Saturday, March 31, 2012

Spark on Taubes/Guyanet

I would argue that the rapidly growing health problem is not simply obesity, but metabolic syndrome (remember obesity is only one symptom, and there are thin people with metabolic syndrome too). We want to understand both how we arrive at metabolic syndrome (so our children can avoid it), and also how to treat it for those who did not avoid it. It is clear "carbohydrates" across the board are not causal in the development of metabolic syndrome. Stephan provides several counter-examples; another is the Tarahumara, who like the old-school Pima subsist largely on corn, beans, and squash, but who have one of the lowest rates of Type 2 diabetes in the world.
But the cure is not necessarily the reverse of the cause when it comes to disease. Metabolic syndrome brings a whole host of issues, not the least of which is broken carbohydrate metabolism. So while carbs in general may not lead to metabolic syndrome, once you've arrived dumping carbohydrates on your broken carbohydrate metabolism is tantamount to doing jumping jacks on two broken legs. I believe the science (along with a massive stack of anecdotal evidence) is pretty clear here, in that the most successful treatment for metabolic syndrome is carbohydrate restriction.

I've enjoyed this reconciliation of the work done by Taubes and Guyanet, along with what I heard from Matt Lalond on a recent Jimmy Moore podcast (well worth listening to). 

In short, the author posits that they may both be right, and wrong.  That is to say, carb restriction may be the only and best treatment for those with metabolic syndrome and it's manifestation as the "pot belly" which is so closely associated with non-alcoholic fatty liver disorder.  That does not mean that we should conclude that carbs are bad for everyone at every time. 

More from the pithy Spark:  "It is important to remember that carbohydrate restriction is successful as a treatment for a disease, but it doesn't necessarily follow that all carbs are bad for everybody."

However, even Spark is willing to bite on the problems associated with, in particular, modern wheat.  Which is to say, as regards wheat, just say no.

I have begun to form a concept of how Guyanet and Taubes may be right, with Guyanet's work applying more to how the metabolic system "should" work for healthy folks.  I have wondered, for example, how some folks can run well and perform well on well under 10% body fat, and others need more.  There are too many variables to be certain of any one answer - variables such as macronutrient ratios, genetics, type of exercise, prior metabolic injury, climate, exposure to cold water, and micronutrient intake to name just a few.  But one model that seems useful is simply that the body adapts to what is demanded of it - so if one demands that one's body run on fat, the body might become more adept at giving up fat for fuel at every lower body fat levels.  In other words, if you run well at 15% body fat, that means the body is at least capable of liberating the body fat you need - amount X per minute - to feed your cells in the event you don't have carbs for several hours.  If you stay in that state - a carb fast so to speak - for longer, you may be successful in getting your body to the point that it can liberate 1.1X per minute.  Etcetera.  And I could very easily see that the "ponderostat" powered by leptin as posited by Guyanet and his mentors might have a role in that process. 

But, what do you do if you have glucose regulation issues?  What do you do if you have the signs and symptoms of metabolic syndrome (big belly and one or more of:  high average glucose, hypertension, dislipidemia)?  Restrict your carb intake, please, since it is the fastest way to right the wrongs you've put your body through (and pay particularly close attention to reducing fructose intake to a MAX of 15g/day).

If you want to fool around with Guyanet's "plain food" ideas after that - low fat, low salt, low sugar - be my guest!  For my money, I can manage eating high fat and high salt just fine, it's the sugars that buggar my appetite, metabolism and health.

