Due to other commitments tomorrow and Monday (see below for the Monday commitment) I more than likely won’t be able to get the promised post up before Tuesday.  I was working away on it this afternoon (actually alternating between writing the post and dealing with comments) when my bride came in and whined for me to go to a movie I didn’t really want to see.  But, being the dutiful and obliging spouse that I am, I went.  And I was glad I did.

MD just finished the book Julie & Julia and was hot to see the movie.  I hadn’t read the book, and don’t plan on it, so I was lukewarm at best on the idea.  But I’m glad I relented because the movie is one of the best I’ve seen in a long while.  MD and I related to it on a number of levels.  We written books and have been through all the publisher snafus that Julia experienced.  We know what it’s like to have a cooking show.  And we’ve been through the blogging experience.  But, unlike the heroine of the blog and book, we’ve actually met Julia.

In the summer of 2000, a couple of friends of ours who own Al Forno, a famous restaurant in Providence, RI, arranged for MD and me to be a part of a huge fundraiser for the Providence Public Library.  It got worked out in such a way that MD and I attended as – get this – celebrity chefs.  Chefs? I still don’t know how it happened because our cooking show hadn’t even been conceived of at that time and we had just published The Protein Power LifePlan a few months earlier.  But there we were as celebrity chefs with – get this, too – Emeril Lagasse, Jacques Pepin, and Julia Child.  And, as they say, that’s not all.  We were there with Billy Joel as well.  Yep, Billie, Emeril, Jacques, Julia, MD and me – the celebs brought out to raise money for the Providence Public Library.  It was kind of surreal.

When I was introduced to Julia, I told her I was delighted to meet her and that my wife and I lived in her home town.  I knew she lived in Santa Barbara, and MD and I had been living there for about a year at the time – if you could call it living there.  We actually lived primarily in Incline Village, Nevada and Santa Fe, New Mexico, but we did spent a fair amount of time in Santa Barbara, where we lived aboard a sailboat in the marina when we were in town.  So, I was more or less honest when I said we lived in Santa Barbara.

Julia Child was a big woman.  And I don’t mean fat, I mean big.  She’s well over six feet tall and is imposing even stooped a bit as she was then at age almost 90.  As we shook hands she replied to my remark about living in her home town in her wonderful, warble-y, quivery voice, “Which home town? Santa Barbara or Cambridge, Massachusetts?”  And she moved when she spoke just as Meryl Streep portrays her in the movie.

Until that moment, I hadn’t realize she lived anywhere but Santa Barbara, but it just so happened that MD and I had just purchased a condo in Cambridge a few months before.  Our eldest son, wife and first grandchild were moving to the Boston area for a year while our son clerked with a federal judge.  We bought the condo and they rented it from us.  So, I answered her that we lived both places.  Which, of course, was a stretch since we lived part time on a boat in one and owned a rental condo in the other, but, hey, I was among real celebrities so I had to act the part.

In the years between that first meeting and her death, we saw her a dozen or so times around Santa Barbara.  She frequented a lot of the same restaurants we did and was a regular at the farmer’s market.  But other than the time we chatted a bit at the Providence Library shindig, neither MD nor I ever spoke with her again.  We would say hello if we passed one another, but that’s it.  I’m sure she didn’t have a clue we had met before.  Having had the interaction with her that we did, made the movie a little more poignant for us.  I now wish we had made the effort to get to know her while we had the chance.

Julia had to deal with her publisher and with promoting her various books.  And we do too.  One of the things authors agree to when they sign a publishing contract is to make themselves available for various publicity events.  MD and I have done the book tour routine (which is miserable), appeared on countless TV shows and radio shows, and shown up for innumerable book signings.   None of these PR events are particularly fun, but the most loathsome PR event of all takes place this coming Monday.  It is the dreaded radio satellite tour.

There is a certain type of PR agent that books these kinds of things, which involve scheduling numerous radio shows one right after the other with military precision.  The shows start on drive time radio on the East Coast and move west with the sun.

We will start at 6:50 AM Eastern, which is 3:50 AM our time, and be on the radio pretty much non-stop throughout the day.  A number of you have asked in the comments if we are going to be appearing anywhere.  Right now, this is all that is scheduled.  I’ve posted the schedule below so that if we’re on a station in your neck of the woods, you’ll be able to listen should you chose to.

It will be a grueling day for us, but somehow we’ll manage to keep our good cheer through it all.  A thousand cups of coffee will help.  Hope you get to listen in to part of it.

Don’t panic.  I don’t have a paid ad for the RealAge Test stretching across the top of my blog post today.  This one is for illustration purposes only.  If you are like me, however, you’ve run across this banner countless times in your online surfing.  It seems to pop up everywhere.  Or at least it used to.  It hasn’t too much lately since the big New York Times exposé, more about which later.

