The subtitle of this post could just as easily have been: Feed your mitochondria right.

The two videos below pretty much tell the whole sad tale of doctors and nutrition.  Taken together, they confirm the widespread notion that doctors, in general, know very little about nutrition and seem to be proud to keep it that way.

This first video has made the rounds on the internet.  I’ve had it sent to me or recommended to me a dozen times, but I had never watched it until just a few days ago.  I was put off because of its length, which, at a little over 17 minutes, seems like an eternity in internet viewing time.  But I hope anyone reading this post doesn’t make the mistake I did and avoid watching because of the length.  It is a spectacular talk given by Dr. Terry Wahls, a female physician who was struck down by a relentlessly progressive neurodegenerative disorder.  She describes how she was able to restore her health by revamping her diet in in a way designed to properly feed her mitochondria.*  The transformation is almost unbelievable, especially considering the disease she was battling.  If you haven’t already seen this video – watch it.  I guarantee you’ll be glad you did.  And while you watch, pay careful attention to what her diet doesn’t contain much of.

Click here to view the embedded video.

After you’ve seen the above video, take a look at the one below.  It is a little over 2 minutes long and was developed to give doctors – who, for the most part, don’t give a flip about diet – advice they can pass along to their obese or overweight patients.  Watching the longer video above first will give you more context to better appreciate the one below and show you just how lame mainstream medicine can be.

This video came from Medscape, a subscription service for doctors to keep them abreast of all the latest and greatest news and updates from the world of mainstream medicine.

Click here to view the embedded video.

Pitiful, isn’t it?

Links:

The Medscape article containing this video.  (Although Medscape is a free subscription service for physicians, non-physicians can sign up as well.  For free.  Register if you would like to see the article, which is nothing more than a transcript of the video above.)  It is amazing to me that an online newsletter designed for physicians would regurgitate dietary information from a newsweekly and pass it off as serious medical information.  Especially in such a condescending and patronizing way.  The whole thing is infuriating.

The list of the 22 nutritional ‘experts’ who came up with the dietary rankings mentioned.

The US News and World Report article that inspired the video.

Power, Sex and Suicide  A pretty thorough book on mitochondrial function that is accessible to the non-scientist.  I read this book 6 or 8 years ago and learned a fair amount about mitochondrial DNA.  I had been interested in the issue of mitochondrial rehab for a while, and this book filled in some, but not all, of the blanks.  A good place to start if your interested.

Why Are Cells Powered by Proton Gradients?  Full text of a paper written by Nick Lane, the author of the above book, discussing how mitochondria work by creating an energy gradient across the inner membrane.  Accessible to non scientists.

Source of photo of mitochondria at top of post.

* Mitochondria are the little sausage-shaped organelles inside the cells that convert the energy stored in food to ATP, the energy currency of the body. I think the idea of correctly feeding mitochondria is an important one.  If your mitochondria don’t work well, you don’t work well.  I’ve got a couple of posts in the works on this subject of just what does keep the mitochondria fit and what happens when they become unfit.  And what it takes to rehab them if broken.  Based on my own pretty extensive review of the scientific literature over the past few years coupled with my clinical experience, I have a few minor quibbles with Dr. Wahls’ notions of what constitutes a perfect diet for the mitochondria, but I’ve got to say that her results speak for themselves.  I just think her diet could be even better with a little judicious tweaking.

Over a half decade ago Professor Jared Diamond, in his Pulitzer Prize-winning book Guns, Germs, and Steel, famously wrote

“The adoption of agriculture, supposedly our most decisive step toward a better life, was in many ways a catastrophe from which we have never recovered.”

Dr Diamond was referring, of course, to the devolution of human health that took place as mankind suffered the corporal transformation driven by the mismatch between hunter-gatherer genes and an agricultural diet and lifestyle. Smaller stature, decreased cortical bone thickness, obesity, increased incidence of infectious diseases, dental caries, periodontal disease, vitamin deficiencies, and even famine – all common in agriculturists – were not, for the most part, the lot of pre-agricultural man.

Humanity doubtless gained more than it lost in this hunter to farmer changeover when viewed in a big-picture sort of way.  Farming made possible larger communities filled with workers, workers who, for the first time, made specialization of labor a possibility.  And fewer people could till the fields and provide food for the many, freeing the others to pursue the arts, business, politics, and warfare.

Stephen Budiansky, author of one of my favorite books, Covenant of the Wild, describes how domestic animals formed a pact with humans in which the animals traded a period of safety and survival for their lives.  Had this covenant not been made, it is highly likely – virtually a certainty – that cows would now be extinct.  Big, slow, stupid and tasty, had they not been amenable to domestication and entered into the covenant with their domesticators, cattle would have been hunted to extinction long, long ago.  But they did – however unwillingly – make the covenant and so exist by the tens of millions today.  The deal they cut was a phenomenal deal for cattle as a species, but not a particularly good deal for the individual cow when the time comes to pay up at slaughter.

Homo sapiens entered an almost mirror image of this same covenant when they domesticated cereal grasses.*  We gave up our independence and mobility for the promise of a constant and plentiful food supply.  But, as with our covenant with domestic animals, there is a catch.  And this time it’s with us.  Humans emerged from this deal with the short end of the stick.  In the same way as did cattle, we made a good-for-humans-as-a-species/bad-for-the-individual-human trade.  Like it or not, we traded the health of the individual human for the overall good of mankind and the development of civilization.

We traded a diet based primarily on fat and protein with a little carbohydrate thrown in from roots, shoots and tubers for one centered predominantly on carbohydrate.  The main source of the carbohydrate was cereal grains, chiefly ancient forms of wheat, the predecessor of the wheat that now occupies a large part of the human diet everywhere.  Ancient forms of wheat didn’t do our forebears a lot of good, and, according to Dr. William Davis’s new book Wheat Belly, the modern forms of the grain do us even less good.

Before we get to the problems modern hybrid wheat causes us, let’s take a look at the afflictions a diet of primitive wheat visited upon our predecessors.

The ancient Egyptians consumed a diet that would be considered optimal by many people today.  Both wealthy and poor Egyptians consumed primarily bread and a type of cloudy, almost gruel-like beer.  To these staples were added a variety of vegetables (mainly onions), and a small selection of game, fish and meat.  The bread was made from coarse ground, whole grain emmer wheat, a primitive, high-protein wheat.  Sugar didn’t come on the scene until about 1000 AD, so the Egyptians used honey sparingly (it was expensive) as a sweetener along with figs.  In short, these people consumed a diet the vast majority of modern nutritionists would prescribe to people to prevent obesity, heart disease, obesity and the rest of the diseases associated with the Western diet.

But, as their mummified remains and their contemporary artwork demonstrate, the ancient Egyptians were often fat and were riddled with heart disease, dental caries, bad periodontal disease and no doubt diabetes and hypertension.  Many people have argued that since only the wealthy were mummified, the mummy data applies only to them, and since the wealthy ate more red meat, the rates of obesity, heart disease and the other disorders common to them didn’t apply to the rest of the population.  Even the common man, however, was often portrayed as obese in Egyptian artwork, and despite greater consumption of meat, the main staple of even the wealthy was bread and beer. And it didn’t do them a lot of good.

The 5,300 year old mummy of Ötzi the Iceman found in the Italian Alps showed a bad case of dental caries and periodontitis along with a stomach-full of einkorn wheat (another primitive variety). Said the researchers who examined Ötzi:

Although the Iceman did not lose a single tooth until the his death at an age of about 40 years, he had an advanced abrasion of his teeth, profound carious lesions, and a moderate to severe periodontitis.

In particular, the molars of the upper jaw showed loss of alveolar bone as a sign of periodontitis (inflammation of the ligaments and bones that support the teeth), while evidence of “mechanical trauma” was found on two teeth.