Friday, March 30, 2012

Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)–Germany study

Background: Early studies suggested that coffee consumption may increase the risk of chronic disease.
Objective: We investigated prospectively the association between coffee consumption and the risk of chronic diseases, including type 2 diabetes (T2D), myocardial infarction (MI), stroke, and cancer.
Design: We used data from 42,659 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC)–Germany study. Coffee consumption was assessed by self-administered food-frequency questionnaire at baseline, and data on medically verified incident chronic diseases were collected by active and passive follow-up procedures. HRs and 95% CIs were calculated with multivariate Cox regression models and compared by competing risk analysis.
Results: During 8.9 y of follow-up, we observed 1432 cases of T2D, 394 of MI, 310 of stroke, and 1801 of cancer as first qualifying events. Caffeinated (HR: 0.94; 95% CI: 0.84, 1.05) or decaffeinated (HR: 1.05; 95% CI: 0.84, 1.31) coffee consumption (≥4 cups/d compared with <1 cup/d; 1 cup was defined as 150 mL) was not associated with the overall risk of chronic disease. A lower risk of T2D was associated with caffeinated (HR: 0.77; 95% CI: 0.63, 0.94; P-trend 0.009) and decaffeinated (HR: 0.70; 95% CI: 0.46, 1.06; P-trend: 0.043) coffee consumption (≥4 cups/d compared with <1 cup/d), but cardiovascular disease and cancer risk were not. The competing risk analysis showed no significant differences between the risk associations of individual diseases.
Conclusion: Our findings suggest that coffee consumption does not increase the risk of chronic disease, but it may be linked to a lower risk of T2D.

By the Paleolithic Model, one would have to conclude that sucking down pots full of coffee is bound to cause trouble at some point.  But I'm not ready to cross that bridge - yet.  So I drink quite a lot and even if I cut back by half, it still might be "too much."  That said, the conclusion is comforting.  One day I will tackle the coffee cutback campaign because I think I'll feel better when I do.

Today, it's my birthday (48th) and I'm drinking all the coffee I want, and will relish a cheesecake later today also!

Thursday, March 29, 2012

Big Kill, Not Big Chill, Finished Off Giant Kangaroos: Scientific American

So, uh, I guess this means The Matrix was right, we are like a virus.

Interesting to see how they teased apart the sequence of events to try and determine what caused what.

Wednesday, March 28, 2012

Minger via Sisson on the Red Meat Scourge

We’re already 74 days into the new year, which can only mean one thing: it’s high time for our latest episode of Science Says Meat Will Kill You, complete with a brand new study and commercial-free viral media coverage! Have a seat and tune in (or at least set your DVR for later viewing).
If you haven’t had at least one family member, coworker, or soon-to-be-unfriended Facebook acquaintance send you this study as a reminder that you’re killing yourself, you’re either really lucky or your inbox is broken. Thanks to an observational study called Red Meat Consumption and Mortality freshly pressed in the Archives of Internal Medicine, a slew of bold headlines exploded across every conceivable media outlet this week:
Media sensationalism aside, the study does seem to spell trouble for proud omnivores. Unlike some similar publications we’ve seen on meat and mortality, this one says that red meat doesn’t just make you die of heart disease and cancer; it makes you die of everything.
Read more:

Read on at Mark's Daily Apple" if you have not had your fill yet of epidemiological beat down.  I like Minger's style!

Those numbers thrown around in the fear-mongering news clips—20% increased risk of death from all causes for processed meat and 13% increased risk of death from all causes for unprocessed meat—are classic examples of how even the most ho-hum findings can sound dramatic if you spin them the right way (and remember to attribute them to Hahhh-vard). If your risk of dying from a particular disease is 5% to start with, a “20% increased risk” only bumps you up to 6% in the grand scheme of things. That’s a lot less scary. Especially when delectable foods are involved.

Tuesday, March 27, 2012

Epidemiology 101

The figure is pretty self-explanatory, so let me get to the part where nutrition science is making the biggest mistakes: “Conduct an experiment.”  There is no shortage of observations, questions, or hypotheses in the nutrition science world – so we’re doing well on that front.  It’s that peskyexperiment part we’re getting hung up on.   Without doing controlled experiments it is not possible to distinguish the relationship between cause and effect.  [Just a heads up – this is going to be a recurring theme this week.]

In response to the "red meat is killing you" study which has received so much press, Attia makes the case for why observational/epidemiological studies can't tell us "what causes what."  