But first let’s take a look at something else brought to the public by the team of Roizen and Oz.  I came across this page on their RealAge website while I was googling something else.

According to these two (or their team of ‘world-renowned scientists and doctors’) we should all avoid fructose and load up on glucose, the ’sugar that staves off hunger.’

Sugar is sugar, right? Maybe not. Turns out that there is one type of sweetener that helps fill you up, while another leaves you craving more.

The two sugars in question: glucose and fructose. Glucose appears to quell hunger, and fructose seems to ramp it up.

The sugars may affect your appetite differently because of the unique ways in which they affect malonyl-CoA, an important appetite-suppressing molecule in the brain. Glucose causes malonyl-CoA to rise, resulting in less food intake. Fructose, on the other hand, lowers malonyl-CoA, resulting in more food intake.

The implication of their message is that if you eat glucose you won’t be hungry, but if you eat fructose you will.  They go on to discuss how important it is to cut fructose from the diet since fructose makes you eat more.  And, by implication, to add glucose.

I agree that we should all cut most of the fructose from our diets, but not for the reasons these guys (and their team of purported experts) give.

I would assume that both of these docs went to medical school and had many years of post-medical school training.  I would also assume the same about their ‘world renown’ staff of experts.  What I don’t understand, then, is how they can make such stupid statements that have no grounding in actual biochemistry.

The ‘important appetite-suppressing molecule’ under discussion is malonyl-coenzyme A (malonyl-CoA), which is one of the major signaling molecules in the body.  Malonyl CoA sits at the crossroad of fat storage and fat burning and drives the reaction one way or another.

If we’ve eaten a lot, especially a lot of carbohydrate, malonyl-CoA levels increase.  Increased levels of this substance then shift the flow of fat away from burning and toward storing.  Among its activities, Malonyl-CoA stimulates fatty-acid synthase (FAS), the enzyme that converts carbohydrate to fat.  And it inhibits the enzyme (CPT-1) that carries fat into the mitochondria where it is burned for energy.

If we haven’t eaten, or if we have been eating a low-carb diet, the opposite happens.  Malonyl-CoA levels are low, which removes the inhibition of CPT-1.  Fat is shunted away from storage in the fat cells and instead is transported into the mitochondria where it is burned.

Since malonyl-CoA is one of the main substances in the body that determine what happens to fat, it would make sense that this molecule would somehow be involved in the regulation of hunger.  Elevated malonyl-CoA levels indicate that we’ve got plenty of fuel aboard and that the body is in the process of getting it stored away, so it would stand to reason that these elevated levels may affect the hunger centers in the brain, sending the message not to eat any more.

Researchers have looked into this notion, and it indeed appears – in rodents, at least – that elevated levels of malonyl-CoA do suppress the hunger centers in the hypothalamus.

If you do a quick thumb through any decent medical biochemistry textbook looking for what makes malonyl-CoA go up, you’ll find that it is driven up by insulin and glucose, the surrogates for being well fed.  But here is where Roizen/Oz and the team of experts go off the rails.  The glucose in question isn’t dietary glucose – it’s blood glucose.  As I’ve written about before, the entire amount of glucose we have circulating through us if we have a normal blood sugar level is around 4 grams, a little less than one teaspoon.  If we eat a medium-sized baked potato, we ingest about 50 grams of glucose (potato starch is made of pure glucose), which is more than ten times the amount regularly circulating in our blood.  Our bodies quickly deal with this excess by increasing insulin and driving the glucose into the cells.  As a practical matter, dietary glucose never really impacts malonyl-CoA.  What does impact it is the level of blood sugar.  So if blood sugar is higher than normal, then more malonyl-CoA is made, and more fat is stored.  Which is one of the reasons type II diabetics are usually obese to some extent.  These people have the double whammy of too much sugar and, since they’re almost always insulin resistant, too much insulin.

Any readers who have type II diabetes will have increased levels of malonyl-CoA.  I will ask those of you who have this condition: are you less hungry?  I didn’t think so.  Despite the fact that in rodents (and probably in people who are normal weight) malonyl-CoA may suppress hunger, it doesn’t seem to do so in those who are overweight and insulin resistant.  It may a little, but there are other forces driving hunger more than the malonyl-CoA suppresses it.  And in any case, it doesn’t have anything to do with dietary glucose – a fact our illustrious crew of ‘world renowned’ experts should have known.  Their implying that adding glucose to one’s diet will decrease hunger is just plain stupid.

But let’s look at something a little more sinister than just plain ol’ stupid.

These same guys are behind the RealAge test that (until fairly recently) was popping up every time you turned on your computer.  I saw the ads for this test over and over and over again, and I wondered what they were selling to justify the huge expense such unremitting advertising requires.  Then I read a New York Times article that explained it all.