…the most surprising find is the high frequency of cavities.

These dental pathologies are a sign of change in the Neolithic diet.

We already know that he was eating grains, such as einkorn or emmer. The contained carbohydrates clearly increased the risk of developing dental diseases

One would assume these findings would be common among the rest of Ötzi’s contemporaries, who doubtless consumed a similar diet.

Sadly, these same findings are also common among modern man who consumes a more malign version of primitive wheat.

Until I read Dr. Davis’s book Wheat Belly, I didn’t really think much about wheat other than its being a major source of carbohydrate in the American diet.  It never had occurred to me that the wheat we eat today is not the same wheat of our great-grandmothers cooked with nor probably even our grandmothers.  And it really hadn’t dawned on me how pervasive wheat is in the diet.  Since reading Michael Pollen’s The Omnivore’s Dilemma I had been conscious of the amount of corn in our modern diet, but I hadn’t thought much about wheat.  As Yogi Berra supposedly said, “You can see a lot just by looking.”  So I went out and looked.  And I can tell you that we are much more Children of the Wheat than we are Children of the Corn.

In most grocery stores, an entire aisle is devoted to nothing but bread in all its forms.  Then there is typically another large aisle full of cakes, cupcakes, cookies, pies, tarts, sweet rolls, bagels, croissants, brownies, and other sweet baked goods.  The vast majority of the cereal aisle displays products containing primarily wheat.  And if you look at processed foods of all kinds, you’ll find wheat in there.  If you make or buy gravy, roux, or just about any kind of sauce, you’ll find it’s thickened with wheat flour. (MD bought some demiglace a few days ago, and noticed as she was removing it from the container that even it had added wheat.) Then there is the aisle full of different beers, many of which are made with wheat.  These are just a few of the items you can find containing wheat in a grocery store; don’t even get me started on restaurant fare.  Wheat is everywhere – corn should be so lucky.

When I was roaming around looking for pictures of dwarf wheat (more about which later), I came upon the website for the Kansas Wheat Commission that listed a few facts about wheat.  Here are several that caught my eye.

Wheat is the primary grain used in U.S. grain products.  Approximately three-quarters of all U.S. grain products are made from wheat flour.

More food is made with wheat than any other cereal grain.

U.S. Farmers grow nearly 2.4 billion bushels of wheat on 63 million acres of land.

About half the wheat grown in the United States is used domestically.

A little back-of-the-envelope calculating using the above statistics tells us that each of us in the United States consumes about four bushels of wheat per year.  Another statistic from the linked website states that each bushel of wheat makes about 90 one-pound loaves of whole wheat bread.  So, we all eat the equivalent of 360 loaves of bread per year, or approximately one loaf per person per day. That’s a lot of wheat, in fact, it’s almost approaching ancient Egyptian levels. (Moreover, since MD and I don’t eat any, that means two other people out there are each eating two loaves per day.)

It would be bad enough if we consumed all this wheat as emmer or einkhorn or other primitive varieties, but we don’t.  We get most from a hybrid of Triticum aestivum – our great grandmother’s wheat – called dwarf (or semi-dwarf) wheat, which now comprises more than 99 percent of all wheat grown worldwide.

As Dr. Davis tells it, the hybridization of wheat came about in an effort to improve yield, which is now about tenfold greater per acre than it was a century ago. Older strains of wheat were taller and more prone to damage from wind and rain.  And

When large quantities of nitrogen-rich fertilizer are applied to wheat fields, the seed head at the top of the plant grows to enormous proportions.  The top-heavy seed head, however, buckles the stalk.  Buckling kills the plant and makes harvesting problematic. A University of Minnesota-trained geneticist…is credited with developing the exceptionally high-yielding dwarf wheat that was shorter and stockier, allowing the plant to maintain erect posture and resist buckling under the large seed head.  Tall stalks are also inefficient; short stalks reach maturity more quickly, which means a shorter growing season with less fertilizer required to generate the otherwise useless stalk.

In the photos below you can see the difference between wheat grown in the Middle Ages and the dwarf wheat grown today.

Dr. Davis writes that modern wheat is approximately 70 percent carbohydrate by weight.  The carbohydrate is in the form of a starch called amylopectin A.

The most digestible form of amylopectin, amylopectin A, is the form found in wheat.  Because it is the most digestible, it is the form that most enthusiastically increases blood sugar.  This explains why, gram for gram, wheat increases blood sugar to a greater degree than, say, kidney beans or potato chips.  The amylopectin A of wheat products, “complex” or no, might be regarded as a supercarbohydrate, a form of highly digestible carbohydrate that is more efficiently converted to blood sugar than nearly all the other carbohydrate foods, simple or complex. [Italics in the original.]

But what about the much vaunted whole grains.  Won’t ‘whole grain’ bread or wheat products be better?  Not according to Dr. Davis:

…the degree of processing, from a blood sugar standpoint, makes little difference: Wheat is wheat, with various forms of processing or lack of processing, simple or complex, high-fiber or low-fiber, all generating similar high blood sugars.  Just as “boys will be boys,” amylopectin A will be amylopectin A.  In healthy, slender volunteers, two medium-sized slices of whole wheat bread increase blood sugar by 30 mg/dl (from 93 to 123 mg/dl), no different from white bread.  In people with diabetes, both white and whole grain bread increase blood sugar 70 to 120 mg/dl over starting levels.

And aside from the blood sugar and, consequently, insulin problems caused by the consumption of too much wheat, there are other problems.  As with almost any food, the newer the food, the greater the likelihood that it will be problematic to some humans who consume it.  Since dwarf wheat has been around for less than 50 years, it should come as no surprise that it does indeed cause it’s share of problems.  Dr. Davis spends the better part of his excellent book detailing many of these problems and describing his clinical experience in helping many of his patients shuck their wheat habit.  He describes the increase in celiac disease over the past 50 years and believes, as I do, that celiac disease is a continuum.  The severe form of it that is recognized as celiac disease is pretty easy to diagnose (if a doctor has sense enough to look for it), but there are milder forms that manifest themselves as anything from mysterious rashes that come and go to diarrhea and other GI disturbances to arthritic aches and pains. And we can’t forget a number of other afflictions that may well have their basis in wheat intolerance that include osteoporosis, acne (bagel face?), neurological disorders, and the creepily- dubbed ‘man boobs.’

It’s good to learn in Wheat Belly that Dr. Davis has finally shucked his bred-in-the-bone cardiologist’s antipathy toward fat in general and saturated fat specifically and has come over to what most of his peers must view as the dark (read: low-carb) side:

The fat phobia of the past forty years turned us off from foods such as eggs, sirloin, and pork because of their saturated fat content — but saturated fat was never the problem.  Carbohydrates in combination with saturated fat, however, cause measures of LDL particles to skyrocket.  The problem was carbohydrates more than saturated fat.  In fact, new studies have exonerated saturated fat as an underlying contributor to heart attack and stroke risk. [Italics in the original.]

Dr. Davis wraps up his meticulously researched book with a straightforward plan to help free the reader from the tyranny of wheat, while at the same time providing instructions for a delicious and satisfying wheat-free diet.  He furnishes an extensive list of wheat-containing foods that should be avoided and imparts his caveats about going facedown in products advertised as being gluten-free.  And best of all, he provides a short section filled with matchless wheat-free recipes for many meals that would otherwise be wheat-laden. (MD and I have tried a few of these recipes and found them to be superb.  I especially enjoy his wheat-free granola recipe even though I go a little easy on the rolled oats part of it.)

Wheat Belly hit the New York Times Bestseller list shortly after it came out (and has been there for two weeks now), which I can tell you from experience, is not an easy thing to do.  As a result (because being on the NY Times list means a book has had big sales numbers), the wheat producers have not taken their hits lying down.  They’re fighting back with full venom, because a book like this one can do them serious economic damage. Expect it to get worse. (Remember all those shelves in the grocery stores stuffed with wheat-containing products? They don’t want to see that go away.)  You can read about some of their tactics here and read Tom Naughton’s interviews with Dr. Davis here and here.

