The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

_I asked Martin what he had for breakfast: a whole wheat bagel with no-added-sugar jam. Lunch: a turkey sub on whole grain bread, no mayonnaise. Snacks: baked chips, pretzels ("a low-fat snack!")._

What do you think of Joel Fuhrman's approach? He would not allow people to eat bagels, jam, bread, chips, and pretzels. The base of his diet is veggies (half raw, half-cooked), then fruits, beans, potatoes, raw nuts, and raw seeds. Grains are at the top of Fuhrman's food pyramid.

http://www.nutritionforwellness.org/img/food_pyramid.gif

Also, when he says "whole grains", he means unbroken grains like brown rice, oatmeal, etc. Not flours, or pastas, or breads made with flour. The only breads he would allow are things like sprouted grain breads, made without any flour.

Most people who eat a low-fat diet eat bad foods. They don't eat high quality foods. Dr. Fuhrman claims to lower triglycerides and improve all other health markers, because he stricly limits foods like flour, fruit juice, vegetable oils, sugar, etc. Maybe a low-fat diet based on grains (esp flours) will raise the triglycerides, but a low-fat diet based on vegetables, fruits, beans, nuts, and seeds (Fuhrman's) wont.

Fuhrman emphasizes nutrient-density far more than people like Dr. Dean Ornish. Whole grain flours are very perishable and quickly turn rancid. Weston Price pointed this out, but most people didn't bother to listen and still don't. Here's an article about how whole grain flours cause sterility if they are stored for as little as 15 days, while flour and bread that is fresh-ground doesn't. How many are eating fresh flour? I would say <1%, maybe zero.

http://eap.mcgill.ca/Publications/EAP35.htm

Just a small correction - Dr Fuhrman's diet is not really low fat like Ornish/McDougall, the only similarity to those diets is the predominance of plant based foods.

It eliminates/restricts saturated fat and plant oils but he is VERY pro 'good' fat in it's natural packaging i.e. nuts, seeds, avocado and fish oil in some cases (he prefers DHA from algae due to mercury in fish for most people and esp pregnant/lactating/babies but for high doses still recommends high quality fish oil especially for autoimmune patients). Re the nuts/seeds/avocado - in his weight loss strategy he does limit them but a minimum level is compulsory on a daily basis and he actively encourages people to have them while maintaining ideal weight i.e. can go very high if very skinny, lower if overweight but cannot eliminate them.

Yes, a reduction in unhealthy fats (saturated, trans, polyunsaturated) helps. But a reduction in fats of all sorts is not necessary and can, in fact, worsen the problem. We learned this lesson years ago with the Ornish diet and similar ultra low-fat approaches. When you reduce fat intake significantly to <10% of calories, triglycerides go way up. In those days, it wasn't uncommon to see triglycerides skyrocket past 200 or 300 mg/dl on these diets.

Do saturated fats elevate triglyceride levels in the body?  Jim

While I certainly enjoyed your book and am extremely grateful for your generous sharing in your daily blog, I am very troubled by this blog entry. Over the last day I have been thinking quite a lot about it off and on, and that would be because I have three stents implanted; two Cypher and one Taxus.

Since my dates in the hospital cath lab in early 2004 I have been following along with TYP principles carefully with the hope of being additional plaque neutral or even a bit of regression, but I see from this entry my hopes might be dashed.

Your statement in the blog entry "I've seen this phenomenon several times now", does this mean it happens most always, or sometimes, or occasionally? What is the game plan now for these patients? Do they (or did) have any similarities that might be contributing to their plaque growth (LPa, diabetes, vit. D, BMI, gender, etc), or are their lipoproteins and assays corrected to perfection?

Thanks again for all that you do, your program and willingness to share is unique and very special to many of us. If you could follow up sometime on this situation with a future blog entry or observations, I would be most appreciative.

With concern,

Neil

Neil--
All this means is that the presence of a stent may modify the potential for reversal ONLY IN THE VICINITY OF THE STENT. Other areas, meaning the majority of your other arteries' lengths, are still subject to your control and the benefits of your prevention program.

Keep in mind that this is an experience involving just a handful of patients. To my knowledge, there are no formal published experiences like this to compare to. All patients had their patterns corrected to perfection by Track Your Plaque standards and don't seem to be distinguished by any one single lipoprotein pattern.

My "gut sense" is that the sort of plaque growth that we see around stents and tracked by heart scanning does not carry the same implications that non-stent associated plaque does.

I just found your site recently and have been reading through the posts.  I find it very educational.  Thanks!  

I'm curious.  Were the stents medicated stents (since it is my understanding that they prevent this kind of thing)?

Thanks for the excellent post! Bookmarked! Will come back again…

Do you take the 8,000 units *daily*?  I started out with a serum vitamin D level of 12 ng/ml and was prescribed 50,000 units per *week*.  That got me up to 27 ng/ml (which the doctor considered acceptable).  At that point, a different doctor advised me to take 1,000 units a day, but I started taking 2,000 units and have now reached 60 ng/ml.  I was concerned that 2,000 might be excessive, and now that I have reached a good level of serum D, I thought maybe I should cut back to 1,000.  But you take 8,000 daily?

D.S. 8000 daily x 7 days = 56000 weekly, not all that different from 50000 weekly.

Love the post Dr. Davis.
I have NOT been sick in 2+ years... seriously.  I tell people, I don't know if it's the 'low carb primal' meal plan ... or the almost daily exercise ... or the daily D3.  Most likely a combination of all 3.    I take 4-8k daily depending on the season and 'sunlight' exposure.

Thriving!... not just surviving.

Steve

This may be another case of everyone being different. Over the course of three years on 2,000, then 4,000 units a day I got to 48 then 63 ng/ml. When I upped it to 6,000 units I hit exactly 100 ng/ml. When I was at the lower levels I felt fantastic, at 100 I did not.  I recommend frequent testing to see what amount brings you to the ideal level and keeps you there.

Would it be beneficial to take K2 along with D3 just in case ?
Vitamin D boosts calcium availability and I wouldn't want it to finish on wrong places.

Yes, K2, magnesium and zinc should also be taken if you  suspect that your diet might be low in these. I discovered that I do not absorb supplements very well unless they are in liquid form.

DS and Johan--

Be careful: You're confusing cholecalciferol (D3), the human form of vitamin D, with ergocalciferol (D2), the non-human plant or mushroom form.

Vitamin D is a (pro)hormone. Humans should ONLY take the human form, never the plant form. For one thing, 50,000 units of D2 is apprximately equivalent to 15,000 units D3, because it's different. It is inferior.

If a doctor prescribes D2, it's because he has no idea what he/she is doing. There is absolutely NO reason to favor D2 over D3.

Great, Steve!

I've personally been enjoying the same experience.

Absolutely. Checking every 6 months has worked out very well for us.

There are reports that high intake of D3 will cause calcification of arteries and heart valves. The reported levels are over 50-60 ng in the serum D3. So there seems to be s diminishing effect of high D3 intake. Also it seems that taking K2 will mitigate or offset this effect. There are conflicting reports on this though. Any thoughts?
Renfrew

That's true of the plant forms of all the fat-soluble vitamins.  We have been badly misled.

The statistics and study summaries I've read seem to indicate that somewhere between 40 and 50 percent of the population cannot convert beta carotene to vitamin A in large enough amounts for BC to be useful as an A source.  If the respondents in those studies were only healthy people, the total percentage is far higher;  diabetics and hypothyroid people can't make the conversion.  And that's only adults.  Infants and young children can't make the conversion either, which pushes the percentage even higher.  Vitamin A has many tasks it performs in the growing fetus; helping the urinary tract develop is one of those tasks.  The Mayo Clinic tells us on its website that urinary tract defects are the most common class of defects in the United States.  Vitamin A is also important in eye and tooth enamel development, among the many, many other functions it performs.  How many people are walking around with eyeglasses, and how many young children are getting cavities now?

The Rotterdam study showed that vitamin K1 in plants does nothing to mitigate heart disease risk, whereas K2 from animal organs and dairy does.  I have heard from other sources that the K2 in natto (mk-7) does not cross the placenta, telling me it's less important to our health than the K2 from organs and dairy (mk-4 or menatetrenone).  K2/mk-4 is important in insulin sensitivity as well as heart health and bone and tooth strength.  But most experts focus on K1 or on the K2 in natto, to our detriment.

