MD and I just got back from yet another cross-country trip, which gave me the opportunity to catch up on my reading.  While reading a golf magazine, of all things, I came across an article that demonstrates why all such articles should be taken with a grain of salt.  I can’t tell you how many letters MD and I get from people who become concerned because they read a piece in a magazine or newspaper that, for whatever reason, got under their skin.  So, I thought dissecting this article like I did a while back with a scientific study would be instructive.

Before taking these kinds of pieces seriously, you’ve got to realize how they are structured.  And believe me, they are as structured as a sonnet.

Freelance writers are always trying to get their pieces sold, and they write them to a formula that most magazines demand, which is why most of them are pretty much the same.  Just switch the experts and the subjects and you’ve got an article on most anything.  Magazine editors give writers assignments often telling them what they want the article to say and how many words they want it said in.  The writer’s job is to follow the format, cram the info into the required number of words and sound authoritative.

Your job as a reader is to realize this structure and plumb it for any valid info while not being distracted by the authorial sleight of hand.

This particular article, appearing in the July 2009 edition of Golf Digest, is cleverly titled “The vitamin D-bate,” and was written by an author with the initials RK.  I’m not trying to hide the name of the author to prevent embarrassing him or her – that’s how the author was listed at the end of the article

These pieces typically hew to the following format: they start with a lede that poses a dilemma followed by an introductory paragraph or two expanding upon the problem; they then have a statement from one ‘expert’ followed by a dissenting statement by another ‘expert;’ then they neatly tie the whole thing up with a pronouncement by the ultimate ‘expert’ who sagely answers the question posed in the lede.  All neat and tidy – and typically wrong.  In the case of the article under discussion, not only wrong, but breathtakingly stupid.

The lede for The vitamin D-bate is the subtitle of the piece.

Sun exposure is a source, but how much is necessary to stay healthy?

Since most golfers spend a fair amount of time in the sun, this should be of interest to them.  So, let’s read on to see how much vitamin D we really need.

After the lede we get the introductory paragraph.

In the vitamin world, D has become a rock star of late, with some experts claiming it might protect against cancer and reduce high blood pressure.  And we already know it’s essential for maintaining bone density and a functioning immune system.

Okay, articles are popping up all over about the benefits of vitamin D, and we’re convinced of its importance.  So how do we get it?

RK turns to the first ‘expert’ for advice.

It’s such an important vitamin that in May, the Skin Cancer Foundation doubled the recommended minimum daily intake from 10 micrograms to 25 (or 1,000 iu) for anyone younger than 50 who has limited sun exposure (including those who always wear sunscreen to protect their skin against the sun’s harmful rays). Ideally, the SCF says, people 18 or older should get up to 50 micrograms [2000 IU] per day.

Although the sun’s ultraviolet B rays help the body synthesize vitamin D, the SCF insists that the sun is not necessary to obtain sufficient amounts.  It suggests getting vitamin D from supplements and food such as milk, yogurt, egg yolks and oily fish (salmon, mackerel, cod).

At this point we need to ask ourselves ‘what is the expertise of the Skin Cancer Foundation?’  If we go to the SCF website, we discover that this foundation has been around for about 30 years and is underwritten by the cosmetics and skin care product companies.  Hmmm.  Maybe not the most reliable ‘experts’ on vitamin D.

But our freelancer has the needed quote to set up the debate.  Now RK decides to call the Vitamin D Council to come down on the opposite side of the debate. (The vitamin D Council really is the expert in this debate.) To get the debate going, however, RK needs to ask something provocative of whomever he speaks to at the Vitamin D Council. If this spokesperson tells RK essentially the same thing that the spokesperson from the SCF did, then there is no debate.  So, RK has to ask the right question to get the needed quote.

RK probably tees the question up much like this: I’ve been told by others that sun exposure isn’t necessary and that all one has to do to get enough vitamin D is to take a daily multivitamin and drink plenty of milk.  Is this true?

Of course the Vitamin D Council spokesperson is going to heartily disagree (and rightfully so) because it takes much more than that if there is no sun exposure.  (The Vitamin D Council recommends somewhere in the neighborhood of 5,000 IU per day, followed up with blood tests for levels.)  Now RK has the other side of the debate because the Vitamin D Council obliges.