I can’t recommend this terrific book highly enough.  Wheat Belly is fully referenced and indexed (unless you somehow got the little freebee paperback review version that I received from the publisher), and is a must have for the library of any serious low-carber or anyone concerned about health.

*MD and I wrote about this domestication of humans by grains in The Protein Power LifePlan.  In that book we referenced an interesting paper by a couple of Australian researchers on the hypothesis that the addictive nature of cereal grains helping this domestication along.

Image credit: Nature Reviews Cancer

The latest newsletter from Dr. Cannell, President of the Vitamin D Council, on vitamin D and the swine flu (and influenza in general).  Well worth reading.

If you are interested in a free subscription to this newsletter, go to the Vitamin D Council site and sign up.

John Cannell, MD
Vitamin D Council Newsletter
May 16, 2009

I have received hundreds of emails from readers, asking what they should do about the possibility of an H1N1 flu pandemic.

Dear Dr. Cannell:

1.    Should I take Vitamin D to prevent the H1N1 flu?  If so, how much?

2.    What role did Vitamin D play in the 1918 pandemic?

3.    If I get this flu, should I take very high doses of vitamin D?  Is so, how much?

4.    Should I take the special flu vaccine the CDC and others are developing?

5.    What are you going to do for your family about the 2009 flu?

6.    Why do the CDC and NIH ignore the Vitamin D studies?

The Public, USA

Dear Public:

First read what I have written about influenza.  Both papers can be downloaded and printed out in their entirety:

Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E.  On the epidemiology of influenza. Virol J. 2008 Feb 25;5:29.

Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E.  Epidemic influenza and vitamin D. Epidemiol Infect. 2006 Dec;134(6):1129-40.

My short executive answers:

1)    Take enough Vitamin D3 to get your 25(OH)D level above substrate starvation levels (50 ng/ml or 125 nmol/L).  Levels of 50 ng/ml usually require at least 5,000 IU per day for adults, some adults will require more.  Children should take 1,000 IU per every 25 pounds of body weight.  After taking this dose for 3 months have a 25(OH)D level.  Individual variation in dose response is great and natural 25(OH)D levels (50-70 ng/ml) are not assured by these doses.  For reasons I will discuss below, I think it possible that Vitamin D levels of 30 ng/ml, which are often obtained by people taking low doses of Vitamin D (1,000 to 2,000 IU/day), may increase your risk of death from a 1918-like influenza virus.

2)    It is clear to me that Vitamin D did not play a controlling role in 1918.  The lethality of the 1918 virus easily overwhelmed innate immunity although I am unwilling to impair my innate immunity by taking inadequate doses of Vitamin D.

3)    Stock you homes pharmacy with several fresh bottles of 50,000 IU capsules of Vitamin D3,  a medicine, not a supplement, and if you get this flu, take 2,000 IU per kg of body weight per day for a week.  As I weigh 220 pounds, I would take 200,000 IU per day for seven days if I thought I had an infection with a 1918-like influenza virus.

4)  Get the H1N1 flu shot as soon as it is available in the fall, especially if the virus shows evidence of lethality this summer in the southern hemisphere,  For reasons I will discuss, a flu shot probably will not generate an immune response in people with 25(OH)D levels above 50 ng/ml but that is simply conjecture.  That is, the flu shot may not work, may not generate antibodies, in people with 25(OH)D levels above 50 ng/ml.  In my opinion, the risk of a lethal virus is higher than the risk of Guillain-Barré Syndrome.  In fact, the risk of Guillain-Barré Syndrome is probably the highest in non-vaccinated people who are infected with the virus and quite low in those who take a modern flu vaccine.

5)   Besides the above actions, stock up on TamiFlu in your home medicine cabinet so you have it next fall and winter.  And follow common-sense precautions, especially frequent hand washing.

6)   Most medically trained physicians, scientists or practitioners think in terms of something bad causing illness, not something good preventing it.  Ask any physician what George Bernard Shaw meant when he said, the characteristic microbe of a disease might be a symptom instead of a cause.  The idea that seasonal influenza or the common cold is a symptom, even the presence of the virus itself being a symptom of an underlying condition, is foreign to modern medical thought.  Influenza researchers at the CDC and NIH think only in terms of vaccines and anti-virals, mainly because most of them have such strong economic affiliations with some aspect of the influenza industry.  The idea of diagnosing and treating Vitamin D deficiency as one part of influenza preparedness is simply foreign to them. Unfortunately, their attitude contributes to the 36,000 deaths every year in the USA from seasonal influenza and leaves American’s innate immune system naked in facing a pandemic.

Detailed answers:

Again, for me to fully answer your questions, and for you to understand my reasoning, the first thing you need to do is to read the articles I have written about influenza.  Neither article is about pandemic influenza, rather epidemic influenza.  Both are full access articles.

Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E.  On the epidemiology of influenza. Virol J. 2008 Feb 25;5:29.

Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E.  Epidemic influenza and vitamin D. Epidemiol Infect. 2006 Dec;134(6):1129-40.

Next is to read additional papers on our website.  We have attempted to get full copies of the most important articles when possible:

Vitamin D Council/Science/Influenza

The WHO reports:

“H1N1 appears to be more contagious than seasonal influenza. The secondary attack rate of seasonal influenza ranges from 5% to 15%. Current estimates of the secondary attack rate of H1N1 range from 22% to 33%.  With the exception of the outbreak in Mexico, which is still not fully understood, the H1N1 virus tends to cause very mild illness in otherwise healthy people. Outside Mexico, nearly all cases of illness, and all deaths, have been detected in people with underlying chronic conditions.

In the two largest and best documented outbreaks to date, in Mexico and the United States, a younger age group has been affected than seen during seasonal epidemics of influenza. Though cases have been confirmed in all age groups, from infants to the elderly, the youth of patients with severe or lethal infections is a striking feature of these early outbreaks.  In terms of population vulnerability, the tendency of the H1N1 virus to cause more severe and lethal infections in people with underlying conditions is of particular concern.”

Virologists are concerned with three aspects of any influenza virus: (1) novelty, (2) transmissibility, (3) lethality.  The current H1N1 is novel, that is, we have no antibodies to this strain.  Its transmissibility is high but its lethality (percent who die after infection) is still low, except in Mexico.  Why it was so lethal in Mexico, no one knows.  Will that lethality return as the virus mutates this summer?  Keep in mind that the lethality of the 1918 flu was high, perhaps a billion people infected, a half billion became ill, and, at the most, one tenth of a billion died.  Until the 2009 virus exposes its lethality, and it may not do so until next fall or winter, we are all playing an involuntary game of Russian roulette.

Pandemics imply widespread infection thus transmissibility, but do not specify the virus’s lethality.  However, this virus was transmitted in May, near the equator, at 7,000 feet altitude.  May is the time influenza transmission usually stops because population 25(OH)D levels are rising quickly. Lethality of influenza viruses change over short periods of time (weeks to months).

That is, the WHO and CDC have no way of knowing if this virus will acquire lethality.  Lethality is how quickly this virus will bore holes in your lung cells, hijack that cells genetic machinery, burst the cell, and spew out hundreds of thousands of swarming viruses to do the same thing to the next respiratory cell, perhaps triggering a cytokine storm response by your body’s immune system that quickly strips your lungs of the cells you need to breath.