As it turns out, the RealAge test is a means for Roizen/Oz et al to gather health information from those who take the test.  I’ve taken the test, which requires many pages of questions, and discovered that I am about 8 years younger than my chronological age.  I also discovered that I would be younger yet if I didn’t eat so much red meat.  You can guess how to perform well on the test: tell them you eat no red meat and a lot of soy.  (My choices on the red meat were: no red meat; red meat once per week; or red meat more than once per week.)

During the course of the test, after a long list of medical problems that are to be checked if the test-taker suffers from them, this question pops up:

If the answer is yes, you may be bombarded with information from various pharmaceutical companies that make drugs to treat the checked diseases. Or if, according to the Times, you decide to become a RealAge member.

Yep, that’s right.  These guys who seem so compassionate and are giving away their RealAge test (after capturing your email address) and providing all kinds of lifestyle change recommendations are really capturing your info and peddling it to Big Pharma.  Which, of course, is how they can afford the many ads for their ‘free’ RealAge test.

Says the NY Times:

But while RealAge promotes better living through nonmedical solutions, the site makes its money by selling better living through drugs.

Pharmaceutical companies pay RealAge to compile test results of RealAge members and send them marketing messages by e-mail. The drug companies can even use RealAge answers to find people who show symptoms of a disease — and begin sending them messages about it even before the people have received a diagnosis from their doctors.

While few people would fill out a detailed questionnaire about their health and hand it over to a drug company looking for suggestions for new medications, that is essentially what RealAge is doing.

Pretty sleazy, if you ask me.

They still provide their RealAge test, but as far as I can tell, only if you go to their website.  They are probably waiting for the fallout to be over from the Times piece.  Until then, they are dragging people to their website with idiotic pieces such as the one I discuss above.  If you are googling a health problem, nutrient, diet, etc., you may come upon their website and be presented with the RealAge test.

But, if the article I read is any indication of the value of their advice, I would be real leery.  The advice may be stupid, but the strategy behind the RealAge test is definitely sleazy.

Applebee's Quesadilla Burger

One of my readers sent me a link to a segment on ABC News with Charlie Gibson showing just how disgustingly slanted and inaccurate mainstream media reports can be.

Gibson leads into the segment about two reporters who underwent self experimentation on the adverse effects of unhealthy eating.  The reporters, ABC’s Yuji de Nies and Jon Garcia, set out to see what would happen if they consumed a giant meal containing over 6,000 calories.  Here is the result as they reported it.

Pretty brutal, eh?  But let’s shine the piercing light of good sense on what is going on here.  As you might expect, the reality is vastly different from that portrayed by ABC.

First off, let’s look at the actual nutritional content of the food eaten.  As reported in the piece, the total energy content of the meal was 6,190 calories, which included 187 grams of saturated fat.  These were the only parameters reported.  I took the time to go through the links in the article accompanying the video to find exactly where these foods came from.  Here’s what I found.

The burger is an Applebee’s Quesadilla Burger (served with fries, of course); the snack is The Cheesecake Factory Fried Macaroni And Cheese; and the dessert is Uno Chicago Grill Mega-sized Deep Dish Sundae (listed as cookie below).  How do I know these are the exact ones?  These were the ones referenced in the CSPI’s List of Most Unhealthy High-Calorie, Fat and Salty Restaurant Foods That May Clog Your Arteries.  After seeing the photos and comparing to what I saw on the video, these selections are the ones the reporters ate.

I then tracked down the Nutritional Facts for the foods involved (here, here, here and here) and put them into an Excel spreadsheet.  Take a look.

The first thing you might notice is that the total calorie count is 5,708, which is considerable, but is actually 482 calories fewer than the 6,190 reported.  Second, and this is a biggie, the saturated fat content of this meal is only 88 grams, not the 187 grams reported.

The reporters stretched the truth a little in that they reported as if the Mega-sized Deep Dish Sundae were a single treat to be consumed by one person at a sitting.  I’m sure it could be so eaten, but it’s actually designed for four people to share.  The Nutritional Facts list the calories per serving as 690 and the saturated fat as 17 grams.  I’ve used the amounts in all four servings, i.e., one entire four-person dessert, in my spreadsheet.

As you may have noticed, the total carb content of the meal is 745 grams, which converts during digestion to a little over three cups (3.1 cups to be exact) of sugar.  The ABC report, of course, failed to mention the carb content of the meal and ignored any immediate effect this huge intake of carb might cause.  One of the reporters, Jon, claimed that he was ’sluggish’ and ‘tired’; the implication being that this sluggishness resulted from his huge saturated fat intake.  No mention, naturally, of the enormous amount of carbohydrate and the large increase in insulin release it might cause.  From what I can see from the video, Jon looks to be sporting a little abdominal obesity, which would imply a degree of insulin resistance and hyperinsulinemia.  People with this disorder tend to over secrete insulin in response to carb intake causing an overshoot and reactive hypoglycemia (low blood sugar), which will indeed result in sluggishness.