A, D, and K are so vitally important to good physical development and avoiding chronic disease.  The information is out there, in study after study.  If the experts won't admit to it, we need to educate ourselves.

100 ng/ml is too high for anybody.  Dr. Davis probably hits the high end of acceptable.  No wonder you felt bad.

I insist on supplementing three of the four fat-soluble vitamins because I've found out the hard way that the plant precursors of those vitamins DO NOT work well for me.  I suspect my experience is more in the majority than the minority, too.  Here's my regimen:

Vitamin A from fish liver oil (read the label):  8000 IU
Vitamin D3: 5000 IU
Vitamin K2, analog mk-4 (menatetrenone): 1-5 drops of a liquid supplement in MCT oil.  This company suggests taking 15 drops a day, which is over 10,000 of the recommended daily intake, and I see no point in going that high.

If I could afford no other supplements, I always take these.  I suffered from a subclinical (at least according to mainstream medical practice) vitamin A deficiency from 2004 on up to 2007 or 2008 that manifested as reproductive health problems and also birth defects in my daughter.  No one suspected an A shortage as the problem.  I figured it out by happy accident.  I am apparently not a good converter of beta carotene and my daughter paid the price.  I don't like liver, and dairy and eggs are not high enough in the vitamin, so this is what I do.  And this way the vitamins all work together synergistically  and I don't have to worry about toxicity.

Yeah, I know, but I was taking 50,000 units weekly to rectify a profound *deficiency*, not as a maintenance dose.

I don't know if it was D2 or D3 when I was taking 50,000 units per week (by prescription; this was over a year ago), but the 2,000 units (OTC) I now take daily are D3.  If this dose has me maintained at 60 ng/ml, it's amazing how the 8,000 units you (Dr. Davis) take isn't too much.  I guess this goes to show that monitoring is crucial, and there's no one-size-fits-all in supplements.

vit D and sleep apnea
http://www.musclechatroom.com/forum/showthread.php?18736-quot-Vitamin-quot-D-is-a-Hormone.-It-Cures-Sleep-disorders-amp-many-ailments

Long time followers of this blog will recall that Dr Davis has discussed vitamin D and K2-related issues many times here. You can find many answers to your questions by following the search links http://www.trackyourplaque.com/blog/category/vitamin-d and http://www.trackyourplaque.com/blog/category/vitamin-k2. Not all posts will be directly related to this discussion, but you will know what is related and what is not.

I guess Vit D can also be gained freely from the nature.

To Jack K. ... posted here since Server blocked this where belongs.
Hi Jack K.,
You once mentioned being ApoE4 (I think), thus are specially interested; and are in your "prime" dedicated to physical culture. Frankly I have no insight into how modified fasting or limiting snack fuel would let a body builder achieve their goals. (Doc recently stated how hard it was for athletes to restrict quick energy foods, like carbs.)

HDL heritability  in the Dutch ERASMUS study was put at 43% and the study of isolated Italian's from Linosa put HDL heritability at 54% (and for those Italians having both high triglycerides and low HDL that dual heritability was 31%). When one considers the ApoA2 percentage in HDL in relation to the amount of ApoA1 in HDL then that detail is going to involve the copy number of ApoA2 genes the individual has; and what is eaten, but not the type of protein one chooses, because it is more lipids (as fatty acid derivatives) that are involved in key signaling roles.

Doc & others ( ex: WholeHealthSource) tell us saturated fat intake boosts total cholesterol, but more so HDL than LDL; conversely when restrict saturated fat HDL level falls . For those with ApoE4 however Doc repeatedly has mentioned that for them it may be best to decidedly limit fat. In which case triglyceride levels are seemingly something one must work around.

Restricting saturated fat intake sees a decrease in  ApoA1 because without those fatty acid derivatives (lipid signalers) ApoA1 undergoes more breakdown, and in addition there is less ApoA1 secretion (not only does ApoA1 degrade faster than ApoA2 but the kidneys apparently don't excrete ApoA2, like the kidneys do to ApoA1). This is how statistically low HDL is associated with a higher percentage of ApoA2  in it's make up. Yet genetics can conceivably tweak this dynamic because fatty acid derivatives (lipid signalers) have to up-regulate PPAR alpha (subject to genetic variation), which then acts on the ApoA2 gene regulatory  element "J" (subject to genetic variation) before ApoA2 gets made in the liver (& a bit in intestine).

Experimentally when PUFA  made up 40% of total dietary fat intake there was less measurable ApoA1 mRNA & less liver secretion of ApoA1; while if 30% of total dietary fat is mono-saturated & PUFA there is usually no change in amount of ApoA1 mRNA, nor less liver secretion of ApoA1. When diet is classified as low fat and fat only 9% of total calorie intake ApoA1 levels usually decrease; I don't know if this is the fat level Doc advises his ApoE4 patients to try. I am not aware of any relevance of dietary protein to ApoA1 levels; however there is some recent indication that iso-flavone plant phyto-sterols (ex: genisten & daidzein from soy) may alter ApoA1 & ApoA2 levels (in contrast to older studies showing no benefit). I garnish food with a dry palmfull of Japanese black soy  fermented 1 year in Koji, called "Tochi", specially imported from Japan for Japanese restaurants by Miyako Foods  626-962-9633 (no financial interest for me); they also make this into a nice specialty miso - but I do not know how it compares in iso-flavone content to other soy forms.

2011:  Male rhesus monkey's  ApoA1 g/l went up from 2.34 when fed soy stripped of iso-flavones to 2.75 when their soy had iso-flavones; and their ApoA2 g/l went up from 0.20 when fed  iso-flavone free soy to 0.22 when their soy had iso-flavones....Female rhesus monkey's ApoA1 g/l went from 2.19 when fed iso-flavone free soy to 2.75 when fed soy with iso-flavones; and their ApoA2 g/l went up from 0.16 on iso-flavone free soy to 0.19 on soy containing iso-flavones. (As for Lipo-a : that also went down with iso-flavones.) The female 15% boost in HDL (90% of HDL = ApoA1 + ApoA2) being greater than the males is attributed to the fact that some of the males went from pre-puberty to puberty during experiment and there are often sex related variations in HDL; and to be precise the authors stipulate that iso-flavones may not work the same when the subject has either familial hyper-cholesterol or those with ApoE4.

Doc has given those with ApoE4 and low HDL a little appreciated strategy when he exhorts them not to eat oats, potatoes and wheat bread; these are common foods that increase levels of an asymmetrical lipid called lyso-phosphatidyl-choline (lysoPC). Remember that HDL also contains glycero-phospho-lipids; well, inside a cell the enzyme cPLA2 (cytosolic phospholipase A2) spins off phospho-lipids (another fatty acid derivative). And unfortunately it is usually individuals with low HDL tend to have more lysoPC than normal; which is considered pro-atherogenic when the lysoPC is configured in a "bad" molecular form (and yet other "good" lysoPC  configurations carry desirable DHA across the brain blood barrier).

It was shown that eating fatty fish 4-5 times a week decreases the total level of lysoPC, and both lowers the amount of  "bad" lysoPC, while raising the "good" configurations of lysoPC; which is another reason to follow Doc's high fish oil suggestion (inter-daily fatty fish might be a lot of mercury intake). I believe Doc is allowing fish oil and  maybe some fish for his ApoE4 patients. This experiment ruled out saturated fat beneficially influencing those lysoPC  molecular variations because subjects avoided all dairy fat, cream or butter.

The lysoPC that is carried in oxidized LDL molecules negatively affects one's tricky macrophages and also the smooth muscle cells of the artery; lyso-lipids not only invoke signals but can themselves be transformed. Certain lysoPC  yield a lot of  the platelet activating factor (alkyl-acetyphosphatidyl-choline) which contributes to sustaining inflammation, and so sets stage for atherosclerotic plaque. High levels of HDL usually conveniently equates with reduced levels of TNF alpha, a condition resulting in fewer undesirable adhesion proteins on the blood vessel's endothelium;  so, conversely those individuals with ApoE4 related low HDL are statistically prone to more endothelial adhesion proteins, and thus should try to do what they can to keep as much "bad" lysoPC controlled with diet.