If that does not kill you within a few days, it leads to pneumonia, the “Captain of the Men of Death,” who finishes the job in a few weeks.  Some viruses, even novel ones, even novel pandemic ones, are not very lethal.  The 1918 virus was an expert driller and was thus highly lethal, but it was its transmissibility combined with lethality that lead to the massive deaths.  It was able to eventually infect about half the world, maybe more; its combined lethality and transmissibility showed itself during its second wave, the autumn wave of 1918.  The Asian pandemic of 1957 started mild, and returned in a somewhat more severe form the following winter. The 1968 Hong Kong pandemic began relatively mild and remained mild in its second winter wave in most countries.

Dear Dr. Cannell:

How does Vitamin D work in the immune system?

Philip, Texas

Dear Philip:

Two systems exist in your body to fight infections, the innate or immediate system and the acquired or adaptive immune system that makes antibodies.  Recent evidence indicates seasonal impairments of the antimicrobial peptide (AMPs) systems are crucial to impaired innate immunity, impairments caused by seasonal fluctuations in 25-hydroxy-vitamin D [25(OH)D] levels.  The evidence that vitamin D has profound effects on innate immunity is rapidly growing.

Janet Raloff. The Antibiotic Vitamin, Science News

Unlike adaptive immunity, innate immunity is that branch of host defense that is “hard-wired” to respond rapidly to infections using genetically encoded effectors that are ready for activation by an antigen before the body has ever encountered that antigen. Of the effectors, the best studied are the antimicrobial peptides (AMPs).

Both epithelial tissues and white blood cells produce AMPs; they exhibit rapid and broad-spectrum antimicrobial activity against bacteria, fungi, and viruses. In general, they act by rapidly and irreversibly damaging the lipoprotein membranes of microbial targets, including enveloped viruses, like influenza.

Antimicrobial peptides protect mucosal epithelial surfaces by creating a hostile antimicrobial barricade. The epithelia secrete them constitutively into the thin layer of fluid that lies above the apical surface of the epithelium but below the viscous mucous layer. To effectively access the epithelium, a microbe must first infiltrate the mucous barrier and then survive assault by the AMPs present in this fluid. Should microbes breach this constitutive cordon, their binding to the epithelium rapidly mobilizes the expression of high concentrations of specific inducible AMPs, which provide a backup antimicrobial shield.

The crucial role of vitamin D in the innate immune system was discovered only very recently. Both epithelial cells and macrophages increase expression of the antimicrobial cathelicidin upon exposure to microbes, an expression that is dependent upon the presence of vitamin D. Pathogenic microbes stimulate the production of an enzyme that converts 25(OH)D to 1,25(OH)2D, a seco-steroid hormone. This in turn rapidly activates a suite of genes involved in pulmonary defense.

In the macrophage, the presence of vitamin D also appears to suppress the pro-inflammatory cytokines. Thus, vitamin D appears to both enhance the local capacity of the epithelium to produce endogenous antibiotics and at the same time dampen certain destructive arms of the immune response, especially those responsible for the signs and symptoms of acute inflammation, such as the cytokine storms operative when influenza kills quickly.

Because humans obtain most vitamin D from sun exposure and not from diet, a varying percentage of the population is vitamin D deficient, at any time, during any season, at any latitude, although the percentage is higher in the winter, in the aged, in the obese, in the sun-deprived, in the dark-skinned, and in more poleward populations. However, seasonal variation of vitamin D levels even occur around the equator and widespread vitamin D deficiency can occur at equatorial latitudes, probably due to sun avoidance, rainy seasons, and air pollution.

For example, a study of Hong Kong infants showed about half had 25(OH)D levels less than 20 ng/ml in the winter. Even in the summer, few of the infants had levels higher than 30 ng/ml, which many experts now think is well below the lower limit of the optimal range. As 25(OH)D levels affect innate immunity, then a varying percentage of most populations even equatorial ones will have impaired innate immunity at any given time, together with distinct seasonal variations in that percentage. The effects such impairments have on influenza transmission are unknown.

Dear Dr. Cannell:

Will Vitamin D protect me against acquiring the H1N1 flu?

George, Utah

Dear George:

I don’t know; no one does.  I am concerned about people who take low doses of Vitamin D (1,000 – 2,000 IU/day) and only achieve a 25(OH)D blood level of 30 ng/ml.  If the virus mutates into a virus as lethal as the 1918 virus, I doubt Vitamin D will totally protect you. Several facts about the 1918 pandemic concern me.

1. Blacks were less likely to contract the flu or die from the flu than whites in 1918.

2. Young people, presumably with the highest 25(OH)D levels, were the most likely to die in 1918, as they have been in Mexico to date.

3. In October of 1918, the Spanish flu erupted simultaneously in both Northern and southern hemispheres.

4. Significant deaths occurred in the Northern hemisphere during the summer of 1918 although the extraordinary killing erupted in October of 1918 in the Northern Hemisphere.

5. One of the worst affected countries was Western Samoa. A crippling 90% of the population was infected; 30% of adult men, 22% of adult women and 10% of children were killed.  This devastation occurred during their summer.  I doubt 90% of the population of Western Samoa had levels below 50 ng/ml in 1918 but I have no way of knowing.  More likely, the population had little acquired immunity to any influenza virus.

Jordan EO: Epidemic Influenza, a survey. Chicago: American Medical Association; 1927. [you'll have to follow the links to get to this one]

After rereading Jordan, I doubt vitamin D was the controlling factor in the 1918 Pandemic.  Furthermore, some of the above data – highest death rates in whites and young adults suggests having some vitamin D was a risk factor for death.  Thus, take enough Vitamin D.

However, other facts suggest Vitamin D was protective in 1918:

1. The mass of deaths in the Northern hemisphere occurred when Vitamin D levels were low (fall and winter).

2. While infection rates were similar for sailors and troops on infected troop transport ships, the sailors had 1/4 the mortality of the troops.  One has to assume the 25(OH)D of sailors aboard 1918 troop transport ships was higher than the troops inside.

3. Underground coal miners in North America had the highest mortality of any occupation.

4. The incidence of influenza in the French army was much higher in troops away from the front (probably in barracks) than in front line troops.

5. Open air hospitals in North America allegedly had lower mortalities than regular hospitals.

6. Mortality for sailors at sea was markedly lower than sailors ashore, despite the crowed conditions on board.

7. In the Western Front, the 1918 flu disappeared in August (when 25(OH)D levels reach their peak) only to return in September, when 25(OH)D levels fall rapidly.

My best guess is that 5,000 IU/day and a 25(OH)D of > 50 ng/ml will be at least partially protective.  Remember, at 50 ng/ml, you are assured that you are not suffering from substrate starvation, that is, your body has enough Vitamin D for its needs and some left over to store.  At a level of 30 ng/ml, most people are still suffering from Vitamin D substrate starvation.

Heaney RP, Armas LA, Shary JR, Bell NH, Binkley N, Hollis BW. 25-Hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions. Am J Clin Nutr. 2008 Jun;87(6):1738-42.

As I have written before, 25(OH)D levels are like water from a mountain spring.  The topmost pool is the calcium economy.  When that pool is full, excess 25(OH)D flows down to hundreds of pools below, cancer, heart disease, infection, etc.  In a lethal pandemic, you want Vitamin D to do two things, increase production of natural antibiotics (AMPs) and quell excessive immune responses.  Are these two pools at the same level?  Is the AMP pool above the cytokine dampening pool?  If so, people with 25(OH)D levels of 30 ng/ml may have enough D to strengthen their innate immunity but not enough to prevent the cytokine storm that kills in a lethal pandemic.  Thus, people taking only 1,000 – 2,000 IU/day, with levels around 30 ng/ml, may risk death from a cytokine storm their body is unable to prevent.  While only a theory, it would explain why the people with the allegedly highest 25(OH)D levels in both Mexico and 1918 (young adults) were the most likely to die.  That is why I caution people that, if you are going to take Vitamin D, take enough, take 5,000 IU/day, which is usually enough to get your 25(OH)D levels into the mid range of the reference range (30-100 ng/ml), which would be 50-70 ng/ml.