However, the Vitamin D Council disagrees: “If one regularly avoids sunlight exposure…to obtain this amount from milk, one would have to drink 50 glasses.  With a multivitamin, more than 10 tablets would be necessary.  Neither is advisable.”

MD and I have played this little game countless times with freelancers.  So much so, in fact, that we’re really reluctant to speak with them because we never know where we’re going to end up in the article.  Usually the interviews are 20-30 minutes long, and end up with one sentence being quoted, and often quoted out of context.  I imagine RK spoke with someone from the Vitamin D Council for that much time, if not longer.  And used this one short quote.

RK really had to work to make this a debate to follow the format. The SCF spokesperson said that people who got little sun exposure needed to take supplements, and, in fact, recommended that ideally people should get up to 2,000 IU per day, which is way more than any daily multivitamin contains.  So, the SCF and the Vitamin D Council are more in agreement than they are apart, but RK has selectively quoted to make it seem like a disagreement.

Now, following the format, RK has to bring in a moderator and give us the final answer we’ve all been waiting for.

So, what should you believe?

Are you ready?

According to dermatologist Michael Kaminer, who treats hundreds of patients with skin cancer annually, the best thing to do is find a middle ground.

Well, the SCF recommends 2,000 IU per day and the Vitamin D Council recommends 5,000 IU per day, so is the middle ground 3,500 IU per day, an amount that splits the difference?

Not quite.

“During long, dark winters where we are covered in clothes, I take vitamin D supplements,” says Kaminer. “But in the summer, grease up with sunscreen, drink some milk, and hit the golf course! You’ll be swimming in vitamin D.”

Oh, really?

I told you it was breathtakingly stupid.

Does this guy understand that ultraviolet B (UVB) rays are what both make vitamin D and burn the skin?  If you put on sunscreen that blocks UVB, then you block the production of vitamin D.  Pretty much completely. Even weak sunscreens with an SPF of 8 block 95 percent of vitamin D synthesis.  So greasing up with sunscreen is definitely not going to have you “swimming in vitamin D.”

In fact, if you’re not careful, you’ll end up more prone to the worst kind of skin cancer: melanoma.  Why?  Because a sunburn is nature’s way of telling you you’re getting too much sun.  Unless you’re a moron, you get out of the sun before you get badly burned.  With graduated sun exposure you develop a tan, which prevents burning because the tan blocks the UVB much like a sunscreen does.  But the tan blocks UVA also.  UVA is the wavelength that doesn’t really burn but does stimulate the melanocytes (the pigment producing cells), which can cause melanoma.  If you slather on the sunscreen and stay out in the sun all day, you don’t get burned, but you do get a ton of UVA, which, until fairly recently, wasn’t blocked by sunscreen.  Now sunscreens contain agents that block both UVB and UVA, but no one knows yet whether these will prevent melanoma in the long run.

The paradox of melanoma is that this cancer typically develops as a response to too much sun but people with chronic sun exposure incur it less frequently than those with sporadic sun exposure.  This paradox can be easily explained.  Those who are out in the sun a lot develop a tan.  The tan blocks UVA, so there is less of the simulation for melanoma.  Those who go into the sun occasionally – office workers who vacation at the beach for a week – use sunscreen and stay out too long, receiving way too much UVA. UVA that increases the risk for melanoma.

I didn’t intend this to be a discourse on melanoma, sunscreens and vitamin D, but the idiotic response given by the ‘ultimate’ authority in our Golf Digest article got me going.

The take-home message from this post is to look for the pattern in these kinds of articles because they’re pretty much all the same.  You end up with a freelance writer arranging the experts to prove whatever the freelance writer – who is certainly no expert – wants to prove.  Or it may not even be what the freelancer wants to prove, but it is a function of how the best quotes fit with the structure of the piece.  “Grease up,” “hit the golf course,:” “swimming in vitamin D” – all are more pithy and memorable than any of the quotes above them.  Chances are RK wanted to end the piece with a bang, so he/she used the better quote giver as the ultimate expert.

Just remember, these kinds of pieces are put together more for their style than their content, so don’t put much faith in their accuracy.

More on vitamin D:

For info on the sun, vitamin D and its relationship with folate, click here.

Also, here is a great calculator designed by Norwegian scientists to determine how long you need to spend in the sun at various times of the year and various latitudes to get 1000 IU of vitamin D.  I recommend at least 5 times this amount to get 5,000 IU.