Precisely, DS. I've got people who require 20,000 units to achieve this blood level, I've got a rare person who needs none.

The individual variation in need is quite wide. That's why the concept of an RDA for this hormone is, in a word, absurd.

I find that even low doses of vitamin D leave me feeling terrible. I get these weird chest pains and lower back pain as well. It also causes pretty bad breakouts for me. I've tried different preparations and brands but it all ends up leading to the same symptoms. This usually happens after I've accumulated a couple of weeks of supplement usage. I haven't experimented with different dosing strategies yet(weekly, bi-weekly or even monthly). I made sure to supplement with magnesium and K2 as well. It sucks because I really like all of the preventative benefits that D3 has to offer but it just doesn't seem to agree with me.
Mike

Dr. Davis:

Any chance that you'll be writing more about the positive results you're seeing in your clinic from increased doses of vitamin D on aortic insufficiency?

Joe

Since D activates immune function a lot, could it be that you have some chronic infection and effects you are experiencing are because of bacterial endotoxins which are released when bacteria dies ?

Have you done the D test ?

If so, perhaps taking some detox supplement would help like huge doses of Vitamin C, clay, NAC etc...

Sure, good idea. However, the majority of experiences have been in aortic stenosis, not insufficiency, only because I've got about 10 people with stenosis for every 1 with insufficiency--just too uncommon.

Hi, Mike--
Sorry about your struggles. I've seen this once or twice, but I'm not sure about why. You might ask your doctor to at least investigate parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols. These might booby trap a vitamin D effort. After all, taking vitamin D should be no more dangerous than getting a nice tan.

Are you suggesting that my reaction could be from some sort of bacterial "die off?"

Interesting. I never really thought about it. I did get my levels checked during the few months I was supplementing and it was only 52ng/ml.

Mike, are you getting enough quality Vitamin A? Vitamin A and D work together. Chris Masterjohn had a post about it on the Weston A. Price website, they have a lot of info there about A and D levels and how they work together. Other people have had reactions to D also and found that they deficient in A, mostly, I think, by evaluating their diet and seeing there were few good sources of A there. Also, older people and some just not so lucky folks don't process beta carotene into vitamin A, it's age and genetics.

It was recommended that I take additional magnesium and vitamin k2 to see if it would make a difference. I've never taken additional vitamin A though because according to the  vitamin d council, additional vitamin A can be toxic.

I have read that Masterjohn article before though.

I just wanted to add my experience on Vit. D3 supplementation.

Two years ago in July I started supplementing 5,000 i.u. Vit. D3 a day.  My sister had been found low, I live relatively the same lifestyle, and thought, "what the heck, I'll start and get my blood tested in late winter next year".  

That next March I had a blood test and found my blood levels to be at a whopping  32 ng/ml.  My doctor said "fine, you're within range" and I thought, "no, that's not fine" and started to take 15,000 i.u. a day.  In March again this year I had a blood draw, and expected to see a very high ng/ml of Vit. D.  My actual result?  It had raised to 45 ng/ml.  I was floored that with that amount, my levels had only raised such a small amount.  

I will add that I am obese.   I just wanted to give you my experience with D3 supplementation in case it helps someone else.  I have now upped my supplementation once more to 20,000 i.u. a day, and if my next blood test is appreciably better, will hold at that level or drop back some.  I will add that I haven't had many if any colds this past year, so even if I have not attained a more optimal level (perhaps I can't due to obesity)  it's still doing me a lot of good.

Oh, I forgot to mention. A friend of mine suggested I try applying liquid vitamin D on my skin and then checking to see if that raises/maintains my blood levels.

I'm thinking about applying 5 to 8k per day to the skin AFTER I shower so that it gets plenty of time to absorb in the skin. Then re-test my levels after a few months to see if it works.

Please let me know what becomes of your experience! We've not tried this specific strategy.

Hi, Jennifer--

Yes, indeed: The individual experiences with vitamin D can vary widely. You may also note that, 3 or so years into the experience, your needs will diminish, sometimes dramatically, with less vit D required to generate the same blood level.

I began experiencing tightness and soreness in my hips and lower back this year. Have been low carbing for over three years, and, except for a short period of stupidity earlier this year, have not consumed any flour products. My multi-vitamin contains only 500 IU of D3, so I am adding this to my daily supplementing. Should I start slowly, 1000 IU a day for a month, and slowly increase? Is D3 toxic? BTW I am in my late 60's, and I do exercise 5-6 days a week as well.

I have read that 20-25ng/ml is optimal.
"Although numerous studies have not
observed any adverse effects of higher
vitamin D status, a few have. Historically,
the main health risks associated with
excessive vitamin D are linked with
abnormal plasma calcium concentrations.
Excessive vitamin D is recognized to
cause hypercalcemia by increasing intestinal
calcium absorption or by increasing
mobilization of bone calcium. Although
hypercalcemia is uncommon with intakes
less than 10 000 IU/d,3 knowledge of
non-calcium-related adverse events is
limited. At least some evidence suggests
that high vitamin D status may be associated
with increased risk of some cancers.
In a large case control study of prostate
cancer in Finland and Norway, both
low (32 ng/mL)
25(OH)D concentrations were reported
to be associated with an increased incidence
of prostate cancer (50% and 70%,
respectively) compared with individuals
with serum 25(OH)D concentrations
between 16 and 24 ng/mL.4 A direct relationship
between higher vitamin D status
and the development of esophageal
carcinoma also has been observed in
Chinese men.5 Interestingly, all the participants,
including those in the highest
quintile, were vitamin D deficient (26.2
ng/mL) with a 3-fold increased risk of
pancreatic cancer compared to individuals
with the lowest baseline status (<12.8
ng/mL). Overall, these studies suggest
there may be an optimum status and that
values below or above may increase risk
of certain types of cancer.
Adverse events associated with high vitamin
D status other than cancer also have
been observed. Recent data from large
epidemiologic studies, including the Third
National Health and Nutrition Examination
Survey (NHANES III) and the Framingham
Heart Study, suggest that a “U-shaped
curve” relationship exists with all-cause
mortality and the incidence of cardiovascular
disease because both low and high
25(OH)D concentrations elevated risk.7,8
In the NHANES III study, higher mortality
risk was observed in participants
with 25(OH)D above 49 ng/mL. In the
Framingham study, the lowest cardiovascular
disease risks were found in
participants with baseline 25(OH)D levels
of 20 to 25 ng/mL but increased with both
lower and higher values,8 thus suggesting
that increased cardiovascular risk occurred
at levels below 30 ng/mL. Furthermore,
the optimal 25(OH)D levels for protection
against cardiovascular disease and certain
types of cancer may differ from those
for bone metabolism or normal parathyroid
hormone physiology."
from 'too much.pdf' in http://is.gd/vT4Ogh Studies from DrGreger collection.

DrGreger has since changed his recommendation from 4000IU to 2000IU/day:
http://www.facebook.com/NutritionFacts.org/posts/193068787424836 yesterday's update

As knowledge marches forward, there will always be differing observations made, some good, some bad, some indifferent.

However, if we weigh the totality of evidence (and I throw in my experience that now amounts to several thousand patients), there has never been any strategy as powerful as vitamin D--except for elimination of wheat in the human diet, the two most spectacular new health strategies I have encountered in my career.

what happened to my post?

I posted 30Aug11 about a concern I have concerning D3 toxicity, but the message disappeared. I have been following for some two years a daily D3 regimen (4000-8000mg) without incident. I recently experienced unusual chest pains over a week and ended up getting a thorough checkup which found no apparent heart problems. However upon disclosing my protracted D3 intake (considered “very high!") it was suggested I suspend D3 for awhile on the off chance D3 toxicity may be the source of my symptoms. I was wondering if anyone else here has had this experience. As I look into this more, I have learned that D3 toxicity is more subtle and prevalent than I had thought, and is not something to be taken lightly. Clearly as Dr Davis has cautioned, adjusting to the right dosage varies from person to person, and given the latent build up of D3 in fat tissue over time, it is not as straight forward getting it right as one might think. In my case the jury is still out.

re previous message: 4000-8000 mg = 4000-8000iu's

I swear by vitamin D3. It helps me avoid asthma flare ups and kick bugs before they can make me wheeze. In the warm months, I make sure to get outside as much as possible as there are other things produced by the sun in addition to Vitamin D, some of which may be important. Then in the winter, I supplement 2-5k ius a day, increasing to 20k ius when sick.