Dear Dr. Cannell:

Will this H1N1 flu reappear next fall?

May, Washington DC

Dear May:

Million dollar question!  Flu viruses constantly mutate.  Right now it lacks an amino acid sequence that confers lethality.  Will it acquire that amino acid by next fall?  I don’t know and if anyone one tells you they know then you know a fool.

Dear Dr. Cannell:

Will you and your family take the flu shot they are developing?

Jerry, North Carolina.

Dear Jerry:

Yes.

However, it will probably not do much as it may be unable to generate an immune response in those with high 25(OH)D levels.  Two Russian studies, the only such studies in the world, suggest higher vitamin D levels prevent the immune response flu shots attempt to generate.  Dr. Scott Dowell, at the CDC, has known about these two studies for at least five years.

In 1977, Russian scientists inoculated 834 non-immune males with live attenuated influenza virus in St Petersburg (62 N) and Krasnodar (45 N), Russia during different seasons of the year, comparing them to 414 vehicle placebo controls. In St Petersburg, they found that the attenuated virus was about eight times more likely to cause physical evidence of infection (fever) in the winter than the summer (6.7% vs. 0.8%). In Krasnodar, 8% of inoculated subjects developed a fever from the virus in January, but only 0.1% did so in May.

Shadrin AS, Marinich IG, Taros LY. Experimental and epidemiological estimation of seasonal and climatogeographical features of non-specific resistance of the organism to influenza. Journal of Hygiene, Epidemiology, Microbiology, and Immunology 1977; 21: 155161.

Different Russian scientists found that fever after inoculation with attenuated virus was twice as likely in February (10.7%) as in June (5%), compared to vehicle placebo controls. They also confirmed that sero-conversion varied by season, with the lowest rate of antibody formation in summer. When they attempted to recover the virus 4872 h after inoculation, they found subjects were more likely to shed the virus in December (40%) than in September (16%), and the quantity of virus shed was significantly lower in summer than winter.

Zykov MP, Sosunov AV. Vaccination activity of live influenza vaccine in different seasons of the year. Journal of Hygiene, Epidemiology, Microbiology, and Immunology 1987; 31: 453459.

These two studies suggest higher Vitamin D levels may prevent a vaccine from causing an immune response, the whole idea of a vaccine.

Dear Dr. Cannell:

What about Guillain-Barré Syndrome if I take the flu shot?

Jeanne, California

Dear Jeanne:

Influenza or influenza like illness usually precedes the autoimmune process of Guillain-Barré Syndrome.  Thus, a recent study found a seven-fold risk for those who contracted the flu but a slightly decreased risk for those getting a modern vaccine.

Stowe J, Andrews N, Wise L, Miller E. Investigation of the temporal association of Guillain-Barre syndrome with influenza vaccine and influenza-like illness using the United Kingdom General Practice Research Database. Am J Epidemiol. 2009 Feb 1;169(3):382-8.

This appears to be much different than the 1976-77 swine flu experience, the last time a swine flu virus caused this type of consternation.  Then, the vaccine was associated with a seven-fold risk of Guillain-Barré Syndrome, but the feared pandemic never materialized.  That is, as Guillain-Barré Syndrome is a complication of the flu and the flu failed to materialize that year, we will never know what the risk of Guillain-Barré Syndrome would have been in 1978 in those who got the flu but no flu shot.

Safranek TJ, Lawrence DN, Kurland LT, Culver DH, Wiederholt WC, Hayner NS, Osterholm MT, O’Brien P, Hughes JM.  Reassessment of the association between Guillain-Barré syndrome and receipt of swine influenza vaccine in 1976-1977: results of a two-state study. Expert Neurology Group. Am J Epidemiol. 1991 May 1;133(9):940-51.

As Guillain-Barré Syndrome is an autoimmune process, those on 5,000 IU per day should not have to fear it.

Dear Dr. Cannell:

Why does the CDC and WHO ignore all the work on Vitamin D and flu?

Sally, California

Dear Sally:

I’m not sure.  A randomized placebo controlled trial showed vitamin D prevents colds and flu.

Aloia JF, Li-Ng M. Re: epidemic influenza and vitamin D. Epidemiol Infect. 2007 Oct;135(7):1095-6;

However, when these same authors attempted to reproduce their findings by giving 2,000 IU/day for four months, they found no protective effect of Vitamin D.

Li-Ng M, Aloia JF, Pollack S, Cunha BA, Mikhail M, Yeh J, Berbari N. A randomized controlled trial of vitamin D3 supplementation for the prevention of symptomatic upper respiratory tract infections. Epidemiol Infect. 2009 Mar 19:1-9.

However, these same authors have since concluded that 2,000 IU/day for four months is an inadequate dose and 5,000 IU per day is generally required to assure 95% of the population has adequate levels.

Aloia JF, Patel M, Dimaano R, Li-Ng M, Talwar SA, Mikhail M, Pollack S, Yeh JK. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Am J Clin Nutr. 2008 Jun;87(6):1952-8.

At least 5 studies show an inverse association between lower respiratory tract infections and 25(OH)D levels or sunshine.  That is, the higher your 25(OH)D level, the fewer colds and flu:

Laaksi I, Ruohola JP, Tuohimaa P, Auvinen A, Haataja R, Pihlajamäki H, Ylikomi T.  An association of serum vitamin D concentrations < 40 nmol/L with acute respiratory tract infection in young Finnish men. Am J Clin Nutr. 2007 Sep;86(3):714-7.

Karatekin G, Kaya A, Salihoğlu O, Balci H, Nuhoğlu A. Association of subclinical vitamin D deficiency in newborns with acute lower respiratory infection and their mothers. Eur J Clin Nutr. 2009 Apr;63(4):473-7.

Ginde AA, Mansbach JM, Camargo CA Jr. Association between serum 25-hydroxy-vitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2009 Feb 23;169(4):384-90.

Wayse V, Yousafzai A, Mogale K, Filteau S. Association of subclinical vitamin D deficiency with severe acute lower respiratory infection in Indian children under 5 y. Eur J Clin Nutr. 2004 Apr;58(4):563-7.

Termorshuizen F, Wijga A, Gerritsen J, Neijens HJ, van Loveren H. Exposure to solar ultraviolet radiation and respiratory tract symptoms in 1-year-old children. Photodermatol Photoimmunol Photomed. 2004 Oct;20(5):270-1.

Despite these studies, the scientists at CDC and WHO are thinking only in terms of a vaccine or TamiFlu.  The idea of strengthening the innate immune system with Vitamin D is simply not on their radar.  Many of these scientists have financial connections to the influenza industry.  However, It is not a conspiracy.  When I was young, I thought most things were conspiracies.  Now that I am older, I know it is not a conspiracy, only incompetence.

If this virus mutates this summer and acquires more lethality and maintains its transmissibility, we may experience another 1918 pandemic.  If so, I plan to be fully armed, with both Vitamin D and the best modern conventional medicine has to offer.

John Cannell, MD
President
Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency.  Please reproduce it and post it on Internet sites.  Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.  Send your tax-deductible contributions to:

The Vitamin D Council
585 Leff Street
San Luis Obispo, CA 93401

Image from Nature Reviews Cancer

Since I’ve been asked about my take on the swine flu situation a few times in the comments section and numerous times by other people I know, I figured I would post on the subject.  Re the above cartoon: I agree with the President.

I don’t think the situation is nearly as bad as many people – including our esteemed Vice President – seem to think it is.  Whenever I hear reports of panic like those we’ve been bombarded with over the past week, I always think of what H.L. Mencken had to say in such circumstances:

The whole aim of practical politics is to keep the populace alarmed (and hence clamorous to be led to safety) by menacing it with an endless series of hobgoblins, all of them imaginary.