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal.  There is a lot of fat swimming in the serum, that’s for sure.  What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood.  And how can you argue with them?  It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates.  The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate.  It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route.  The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs.  Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells.  Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature.  Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest.  The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.  As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

But what about the ultrasound showing the blood vessels had changed?  Wasn’t that because of the fat?

I’m afraid not.  The fat from the diet wasn’t in the blood vessels yet, so it couldn’t be the dietary fat causing the change.  So what was it?

How about a little normal physiology.  Let me explain.  The body gets blood where it needs to get it by opening certain blood vessels while closing others.  Let me give you an example.  Have you ever jumped into cold water to go swimming and noticed that not long after jumping in you have to urinate?  What happened?

Your arms and legs have a radiator effect.  Since these appendages have little padding the blood circulating there is exposed to the cold water, and if nothing is done, the cold water cools the blood creating a big problem.  Your body compensates by shutting down the circulation to the skin and areas close to the surface in your arms and legs and shunts that blood to your core.  Your core already has plenty of blood when this happens, so it has to get rid of some.  It does so by sending it through the kidneys where the liquid portion is filtered out and becomes urine.  Suddenly your bladder is full and you have to go.

The body has the ability to direct blood wherever it needs by its manipulation of blood vessel size.  Where do you think blood is needed after an almost 6,000 calorie meal?  That’s right.  The digestive tract.  It takes a lot of work to deal with 6,000 calories, and a lot of work requires a lot of oxygen, which comes from the blood.  So after a heavy meal, the body shunts extra blood to the guts where the works is being done.  It does this by opening or dilating the arteries carrying blood to the intestines and by narrowing the blood vessels in other parts of the body.

Now, think back to the video of the woman whose blood vessel (in her arm) is being examined by ultrasound.  When it’s compared to the previous ultrasound, the one before she ate, notice how much faster the heart is beating.  (The little swishing sounds you hear, each of which represents a heart beat, are spaced much closer together.)  The heart is beating faster because the body is working to digest an enormous amount of food, and this work stresses the heart in the same way that running down the street would stress the heart.  Work is work.

The digestive tract needs extra oxygen to do its work, this extra oxygen can get there only via the blood, so the intestines require more blood than normal.  This extra blood gets shunted there by opening the arteries that feed the gut and narrowing those that go other places where a lot of blood isn’t needed at the moment.  Such places as, say, a relaxed arm.

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better.  It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story.  Kind of sad, isn’t it.

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.

Here is a copy of the press release:nutritional-guidelines-press-release

Take a look at the names and resumes of those on the committee, and you’ll see that they are all lipophobes and carbophiles of the deepest dye.  Based on this cast of characters, it doesn’t look like much will change over the next five years. God help us all.

Let’s take a quick look at just one member of this illustrious panel that will decide how over 50 million people per day will be fed between 2010 and 2015.

Joanne L. Slavin, PhD, RD, a professor in the Department of Food Science and Nutrition and the University of Minnesota, is an expert in carbohydrates and dietary fiber. Her research expertise focuses on the impact of whole grain consumption in chronic diseases, such as cancer, cardiovascular disease, and diabetes, as well as the role of dietary fiber in satiety.

Before we even get to Dr. Slavin herself, you should be aware that this department at the University of Minnesota is a hotbed of high carbery. In fact, this is where the dietitians came from who piled on the Atkins’ diet in the commentary to the bogus Lancet article I posted about a couple of years ago. (If you haven’t read it already, this is a post well worth reading just to see how screwed up the nutritional establishment really is.)

What do you think Dr. Slavin’s take is on whole grain consumption in chronic disease?  Do you think she believes that whole grains are bad?  How about fiber?  Do you think she is aware that the idea of fiber as a protective factor against cardiovascular disease and other chronic diseases has never been proven?  Or do you think she blindly promotes fiber despite the lack of evidence that it’s good for anything?

Let’s take a look at one of her presentations and see. slavin-handout

From her material, it’s easy to see what her fixation is.  I’m glad I’m not her child, I can tell you that.

Other than the fact that they’re incorrect, I have a couple of real problems with the nutritional guidelines.

First, they are presented as if they are the latest in scientific thought on the subject of nutrition.  They aren’t.  They start out as guidelines put together by the most mainstream of the mainstream, which is a strike against them in the first place.  Then the lobbying starts.  That’s right.  The food industry gets into the act.  The officials in the Department of Agriculture ultimately referee the fight between the scientists (such as they are) and Big Sugar, Big Corn, Big Wheat and the rest of them.  What emerges is a sort of compromise between science and industry.  But it is foisted off as pure science.