Click here to get a chart of US latitudes and longitude.

H/T to Annlee Hines for providing the link.

Changes in diabetic nephropathy

I received a short paper from a colleague in Portugal a couple of days ago that demonstrates in just a few pages how science should really work.

The paper from the journal Diabetologia reports on a study done in Pakistan showing that high-dose thiamin (vitamin B1) may be a valuable therapeutic agent in the treatment of diabetic nephropathy.   This small study certainly isn’t the final word, but it does show how medical science should work.

First, the paper starts off in the introductory paragraphs discussing how the idea for high-dose thiamine therapy came about.  Before we get into that, however, let me digress briefly to discuss diabetic nephropathy for those who are unfamiliar with it.

The main job of the kidney is to remove waste products from the blood while keeping the non-waste products, i.e., proteins, sugar, etc. in the blood.  You can think of the kidney as a sieve with tiny holes.  All the waste that needs to be filtered is small enough to fit through the holes while the substances meant to remain unfiltered are large enough to not fit through the holes.  If you were to pour liquid containing both waste and non-waste matter into a long tube with your sieve somewhere in the middle in a place non-visible to you, you could check to see if your sieve were damaged by looking at what comes out at the bottom of the tube.  If you find only waste, then you can be pretty certain that your sieve is functioning.  If, on the other hand, you find material coming out the bottom that should have been caught by the sieve, you can be pretty sure there are holes torn in your sieve.

This in very simplistic terms is what happens in the kidney.  Proteins are large molecules and should never make it through the kidney into the urine.  Protein in the urine in any significant amount tells you the kidney has a problem.  With simple lab tests we can identify microscopic levels of protein in the urine, and anyone having a certain amount is said to have microalbuminuria, which means microscopic levels of albumin (the main protein in blood) in the urine.

In people with diabetes, microalbuminuria means the kidneys are starting to develop nephropathy, or pathology (or disease) of the nephron (the basic unit of the kidney).  To go back to the sieve analogy, they’ve developed bigger holes in their sieve. This condition afflicts about 40 percent of those with diabetes and can (not that it always does, but it can) progress to complete kidney failure, requiring dialysis or kidney transplant.

Diabetic nephropathy is most likely caused by the toxic effects of too much sugar in the blood and is helped, and even reversed, by careful control of blood sugars.  Despite this common knowledge, many unenlightened people continue to treat the condition by limiting dietary protein instead of focusing on the continuing damage caused by elevated blood sugar.  In order to keep caloric intake up, what do people substitute for protein?  You got it.  Carbohydrates.  And since dietary carbohydrates become blood sugar fairly quickly, they end up damaging the kidney more than the protein they are replacing.

Now that you’ve got at least a working notion of what diabetic nephropathy is, let’s look at our paper.

The authors start off with a description of the research on thiamin to date that gives us a nice picture of how the various types of studies all tie together to make real science.

First off, someone noticed that people with diabetes and protein in their urine had low blood levels of thiamine.  This observation prompted researchers to do observational studies of this phenomenon.

In evaluating large numbers of subjects with and without diabetes and protein in their urine, scientists determined that the diabetics typically had lower blood thiamin levels than the non-diabetics.

But, at this step, these studies are simply observational studies and can’t possible prove causation.

The next step in the scientific evolution is to hypothesize that low thiamin levels are somehow involved in the development and/or progression of diabetic nephropathy.  If this hypothesis is valid, then giving thiamin should improve the condition.

Researchers gave thiamin to rodents with diabetes and discovered that increasing blood levels of thiamin reduced or eliminated proteinuria in the animal model.

Here is where the tricky point arrives in the study of drugs – trying them in humans.  As I’ve written many times in these pages, rodents are not just furry little humans.  What often causes no problems for them causes huge problems, including the ultimate problem – death – in humans.  So it is a difficult business to start giving experimental drugs to humans.

In this case, however, it isn’t so bad because thiamin – even in high doses – is non-toxic to humans.  The next step is the randomized, double-blind, placebo-controlled clinical study, which the authors of our paper under discussion performed.