In this case, I don’t think it is the government that is spreading the panic – Biden’s gaffs notwithstanding – instead I believe it is the press.  The same Mencken quote could easily apply to the media.

You didn’t hear about Biden’s gaff?  Well, the spinmeisters got to it pretty quickly.

If, instead of running for their lives, people are running to the internet, glued to CNN, and the other 24/7 news channels and reading every newspaper and news magazine that comes along, the press is extremely happy.  It’s what they live for.  When they get a hot story like this one, they are loath to let it go until they’ve milked it for maximum exposure.  And they are milking this one for all it’s worth.  But remember, the media did this same thing a few years ago and inspired the same kind of panic over SARS, which ended up not amounting to much in terms of a real pandemic.

By now everyone knows that the swine flu in question is the H1N1 influenza A virus that was first thought to be similar genetically to influenza viruses that are found in pigs in North America.  More research has demonstrated that some of the genes involved are those that are found in pigs in Europe and Asia as well as birds and humans.

Based on the recent cases, this influenza doesn’t appear to be all that virulent.  In fact, it looks to be much less virulent than the standard old garden-variety flu that is common in the winter.

This influenza virus, like all influenza viruses, can mutate via a process called antigenic drift, which can make it either more or less virulent.  When we get the flu, we develop antibodies to the particular strain of influenza virus that infected us.  As this virus mutates a little, our antibodies can continue to beat it back because it is similar enough to the strain we got that our immune system recognizes it.  After a number of years of antigenic drift, the virus will have changed enough that our immune system no longer recognizes it, and we get infected again.  Measles, mumps and chicken pox are common viruses that don’t go through antigenic drift, so once we have them, we pretty much have immunity against then forever, but not with the flu.  Which is why once you get it, you don’t get it again for a number of years, then you come down with it once again.
Based on my own experience both being infected with the flu and taking care of patients infected with it has led me to believe that the influenza virus is becoming less virulent in general over time.  Why?  Natural selection.

Remember, natural selection works by spontaneous mutations that confer a survival advantage to the organism that carries them.  Such an organism has a better chance of surviving and passing the mutation along to its offspring.  With this in mind, consider the influenza virus.  It lives in humans, birds, pigs, etc.  It typically spreads via droplets disseminated by sneezing and coughing or close physical contact.  Think about what happens if a virus is extremely virulent.  The person (or animal) infected with it gets extremely ill, stays put, and maybe even dies.  This behavior reduces the chance of the virus’ spreading.  If however, the virus mutates to a much less virulent form, people who are stricken with it continue to work and socialize and don’t die.  The virus lives longer in the host and has a much greater chance of being spread, which is better for the virus.  So a lesser virulence confers a survival advantage to the virus, which is why I think the flu has become less and less problematic over time.

What can we do about this strain?

First, I don’t think it will amount to much because of the season.  I’m a firm believer in the notion that reduced vitamin D levels in the winter predispose us to the flu and other viral infections at that time.  Right now, it is late spring and nice and sunny with longer days.  People are getting out more and building their vitamin D.  For this reason alone, I don’t believe we’re going to see a pandemic.

It takes about 12 weeks to grow the virus in culture and use it to develop a vaccine, which is why the CDC can’t just crank out vaccine on the spur of the moment when a virus such as this one shows its face.  And even if a vaccine could be cranked out, it takes a while after the vaccination to develop the immunity, so it wouldn’t help immediately anyway. Since there will be no vaccine, we need to turn to other techniques to protect ourselves.  How can we do that?  By doing all the things we need to do to bolster our immune systems.

This swine flu is a type A influenza, which is a type that can usually be warded off prophylactically with amantidine (Symmetrel), an inexpensive drug that is readily available.  But from my reading, it looks like this particular strain of influenza A is resistant to that drug.  There are a couple of other drugs that are effective in the treatment of this flu – Tamiflu and Relenza – but I wouldn’t use them as a prophylactic.  Keep them in reserve in the unlikely event that you should actually contract this flu.  MD and I have gotten calls from friends and family all over the place wanting us to call them in prescriptions for these drugs, but we have refused because we don’t want to deplete supplies (which are limited) for those who actually get the flu.

As far as I’m concerned, the single best thing you can do is to make sure your vitamin D levels are where they are supposed to be.  On days that I’m not in the sun, I always take a 5,000 IU vitamin D3 capsule.  If I feel like I’m coming down with something or if I’m going on a long flight, I’ll take a 50,000 IU capsule.

In addition to the vitamin D, the other things you can do are as follows:

Eat plenty of good quality protein and fat.  Your immune system is made of protein and fat, so eat what it needs.

Avoid sugar and refined carbohydrates.  A number of scientific studies have shown that sugars and refined carbohydrates increase inflammation and, consequently, occupy much of the capacity of the immune system.

Get plenty of sleep.  Sleep is a great immune enhancer.  Remember all the times you’ve shorted yourself sleep and ended up catching a cold.  Get your rest.  If you have trouble falling asleep, try some sublingual melatonin.  It’s available at any health food store.  Put 1 or 2 mg under your tongue when it’s lights out.  Don’t use the melatonin unless and until you’ve turned the lights out and are ready to sleep.

Wash your hands frequently and keep them away from your nose and eyes.  This is especially good advice when you are traveling or even just out and about.  Someone with the flu (or other virus) sneezes into his/her hand, touches a door handle, you grab the same door handle, then rub (or pick at) your nose, and Bingo! you’re inoculated.  So I repeat: wash your hands and keep them away from your nose.  Hand sanitizers help.  And, as if I need to tell anyone this, try to avoid having someone sneeze or cough in your face.

I would avoid kissing pigs and strangers.  Wait until this scare recedes into your rear-view mirror before you follow the lead of this youngster.

Follow the above recommendations, and I think you’ll do all you can to minimize your chances for infection.

If you do get the flu, have your doctor give you a prescription for one of the two drugs mentioned above.

But I doubt you will get infected.  And I suspect this whole thing will blow over in fairly short order.

When I took my parasitology course in medical school I was exposed for the first time to all the loathsome diseases that are unheard of here but are a part of daily life in other parts of the world. Here people go nuts and rush to the emergency room if they find pin worms in their kid’s stool; there having a Loa loa worm creep across your eye is a common occurrence and only a minor bother.

I was fascinated with my study of liver flukes, roundworms, tapeworms and all the other parasites afflicting primarily those in tropical areas. The most vile yet amazing of these creatures was to me Dracunculus medinensis, the Guinea worm. This parasite causes untold misery to those it afflicts, and is now, as this BBC piece relates, on its way to extinction. For people living in areas the Guinea worm infests, I’m sure this is wonderful news.

What the BBC neglected to mention is that the eradication of the Guinea worm has been effected in large measure by none other than our former president, Jimmy Carter. Carter, in my opinion, wasn’t much of a president, but he has been a terrific ex-president when he avoids politics and sticks to humanitarian issues. This Carter Center he and his wife founded has been instrumental in educating people in areas where the Guinea worm is common to take the needed steps to intervene in the parasite’s life cycle and disrupt its ability to reproduce. The BBC reports:

A tropical worm disease that has plagued people since ancient times could be eradicated in less than two years, experts predict.

The World Health Organisation said Guinea worm disease, or dracunculiasis, now only affects around 25,000 people in nine countries.

To have this worm beaten back to only the point at which it affects only 25,000 people is a stupendous achievement. I broke out my old med school parasitology text, which was published in 1975, and found that at that time there were an estimated 48 million people infected with the Guinea worm. From 48 million to 25,000 in about thirty years is a real triumph.

The thing that intrigued me the most about the Guinea worm was its inbred ability to do what it needed to do to reproduce itself. As anyone who has read much of my writing knows, I’m driven by the idea that the best diet for man today is the one he cut his evolutionary teeth on. The forces of natural selection mold our genome in ways that we are barely starting to even think about. Our genome not only responds to the foods we eat by turning on or off particular genes, it affects our thinking and emotions as well. Nowhere is this genomic force more well demonstrated than in the Guinea worm.

