to do with identification of this variable:
But let's for a moment pretend that the data was in fact accurate and that you could fairly extrapolate that your style of eating today will remain the same for the next 15 years. My next question would be do you think the quality of your diet's various proteins, carbohydrates and fats might have a bearing on your risk of developing cardiovascular disease over the next 15 years? Would eating a diet higher in trans-fats confer a different degree of risk than a diet higher in unsaturated fats? Would eating a diet rich in whole grains confer a different risk than a diet rich in ultra processed pulverized flours? How about if you ate out regularly versus cooked from scratch? Deep fried versus baked? Sausages versus salmon? Quinoa versus white rice? Kale versus potatoes?  Of course it would matter, and thats a fact that I'd bet even a straw poll of 10 year olds would agree with.

One of the factors in the study is simply goofy, but it is a mistake often made by those who fear low carb but do not understand low carb diets.  The mistake is thinking of low carb as "high protein."  It is quite difficult to eat a truly high protein diet, because most of the ways a human can down a lot of protein require that a human also eat fat.  Also, truly high protein diets are not the best weight loss diets, as they preclude ketogenic metabolism; the gluco-neogenesis associated with protein intake interrupts ketogenesis.
It always makes me wonder - why does anyone fund studies like this?  There are good intervention studies that show a better result in the short term for carb restriction.  There is no possible factor yet identified that could account for why eating low carb short term might be good but that would make it bad for the long term.  There have already been plenty of observational studies that show all kinds of correlations.  All that's left is to fund good, long term, intervention studies.  Expensive?  Yes, expensive as all get out.  But the cost benefit of another cleverly designed observational study is zero.  Just stop it folks.
The other thing I wonder is - why do folks publish these mis-informative articles?  Easy news?  No one understands even the basics of the scientific method?  There are many reasons, none very satisfying.
In summary, I don't think the Swedish ladies in question were killed by their "high protein low carb" diets.
Eat meat, eggs, vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.  If you are lean, feel good, perform well, have little hunger, and demonstrate good glycemic control, you'd be crazy to let studies like this deter you.

Hero WOD: Tumilson

8 rounds for time of: Run 200 meters 11 Dumbbell burpee deadlifts, 60 pound dumbbells


U.S. Navy Special Warfare Operator Petty Officer 1st Class (SEAL/Enlisted Surface Warfare Specialist) Jon "JT" Thomas Tumilson, 35, of Rockford, Iowa, assigned to an East Coast-based Naval Special Warfare unit, died on August 6, 2011, in Wardak province, Afghanistan, of wounds suffered when his helicopter crashed. He is survived by his parents George and Kathy Tumilson, Joy and Scott McMeekan, sisters Kristie and Joy, and his dog Hawkeye.
HT:  www.crossfit.com






Fair winds and following seas on your journey warrior!

"What Really Makes Us Fat"

The calorie-is-a-calorie notion dates to 1878, when the great German nutritionist Max Rubner established what he called the isodynamic law.

It was applied to obesity in the early 1900s by another German — Carl Von Noorden, who was of two minds on the subject. One of his theories suggested that common obesity was all about calories in minus calories out; another, that it was about how the body partitions those calories, either for energy or into storage.

This has been the core of the controversy ever since, and it’s never gone away. If obesity is a fuel-partitioning problem — a fat-storage defect — then the trigger becomes not the quantity of food available but the quality. Now carbohydrates in the diet become the prime suspects, especially refined and easily digestible carbohydrates (foods that have what’s called a high glycemic index) and sugars.

UNTIL the 1960s, carbohydrates were indeed considered a likely suspect in obesity: “Every woman knows that carbohydrate is fattening,” as two British dietitians began a 1963 British Journal of Nutrition article.

http://www.nytimes.com/2012/07/01/opinion/sunday/what-really-makes-us-fat.html?_r=1&src=me&ref=general

In this article, Gary Taubes goes into what the study I cited in this post - Limits of the JAMA "Metabolic Advantage" Study - did that was unique, and puts it in the historical perspective of scientific investigation into obesity that very few others could.

Read it.  

I'm hopeful that I can finish my critique of AC's criticism of the study; if you don't know AC yet, it'll be fun to meet him.  He's a crossbreed between banty rooster and a bone gnawing terrier.

Limits of the JAMA "Metabolic Advantage" Study

Based on the study discussed yesterday, it's worth weighing in on the limits for even a study as good as that one.  First, the weight maintenance portion of the test only covered 1 month.  That's barely long enough for people to adapt to low carb intake - meaning, it generally takes 1-3 weeks to regain the quantity of enzymes needed at the cellular level to allow fat burning in the absense of excess carbohydrate.  Maintaining the stores of catalysts at the cellular level seems to be a "use it or lose it" function like most in the human body - if you over-eat carbs all the time, you are in a chronic state requiring priority sugar disposal.  Part of that is accomplished as the cells of the body burn sugar in priority before using fatty acids.  In short, if you seldom run on fat, you lose the ability for a day's worth of running on fat. 

As an aside, I'm thinking this might be a problem for fat loss.

So, there's a possibility that the metabolic advantage that was shown over a month of low carb consumption might not be as significant if the subjects continued their low carb eating for longer periods.  I'll bet the body adapts and regains some efficiency in burning/using fat over time - meaning the metabolic advantage may have limited period of effectiveness.  If so, that's still better than being the person who's continuously bombing their metabolism with excess carbs/sugars. 

It would be interesting see what the numbers would say about the low carb intake and "metabolic advantage" over the course of a year long test.  I think it's also worth exploring whether those who are tall and thin - ectomorphs - respond differently to the MA of very low carb than do endomorphs and mesomorphs.  Ever notice that all the Biggest Loser contestants have very generous pelvic girdles?  In other words, to get Biggest Loser large, you have to start with a "large base."  This fits a generally observed pattern you are likely to recognize if you think about it - the endomorphs put on fat all over, and the ectomorphs put on fat, if at all, only on the belly.  Endomorphs have a generous helping of subcutaneous fat, ectomorphs very little.  It could be said that ectomorphs have fat averse metabolism, and endomorphs have fat loving metabolism.  If you look at the charts in the JAMA study, there is considerable variation in the individual responses to the diets.  On average, the low carb folks enjoyed a large benefit in "metabolic efficiency."  But individuals saw higher or lower result - based on their body types?  I'd like to know.  I'll be the ectomorphs benefitted less from the low carb approach.

What does all that mean in practical effect?  Almost nothing to you dear reader.  All you need to know is whether some degree of carb restriction can be made to help you reach your health and appearance and performance goals.  If your body has piled on a lot of excess fat, low carb is likely to be a great benefit.

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.
http://www.usatoday.com/news/health/story/2012-06-27/calories-low-carb-weight-loss/55843134/1

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:
http://jama.jamanetwork.com/article.aspx?articleid=1199154

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:

The Art and Science of Low Carbohydrate Liv...

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.

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).

http://eatingacademy.com/how-low-carb-diet-reduced-my-risk-of-heart-disease

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.