Researchers randomized a group of 40 subjects who had diabetes and microalbunuria into two groups.  Subjects in one group got three 100 mg thiamin capsules per day; subjects in the other group got placebo.  (I couldn’t tell from the paper whether the three capsules were spread out over the day – I would assume they were – or were taken all at once.)  The two groups remained on their supplement regimen for three months followed by a two month washout (a period in which no one either thiamin or placebo).

The results were pretty spectacular.

There was a significant drop in the amount of protein in the urine of subjects taking thiamin as compared to those taking placebo.  Even more exciting was the following:

After [thiamin] therapy for 3 months, regression of microalbuniuria to normal urine albumin had occurred in 35% of the patients.

Over a third of the patients on thiamin had no more evidence of diabetic nephropathy, at least as demonstrated by protein in the urine.  This is a spectacular result, especially for a natural substance with virtually no toxicity.

I appreciate the way the authors of this paper presented their data.  It is much more informative than simply providing the average differences between the study group and the control group.

Take a look at the graphs below.  The upper figure is the overall change in microalbunuria between the groups.  The middle graph is the change in the subjects on placebo; the bottom graph shows the changes in subjects on thiamin.

As you can see, the results of each subject are presented a single line.  You can tell a lot from these kinds of graphs.  For example, you can see that in the thiamin group there was a generalized downward slope to all the lines, which means that all the subjects improved on the regimen, a fact that is most important.  The middle graph, the one showing the results from the placebo is interesting as well.  You can see that the vast majority of subjects had no change while a couple had significant changes.  Why would there be improvement on the placebo?  Who knows?  If I had to guess, I would guess that those subjects taking the placebo who showed the major improvement may have changed their diets on their own.  These were patients at a diabetic clinic who were being treated for their condition, so maybe these subjects were more aggressively treated.  But, it really doesn’t matter because we can see from the flat lines of most of them that there was no change due to the placebo.  This type of graph at least allows us to speculate and to realize why there was a slight drop in the average level of protein in the urine of even those subjects on placebo.

The authors note in their discussion that

this is an encouraging pilot-scale outcome that high-dose thiamin reverses early-stage nephropathy in type 2 diabetes.

They go on – as they should – to recommend larger scale studies to see if their findings hold up.

Based on this study, would I, myself, take thiamin in 300 mg per day doses if I had diabetic nephropathy?  Absolutely.

Although it is only a pilot study, the results are pretty stunning.  But the ‘drug’ is harmless.  So what is the risk?  A few pennies per day for the thiamin?

If this were a study in which, say, statins were used as the agent, I wouldn’t be quite as eager.  I would probably wait until other larger studies had replicated these findings.  Why?  Because statins aren’t harmless.  One can die from them. Or can have miserable generalized muscle aches and weakness.  In other words, there is a lot bigger downside to taking statins than there is to taking thiamin, so I need a much greater level of comfort to make the risk/reward calculation in favor of taking a statin.

The only weakness I can find in this paper is that the authors spent no time discussing the possible mechanism for the benefits of thiamin on diabetic nephropathy.  Perhaps they ran out of time and are saving it for another paper. Alas that is what has happened to me as well.  MD’s group is performing with the symphony today, and I’m being badgered to get ready to leave.  So, I, too shall leave a discussion of the potential mechanism to a future post.

Hat tip to Pedro Bastos for sending me this paper.

Happy with these results MD, our partner and I decided to take the next step and get an actual product made.  We did, and let patients try it.  Again, the patients liked the supplement and though they lost weight better on it.  Although we, too, thought the patients did better, we couldn’t really say because we hadn’t compared the supplement with a placebo in a controlled fashion.  We decided to take that next step.

We contacted a clinical lab that does testing for a fee (a substantial fee, I might add) and talked to the director of the facility, who was pretty discouraging.  He told us that he would be happy to take our money and test our supplement, but that we shouldn’t get our hopes up.  He related that his company had tested scores of nutritional supplements and had never found one that really did much.  And that he figured ours wouldn’t do well against placebo either.

We arranged for the plant that made our product to make a placebo that looked and tasted the same.  We sent it along with a large check to the clinical testing facility to do the double-blind, placebo-controlled trial.  In an interesting side note, the guy who ran the lab told us during our first call that he wasn’t going to do the test unless we used a low-carb diet as the control diet.  He hadn’t a clue who I was, so he wasn’t saying this for my benefit.  He had found in all his testing that neither the control arm nor the study arm ever lost any weight unless both were on low-carb diets.  We, of course, agreed.  In fact, we wanted it tested by people using low-carb diets because that was our target audience.