A gritty summary:
I trust by now you have a better understanding of why the “science” of nutrition is so bankrupt.  It is based on almost a complete reliance on these observational studies. Virtually every piece of nutritional dogma we suffer from today stems from – you guessed it – an observational study.   Whether it’s Ancel Keys’ observations and correlations of saturated fat intake and heart disease in his famous Seven Countries Study, which “proved” saturated fat is harmful or Denis Burkitt’s observation that people in Africa ate more fiber than people in England and had less colon cancer “proving” that eating fiber is the key to preventing colon cancer, virtually all of the nutritional dogma we are exposed to has not actually been scientifically tested.   Perhaps the most influential current example of observational epidemiology is the work of T. Colin Campbell, lead author ofThe China Study, which claims, “the science is clear” and “the results are unmistakable.”  Really?  Not if you define science the way scientists do.  This doesn’t mean Colin Campbell is wrong (though I wholeheartedly believe he is wrong on about 75% of what he says based on current data).  It means he has not done any real science to advance the discussion and hypotheses he espouses.  If you want to read the most remarkable and detailed critiques of this work, please look no further than here (Denise Minger) and here (Michael Eades).

Monday, March 26, 2012

Epidemiology: Killing Thousands With Science

This latest variation does come with a caveat, however, which could have been made at any point in this history. While it is easy to find authority figures in medicine and public health who will argue that today’s version of H.R.T. wisdom is assuredly the correct one, it’s equally easy to find authorities who will say that surely we don’t know. The one thing on which they will all agree is that the kind of experimental trial necessary to determine the truth would be excessively expensive and time-consuming and so will almost assuredly never happen. Meanwhile, the question of how many women may have died prematurely or suffered strokes or breast cancer because they were taking a pill that their physicians had prescribed to protect them against heart disease lingers unanswered. A reasonable estimate would be tens of thousands.

Does this mean I hate epidemiologists?  No.  Does it mean I think that epidemiologists and the entire medical profession that began selling these "killer" pharmaceutical products hate women and wanted to profit by injuring their health?  No.  It also does not mean that I think there's no role for their work.  I'm also not convinced anyone should care what I think, but what I think is that if you happen to be a highly paid, influential epidemiologist, you can only remain one if you get funding and do studies.  And even if the studies you do are not needed, you will do them.  And having done them, it's not likely that you will then say to the clueless "reporters" (aka those employed by the profit seeking publishers who need a story, dammit, any story) "You know, it's actually not possible to determine causality from this study, and it was really just a waste of time and money, but I sure enjoy these things, it's what I'm good at."

Although, this one sort of did:
Richard Peto, professor of medical statistics and epidemiology at Oxford University, phrases the nature of the conflict this way: “Epidemiology is so beautiful and provides such an important perspective on human life and death, but an incredible amount of rubbish is published,” by which he means the results of observational studies that appear daily in the news media and often become the basis of public-health recommendations about what we should or should not do to promote our continued good health.

In short, it's the misrepresentation that I hate.  Epidemiologists should admit the limitations of their work (as Peto did/does).  Reporters are great, but we should all just call them what they are - information entertainers, hustling for a buck like the rest of us.  Likewise, I'm all good with the "media" being for profit and behaving however they legally can to make a buck - but shame on us for ever thinking they were anything but that.  I remember announcing to a casual lunch conversation the obvious - ""News Company X" is owned by General Electric, and its purpose is to make a profit." The stunned stares followed, and even one awesomely naive person said "You ARE a cynic!"  No, I have the totally unremarkable ability to recognize the blatantly obvious.  For an inexplicable reason, many of our fellow citizens look at the news and believe the claims they make about themselves that they have more than an accidental relationship to truth.  This is as strange to me as believing General Mills' claims that their foods are "healthy".

So when the epidemiologist looks earnestly at the reporter and says "the data say red meat is killing you" take it for what it is worth.  And if you leave all the red meat for me, thank you.

Sunday, March 25, 2012

Wolf River CrossFit

Presenting my training on the Paleo Model at Wolf River CrossFit in a couple hours - can't wait!  It's the best one yet.