M

Is taking a high dose of Vitamin D3 during pregnancy safe? I know most of the "recommendations" are to take 200 IU, but I have some 5000 IU pills in my cabinet, and am wondering if those would be safe or not. Or should I find a lower dosage pill?

Hi, Melinda--

Sadly, there are next to no data for how to best manage vitamin D and pregnancy. However, common sense would suggest that achieving a desirable blood vitamin D level should not be harmful, else getting a tan while pregnancy would be harmful, too.

A dose of 5000 units typically yields a healthy blood vitamin D level in the majority of females.

Hi Mike & Dr. Davis!

Can you please tell me, has anything worked for you yet? I too do not like the feeling I get on Vit D3 but I am only at 31 and need  to start taking 8,000 a day as well.

Also Doctor Davis can you please please elaborate on these: "parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols". and why they would booby trap the Vit D3 efforts? How does someone work around this ang take Vit D3?? I found out yesterday I happen to have a high Reverse T3 and need to go on thyroid meds and also have adrenal issues. As well as low insulin levels. So I might be the one who is getting booby trapped.

Any help appreciated

Thank you!

Hi Mike & Dr. Davis!

Doctor Davis can you please please elaborate on these: "parathyroid and adrenal status, e.g., PTH, calcium, and salivary cortisols". and why they would booby trap the Vit D3 efforts? How does someone work around this ang take Vit D3?? I found out yesterday I happen to have a high Reverse T3 and need to go on thyroid meds and also have adrenal issues. As well as low insulin levels. So I might be the one who is getting booby trapped.
My Vit D3 is only at 31 and have been prescribed 10,000  a day. I really want to start but I have not liked how I have felt in the past on Vit D3.
Any help appreciated

Thank you!

Hi, Rose--

The key here is to find someone who can guide you along while monitoring and interpreting these factors. The greatest difficulty: finding a healthcare practitioner with the knowledge, experience, and interest in doing so.

As crude as it is, you are still best with word of mouth: asking friends and family who has been a helpful advocate with health problems, especially those involving vitamin D.

See below.

Hi Dr. D,
I posted a question on another thread about vitamin D and calcium levels and now I think this thread is more current and probably relevant .
I am being worked up at the moment for a possible parathyroid adenoma. My serum calcium has been trending up for the past few years and is now 10.3 (x2).
  Way back in 2005 I started reading about the benefits of supplementing with D and used 1000iu/day, as well as 400-800 magnesium and Life Extension's K2. Fast forward to 2009 and imagine my surprise at my D levels being 26!  Increased it to 5-6k per day and went to 43.
Dr. James Norman is considered to be the foremost expert on all things parathyroid here in the US , and his website : parathyroid.com.  was very informative for me, but concerned me regarding blanket supplementation of vitamin D.
I respect your opinions greatly and would like your thoughts as to his information.

Thanks!
Reikime (RN)

Hi, Reikime--

I am obviously no authority on parathyroid tumors. Dr. Norman's website is very interesting and makes great sense. I, too, in looking at vitamin D, calcium, and PTH levels have uncovered several parathyroid tumors. It appears to be a lot more common than previously thought.

The only issue I would disagree strongly with is the statement that the ONLY purpose of vitamin D is to increase intestinal absorption of calcium. In fact, among the most exciting areas of research with vitamin D are a new appreciation for the widespread, multi-faceted effects vit D has in multiple, perhaps all, organ systems.

Hi Dr Davis,
It seems that a finnish University is doing a major study on Vitamin D, check this out!

"The FIND will be a randomized, double-blind, placebo-controlled, 5-y supplementation study of the benefits and risks of vitamin D in the primary prevention of CVD and cancer among 18000 men ≥60 y and women ≥65 y. The participants will be randomized to 3 groups with 6000 in each, with daily supplementation of either: 1) 40 µg/d (1600 IU) of vitamin D3, 2) 80 µg/d (3200 IU) of vitamin D3, or 3) placebo. Compliance, use of non-study drugs or supplements, diet, development of endpoints, and CVD and cancer risk factors will be assessed by questionnaires. Blood samples will be collected for assessment of effect modification by baseline 25-hydroxyvitamin D, as well as for future ancillary studies of genetic/biochemical hypotheses."

https://www.uef.fi/nutritionepidemiologists/find2

Looks awesome to me. What do you think? Highest dose arm 80 µg a day for 5 years is more than VITAL.

Hi, Johnny--

Excellent!

In the meantime, the effects I continue to witness are so powerful that I still advocate correcting vitamin D to 60-70 ng/ml.

Hi Doc,

A quick question on vitamin D:
I recently tested at 17 ng/ml for vit d.  (had been supplementing w/ 2000 iu of D3 for 2 weeks previous to that).
The doc is recommending I take 40,000 IU once a week for several months until it stabilizes, and then switching to lower supplementation.

A few questions:
(1)  Obviously this will be D2 not D3 since it's prescribed - just go with it?  I believe I read a study somewhere that showed D2 ended up being as effective as D3 despite being slower.
(2)  Thoughts on taking these large "catchup" doses rather than a more consistent 10,000 IU/day regimen?

My other stats:  Age 31, 160lbs, Total Cholesterol = 204, HDL = 60, Triglycerides around 100.

You are closer to the truth, N, than your doctor. Clearly your doctor is fairly ignorant of the emerging issues with vitamin D.

While dosing can vary, depending on body size, race, genetics, etc., 10,000 units per day of D3 would be a typical effective dose.

I had read that about 20-30 minutes of sunlight daily were required for Vitamin D absorption.    Having already gone through Mohs surgery for a tiny basal cell carcinoma on my nose - and being "melanin challenged" - I have always tried to cover up or stay out of direct sun.  Sun blocks apparently have some questionable compounds in them.  I jog 2 miles every day if its not raining or snowing.  So on a sunny day that's 20-30 minutes of exposure.  Should Vitamin D dosage be varied according to daily sun exposure ?   Self-prescribing dosage of supplements is a real headache for me.  I don't have a clue.   It would sure help if there were affordable food sources of sufficient Vitamin D.   What about dairy ?

Is there an inexpensive way of finding out which form you have?

is there any truth to the idea that if your trig/HDL ratio is under 2.0 that your LDL type is predominantly large/buoyant?

Is there a way to determine whether small LDL production is carb- or genetics-caused?

Is this the same for poly/mono unsaturated fatty acids?

Dr. Davis,

Does the form of saturated fat have any impact on this in the case of genetic predisposition to small LDL formation? For example, does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?

Rick Braden

Dr. Davis,
That's very interesting!!  Any chance you could provide the reference?
Thanks, Dan

This naturally leads to the question about understanding our personal genetic coding.  Without that coding information it seems difficult make an informed decision about the consequences of lowering carbohydrate and increasing fat (and saturated fat) until the consequences are upon you!

This definitely needs a follow-up post. I've not seen this distinction until now. If true, Dr. Davis, does it not present a difficult dilemma for those who have both genetic sdLDL and Lp(a)? If saturated fat needs to be restricted for genetically high sdLDL, would this not leave the Lp(a) (which responds best to saturated fat intake) unopposed? What is your proposal to address this?

Interesting post, Dr. Davis. How would one find out if they are genetically predisposed to react to saturated fat intake with an increase in small LDL?

Do you have some specific references for LDLa and saturated fat? Is it essentially congenital hypercholesterolemia that reacts with the sat fat?

this is a long overview discussion. thank you!  What would dietary recommendation be for someone if small LDL is genetic in origin?  Also, wouldn't this pattern possibly require statins to get LDL particle count as low as possible since it is unlikely that diet will do the job?  In my case, i need Lipitor and Zetia; otherwise my particle count mostly small remains high despite Vit D, normal weight,no wheat cornstarch or sugar.  Great post!