We helped set up the test protocols and turned the lab loose on the study.  The lab was in Bangor, Maine, and none of us ever set foot in it while the test was going on.  The study was a 6 to 8 week study (I can’t remember which because I don’t have the study with me) looking at a number of parameters, including weight loss.

I was in the Harvard Coop when I got the call from the lab director that the study had been completed and the double-blind codes broken.  It was a memorable call.  He started out by saying: “Well, I’ve got some good news for you and some bad news for you.  Which do you want first?”

Being the eternal optimist, I said, give me the good news.

He said:  “You have got a phenomenal product.  It works like nothing we’ve ever seen.  It works better than some drugs we’ve tested.”

The people on the supplement had lost almost double the weight (71 percent more, to be exact) than those taking the placebo.

As you might imagine, I was thrilled. But not all that surprised based on our reports from our own patients.

“So what’s the bad news?,” I asked.

The bad news, he told me, was that we didn’t have what he thought was a commercial product.  He said that he had to practically horsewhip some people to keep them on it.  He said he thought it didn’t matter how efficacious a supplement was if people wouldn’t take it.

He had a point.  And, admittedly, the first primitive version of our product was pretty rough.  The product, which we later named Pentabosol,  is a powder that you dissolve in water (cold or hot like a tea) and drink.  The early study version mixed about like sand mixes with water.  You had to put it in the water, then swirl the water in the glass while you drank the stuff.  And it didn’t taste all that great.

We went through a couple of manufacturers before we finally found one who figured out how to make Pentabosol so that it actually mixed into the water and tasted good.  The ultimate version is a lemon lime sort of flavored drink that is reminiscent of Country Time Lemonade (at least it is to me).  You take a serving of it on an empty stomach in the morning and at bedtime.  It has no ephedra, no stimulants, and no real side effects to speak of.

We ended up marketing it successfully and have sold, I would guess, close to a million cans of it.  Due to circumstances that arose in 2003 (circumstances worthy of a long post all on their own), we decided to quit promoting Pentabosol so heavily and turn our attention to another supplement for brain health that we had just gotten through an extremely expensive and lengthy clinical test.

With that preamble, let me now make the call for help.

If anyone reading this post has used Pentabosol and lost any significant weight, we would love to use you as a testimonial.  We are cranking up the promotion of Pentabosol again and really need some good before and after photos.  If you are willing, contact me via the comment section and leave your email.  Your email won’t be posted and your comment won’t be posted if you tell me not to.  If you’ve had experience with Pentabosol and would simply like to comment about it, be my guest.  I’ll post all comments.  The good, the bad and the ugly.

To give you an example of what I’m talking about as far as before and after photos, here are some before and after photos of our faithful assistant Kristi, whom we rely on for just about everything.  If Kristi took a powder, our operation, such as it is, would be dead in the water.  I hope she doesn’t read this or she’ll be whining for a raise.

Here are a couple of photos of Kristi and her husband taken not too long ago.  In fact, the one was taken at our place in Tahoe.

Kristi decided to go on a low-carb diet and take Pentabosol religiously, and here are the results.

These changes didn’t happen overnight, but they did happen.  And, based on what we found in our study, they happened more quickly than on diet alone.

Kristi accompanied us on our trek to Expo West that I wrote about in the last post.  In one of the photos I posted, you could see a woman in front of a vegetarian booth.  If you wondered how I brazenly took that photo, here’s how I did it.  I had MD and Kristi pose in front of and off to the side of the booth, and I pretended to take their photo.  The photo I posted earlier had Kristi and MD cut out.  Here is the actual photo in it’s entirety.  As you can see, Kristi is still thin.  And even has a little more to lose.  She went from a size 14 to a size 6.

So, once again, if you’ve used Pentabosol and lost weight and are game, let me hear from you.  Thanks in advance.

The standard Western diet is sadly lacking in omega-3 fats. Most of the recommendations we hear are to increase our intake of omega-3s by eating fish a few times per week. Most people who do eat fish eat tuna, the most readily available fish around that contains a halfway decent level of omega-3 fats.