After the scientific committee started pushing for a reduction in sugar in the 2000 guidelines, Senator Trent Lott presented the Secretary of the Department of Agriculture (the agency that sets the guidelines) with a letter signed by himself and multiple other senators from sugar-producing states asking that the recommendations to cut sugar from the diet be lightened.  Which, of course, they were.

My second problem is in how powerful these guidelines are in reality.  Most people think, hey, who cares what the guidelines are?  I eat the way I eat.  I don’t pay any attention to the guidelines.  Problem is the government is required by law to abide by these guidelines in feeding all the people the government feeds.  And the government feeds a lot of people.  Over 50 million per day, in fact.  Schools, the military and prisons are just a few of the institutions the government feeds daily.  Given these numbers, it’s easy to see why the food industry is so keen on how these guidelines end up being written.

In the YouTube below, you can see yours truly trying to explain all this to Bill O’Reilly.

Click here to view the embedded video.

Senator John McCain argues that “the best care is preventative care,” and his health care reform plan claims that “by emphasizing prevention” and other measures “we can reduce health care costs.” Senator Barack Obama’s plan says, “Simply put, in the absence of a radical shift towards prevention and public health, we will not be successful in containing medical costs or improving the health of the American people.”

It may sound like common sense. But it is still a myth.

The term “preventive medicine” no longer means what it used to: keeping people well by promoting healthy habits, like exercising, eating a balanced diet and not smoking. To their credit, both candidates ardently support that approach.

But the medical model for prevention has become less about health promotion and more about early diagnosis. Both candidates appear to have bought into it: Mr. Obama encourages annual checkups and screening, Mr. McCain early testing and screening.

Like most platitudes spouted by politicians, it sounds good.  But is it?  The idea is, of course, that with all these early checkups, tests and screenings, doctors will discover serious disease in its early stages when treatment is easier and less expensive. Were that all that happened, preventative medicine might be worthwhile.  But that’s not all that happens.  Unfortunately, today’s doctors use physicals, tests and screenings to pinpoint diseases that aren’t really diseases.  And these non-diseases are not inexpensive to treat.  Let me give you an example.

I have a friend who recently turned 49.  He is to all outwards appearances health as a horse.  He hikes, he works out, he plays a lot of golf, always walking and carrying his bag, he isn’t overweight, and he has a good family history.  His father died in his late 70s and his mother, age 84, is still living and drives her car everywhere.  This guy is your basic active healthy middle-aged male with no obvious problems.  Then he goes to the doctor to get a physical exam.

All the tests and screenings come out normal except for one.  You probably guessed it.  His cholesterol was a little high.  At 215 mg/dl it came in over the magic cutoff of 200.  And like all ‘good’ doctors, his recommended that he go on a statin drug.  So he went on Lipitor.  And promptly got muscle aches and felt lousy.  He called his doctor about the pain, and his doctor told him to keep on taking the Lipitor.  He said the aches should subside with time.  So my friend soldiered on and took his medicine.  But his pain continued.  After several months of this aggravating pain, my friend asked me about it.  I was stunned to learn that with his age, condition, and family history, his doctor had started him on a statin.  I suggested that he discontinue the drug and load up on some CoQ10, which he did.  His muscle pain went away and he was soon back to his old self.

But, he had had the fear of high cholesterol laid upon him.  He asked me about it and told me that he was a little worried.  I gave him the talk that I have given ad nauseum on the pages of this blog about the lipid hypothesis being only a hypothesis and that cholesterol doesn’t mean squat and that a statin wouldn’t help him improve his overall chances of not dying.  He was reassured but not totally convinced.  I suggested an EBT scan of his heart for a calcium score, an actual indicator of coronary plaque.  We went for it and ended up with a calcium score of zero, which indicates virtually no coronary plaque.  The doctor who gave him his physical was treating him for a non-existent disease.  An elevated cholesterol isn’t a disease – it’s a lab value.

So, we have a healthy guy who goes in for a little preventative care and comes out with coronary angst and a prescription for a medicine that does him absolutely no good and that even may have been doing him harm.  He then underwent yet another screening procedure to allay the fears that had been created by the first round of preventative care.  He (or his insurance company: read you and I) paid several hundred dollars for the first go round, another couple of hundred for the three month’s worth of Lipitor, and another $700 for the heart scan.  After at least $1500 of someone’s money, the guy isn’t any better off than he was before he went for his physical exam.  In fact, he would have been much better off had he never gone to the doctor in the first place.

The above example is preventative care as we know it today.  And it doesn’t save money overall; it costs money.  A lot of money.  Had I not entered the picture, this guy may have been on Lipitor for years at God only knows what cost. Preventative medicine today doesn’t reduce medical spending – it increases it.