Doc -

Good post but -

Hard to understand post without the background basis on which the statement is made.

Is your statement based on clinical observations? Or is it based on opinion only?

Yes, references supporting your premise in this article would be very welcome.

This post concerns me because as a low carber I find it difficult to maintain a low carb diet without saturated fat sources. Perhaps this is driving the concern and questions from others also.

Count me in those who are waiting to see data where this is coming from.
Thanks for all your blogs posts.

Yes, I hope this isn't a hit and run post. Many learned people, such as Peter at hyperlipid would probably disagree. Do you have any references?

So what do we do if we should not eat but a few carbos and up to certain amount of protein?

The rest have to be saturated fats, isn't it?

Please, some more practical information before we all run over the cliff.

Harold, I am also interested in the familial hypercholesterolemia question.  After a quick search, I found this http://www.jlr.org/cgi/reprint/23/8/1196.pdf with a quote: "LDL has been
found to be cholesterol-enriched and triglyceride-poor
(5, 6), and in one study, the peak flotation rate of FH LDL
has been found to be higher than in normals (6),
implying decreased density, increased size, or both.
However, these results are difficult to assess, since there
is considerable heterogeneity of LDL in normal subjects,
although size, flotation rate, and composition"

So, FH people may be predisposed to large, fluffy LDL.  However, I do not know whether FHs handle saturated fats better than normals, and this is an important question.  

-Aaron

A question on triglycerides...if high TGs are a trigger for small, dense LDL and should be minimized, are there any ways to reduce area-under-the-curve TGs after a meal (other than the usual low carb, omega-3, etc. recommendations).  Are large, infrequent meals better than small, frequent meals?  Does fiber change the shape of the post-meal TG curve?

Also, does fasting TG tell the whole story?  Could one have, say, <50 mg/dL fasting TG but have elevated TG throughout the day as a result of large, high-fat meals?  

-Aaron

Thank you Dr. Davis!  Finally a voice of sanity in this whole sat fat hoopla.

I for one, although not neurotic about it, do not favor saturated fats and will eat a good non-hydrogenated margarine (like Smart Balance) over butter any day.

Please keep up this sane blog and give us the WHOLE enchilada, not just what some want to hear.

Search PubMed or Google Scholar and you will find NO data on this issue. To my knowledge, there are none that distinguish genetically -driven small LDL vs. lifestyle-induced.

This is based on having tested lipoproteins in thousands of people over the past 10+ years.

Prototypical "genetic small LDL" person: 5 ft 10 inch, 140 lb male who eats low-carb. In other words this person is at ideal weight and does not eat foods that trigger small LDL--yet has 90% small LDL by NMR (e.g., 1200 nmol/L, LDL particle number 1550 nmol/L). Should this person overindulge in saturated fat, small LDL will go up.

Dr. Davis, how do you know it is saturated fats that are the cause? For example, most low-carbers also have elevated intake of inflammatory polyunsaturated fatty acids, which I would be much more likely to blame.  But, in either case, it seems there are too many uncontrolled variables involved (as far as food intake) to pin any of them to the wall.

It's very difficult for me to believe saturated fat is the cause, while other possibilities exist.

For everyone worrying about this, just get yourself a VAP or NMR test.  If you have LP(a) or sdLDL, that will show it.  You don't need genetic testing.

What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?

Thanks Dr. Davis for another insightful post from your clinical experience, giving the kind of information that helps elucidate why saturated fat works for some and not for others - and the kind of information you can't get anywhere else.  Ignore the pro saturated fat/anti-polyunsaturated fat zealots, who can't be persuaded by any evidence or logic.

"What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?"

I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?

Hello Dr. Davis

You said:

"Should this person overindulge in saturated fat, small LDL will go up."

Just to be clear, are you saying you have observed low carb subjects (how low?) that have added saturated fat to their diets and then on subsequent testing you have seen sdLDL rise in absolute and percentage terms?

If they were truly LC, were they already high sat fat at the time of the NMR or were they high PUFA (South Beach?)

May I ask how many such cases you have seen?

You should definitely publish this, or if you don't think it is publishable maybe you could give us all the data in a blog post.

Thanks, this is very interesting.

In people with presumptive genetically-determined small LDL, HDL can be 70 mg/dl or greater, triglycerides 45 mg/dl or less, yet small LDL persists, usually at 600 nmol/L (NMR).

I have approximately 100 patients like this. They tend to be very thin with BMI's of 23 or so, yet small LDL persists.

Hi Dr. Davis,

This post really intrigues me. I am a first year medical student (24 yo) with familial hypercholesterolemia. I am on a low carb paleo diet, taking omega 3, vit D and just recently added magnesium to the mix as well. I went off Lipitor two months ago just an experiment to go along with this new eating plan, and received blood work only a few days ago. Numbers about 450 on total and 285 for LDL. My CT scan already showed plaque buildup in the coronary arteries, aorta, and one valve. While I am not looking for medical advice per se (since I know you prefer not to give it over your blog) I was just curious as to how your track the plaque plan and recommendations are effected with this type of genetic disorder. My cardiologist says if I dont go on drugs immediately I'll have a cardiac event at 40 years of age. I could use some advice and direction to persue. Is it impossible to avoid genetics, and the use of drugs are unavoidable? Thanks. Really appreciate it.

How do you know how much small LDL you have?

""I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?""

Well - just speaking for myself, I have high HDL and low trigs, and always had a mix of small/large (A/B) pattern LDL.  When I stopped eating wheat, my LDL all became large.  

I also have high Lp(a), which was uneffected by my eliminating wheat.

You can drive yourself crazy figuring out what's OK to eat and what's not.  I don't worry about it anymore.  I rarely eat wheat because I've seen results from Not eating it, try not to overdo the sugar and fruit, get plenty of veggies and protein.  

I get my VAP test once or twice a year to make sure everything is where it should be, more or less.

I'm just not going to worry about it beyond that.  

Bonnie

Dr. Harris:

Are these customers of yours lean lowcarbers eating plenty of LA or very, very much protein in their diet? If not, then what do they eat?

With regards,
LeenaS

Interesting, and concerning, since I fit that description:

Chol: 6.35mmol/L
HDL: 1.88
LDL: 4.2
Triglycerides: 0.66
Chol/HDL ratio: 3.4
American Values:  TG 58.47 LDL 162.54 HDL 72.75
Triglyceride/HDL ratio: 0.8
Hieght: 6'0
Wieght: 165lbs
BF 8%

I've had other opinions on these numbers; should I be pursuing more accurate particle numbers?  I go out of my way to consume large amounts of red meat, coconut oil, butter, and eggs.  I'm fitter and healthier (subjectively) than I ever have been at 36 than I was in my 20's.  I find it disconcerting than I could potentially be doing something detrimental.

Hi Dr. Davis

In the original post you said:

"saturated fat will increase small LDL.  In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL."

So, if I follow this correctly, you are saying that these 100 patients all had increases in their sdLDL after documented increases in saturated fat in their diets? In other words you had two data points for each subject, correct?

If the subjects did not all have documented increases in sLDL then by "persist", do you mean their sdLDL went down with LC eating (like 800 to 600, say) or do you just mean that they had a single high value and it was only measured once, but it was high?

If it is the latter, I could see how it's fair to say that some LC eaters have a higher sdLDL than we might predict (for whatever reason) but it seems like a non sequiter to conclude that the sdLDL would be made higher with more sat fat consumption.

I just want to make sure I get this straight so I understand it correctly.

Thin. Nice. I'm less concerned. lol

Does this group of people also have elevated blood sugar, as might be predicted by another of your blog postings?

http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

Dr. Davis,

I concur with Dr. Harris in that more details would be nice to better understand exactly what you're saying.

Are other variables accounted for? Were many, most, or all of these patients on statin drugs, which could have prevented a shift in particle size if triglycerides were low and insulin sensitivity was high?

Again, if there is such a phenomenon going on, is the "genetic sdLDL" clearly atherogenic in the same way that "environmental sdLDL" seems to be?