But news reports over the past several years have put a lot of us off of tune, at least the canned variety, with reports of how much mercury such tuna contains. MD and I have opted to get our tuna as sushi grade tuna that we get either at Japanese restaurants or by purchasing it at a natural foods grocer and making our own sashimi. Now comes a report that gives us pause.

The International Herald Tribune published an article story showing that even sushi-grade tuna is crawling with mercury, which makes fish eating now a Faustian bargain. We can get the omega-3s, but at the expense of a ton of mercury.

Recent laboratory tests found so much mercury in tuna sushi from 20 Manhattan stores and restaurants that at most of them, a regular diet of six pieces a week would exceed the levels considered acceptable by the Environmental Protection Agency.

Sushi from 5 of the 20 places had mercury levels so high that the Food and Drug Administration could take legal action to remove the fish from the market. The sushi was bought by The New York Times in October.

But maybe this is just a freaky sample. I’m not so sure. And the article goes on to state that the more expensive the tuna, the greater the contamination.

These findings reinforce results in other studies showing that more expensive tuna usually contains more mercury because it is more likely to come from a larger species, which accumulates mercury from the fish it eats. Mercury enters the environment as an industrial pollutant.

Now, I love sushi (actually, MD and I almost always opt for sashimi, which is the raw fish without the sticky rice, as shown in the photo above), but I’m not really willing to sacrifice my health for it. I get most of my omaga-3 fat from the krill oil that I take daily. Krill are tiny shrimplike creatures that are at the bottom of the food chain, and, thus, don’t concentrate mercury in the same way that fish do. And krill have a unique phospholipid structure to their fatty acid bonds that makes them much more absorbable, preventing the fishy smelling belching that fish oil capsules sometimes cause. If you want to get your omega-3s as tastelessly and painlessly as possible – and without the risk of mercury toxicity – you can’t go wrong with krill oil.  Even a few years ago krill oil wasn’t readily available, but now you can find it all over the place.  And it’s not all that expensive.   So, to get your daily dose of omega-3, down a krill oil gelcap or two and forget the recommendation to eat fish several times per week.

This issue reminds me of a talk on the mechanism of action of statins that I sat through at a medical meeting in Napa, California about 10 years ago. At that time researchers knew that along with their cholesterol-lowering capabilities statins also acted as anti-inflammatory agents. Statins increase the production of nitric oxide, an extremely short acting substance that has relaxing and anti-inflammatory effects on the lining of the arteries. The researcher giving the talk was from Harvard, and he had done a study in which he compared the nitric oxide releasing ability of l-arginine (an amino acid) and a statin drug. He found that the way that statins increased the production of nitric oxide mimicked the way l-arginine did the same thing. He proudly announced that his research showed for the first time how statins really worked to exert their anti-inflammatory effects. I wondered at the time why he didn’t just recommend that patients be given l-arginine – a natural substance with virtually no side effects – instead of statins? I would have asked the question, but this was a mainstream medical meeting, and I figured if I asked that question I might be stoned.

Thanks to this and subsequent research, we know that the anti-inflammatory benefits provided by statins can be had cheaper and more safely by taking l-arginine, available at health stores everywhere. ( Incidentally, know what the best natural source of l-arginine is? Wild game. Just another piece of evidence in favor of a Paleolithic diet.) And now we know that statins increase production of vitamin D, another heart-healthy substance.

Dr. John Aloia and his group (who did the study I posted about previously) noted that their African American subjects who were on statins had significantly higher levels of vitamin D than did those who weren’t on statins.

A total of 208 women were randomized to receive vitamin D3 (n=104) or placebo (n=104). 51 women were on statins. At baseline, the subjects on statins had a significantly higher 25-OHD level [a measure of vitamin D in the blood] than the subjects who were not on statins (51.2 ± 20.1 nmol/L versus 43.2 ± 18.0 nmol/L respectively, p=0.008). This was also true when averaging 25-OHD levels across the 3-year study period and looking at active and placebo patients separately. 185 subjects had follow-up 25-OHD levels drawn every 6 months during the study. Higher levels were seen in the statin use subgroup whether they were on placebo or active vitamin D. There was no interaction seen between vitamin D use and statin use, i.e. the impacts are additive (p=0.5502).