As Dr. Welch confirms:

Increasing the amount of testing for an ever-expanding list of problems always identifies many more people as having disease and still more as being “at risk.” Screening for heart disease, problems in major blood vessels and a variety of cancers has led to millions of diagnoses of these diseases in people who would never have become sick.

Likewise, recent expansions in the definitions of diabetes, high cholesterol and osteoporosis defined millions more as suddenly needing therapy. A new definition of “abnormal bone density,” for example, turned 6.8 million American women into osteoporosis patients literally overnight.

These interventions do prevent advanced illness in some patients, but relatively few. Any savings from preventing those cases is dwarfed by the cost of intervening early in millions of additional patients. No wonder pharmaceutical companies and medical centers see preventive medicine as a great way to turn people into patients — and paying customers.

Many of whom pay through the nose for a long, long time.

In a brilliant analogy, Dr. Welch compares early screening for disease to the ‘check engine’ light in your car. When it comes on, it may indicate that a problem exists, but more often than not it comes on due to some trivial cause

like one sensor’s recognizing that another sensor isn’t sensing.

I’ve made many a trip to the mechanic to get my car looked at after the annoying ‘check engine’ light came on, and most of those trips resulted in the mechanic resetting the ‘check engine’ light.  Many times the light came on simply because it was programmed to come on when the car reached a certain mileage.  Just like we are encouraged to have certain screening procedures when we reach a certain mileage.

If when our own ‘check engine’ light comes on, and we head to our doctor, we would be time and money ahead were we given advice to cut the carbs, get more sleep, and quit stressing.  But that’s not what happens.  We get our cholesterol checked and thus begins a life-long fight to get it lower, when all it is is a lab result.  If you don’t believe me about this, search the comments of this blog using the word ’statin’ and you’ll see how many people write telling me that their cholesterol was found to be a little high, and their doctor wants them to go on a statin.  It’s pitiful.  In fact, it’s an outrage.

I’m not saying you should never go to the doctor or never have a screening to see what’s going on.  But I do say that you should undertake these procedures only when they provide some value.  Colonoscopies are worthwhile because colon cancer, caught early, can be successfully treated.  Same with PAP smears and cervical cancer. An EBT scan of the heart for a calcium score is valuable because it measures plaque.  If you see a mole that is changing in shape or color, it’s good to get it checked.  There are a few other screening tests that are of value, most routine lab tests can only steer your doctor wrong.  And put you at odds with him/her.

Take the time to read the full New York Times article.  You’ll never look at the idea that preventative care is the panacea for all that ails us the same again.  Now, if only the candidates could get the message.

These long must-watch videos are in two parts: the first part is by a defense attorney discussing the unbelievable complexity of the law, especially federal law, and the difficulty of simply going through life without knowingly or unknowingly breaking some kind of law.  And he discusses the dangers of talking to the police without a lawyer present.  The second part is a talk by a police detective confirming everything the attorney says and, fascinatingly, discussing his own tricks, learned in over 25 years of police work, to get people to talk to him and even to confess to crimes.

I’ll probably alienate any readers who are involved in law enforcement, which isn’t my intention.  I’m sure that if any law enforcement officials were suddenly under investigation, they wouldn’t say a word without their lawyer present.  The rest of us need these same protections.

I’m not presenting these videos for any criminals who may be reading, but for the average citizen who happens to get crosswise with the police.  Every single police officer I know (and I know a half dozen or so) are hard working, dedicated, responsible, and even kind-hearted folks, but they can make mistakes.  I make mistakes, so I figure they can too.  The officer speaking on the last part of this video says that he doesn’t really interrogate people that he doesn’t think are already guilty.  So, you are basically assumed guilty if you’re under investigation for whatever.  And if the officer is mistaken, you can be in real trouble.  You can’t talk your way out of it; you can only make it worse.  When you watch these videos, you’ll see what I mean.

Martha Stewart spent six months in a federal prison not because she did anything wrong during her alleged insider trading, but because she lied to a federal official.  And it’s easy to lie unintentionally.  Let me give you an example.