Tuesday, March 20, 2012

Lose the Belly

In the six-month weight-loss study, Hopkins researchers found that the more belly fat the participants lost, the better their arteries were able to expand when needed, allowing more blood to flow more freely. The researchers also found that participants in the study who were on a low-carb diet lost about ten pounds more, on average, than those who were on a low-fat diet. Being overweight increases the risk of cardiovascular disease, especially if the fat is accumulated in the belly above the waist.
“After six months, those who were on the low-carb diet lost an average of 28.9 pounds versus 18.7 pounds among those on the low-fat diet,”

There's not much uncertainty that belly fat is an indicator of poor health.  Losing belly fat is good, no matter how.  The question resolves to - what's the easiest way to lose belly fat?  For most, it is by carb restriction, expecially in the beginning. 

However, it gets even better.  Carb restriction reduces kidney injury resulting from chronicly excess carb intake and the resulting hyperinsulinemia.  Carb restriction rapidly reverses sodium retention at the kidney, and uric acid retention as well.  It speedily reduces non-alcoholic fatty liver disease.  It reduces systemic inflammation resulting from the insulin cascade.  It allows for adequate protein and fat intake, preventing or significantly delaying the metabolic slowing that occurs with low carb, low cal (aka, "starvation response").  Carb restriction with decent food quality (IOW, not too much food substitution with pre-packaged foods like bars, shakes, and such) also provides good regulation of lipids - decreased triglycerides, increasing HDL, and production of fewer small, dense LDL. 

Add some magnesium to replace what you should be getting from unfiltered water, make sure you get enough protein from sources which used to have a face and a mother (60g/day MINIMUM), ditch the vegetable oils, and "it's all good."

Monday, March 19, 2012

Heart Disease Models Old and New

I was asked to expound upon the linked article from this post:

 One model for the description of this doctor goes like this.

High carb intake results in high blood glucose which requires high insulin levels to defend the body from “acute glucose toxicity.” High polyunsaturated fat (PUFA) intake results in the cell walls of many cells, ...but most conspicuously LDL particle cells, being easily oxidized (PUFAs are susceptible to oxidation). So mixing the two is a devil’s brew.

First, the body is dumping insulin which has a number of effects, one of which is elevating the inflammatory state in the body. Inflammation helps fight off bugs, and helps begin the healing process by breaking down and clearing out damaged tissue after injury. Chronically high inflammation slows healing and seems to actually create damage – kind of like sending an elephant and rider to clean up a bunch of timbers, but it just keeps pulling down more trees, it never quits working.

Inflammation also accelerates oxidation – the equivalent of tissue ‘rust.’ Oxidized particles become irritating to surrounding tissues – one metaphor is that they are like glass, very useful until broken and then dangerous.

So the fad diet of the last 30 years has resulted in a nation of inflamed bodies, overfed on corn oil and soy oil and similar frankenoils produced cheaply as by products of other agricultural harvests, and sick from excessive chronic intake of carbohydrate.

The LDLs in the body do their think for a while (taking cholesterol to parts of the body that need repair) and then are taken up by LDL receptors for recycling. In a high oxidative environment, and given that the PUFAs are part of the cell walls of the LDL particles for many of us, LDLs oxidize rapidly. They become the little bits of sandpaper the doc referred to, which damage the arteries. The body attempts to repair the artery via cholesterol, forming large plaques.

Why in the coronary arteries? Hard to speculate. Size perhaps?

Bottom line – with carb restriction, you can treat gout, hypertension (80% of sufferers), dislipidemia, abdominal circumference, osteoporosis, abnormal glucose (IOW, all the correlates that describe metabolic syndrome), fatty liver disease, kidney disease, etc. In a way, the “why” doesn’t matter. If you go beyond carb restriction to add a few and delete a few more things from the diet, it gets better – treating hair loss, tooth decay, MS, acne, and more. 

Specific deep dig on the oxidation/LDL model at, in the Chris Masterjohn podcasts.  See More

Saturday, March 17, 2012

Paleo Pop

The Paleo diet refers to what Paleolithic (or Stone Age) people were eating roughly 10,000 to 50,000 years ago. In those days, people hunted for meat, sometimes fished, and gathered a lot of vegetables. They did not eat any grains, processed fats, or sugars (other than occasional honey, which was difficult and painful to obtain). In other words, no one stuffed themselves on breads, pastas, pizzas, muffins, bagels, soft drinks, fries, or desserts.