If so, I ask again, what is the solution for someone who is afflicted by both Lp(a) and genetic sdLDL? The "profile" for genetic sdLDL is similar to the profile for those with Lp(a), and there is probably a lot of crossover. Saturated fat lowers Lp(a), but (presumably) raises genetic sdLDL. This is a fierce dilemma! Would not the better choice be to choose the diet that opposes the more vicious of the two, which is Lp(a)? What is the priority?

Has a high SFA diet only increased sdLDL per NMR, or has it also clearly been shown to increase CAC scores? In other words, does it clearly progress the disease itself?

David

Saturated fats not linked to heart disease: Meta-analysis - American Society for Clinical Nutrition (January 13, 2010). doi:10.3945/ajcn.2009.27725 © 2010

It would really be interesting to know what the primary sources of saturated fat are for these "100 patients".  There may be a single (widely available) common source of sat fat that these specific patients are consuming, do we even know that?  I agree, by what has been revealed, that there are too many variables to know conclusively that saturated fat is the cause of their persistently elevated small LDL.

Mark me down as someone who is not convinced that CLA, n3 rich organic, free range, and wild animal sources of fat could possibly in any way be detrimental to anyone.

When will people stop worrying about cholesterol numbers? They really don't mean anything.

Until someone explains a plausible mechanism through which lipoproteins directly kill me I will ignore it any suggestion that they do. This is what a good scientist would do.

@ Rick Braden
Re does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?
Palmitate is the predominant saturated fatty acid in soybean oil. Soybean oil increases total cholesterol,LDL and LDL:HDL ratio, whilst HDL diminished.
Coconut oil (predominantly Lauric acid) does not cause dyslipidemia and promotes a reduction in abdominal obesity.

That is generally the case,  stearate does not appear to increase LDL... Laurate and stearate reduce the total cholesterol/HDL ratio

I don't know if the genetic predisposition to LDL alters response to laurate, stearate palmitate.

It may help people better understand the difference in cholesterol forms if they look at the photos of VLDL, LDL, HDL,  NED KOCK has kindly provided on his blog

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

buy jeans: I'd love to see clinical evidence supporting that claim.

Heart diseases are a major matter of concern these days therefore all that can be done to correct the diet and make it benefit good health should be taken to.

Dietary Carbohydrate Modifies the Inverse Association Between Saturated Fat Intake and Cholesterol on Very Low-Density Lipoproteins
Interesting full text free paper that may change the way saturated fat is viewed. I wonder if the source of the Saturated fat (butter/coconut oil as opposed to indoor grain fed beef/lard) and the type of carbohydrate (Wheat sweet potato)  may add a further level of complication.

I recently had a discussion with a relative who got a prescription for Vitamin D.  (This after I bought her a Vitamin D test from Grassroots showing a level of 19.)  I told her the prescription was a bad idea as it was surely Vitamin D2.  She looked into it and came back and told me, no, it was D3.  I have not seen it, but I am asking now - is it really true that prescriptions are invariably D2?  She claimed it was 50k IU of D3, once a week.

Separately, I see it stated here and there that the Vitamin D added to milk is D2.  Most milk labels I see show it as D3.

A bit of information that the drug reps don't tell the physician is people need to be on a maintenance dose. I have seen so many people who were prescribed D2 for a few months. Once the vitamin D level rose to over 30, they were told they could discontinue taking the D2.

One person told me that she had started and stopped D2 three times. She said her doctor could not figure out why her vitamin D level keeps dropping when the D is stopped. At least she was retested. The other people who were told to stop taking D2, were never retested once their D hit "normal".  

I have a friend who told her doctor she would get her vitamin D as D3 OTC. She said he expressed surprise that it could be bought without a prescription.

The study you site appears to use the dry form of vitamin D3.

So is D2 a prescription medicine?

Here is an abstract providing an example of the total lack of effect of D2 in a patient.
The lack of vitamin D toxicity with megadose of daily ergocalciferol (D2) therapy:
The maximum daily dose of vitamin D currently recommended is 2000 IU. Ergocalciferol (D2) 50,000 IU orally weekly for 8-12 weeks is often used to treat vitamin D deficient patients (25(OH) vitamin D <20 ng/mL).
The lack of vitamin D toxicity after massive doses of ergocalciferol has yet to be reported in the literature.
We report a case of a 56-year-old woman who received supratherapeutic doses of ergocalciferol (150,000 IU orally daily) for 28 years without toxicity. We discuss the possible mechanisms which may account for a lack of toxicity despite intake of massive daily doses of ergocalciferol in this patient.

The sad aspect to this story is that as Vitamin D2 at that ridiculously high intake didn't do her harm, it's also probable that her body did not recognise it at all, so it probably didn't do her any good either. As there have been other accounts of people taking large (but not as huge as this case) amounts of D2 and it not having any noticeable effect on Vitamin d deficiency symptoms it seems just pointless to risk using it, when there is a cheaper, more reliable, alternative readily available.

I think it is up to the patient who is tuned in to this fine blog and several other like minded blogs who preach as you do, such  as "nephropal.blogspot.com" to bring your information to their primary doctors.  My primary doctor still takes a Staten drug even though he knows and marvels at the health gains that I have achieved through supplementation with high dose vitamin D3 and high dose omega 3fish oil, along with a cave man like diet.  I asked him why he take a Staten drug when they work by increasing his vitamin D level? I said just take vitamin D3 instead of the Staten drug.  His answer was that he only takes a little Staten drug.  When he found my wife to be vitamin D deficient, he in fact ordered a script for vitamin D2.  I insisted that she take OTC vitamin D3 and after a tussle he gave in.  

I am sorry to say that only we the patients can change the system.  I don't blame the very over worked primary care physicians who have no time to read the necessary science.  We the patients have to bring the relevant data to them.  After all it's our health that is being impacted.

Bark--

There is indeed a prescription D3.

Now, why a prescription form is necessary is beyond me. I suppose we could make prescription vitamin C, too, and charge $120 per month.

Hi, Anne-

Yes, I also see this incredible blunder occuring around me.

I'm not sure what they're thinking.

Vitamin D3 1000 IU 240 tablets per bottle x 2 bottles purchased from Costco is dirt cheap.  $5.20 Cdn.  Very cheap $ U.S. dollars.

I take 3,000 to 5,000 IU daily and associate it with stopping hot flashes.

Inadvertently 'experiments' by running out of D3 for several weeks at a time resulted in really terrific hot flashes. Nothing is quite as unpleasant as having a hot flash as soon as I wake up, for example. Clearly I have not done double blind studies.  I am (sort of) menopausal.  No periods from September 2008 to June 2009.  Now, back.

No vitamin D3 intake during summer of 2008:  terrible terrible hot flahses. Then started taking D3 3000 IU in August 2008. Ran out of D3 sometime in Januray.  Hot flashes started up sometime later.  However, no hot flashes since end of March 2009.  No hot flashes from September to January.  Stopped taking D3 because too lazy to go to Costco to buy more.  Then started taking D3 and then stopped with the hot flashes and have not had another one in months even though obviously the hormones are fluctuating.

I used to think that HRT would stop hot flashes.  HRT does nothing for the hot flashes.  Vitamin D3 appears to work much more effectively.  

Dr. G. Kadar
Toronto, Canada

Dr. Kadar--

Fascinating observation!

Any other ladies who've made similar observations? Or perhaps taken vitamin D yet continued to experience hot flashes?

Tony ~ D2 can be bought as an OTC too.

Dr. Kader ~ I have a co-worker who says her hot flashes disappear when she takes vitamin D.
Anne

I wonder if there is any research on your view that the tablets don't work, only the gelcaps, for raising vitamin D levles.  It seems like it would be very easy to show whether or not this is true, and very important since lots of people take the tablets.

Hi, Peter-

To my knowledge, there is no research on this topic. However, having tested vitamin D blood levels thousands of times, I can say with confidence that the tablets are inconsistently absorbed--sometimes they work, often they don't, or they increase blood levels less effectively. Levels also vary widely, due to inconsistent absorption.

Gelcaps--i.e.,oil-based--are absorbed consistently.

What are some good brands of OTC D3?  I see the Costco mentioned, but has it been independently tested?  I know the Costco brand fish oil is supposedly decent, so it would make since that the D3 is as well.