When MD and I lived in Little Rock after we had gone into practice, we lived in two different houses.  In the first house, I played a practical joke on her brother out on the front porch that we’ve all laughed about for years.  The joke involved a wallet MD’s dad had left at our house that her brother was coming by to pickup to take back to her father. (The joke involved inside family information and wouldn’t make sense if I described it.  But it was hilarious – to me anyway.  I’m sure her brother may not have felt the same way about it.  Come to think of it, he never came around much after that.)  MD’s father died a couple of years later, and a year or two after that, MD and I moved into the house we lived in for the last 15 years we were in Little Rock.  Not long ago, MD was telling someone visiting from Little Rock about this joke.  As I listened, it dawned on me that MD was telling this story as if it had happened at the last house we lived in.  Later I asked her about where she thought we lived when this happened.  She said ‘on Riverview Point’ (the last house, #2 Riverview Point).  I told her that it had happened in the previous house.  She told me that I was crazy and that I should know better by now than to question her memory.  (She’s right.  She has a unbelievably phenomenal memory.  Probably the best I’ve ever been around.  Whenever I question it, I am almost invariably wrong.  So I seldom question it any longer.)  She said she remembered her brother coming to the door, the joke, and us laughing about it in the Riverview Point kitchen.  I then told her that it couldn’t have happened in the Riverview Point house because her dad had died before we ever moved there.  After a long pause, she said, I know you have to be right, but I remember so clearly that all happening on Riverview Point.

The above story is a benign example of the kind of misremembering that we all have done.  But what if MD were being questioned by the police about the incident and she swore it happened on Riverview Point?  When she would be found to be wrong, it would look like she were intentionally lying.  And if she did so to a federal investigator, she could go to prison.  Remembering incorrectly and lying are two different things, but it’s easy for law enforcement officials trying to make a case to believe that a flaw of memory is an intentional lie. Especially if spoken with authority.

The tragic Jon Benet Ramsey murder took place right after MD and I had moved to Boulder, CO, so we were keenly aware of all that went on with that. Living in Boulder, you couldn’t avoid it. I’ve driven a hundred guests by the Ramsey house, which, by the way, isn’t a mansion as was reported by virtually all the national media, as in ‘the Ramsey mansion.’  It’s smaller than our house, which certainly isn’t a mansion.  The Ramsey house is an upper middle-class house in an upper middle-class neighborhood that sits cheek by jowl with all the other such houses on the street.  There isn’t 30 feet between adjacent houses on the Ramsey’s street, which is certainly not the case for mansions, at least not as I think of mansions.

As I’m sure everyone remembers from the constant media exposure, the Ramsey family wouldn’t speak to the police without their attorney present.  Everyone (including yours truly) figured that one of the Ramsey’s (probably the son) had committed the murder, and that the Ramsey’s were protecting the guilty family member.  Why else wouldn’t they speak with the police?  They were smart.  They did just what the lawyer in this video recommends for all the reasons he recommends.  And it saved their bacon.  I believe that the Boulder police believed that one of the Ramsey’s were guilty, and the Boulder police were under huge pressure to solve the crime.  But the police could never get any traction in the case because of the Ramsey’s attorney.  Had the Ramsey’s spoken freely with the police, one of them may well have been charged with the crime simply because of a slip of the tongue.  A misremembrance that the police categorized as a lie.  As it turns out, DNA evidence has recently exculpated the Ramseys.  But at the time, they were in peril because public opinion had it that one of them was guilty.  And I’m sure the police were predisposed to charge them.

Most clever career criminals know to never speak to the police without an attorney.  The stupid criminals don’t make it long as criminals before they’re locked up.  It’s the non-criminals, the category into which I hope most readers of this blog fall, who need the protections these videos describe.  Don’t think your smart enough or clever enough to intellectually steamroll over an investigator.  They are very, very good at what they do.  It’s their world, and you are totally a fish out of water in that world.

Watch and learn.  I hope you never need the lessons from these videos, but if you do, you’ll be glad you took the time to watch.  Plus, it’s entertaining.  Both speakers are excellent in completely different ways.

In Part I of the 2 video series, Mr. James Duane, a professor at Regent Law School and a former defense attorney, tells you why you should never agree to be interviewed by the police.

In part II, an experienced policeman, Officer George Bruch, who is now a law student, tells you why you should never agree to be interviewed by the police.

Click here to view the embedded video.

I was once told by Reid Buckley (Willaim F. Buckley, Jr’s younger brother and a famous debater in his own right) that the most potent force one has in dealing with a hostile interrogator on TV or radio is silence. Silence is death to them. Silence makes them keep on jibbering and end up looking the fool. But most people fall into the trap of the much more experienced talking heads and end up looking the fools themselves. In the clip below, you can see what I mean about the silence and one word answers. Watch the poor woman conducting the interview struggle.

MD and I have been on many, many TV and radio shows, and what we’ve learned from it all (plus from talking to a lot of people in the biz) is that it’s all entertainment, pure and simple. Bill O’Reilly, Anderson Cooper, Chris Matthews, all of them, are all entertainers. If their shows aren’t entertaining, they lose ratings, and they ultimately go off the air. Many people think of these folks as hard news people, but they’re not, they’re entertainers. So they’ve got to be entertaining. And the way most of them are entertaining – especially the Sean Hannity types – is by attacking their guests.