Nice summary of the concepts, but it reminds me of all of the arguments over details of a "good" paleo diet.  Some get crazy about dairy, some about salt, some about fat.  I eat all of that and do as well as I ever could have imagined.  Robb Wolf and other recommend 30 days of strict paleo, followed by testing via re-inroduction how you react to potentially problematic foods like dairy, wheat or possibly nightshades.  It's a common sense solution, but hard to implement.

Friday, March 16, 2012

FOTG: The Mission

Saw this quote on the web today regarding a large observational study that showed a correlation between higher red meat consumption and some kind of cancer:
"I am tired of hearing this shxx ... eat red meat ... don't eat red meat ... die of cancer ... die of cardiovascular disease .... it is tiring to try and eat a healthy life style when everyone has a study that suggests you will die quicker if you do this or that ... this can really get exhausting".

This person's attitude embodies the mission of this blog.  This blog is successful if it helps people find an answer to the dilemna this writer illustrates.

If you are at this point, let me offer these thoughts on how to move ahead.

I see two outcomes as a result of folks that get to the point of frustration illustrated by this person's post.

One - they quit trying to figure it out and eat whatever they want to eat.  If everything's bad, everything is just as good as anything.

Two - folks adapt a position.  "If you don't stand for something, you're going to fall for anything."  So folks believe "something", because that is better than admitting they don't know, and being subject to doubt, confusion, and the ping ponging of information on the info highway.

The following discussion will offer you a "position" to test, and criteria by which you can test it.

The question:  What is a good diet?  How can I tell if a diet is good for me or not?

The BLUF:  You will gain and maintain glycemic control on a good diet.  If you don't have stable, healthy blood sugar, you don't have health.
*You sleep better on a better diet.  Why?  Stable blood sugar to feed the brain.
*You will have well regulated hunger on a good diet, meaning, you will feel hungry only when you are truly deficient in some nutrient.  By contrast, no matter how much you eat, you will routinely feel hungry on a bad diet.  Why?  Poor blood sugar regulation drives hunger via reactionary hypoglycemia.
*On a good diet, your fasting lipid profile will normalize - HDLs will rise to normal or good, LDLs will rise (but the ratio of total cholesterol to LDLcholesterol will be well under four), triglycerides will fall to under 100.  Why?  The necessity of dealing with excess blood sugar results in the liver producing too many triglycerides and VLDLs.  VLDLs become small, dense (dangerous, easily oxidized) LDL.
*With a good diet, your abdomen will get smaller by establishing glycemic control, which results in a normal appetite, and better fat burning throughout the body.
*A good diet will not make you hypertensive; about 80% of those with high blood pressure can stop taking their meds with carb restriction.  A good diet will also regulate uric acid levels, preventing gout.
*A good diet will lower inflammation levels, allowing you to take fewer pain meds, at lower doses; I was able to drop from 2400mg/day of ibuprophen to only an occasional 200-400mg dose.
*A good diet supports normal human ability to concentrate.  Blood sugar spikes/dips will leave you feeling lethargic, irritable, hungry and unfocused.
*I good diet will support feeling good.  A high sugar/high carb diet, especially in combination with other inflammation producing foods (omega 6 laden "vegetable oils"), creates a chronically high inflammatory state that may lead directly to depression by interfering with serotonin management loops.
*A good diet will result in good "energy levels".  If you are eating such that your blood sugar levels fluctuate, a source of quickly absorbed sugar will give you an "energy" boost.  Of course, those so called energy drinks will also reinforce, rather than helping to break, your cycles of fluctuating blood sugar, and the bigger question is "why do you need exogenous sugar for energy?".  The answer:  a bad diet.

The most unhealthy population is that group which suffers from uncontrolled blood sugars, which is to say, diabetics.  These people age and die about ten years faster than non-diabetics.  They die at greater rates from virtually every affliction we fear - cancers and vascular diseases and the rest.  That fact makes perfect sense.  Glycemic control is the second most critical metabolic function for life  (the most critical metabolic function is respiration), because the brain runs primarily on glucose, and having either too much, or too little, is an emergency.  Just as you would destroy much of the contents of a house with a high pressure water house in order to "save" the house from a fire, it appears that the body does the same thing when defending the brain and nervous system from chronic over-dosing of high blood glucose.