Dracunculus medineses is a simple creature in terms of biological complexity with a less than primitive brain. Yet it is driven by incomprehensible forces to do what it needs to do to propagate. It starts its life as a larva wriggling in the water where it is eaten by a water flea. No water flea meal ingestion, the cycle ends. Once in the flea the larva coils itself tightly and becomes inactive. If the flea dies, so does the larva. But if the flea is consumed by a person drinking the water, the larva gets its next big break. The stomach acid dissolves the flea, but not the larva, which makes its way to the small intestine, then through the wall of the small intestine into the body cavity. Over the next year the female finds and mates with a male Guinea worm larva. The male dies and is absorbed into the body of the female. The impregnated female goes through a growth spurt that ends up with her being an adult worm from two or three feet long and about as big around as a piece of spaghetti. Here’s where it gets interesting.

Up to this point the human host of this worm has no symptoms and hasn’t a clue as to what’s about to happen. The pregnant female begins to migrate toward the victim’s feet. How does it know which way that is? It’s a mystery. Once the worm reaches its destination at the under surface of the skin of the foot or ankle it releases a toxic liquid that causes a blister on the surface of the skin. The blister and the toxic liquid that cause it are extremely painful causing an intense, fiery, burning sensation. The person experiencing this torture is driven to submerge the affected foot into water to help reduce the pain. As soon as the foot goes into the water, the female Guinea worm, with uterus poked out the top of the blister, releases thousands of new larva into the water and the cycle starts again.

Once the female has surfaced and released her larva, she can be seen. The age-old method of treatment at this point is to wrap the emerging worm around a stick of matchstick diameter and slowly, very slowly, roll the worm around the stick. It takes several weeks to fully extract the worm. The extraction must be done with extreme care because if the worm breaks during the process a severe inflammatory reaction takes place causing disabling pain and, in some cases, even death.

The worst part of this ordeal is that if you’ve got one Guinea worm, you’ve probably got another ready to erupt at anytime.

By teaching people in Guinea worm infested areas to at least strain their drinking water to remove the water fleas, the life cycle is disrupted. The Carter Center is educating people to do that and to avoid standing in water when the blisters erupt. If the female can’t eject her larvae into the water, the life cycle also comes to a halt.

The take home message of this story is to be aware of urges and drives to eat. If the forces of nature can drive such a simple-brained, primitive creature as the Guinea worm to do all the things it needs to do to reproduce, imagine how strongly these forces work on us infinitely more complex creatures all the time. If a man with his foot on fire from an emerging worm can be trained to go against all his natural inclinations and not plunge his foot in the water, we can be trained not to succumb to our nature-driven urges to go face down in the carbs.

Now, the real reason I wrote this post: I have to expiate for my own sins. My wife bought a box of chocolate candies from a kid trying to raise money for something. She brought them home and put them in a drawer (why she didn’t just give the kid five bucks and say ‘keep the candy’ I don’t know). They’ve been in the same drawer, one in which I almost never look, for several months. Last night MD made ribs for dinner, which I ate along with a few slices of tomato. I felt full and content. Then for whatever reason, the knowledge that those candies were there began to prey on me. Why last night? why not three months ago or anytime in between? I don’t know. It must be one of those drives like the one that drives the Guinea worm to the feet of its victim instead of the hands.

As Hamlet said:

To hold, as ’twere, the mirror up to nature.

Whatever the reason, I opened the box and threw five or six of those suckers back as fast as I could. A paragon of low-carb virtue I was not.

Of course, I felt like crap afterward. Not emotionally, but physically. God only knows how high my blood sugar went. I like to think I’m more complex than a Guinea worm, able to overcome and out think urges installed by my genome, but last night I wasn’t. And I have no one to blame but my genes…and my wife!

An intriguing article appeared in the Journal of the National Cancer Institute showing a correlation between periodontal disease and the development of pancreatic cancer. There have been a couple of studies correlating tooth loss with pancreatic cancer, but this is the first study I’ve seen that looks at periodontal disease and cancer of the pancreas.

You don’t want to get any kind of cancer if you can help it, but you really don’t want to get cancer in your pancreas. The virulence of cancers are usually defined by their 5-year survival rates, meaning what percentage of people who are diagnosed with a particular cancer are still alive 5 years later. The lower the 5-year survival rate, the deadlier the cancer. According to the latest statistics from the American Cancer Society (ACS), breast cancer has a 5-year survival rate of 88.5 percent, which means that out of 100 patients who are diagnosed with breast cancer, 88.5 of them will still be alive 5 years later. For lung cancer, a pretty deadly cancer, the 5-year survival rate is 15 percent. The 5-year survival rate for pancreatic cancer is 5 percent, making it the most deadly of all the cancers listed in the ACS list. Pancreatic cancer is a good one to avoid.

According to most papers I’ve read the only established modifiable risk factor for pancreatic cancer is smoking. There is evidence is starting to accumulate suggesting that diabetes, obesity and insulin resistance are also associated with increased risk. Recently a number of papers have been published showing that sugar, sugar-sweetened beverages, and high-glycemic-load diets are associated with an increased risk for this deadly cancer.

Now comes this paper showing that male health professionals with periodontal disease have significantly higher rates of pancreatic cancer. And the more severe the periodontal disease, the higher the correlation. Why should periodontal disease predispose to pancreatic cancer? I think the reason is pretty obvious, but the authors of the paper dance all around the issue.

According to the authors

Several mechanisms could potentially explain the observations from this study. Inflammation appears to play an important role in pancreatic cancer pathogenesis, although the inflammatory mediators that lead to the development of pancreatic cancer remain poorly defined. An association between periodontal disease and systemic inflammation has been observed using biomarkers. In the HPFS [Health Professionals Follow-Up Study, the study from which the database for this analysis was drawn], plasma C-reactive protein levels were 30% higher in individuals with a history of periodontal disease than in those with no history. We hypothesize that periodontal disease may promote pancreatic carcinogenesis through inflammation.

Alternatively, periodontal disease could influence pancreatic carcinogenesis through increased generation of carcinogens, namely nitrosamines. Individuals with periodontal disease and poor oral hygiene have elevated levels of oral bacteria and have much higher nitrosamine levels in their oral cavity due to nitrate-reducing bacteria. Nitrosamines and gastric acidity have been hypothesized to have an important role in pancreatic cancer; numerous studies support this hypothesis [I found only one].

To summarize, the authors hypothesize that the inflammation caused by the infection in the gums causes the pancreatic cancer and/or the increased gastric acidity from the nitrosamines produced by action of the infectious bacteria.

I suppose that inflammation and increased gastric acidity could cause it, but I don’t believe those are the most likely causes. Remember, we’ve got a number of studies showing that the consumption of sweets and a high-glycemic diet appears to increase the risk for pancreatic cancer. There is evidence that obesity, diabetes and insulin resistance are correlated with increased rates of pancreatic cancer. And now we’ve got periodontal disease to add to the mix.

What causes periodontal disease? I’ll give you a clue. Just as with dental caries (cavities), periodontal disease doesn’t appear in the remains of pre-agricultural man. Periodontal disease is easily recognizable from skeletal remains, and it just ain’t there in our meat-eating ancestors. Once agriculture took root (no pun intended), dental caries and periodontal disease became common. It’s hard to find an ancient Egyptian mummy without severe dental disease. And remember, ancient Egyptians lived in the days before sugar, so we can’t blame sugar for their dental disease. They ate a huge amount of grain and grain-based foods, a fari amount of fruits and vegetables, and very little meat. In fact they ate pretty much the kind of diet that today’s nutritionists would have us all eat to prevent disease. It didn’t do the Egyptians a whole lot of good. The calculus (tartar) deposits on their teeth were often so extensive that they held the teeth in place after death for 2,000 years. The result of these deposits is early bone loss, loose teeth, infection, and tooth loss. In addition, the ancient Egyptians had arteriosclerosis, obesity, rampant tooth decay, and a host of diseases that we consider ‘modern’ diseases.