(Click here to read Dr. Aloia’s report, published in the American Journal of Cardiology a couple of months ago. )

It has been shown that patients on statins have fewer hip fractures as compared to those patients not on statins. Is this due to the increased levels of vitamin D? Probably, but no one knows for sure yet. And no one knows how statins increase vitamin D levels.

But I do know that I would much prefer to take a few grams of l-arginine and 5,000 IU of vitamin D3 daily than I would to take a statin. All of the benefits and none of the risk at a fraction of the cost. Hmmm. This isn’t rocket science – just common sense.

Just got in from a whirlwind trip to New York, which ended up what with family and business obligations being the busiest trip there I’ve ever experienced. MD and I have just enough time to go through the mail, do laundry and head back to the airport to fly to Dallas for Christmas. Once back, we’ll have some time of our own.

I have to apologize yet again for not answering the many comments that have stacked up. I simply haven’t had time. But I will get to them, I promise.

The photo at the top of this post is St. Patrick’s Cathedral on Madison Ave. taken from our hotel room window a couple of nights ago.

Below is a photo of the two women in my life: wife and granddaughter. And below that is a photo of an exhausted grandfather and an even more exhausted granddaughter taken at about 1 AM, way past both of our bedtimes.

My harried schedule cut short my meeting with Gary Taubes so that I wasn’t able to convey to him the questions that many of you posted. I think I can talk him into either a guest post or a Q & A with answers posted. Gary and I were supposed to get together last Friday late in the morning. He had a lunch scheduled in the early afternoon, so we figured we would have plenty of time before to meet. I caught a cab to head down to our meeting place at 11th and 6th and got snarled up in all the holiday traffic and was abysmally late. By the time I got there, we were able to chew the fat for only 45 minutes or so. I tagged along with him to his lunch meeting, which was with Nina Teicholz, the journalist who wrote the great article on saturated fat for Men’s Health. (Gary and Nina are probably the only journalists who are low-carb friendly in New York.) I could only hang out for a few minutes with them before I had to scuttle back to midtown for yet another appointment. I got smart on the way back and took the subway to avoid the horrendous traffic.

I’ve got a bunch of posts in the works: new low-carb papers, vegetarian diets and free radicals, more Anthony Colpo silliness, the Anthony Colpo disciplinary post, and vitamin D.

While awaiting my scheduling problems to abate so that I can get back at it full force, here is a great article on the importance of vitamin D from the CBN, of all places. Be sure to watch the video. I tried to embed it and ended up crashing my machine. I think I’m the only person who can crash a Mac. If someone out there knows how to embed this video, let me know, and I’ll give it a try.

If you live anywhere in the northern US (and that’s above El Paso, Texas), in Canada or in Europe, you need vitamin D3 in pretty large doses. I take at least 5,000 IU daily during the winter and sometimes a 50,000 IU booster capsule if I’ve been exposed to a lot of sick people (for instance the lady who sat across the aisle from me on the flight last night and coughed the entire way). If you are like most of the New Yorkers I met and are fish-belly white, you need vitamin D. If you are African American you need vitamin D. Don’t leave home without it.

I’ll post again from Dallas. And, if I have my normal airline experience, I should have a lot of time cooling my heals at various airports tomorrow. If I do, I’ll catch up on all the comments that have stacked up. Pray for me.

MD and I have been subsumed by the whirlwind we’ve been in since our arrival in New York a couple of days ago. It seems as if we’ve trekked from first one meeting to the next without a break in between. I haven’t had time to post, and I’m woefully behind on answering and posting comments that have come in (about 80 at last count). If you’ve sent a comment and wondered why it has apparently vanished, now you know why. Don’t despair. I think I’ll have some down time this weekend so that I can catch up.

It’s been a while since I’ve been to New York in December, and I hadn’t remembered how short the days are and how dark and overcast as compared to Santa Barbara and Lake Tahoe, both places of almost constant sunshine. While contemplating this lack of sun I came across an article (actually a letter in response to an earlier article) in the journal Epidemiology and Infection that I found interesting and wanted to pass along. (Unfortunately there is no abstract for this article, so I’m not providing a link.)