Preventative medicine must begin with the issue of glycemic control, and without glycemic control, there's little reason to think you can be "healthy." 

In summary, the premise is thus:  glycemic control is the entering argument for health.
Supporting evidence: every known health marker improves with improved glycemic control; many disease correlates can be treated effectively simply by restricting carbohydrate intake in order to restore glycemic control.

Highlights from my N=1 experiment:  I tested my glucose off and on for 30 days; predictably 85 ng/dl or below regardless of pre-post meal time.  Multiple health factors improved, body composition sustained at ~10% body fat, physical performance has never been better, my doctor tells me "I don't know what you are doing but keep doing it."  This experiment has been a 16 year effort.

At this point, one must ask "what if I'm wrong."  The point of science, the reason we revere it is that humans are notoriously bad at discovering truth.  Science provides a methodology which allows one to identify truth.  The science of diet, after a 100 years of trying, is dodgy (that's a technical term) - at best.  There's absolutely no proof of what is or is not causing disease.  There's a good reason for that - it's remarkably expensive to conduct the intervention studies that would be necessary to discover the answer to the question of what diet is best.  Most likely, there is no one "diet" that is best, because some folks tolerate a fair amount of carbohydrate intake and maintain glycemic control, whereas some tolerate much, much less.  Your N=1 test - you experiment to find out what diet is best for you - is literally the best that science has to offer.

And still, you may be wrong.  Even if your search finds a diet that gives you a good number for every health marker at your disposal, you may still die of cancer.  Which is exactly why "a good diet" is defined by outcomes such as looking, feeling, and performing well.  In other words - if you live to 100 but feel like death warmed over, did you win or lose?

You don't get to have certainty about how long you live.  You can have a good, good shot at enjoying the days you do have if you eat ... a good diet.

I've made my bet based on the paleolithic model of nutrition - eat meat and vegetables, nuts and seeds, little fruit or starch, no sugar/wheat.  I enjoy the food, I love how healthy and lean I feel, and I don't think there's any other formula that better enables a vigourous, active life.  My health markers are the envy of my doctor.  If I cash out early but enjoy every day until then, so be it.

If you are ready to make a change in how you feel, in your health, in your mental and physical performance, and want assistance, call me!  Or come to my next presentation, held at Wolf River CrossFit, more information here.
(Edits for style 16 March 12)

CO2 ... Makes You Fat?

Interesting study, but the only takeaways are: 
-move to the mountains or exercise to help "off gas" excess CO2

Therein lies a highly probably answer to whether or not this is a real phenomenon - we already know that in the majority of studies that have been done, exercise is not shown to be a contributor to fat loss.

In any event, aside from exercise, which you should do because it increases your quality of life in numerous ways, and moving to the mountains - we already know that carb restriction is a very powerful weight loss and health strategy.  I'm not that excited to find that "excess" CO2 may contribute. 

Thursday, March 15, 2012

Science of Human Health - It Is Not Rocket Science

The BLUF:  When prospective/epidemiological studies are used to establish causative relationships, they are no longer scientific, they become editorial.  The fact that most of the science of human health is bad science leads many to accept as evidence science which should be considered interesting at best.

Zoe does a brilliant job of showing why this is true, using the data in this study.

Here's a choice cut from her study:
- The two studies combined, therefore, covered 2,958,416 person years and there were 23,926 deaths in total: 5,910 attributed to CVD and 9,464 to cancer.
The first point to make, therefore, is that the overall death rate was very small:
- In the HPFS, in 758,524 person years the overall death rate was 1.18% and the CVD death rate was 0.36% and the cancer death rate was 0.41%. Over a 22 year period, just over one in a hundred members of the study died.
- In the NHS, in 2,199,892 person years the overall death rate was 0.68% and the CVD death rate was 0.15% and the cancer death rate was 0.29%. Over a 28 year period, approximately one out of 150 members of the study died.
- In the two studies combined, in 2,958,416 person years the overall death rate was 0.81% and the CVD death rate was 0.2% and the cancer death rate was 0.32%. In the combined studies, fewer than one person in one hundred died in a 28 year period.