Sticky, high-carb foods cause periodontal disease. The obesity, diabetes, and insulin resistance mentioned above are probably caused by high-carb diets. The papers mentioned above show that high-carb diets are associated with pancreatic cancer. So, despite the authors speculating about inflammation and increased gastric secretions, I think the periodontal disease data further confirms the hypothesis that excess carbohydrate consumption is more than likely the driving force behind pancreatic cancer.

As if you needed more, this is just another reason to follow a whole-food low-carbohydrate diet.

Let’s engage in a sort of thought experiment. Let’s assume that way back in the early days of medicine doctors always wanted to see us cough up mucus from our lungs. Since mucus is a kind of breeding ground for all kinds of nasty bacteria, it would make sense in the olden, pre-antibiotic days to want patients to hack up as much of this stuff as possible to get it out of the body where the bacteria could no longer wreak their havoc.

Let’s assume that doctors of old–who didn’t realize that the excess mucus was the body’s way of ridding itself of something foreign, i.e., the bacteria or viruses causing the infection–started equating coughing up ‘healthy’ amounts of mucus with good health. It’s not too far a leap to imagine these doctors supposing that if they could get their patients to cough up stuff all the time, the respiratory system would stay clear of the mucus that harbors all the pathogens that cause lung problems. Druggists might come up with concoctions that would cause people to cough, even if they didn’t need to.

Now let’s imagine that the idea that coughing up large amounts of mucus-laden sputum reaches the point of a national obsession. People, especially the elderly for whom respiratory infections are much more dangerous, discuss with one another how much sputum they produce and how often. If they don’t cough as much or as productively as they perceive those around them are doing, they go to their doctors who prescribe a sputum inducing medicine for them. People everywhere are obsessed with keeping their respiratory systems clean.

Now, someone comes along and says, Hey, world, I’ve got the perfect product to keep everyone coughing productively. Use my product and before you know it you’ll be coughing your head off and ridding your lungs of all kinds of nasty junk. Here, try one of these. It’s called a cigarette.

In today’s modern world we all know what cigarettes do. The irritation of the smoke damages the lining of the tubes that carry air into and out of the lungs. As the damage continues, goblet cells (so called because they resemble little goblets), the cells that produce mucus, increase in size and number, producing more mucus to coat and protect the cells lining the airways. As the smoking continues, so does the damage, and so does the double duty of the goblet cells. Ultimately, in far too many people, the production of the protective mucus from the goblet cells isn’t able to keep up with the damaging effects of the smoke and cell injury occurs. As these cells are damaged, they cease to function properly, and ultimately die. They are then replaced by new cells, which themselves go through the same cycle. Somewhere along the way one of these cells, due to the damaging effects from the smoke, undergoes a malignant transformation and starts to reproduce itself. When this happens lung cancer is born.

We know what happens to the lungs with smoking. We know that all the coughing and mucus production isn’t a good thing–it isn’t protecting us from disease; it is the result of disease. But if we lived in a society that worshipped bringing up mucus every day, how long would it take us to figure out that smoking wasn’t particularly good for us?

Into this society of mucus lovers a researcher comes along and writes a paper showing how cigarettes cause an increase in mucus. He talks to the press and tells them about his research, saying, ‘I’ve now figured out how these wonderful cigarettes work to improve our mucus production. They damage the cells, which then make and release more mucus to protect themselves. It’s really wonderful how the body responds thusly. Now that we know how it all works, let’s go out and smoke even more.’

Preposterous, you’re probably thinking. Only if you live in a society that doesn’t worship regular mucus production.

We live in a society that worships regular bowel movements. Doctors for the last few hundred years have focused much of their effort in ensuring the regularity of their patients. Many people, the elderly especially, are obsessed with moving their bowels daily. Most people, if asked, would probably reckon that it’s not good to have fecal matter just sitting around in the colon. Get it out of there, they would say. It can’t be healthy. Just as it escaped the notice of our doctors in the scenario I imagined above that animals in the wild don’t bring up copious amounts of mucus daily, it has escaped the notice of doctors today that animals in the wild, especially carnivorous animals, don’t always have daily bowel movements, and that when they do, such BMs aren’t always huge and loose.

Into our bowel-regularity-worshipping society there has come a substance that ensures regularity. It’s called fiber. It is sold everywhere in diverse forms. All manner of ‘experts’ from our doctors to our grandparents encourage us to consume plenty of fiber. If we can’t get enough from the foods we eat to achieve regularity, we are encouraged to buy supplements. Everyone is on the regularity bandwagon and, by extension, the fiber bandwagon. The much despised Jane Brody has written countless times on the virtues of fiber, WebMD encourages us to get our share, even C. Everett Coop exhorts us to keep the fiber coming. And, despite numerous studies showing that fiber doesn’t really do squat for us healthwise, everyone continues to recommend it.

To paraphrase John Huston: Evidence? We ain’t got no evidence. We don’t need no evidence. We don’t have to show you any stinking evidence.

Into this society of bowel movement lovers a researcher comes along and writes a paper showing how fiber causes an increase in regularity. Our intrepid researcher’s name is Dr. Paul L. McNeil; he is a cell biologist at the Medical College of Georgia. I’ll let him tell how it all works.

When you eat high-fiber foods, they bang up against the cells lining the gastrointestinal tract, rupturing their outer covering. What we are saying is this banging and tearing increases the level of lubricating mucus. It’s a good thing.

Indeed?

He goes on:

It’s a bit of a paradox, but what we are saying is an injury at the cell level can promote health of the GI tract as a whole.

Really?

He goes on to explain that even though epithelial cells usually live less than a week, they are regularly bombarded, in most of us at least three times a day, as food passes by.

These cells are a biological boundary that separates the inside world, if you will, from this nasty outside world. On the cellular scale, roughage, such as grains and fibers that can’t be completely digested, are a mechanical challenge for these cells.

But in what he and colleague Dr. Katsuya Miyake view as an adaptive response, most of these cells rapidly repair damage and, in the process, excrete even more mucus, which provides a bit of cell protection as it eases food down the GI tract.

As reported in ScienceDaily

In research published in 2003 in Proceedings of the National Academy of Sciences, Dr. McNeil showed proof of his then decade-old hypothesis that cells with internal membranes use those membranes to repair potentially lethal outer-membrane injuries. A recent paper published in Nature in collaboration with Dr. Kevin Campbell’s laboratory at the University of Iowa showed how human disease, including certain forms of muscular dystrophy, can result from a failure of this mechanism.

An outer membrane tear is like an open door through which calcium just outside the cell rushes in. Too much calcium is lethal but that first taste signals the vulnerable cell it better do something quick. With epithelial cells, several of the internal mucus-filled compartments fuse together within about three seconds, forming a patch to fix the tear. In the process the compartments expel their contents so, almost like a bonus, extra mucus becomes available to lubricate the GI tract.

And a final telling paragraph.

The scientists aren’t certain how many times cells can take a hit, but they suspect turnover is so high because of the constant injury. Potentially caustic substances, such as alcohol and aspirin, can produce so much damage that natural recovery mechanisms can’t keep up. But they doubt a roughage overdose is possible.

(You can click here to read this study in its entirety in PLoS Biology)

So, we have a situation where a product causes damage to the cells lining a tube, causing them to produce a lot of mucus in an attempt to protect themselves. In the process many of these cells die and are replaced by new cells. And this is perceived as a good thing.

My question is: is it really a good thing?