I usually order online (vitacost.com) and I like the NSI brands.  Are they good?

Dr. Kadar

Thanks for sharing about your success with vitamin D3 bringing relief for your hot flashes.  I have a daughter who was suffering with hot flashes and refused to take the dangerous medically recommended hormones to alleviate the problem.  Instead she started to take black cohosh. when I pulled a negative study from Pub Med she stopped. She continued to suffer and not in silence.  In the meantime, understanding the health benefits, I convinced her to start taking 6000 IU of vitamin D3 soft gels.  It never dawned on me that this could be so positive relative to hot flashes.  This morning I asked her how come I don't hear any hot flash complaints and she answered that she hasn't had an episode in a very very long time.  It seems likely that we now can put a face on the reason why.  Yet another use for the miracle health supporting hormone vitamin D3.  

It truly is a fascinating observation,as Dr. Davis remarked.  Thanks for solving this mystery.

It's just a guess, but the inconsistent absorption of dry  D3 sounds like it's due to fats (or lack of fats) consumed when dosing. So if patients take it with fish oil, or right after a fatty meal, it may work.

But I see no reason to stay on dry anyway as gels are very cheap. There are also liquid drops (usually with a fat carrier) for those who dislike pills.

I'm just waiting for a company to put out a D3/K2 gel next. They seem like logical partners.

I have a blogsite where I am tracking successes regarding the usage of vitamin D.  Will you tell your success story?  I am an advocate and educator for using Vitamin D3.  I personally take 6000-8000 to keep my levels of D3 at the appropriate level.  

I will never stop!  It manages the SAD disorder that I had without knowing for over 25 years.  It has changed my life.  My sense of wellbeing has increased to 100%.  Before, it was always a struggle to shake off the feeling that something always felt off, or wrong. It never felt like depression, and my outlook has always been upbeat.  But I still carried around, what I only know how to discribe as almost a sadness, or a feeling that something was wrong but I couldn't put my finger on it.  After taking the Vitamin D3, it just disappeared.  So, now I am an advocate, and believe firmly that this information must be disemminated out into the communities.  

If you have a story to tell I would appreciate it if you would add it to my blog site:

http://dactionhealth.ning.com/

Best~Diana~

There are also D3 available in liquid form.  It is great for those who can't swallow pills.  I believe it is through Biotics Research.  It is 2000U a drop.  I put 3 to 4 on my finger, and it is done. Nice to have the option and works better for children.

I recently discovered while shopping for my D3 that there is also a D3 version made from sheep lanolin.  Is this as effective as the D3 from fish oil?  Is there any reason why one would be preferred over the other?  I go for the fish oil source because I just don't know anything about the other.

I've been taking anywhere from 4,000 iu to 10,000 iu per day since February 2009 when my test revealed a level of 27 ng/dl. Last month I asked my dr for another test and he said they normally don't test again, which I just don't understand!(kaiser insurance). I still have my hot flashes but now that I think about it they are few and far between and less intense.
Nancy

Probably taking vitamin D3 tablets with a meal containing fat helps with absorption.

I've got patients using the drops.  They butter their toast and add the relevent number of drops of D3 1000 IU per drop to their buttered toast. (I recommend 100% rye sourdough bread for those patients who must eat their bread.)

I am now asking female patients experiencing intrusive hot flashes to take vitamin D3.  I'll wait for feedback from them.  Also for perimenopausal mood fluctuations.

Looked at another way:  D3 is a hormone replacement therapy.  

I do also tell patients about vitamin K2 and how it is also necessary for bone metabolism.  If they take therapeutic doses of
vitamin D3, then they also must eat eggs (and cheese, liver, etc.)  But minimally, they must eat egg yolks.  In Canada, K2 is not available in any serious way as a supplement.  

Dr. G. Kadar
Toronto, Canada

I would love to take my D3 in gelcap form, but have thus far been unable to find any here in Canada.  I sometimes take the liquid, but get hung up on what constitutes 'a drop,'  so usually settle for tablets along with fish or krill oil.  Anyone know of a Canadian source for gelcaps?

Dr. William Davis said...

"I can say with confidence that the tablets are inconsistently absorbed--sometimes they work, often they don't, or they increase blood levels less effectively. Levels also vary widely, due to inconsistent absorption.

Gelcaps--i.e.,oil-based--are absorbed consistently."


I cannot say anything about hot flashes since I'm a man (but can and will tell these interesting observations to PMP women I know), yet I have something to say about tablet versus powder versus gelcaps issue that may be of interest.

I have moderate level Crohn's disease and got great help from D3 supplements for over 7 months now. I started with gelcaps (dosage 25-75 µg/d), then abruptly moved into powder form (Vit D Max, dosage 125 µg/d) and observed GREAT improvement in a couple of weeks. Even my BP dropped so much - from 145/95 to 115/75 and I even got dizzy during daytime. (I also took some melatonin to be fair).

Then - after about 4 months - I changed back to gelcap form and kept the dosage and experienced somewhat more symptoms - if only for a while.

Is it possible that powder form may work more quickly, or did my powder D3 contain more D3 than mentioned? I honestly don't know.

I wrote for Dr B G about my Crohn improvement a while ago but she seems to be on holiday as we're speaking?

- Neo

I buy small easy to dissolve capsules of D3 (dry powder, not oil) made by Bio-Tech from Dr. Eades' Protein Power site (no affliation other than as a reader).  The cost for the dose is very, very good ($8 for 100 capsules) and the bottles are small.  I was able to buy 11 bottles for the same shipping price as 1 bottle, so I stocked up and shared with family members (my experience is that middle aged adults need at least 5000iu per day year round to keep 25 (OH)D levels above 50 ng/mL).  I test at least twice a year, so I know that the D3 is absorbing.  

I also usually take the D3 around the same time I am consuming some fat, which probably helps with absorption.  Other family members take Carlson's oil capsules with good results.  We avoid hard tablets.

Bio-tech also makes a non-prescription D3 in a 50,000iU dose, 12 capsules for about $18 (plus shipping), which is a very competitive price compared to high dose Rx D2.

Hi
Really a nice blog!
Needs stuff to to!

Readers who are using Vitamin D3 for cancer prevention may be interested in this new paper from Vieth
How to Optimize Vitamin D Supplementation
to Prevent Cancer, Based on Cellular
Adaptation and Hydroxylase Enzymology
The hypothesis seeks to answer some of the Dilemmas that challenge the vitamin D/Cancer hypothesis regarding prostate/pancreatic cancers.
1)How can the vitamin D hypothesis explain the U-shaped risk curve for prostate cancer when the data suggest that the average 25(OH)D
concentrations in countries with relatively high rates of prostate cancer are apparently the optimal concentrations for preventing prostate
cancer?
2 What plausible mechanism, other than vitamin D, could account for the association between greater lifetime sun exposure and diminished risk of prostate cancer ?
3 How can latitude and environmental ultraviolet light be associated with increased risk of prostate cancer, and pancreatic cancer, yet not be a significant contributor to the lower average 25(OH)D concentrations theorized to be the key component of the mechanism that relates latitude to cancer risk?
4 Why is summer season of diagnosis, or a higher serum 25(OH)D associated with better prognosis of prostate cancer?
5 If vitamin D is adverse for prostate cancer, then why is the rate of rise in prostate-specific antigen (PSA) slower in summer  than in other seasons and why would vitamin D supplementation slow the rate of rise in PSA ?
6 Why, in regions of the United States where environmental UVB is low, is there a positive association between pancreatic cancer versus serum 25(OH)D, while at the same time, in regions where UVB is high (presumably providing even higher serum 25(OH)D levels), is there no relationship with 25(OH)D ?
7 If 25(OH)D is antiproliferative in cell cultures of prostate cells in vitro  and pancreatic cells, then why would it contribute to the development of cancer in vivo?

Vieth suggests that as circulating 25(OH)D levels rise and fall, 1,25-dihydroxyvitamin D  concentrations  need to be adjusted and the balance between 25(OH)D-1-hydroxylase [CYP27B1](tumor surpressing) and the catabolic enzyme, 1,25(OH)2D-24-hydroxylase [CYP24](oncogene) may for a while become disrupted.