Does this scare you as much as the headline would have?  Me neither.  Lies, damned lies, and statistics.  I encourage you to read the entire article to put your mind at ease about the supposed risks to you and your loved ones.

Here's another of Zoe's great points:
This is what led to the big news story: “adding an extra portion of unprocessed red meat to someone’s daily diet would increase the risk of death by 13%. The figures for processed meat were higher, 20% for overall mortality…”

But what Zoe highlights well in her analysis is that the authors are doing a bunch of fancy math and then guessing.  They guess some corrective factors for other assumed risk factors.  Are their assessments of the other "risk factors" correct?  Yes, and if you don't believe them, well, just ask the authors. 

I'll admit I don't understand this kind of statisitical analysis, but I know this - they are assuming and guessing.  That is what you do to explore conjecture, and to determine what might be done to refine or test a conjecture.  Guessing is not the means by which to establish causality.  Therefore, all that language of "risk" that you see in all of these types of studies (prospective observational studies) is a code word that means "our mathematical games, if correct, predict an outcome that we don't know to be true."  Frankly, if the answer were known, these types of studies would be even "more useless" than they are. 

I have a confession.  I don't really care if you choose not to eat meat.  If you make that choice, to some degree it may lower the price that I pay for meat - the exception being that if you choose to eat grass fed animals, the economies of scale may at some point tip the economics towards better pricing for same.  But I would be sad if, even though you love red meat, you choose not to eat it because you believe these near ludicrous guesses about mortality. 

When you see words like "linked", "associated with" and "risk factors", you are reading the language of statistical gaming.  Make some guesses, re-run the numbers, and "wow, that looks interesting."  If I was an epidemiologist, and I could get a paying gig running numbers like this, I would love it.  Hopefully, though, I would not pretend that the numbers mean what these folks take the numbers to mean.

Human science is nearly impossible to do well, it is much, much harder than rocket science.  That does not mean we should pretend that bad science, isn't.

Sunday, March 11, 2012

Ship Is Still Turning

These recommendations are no longer scientifically or morally defensible. The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated.

The long-established dietary recommendations have created epidemics of obesity and diabetes, the consequences of which dwarf any historical plague in terms of mortality, human suffering and dire economic consequences.

Despite the fact that 25% of the population takes expensive statin medications and despite the fact we have reduced the fat content of our diets, more Americans will die this year of heart disease than ever before.

Friday, March 9, 2012

Paleo v. "Mediterranean" Diet

A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease.
This study can be accessed at:

After 12 weeks the study found:
(a) Those on the old stone age diet lost 31% more weight compared to those on the Mediterranean-like diet.
(b) Those on the old stone age diet lowered their unhealthy high fasting glucose levels 88% more than those on the Mediterranean-like diet.
(c) Those on the old stone age diet lowered their unhealthy high HbA1c levels 4.3% more than those on the Mediterranean-like diet.

The "Mediterranean-like diet" bites the dust again.  Which isn't to say it is a bad diet if it works for you.  But most of the hoopla about the so called Mediterranean diet isn't based on half as much science as some folks would like you to think.

Thursday, March 8, 2012

Coconut Oil, Proven Healthy

In a study published in 1981, the populations of two South Pacific islands were examined over a period of time starting in the 1960s, before western foods were prevalent in the diets of either culture. The study was designed to investigate the relative effects of saturated fat and dietary cholesterol in determining serum cholesterol levels. Coconuts were practically a staple in the diets, with up to 60% of their caloric intake coming from the saturated fat of coconut oil. The study found very healthy people who were relatively free from the modern diseases of western cultures, including obesity and heart disease. Their conclusion: “Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations.”1

This isn't exactly new news - but it still may surprise some.  Eat your coconut oils and other saturated fats if you like them.  Nuff said.  