Dr. John Aloia and his group at the Bone Mineral Research Center at Winthrop University Hospital in New York reported on a three-year study they had done on 208 African American postmenopausal women (a group at great risk of vitamin D deficiency) who were supplemented with either vitamin D or a placebo. For the first two years the active group received 800 IU daily, which was increased to 2,000 IU daily in the last year of the study. In the three years of the study 34 patients reported cold and flu symptoms, eight in the supplemented group and 26 in the placebo group (p<0.002). This showed that participants who got a placebo had a 300-percent greater risk of having a cold or flu, and that vitamin D supplementation provided a highly significant protective effect.

I’ve been planning a major post on vitamin D for over a year now, but it seems as if every time I turn around there is a new paper that I want to incorporate. I’m still planning the post, but for now (especially after experiencing first hand just how weak and watery the sunlight is in northern climes) I wanted to get this brief note up to encourage everyone to take vitamin D3 at least during the winter months. There is abundant evidence that vitamin D helps prevent cancer, heart disease, colds and flus, along with a host of other disorders…and even helps people lose weight. Vitamin D3 is the optimal form in which to take this supplement. I would recommend at least 5,000 IU per day.

We will soon have a 5,000 IU dose up for sale on our website, and lest you think this post is a cheesy attempt at selling supplements, let me assure you that no one ever got rich selling vitamin D3. It is dirt cheap. It’s just that the 5,000 IU dosages are difficult to find, and many people hate taking a handful of large capsules to get that amount, so we searched out a source to make available to our readers. We actually have the supplement in the warehouse, we just don’t have it up on the website yet. And I don’t have a clue how to get it there, but I’ll get someone who does to get it up as soon as I can.

Wherever you get it, just get it and start taking it. And don’t worry about vitamin D toxicity. An excellent review article in the American Journal of Clinical Nutrition about a year ago showed that based on a large number of studies a dosage of 10,000 IU per day would not be toxic in the long run. So, if you only take one supplement this winter, make it vitamin D3.

A recent British Medical Journal article describes the type of folic acid commonly used:

The form of folate in supplements and in fortified foods is pteroylmonoglutamate (PGA), a form that does not occur in nature. It is both cheap and stable unlike most native forms of the vitamin. The body metabolises PGA into methylfolate, the normal form of the vitamin transported in plasma. However, research shows that this absorption and biotransformation process is saturated at doses in the region of 400 µg PGA or less. Thus at doses at or just below 400 µg PGA all this synthetic form of folate is converted into biologically active methylfolate during absorption. At higher doses synthetic PGA is also transported into the blood in a manner that is directly proportional to dose. This raises the possibility of a lifetime’s exposure to unmetabolised PGA where mandatory fortification is undertaken. Although such exposure may present no health risk at all, we cannot know this for certain.

Since PGA is the form of folic acid most commonly used in supplement form, and since many physicians prescribe doses in the 5 mg range (5000 micrograms: more than ten times the amount needed to give maximal blood concentrations), this adds to the dosage one gets through food fortification, from primarily breads and cereals.

When Dr. Lucock, the researcher writing the BMJ article, analyzed patients who were taking large doses of PGA for vascular problems, he found that a number of them had exceedingly high values, which “were mirrored by the corresponding red cell folate values” indicating truly high values and not a measurement error. Upon more sophisticated analysis, Dr. Lucock found

that only around half of the serum folate measured by routine haematological assay was methylfolate. The assumption was that the remainder was unmodified PGA, as only this and other partially oxidised folates do not fluoresce and thus are not directly measurable by high pressure liquid chromatography.

Dr. Lucock then states:

Nobody yet knows what, if any, the long term biological effect of mandatory fortification of grain products would be at a national level. In a recent report on the situation in the United States, more people than expected were subjected to the established tolerable upper limit of exposure to PGA.

I looked at the article in the Journal of Nutrition that was the reference citation to the statement about more people in the US than expected had elevated folic acid levels. The paper points out that most of the people falling into this category were those who both ate fortified foods and took folic acid supplements.

Since bread and cereal products are those fortified in the US at this time, I would be willing to bet that most people on low-carbohydrate diets do not have excess levels of unaltered PGA.

A well designed low-carb diet will contain plenty of green leafy vegetables and colorful fruits, all of which have large quantities of folate. It’s only when the diet shifts from all these healthful foods to mainly refined carbohydrates, that folate fortification is needed. And what better foods to fortify than those that the great hordes of the unwashed masses are adopting as their dietary staples.