Any time there is a delay in cellular adaptation, or lag time in the fine tuning of  1,25(OH)2D  in response to fluctuating 25(OH)d concentrations there is the potential for too little of the tumor suppressor enzyme and too much of the oncogene CYP24.

Regular daily supplementation with D3 keeps levels high.
Regular 25(OH)D testing will enable you to see your levels are remaining steady.
It may be  sensible for people living further North to have a lower summer intake and higher winter amount in order to reduce the amplitude between summer highs and winter low 25(OH)D levels.

Those who go for Winter sunshine breaks may want to think about increasing D3 intakes before they fly off, reducing supplement intake while under the tropical sunshine and resuming supplementing immediately on returning home to prevent sudden changes in status and limit the extent of gains/losses.

25(OH)D levels need to be both high and stable.

The graph Dr Davis shows how D2 levels dropped steeply (indeed levels at the end of the month were  lower than before supplementing started) so the fact that D2 increases the rate at which 25(OH)D depletes making the fluctuation in level more acute, is a further reason to avoid it.

Dr. Davis,
I just got my labs back after 7 months on low-carb, high-fat diet.  Chol was 337 (my labs are here).
I was wondering if you or readers could point me to 5 or 6 links that would help educate me on this issue so I can see if I need to make any changes in the next 7 months.  Thank you for your time.

Why do doctors prescribe Vitamin D2?
They don't very often. Calcitriol (most common brand, Rocaltrol) is the most often prescribed Vitamin D around here (near Philadelphia).

Why do we need a prescription Vitamin D when OTC Vitamin D is just as good?
Two reasons:
1. Without a prescription, patients take medicine less reliably,
2. More importantly, many of my patients are poor, and OTC meds are not paid for, but prescriptions are.

I take D2 (and get as much midday sun as is safe) because of the horrible way the sheep are treated.

http://www.savethesheep.com/animals.asp

I know a nurse practitioner who practices in Phoenix, Arizona. She has done hundreds of blood draws for nutrient levels and has noted that some 99% of people were vitamin D deficient.

She went on to explain that a lot of these people were construction workers and did not even wear sunscreen. Again, this is in Phoenix where the sun shines intensely nearly every single day of the year. If those people are not getting enough D, I think it's pretty safe to say that you are at least at risk.

D2 comes from plant sources. D3 comes from animal sources, primarily animal skins. If you are vegetarian you would not want to take D3.

The primary reason the prescription form is D2 is because D2 is much safer. Too much vitamin D is worse than too little. The standard prescription dose is very high, 50,000 units. High doses like that of D3 would be extremely dangerous. Your body is much better able to regulate it's absorbtion of D2.

I would never take D3. It might take a bit higher dose of D2  to achieve the same result (studies do not agree on this) but I am never going to poison myself. I expect sereous negative health consequences in the future as a result of the marketing of D3. D3 is pretty much all you can find over the counter these days. I assume that it is more about promoting animal agriculture than human health.

It is true that the pharmaceutical industry has at times had undue sway over the medical profession.  To say that physicians are educated by "pretty representatives" is insulting and undermines the credibility of the author.  I agree that vitamin D3 is more "natural" and technically more potent.  The reason why vitamin D2 is more often prescribed is at least three-fold.
1. Vitamin D2 is available in a prescription strength that allows for a more rapid repletion of vitamin D levels.  (It is hard to find a prescription vitamin D3)  In other words, it would take longer to replete vitamin D with over-the-counter doses of vitamin D3.  So why not just take a bunch of D3 capsules?  The dosing schedule for repletion of vitamin D with D3 is not as well worked out as it is with vitamin D2.  As soon as someone does a large scale study using vitamin D3, we will all be willing to switch.  Doctors are hesitant to make up regimens where effective ones already exist (re: risk of patient harm/legal liabilities)  
2. Vitamin D2 has been prescribed for decades. We as physicians are more familiar with its effect on patients.  
3.  Finally, vitamin D3 used to be more expensive--another reason D2 was preferred over D3.  Doctors, like everyone else, are often resistant to change.
One thing is certain.  The author's assertion that physicians are not guided by science is false.  What we need is large scale clinical trial with vitamin D3.  The problem here is funding.  Who will pay for it?  Until then, the most we can say is that vitamin D3 is more "natural" and more potent.  Vitamin D2 however is effective and has not been shown to be injurious.

Dr. J--

Allow me to insult you again: It has been my experience that many of our colleagues are miserably susceptible to the smile of a pretty representative. Perhaps you are not, but I see it all the time.

I'm afraid that I believe you are way off base on the D2. I recommend that you read the existing literature. I believe that there's only one conclusion: D2 is markedly inferior. While better than nothing, why would anyone take a non-human form over a human form?

Having replaced vitamin D in approximately 2000 patients using D3, I can tell you it is safe and reliable. In the handful of patients taking D2, I've seen everything from modest increases in blood level so 25-hydroxy vitamin D to no increase at all.

Twice I have been on prescription strength Vit d2(50,000 units first for 8 weeks since my level was 30  and then rose to 66 with RxI took good quality Vit D3 in between 2000 units daily faithfully,eat a good diet (also take ERT age 65) and after serveral months^ my level again fell to 33 now have beenplaced on Vit D2 for 12 weeks, blood level 64 and will repeat test in 6 months.I am now taking 4000 units of D3. I DO NOT seem to be absorbing Vit D3 and wonder why or if I need even more daily

Why wouldn't you just obtain your Vit D through food sources? sardines, salmon, tuna, liver, egg yolk, cod liver oil, fatty fish, dairy

I HAVE to say something.  There are some valid health related reasons why some people/children have to take D2.  My daughter has to take D2 (her levels are at 33) so her DAN doc wants her D supplemented.  She also has some gastritis/EE he is hoping to heal in her tummy w it.  He wishes and we all wish she could take D3--I know its way better than D2.  BUT--she can't take D3--she is allergic to both fish and lanolin . . . so . . . therefore she has to take D2 right?  No other D3 option out there for her right--please answer if there is another option for her.  She is allergic to all the natural foods with D3 as well--egg etc.  D2 is all thats left.  I PRAY its helping her a little. We use a local company in WI called Cty Line Pharmaceuticals--the D2 is liquid, its D2 dissolved in propylene gycol with NOTHING else added.  Its a bit spicy but my daughter "Gags" it down as she  surely be allergic to anything added to flavor it.

There is no such nutritional supplement representative in the waiting room. This preference for the "drug" D2 over the supplement D3 also stems from the inherent preference of physicians for things they can control, whether or not there is proof of superiority.

I was vit D deficient at a level 12. I was told to take over the counter D3 1,000 a day for 5 mths, retest. It raised to only 23. I was told to take Vit D 3 at 2,000 a day for another 4 mths and the result was I went back down to 18. Finally took the presciption D2 at 50,000 a wk and I am mid normal. My 2 daughters were recently diagnosed with D deficiency as well. I walk a dog daily yet my 85 yr old mother who does not really see the sun and when does wears sunscreen takes no Vit D and is not deficient. Go figure.

P.S. Yes Vit D did reduce hot flashes as well.

In 1972, one year after starting my Medical Education {Psychology}, I attended the yearly "National Health Federation" {Monrovia, California} Convention. I was already prescribing High Doses of Vitamin D, and I attended a lecture by a  Physician who was already known as THE EXPERT in Vitamin D research!! To this day, I don't remember his Name. The Subject of this particular presentation,  was that Vitamin D2 was toxic to the Kidneys & caused Kidney Damage; Primarily Kidney Stones! His Research was solid and alarming! I bought the 90-minute Tape of his entire Presentation, but misplaced it approximately 5 years later. His presentation  was a Classic, and I'd pay $50.00 to $100.00 for a copy of the Tape today! If anyone has this tape, PLEASE contact me!!
Meanwhile, NEVER take any amount of Vitamin D2. He proved that Vitamin D3 was safe, and that Vitamin D2 should never be ingested!

I find this very interesting because on the one hand they are giving up control over what their advertisement says, but on the other hand the ads that people come up with are probably even more relevant to the readers.

Very good blog, support, only the future health!