Wednesday, March 7, 2012

High Fat For Type I

The diets comprised of:
(i) 45% carbohydrate, 34% fat, 32 grams fibre per day (higher carbohydrate diet).
(ii) 38% carbohydrate, 43% fat, 20 grams fibre per day (higher fat diet).
After 4 months, HbA1c levels were 1.8% higher in those on the higher carbohydrate diet compared to those on the higher fat diet.
This study reveals that a higher fat diet enables better blood sugar control than a higher carbohydrate diet in type I diabetics.

I wonder how many people's mind will be changed by the facts.  This isn't a remarkably low carb diet, I look forward to seeing the next level of research in this arena.

Friday, March 2, 2012

Eat Fat To Lower Fat Levels

This guy is a potent analyst, and I enjoyed this reminder of what would be considered a paradox for those steeped in the low fat, high carb diet of the last 30 years:  fat content in your blood increases as you increase the carbohydrate intake in your diet.

Why this happens:
1.  Those eating chronically high levels of carbs lose the ability to process fat as fuel (stores of the requisite enzymes fall within the cells that should be able to burn fat).
2.  Excessive carb intake requires that the liver convert blood glucose into triglycerides (three fatty acids bound together with a type of sugar); these are delivered to VLDL and are shunted around the body in the blood stream.
3.  The liver also turns some of the excess glucose into palmitic acid, a saturated fatty acid which some say is a factor in leptin resistance.
4.  In conditions of excess blood glucose, most cells preferentially burn glucose for fuel as a defensive measure - as this glucose is burned off, more can be taken in by the cells, helping to prevent glucose toxicity.

In short, in a person taking in excess sugars, whether that be from bread, sugar, high fructose corn syrup, or fruit juice, there's an entire chain of downstream effects that generates fatty acids in the blood and then prevents the body from using those fatty acids for fuel. 

This is why a predictable result of carb restriction, starting at 150g/day and increasing as carbs are restricted further, is decreased levels of fatty acids and triglycerides in the blood.  The lipid profile of high triglycerides, low HDL, and high LDL, is being called the atherogenic profile.  You should expect, following carb restriction, to see triglycerides under 100, HDL greater than 50, and LDL should increase or stay the same (beware - LDL numbers for folks on very low carb diets are not accurate - the cheap way to measure cholesterol involves a formula which does not require measurement of the actual number of LDL particles and their cholesterol.  This formula is inaccurate for those eating low carb).   

This is also why it's neither the cholesterol, nor the lipoproteins carrying them around, that are killing you, per se, and why we can't just manipulate these numbers to improve health.  You can use pharmaceuticals to raise HDL and lower LDL, but that does not make you healthy if you are sick from eating too many carbs.  What makes you healthy is to stop eating too many carbs.  Eat meat, vegetables, nuts and seeds, little fruit/starch, no sugar/wheat.

Thursday, March 1, 2012

Exercise/Alzheimer's Link

...when the scientists examined the results for people with the e4 gene variant. Most of those who carried the APOE-e4 gene displayed much larger accumulations of amyloid plaques than those without it.
Unless they exercised. The carriers of the gene who reported walking or jogging for at least 30 minutes five times a week had plaque accumulation similar to that of volunteers who were e4-negative. In essence, the APOE-e4 gene carriers mitigated their inherited risk for developing Alzheimer’s by working out. Or, as the study authors wrote, a “physically active lifestyle may allow e4 carriers to experience brain amyloid levels equivalent to e4-negative individuals.”

This explanation squares well with the carbohydrate hypothesis of disease.  In short, excess chronic intake of glucose leaves too much sugar in the blood stream at abnormally long durations, which creates more glycated proteins, and keeps insulin degrading enzymes busy with too much insulin.  When IDEs are not working on insulin, they help to scavenge the bits of material that become amyloid plaques in Alzheimer's patients. 

So the study shows a correlation between regular exercisers and reduced incidence of Alzheimer's in those with the genetic predisposition.  The walking is likely to either be the result of someone that does not eat too much carbohydrate, or if they do, they are disciplined about other health efforts (IE, eat too many carbs because the health authorities told them to do so, and they comply with a large number of elements of a healthy lifestyle).  Or, it could just be that the consistent walking helps to regulate blood glucose levels even in those that over-carb themselves.

If this article hits close to home, have a look, it is a good read.