Most guests who go on these shows are experts of some kind and they know their stuff, so they figure they can hold their own with O’Reilly, Hannity or any of the rest because the expert knows that he/she knows way more than the interviewer about the subject in which the experts are expert. What the experts don’t count on, though, when they walk into the lairs of O’Reilly, Hannity, Matthews et al are that they are experts in doing live TV and in savaging guests whose opinions they don’t like. And the guests pay the price for their hubris.

The poor expert – who is used to refined academic debate – is devoured alive and made to look the ill-prepared fool despite having incomparably more knowledge of the subject in question than does the interviewer.

One has to be prepared.

The one time I was on the O’Reilly Factor I was prepared. It was kind of a weird experience unlike any other TV I’ve done. I was in a Fox affiliate studio in Albuquerque, New Mexico all mic’d up and ready to go. I was setting at a desk staring at nothing while people milled around in the studio. All of a sudden this whiny, whiny voice (that I didn’t recognize) comes into my earpiece saying: “Hey, Doc, it’s Bill O’Reilly. I’m going to start out asking you about…(whatever it was; I don’t specifically remember), then you give me your answer, then we’ll bat it around a little. I’ll be back in a minute.” (I’ve listened to Bill O’Reilly a thousand times since then with my eyes shut, but he still never sounds as whiny as he did when his voice was suddenly in my ear that day.)

Pretty soon, here he comes and we’re on the air. Now I’ve been told that O’Reilly can see the people he interviews while he interviews them so that he can react to what they’re saying, while those being interviewed don’t have that option. I don’t know if he could see me or not, but I definitely could not see him. There was a monitor to my right, but I worked not to look at it. (You can see inexperienced people on TV looking to their left or right during one of O’Reilly’s interviews because they’re looking at a monitor to see the show in progress. The folks at home don’t know that’s what they’re doing – the folks at home assume the interviewee can see O’Reilly – and it looks like they’re being shifty eyed.) I had to stare directly ahead into the camera as I answered the questions coming in through my earpiece.

I knew I was going to be on the show so I watched all I could of it before my turn came. I realized early on that Bill is a big fan of himself and of his own books. In fact, I think he’s prouder of his books than anything else because he refers to them constantly. I got a copy of his most recent book, read it, and had a few pithy remarks under my belt in case things took a turn for the worse for me. They didn’t ever go bad, but I did slip in a comment, which I’m sure mollified him (it wasn’t really a hostile interview, but I’m sure that many people who go on the show don’t think it’s going to be hostile until he turns on them, so one never knows) and kept things moving along without my getting attacked. Although I know much, much more about nutrition than O’Reilly will ever know, I’m smart enough to know that he is a pro at making people look bad irrespective of how smart they are, so I didn’t want to give him the chance. Thus, I did my homework.

In the clip below the interviewer is totally benign. The interviewee is the winner of a national spelling bee. I’m sure the interviewer figured this would be a piece of fluff, but instead she walked into a buzz saw. The kid being interviewed obviously has Asperger’s syndrome: he’s incredibly intelligent, but can’t really abstract well. He is totally concrete in his thinking. The interviewer is used to throwing out open ended questions and let the interviewees babble on: in this case she got yeses and nos. Which is another good example of what not to do on an interview if you ever want to get asked back. Don’t answer a yes or no question with a yes or a no: ELABORATE. That’s what the interviewer is giving you the opportunity to do.

(What I mean by this kid’s being concrete in his thinking is when the interviewer asks him what his mom said when he won. I’m sure that his mother had a lot to say to him after he won, but right at the moment he won, he was on stage and his mother was in the audience. But the question wasn’t the more precise: What did your mom say to you when she first saw you after you won? The question was the more societally normal: What did your mom say when you won? Watch and listen to his answer. This lack of ability to abstract from what is an imprecise, but commonly structured question is pretty common with Asperger kids.)

Watching this video you can see what happens to the composure of the interviewer when someone doesn’t follow the expected norm. She is desperate to salvage the spot without looking like a total moron, which she ends up doing anyway. You may be wondering why she doesn’t just abort, thank the kid, and move on. Because these shows are entertainment, they are precisely scheduled. Whoever is going on next may not be set up, there is nowhere to go, which is why silence is so deadly. Another thing this spot shows is just how long three minutes can be on live TV. The first time I was told that I had three and a half minutes on a big show, I was totally disappointed. The person setting up the interview told me that that was a huge amount of time. When I was on it seemed to pass in a flash, but as you can see, it can be be an eternity if it’s going badly.

So, here it is. The innocent interviewer thinking she’s going to do a feel-good piece. The interviewee who is bright as all get out, but totally unimpressed with the interviewer and the situation. And who can see no shades of gray: only black and white. The two are on a collision course that I’m sure left the interviewer (who did as good a job as she could under the circumstances) drenched with sweat and running for her Xanax as soon as she could get off the set.

Enjoy and learn.

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!