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!

For a related blog posting, see Jimmy Moore's Diabetes Health Leaders Finally Realizing Low-Carb Diet Has Merit

I wish there were good answers to you questions.

When I controlled my newly diagnosed mild diabetes with elimination of grains, starch, sugar and processed foods from my diet, dropping 70 pounds along the way, my doctor was astounded but ultimately not interested in the details of how I did it.  Same with the diabetes nutritionist.

When I began to explain how I accomplished blood sugar control and weight loss without medication (coming off high blood pressure meds at the same time), and that my methods contradicted the ADA recommendations (and their advice), I was met with 'well, most people can't stick to that'.  End of discussion.  They don't want to know - they really don't want to know.  It's very disappointing because positive personal experience seems to count for nothing with the very people who are tasked with helping.  They actually disapprove of the approach I've taken because it contradicts convential wisdom and advice.  It seems they'd rather write off my experience as 'one of those things' than consider that there are ways to achieve blood sugar and weight control.

Dave--

Thanks. I took a look at Jimmy Moore's blog post from today. It is an excellent update on the changing landscape in carbohydrate restriction.

I do fear, however, a politically correct lukewarm (at best) endorsement of the concept, since there is a great financial stake in maintaining the status quo. The number one monetary contributor to the American Diabetes Association, for example, is Cadbury-Schweppes, the world's number one candy and soft drink manufacturer.

vlm--

What a spectacular result!

I say stick with what works, regardless of the ignorance of those around us. But be sure to educate your friends, family, and neighbors, particularly when they ask why you've looking so good.

Not only is the ADA. AMA and AHA becoming irrelevant so are the doctors who follow these destructive advices. Look for a paradigm shift-Dr. Davis is on the cutting edge of that shift.

Dr Davis,
   I am from South India and the primary diet is white rice. There is a wide spread notion in our region that rice adds up to your weight and wheat is the best alternative. After reading your articles about wheat, I have switched back to rice, but this time, to raw brown rice.
   Are your observations about wheat also applicable for rice and other grains?

-Neelesh

Yes, it does, though rices, particularly the cruder forms like brown, are less of a culprit.

However, the need to make these changes depends on lipid patterns such as low HDL, high triglycerides, and small LDL. If these apply to you, then an across-the-board reduction in high glycemic index foods like wheat and rice improves these patterns. However, if you have none of these patterns, then such a change may not be all that necessary.

I do fear, however, a politically correct lukewarm (at best) endorsement of the concept, since there is a great financial stake in maintaining the status quo.

That's exactly why I haven't included the rumor that the ADA is revising to include low-carb as an option in their upcoming position statement for 2008 - I'll believe it when I see it.

Bravo on this post Dr. Davis!

Dr Davis : You show ADA food pyramid with grains at one end.  Do you have an example of a food pyramid that you would suggest for track your plaque followers.

I've always found the whole idea of a food pyramid kind of goofy. But, just truncating the entire bottom of the pyramid is what I would suggest. There is indeed room for non-wheat grains, such as flax and oats, but I base it on individual lipoprotein patterns.

The new Track Your Plaque diet is still in the works.

Another testimony to this idea: I was diagnosed with diabetes 2 when my retinas hemorrhaged slightly.  (Flashers and floaters.)  My glucose was at 300 and the doctor prescribed strong meds.  It was just after Christmas and everyone had sent me chocolate which I enjoyed.  After this diagnosis, I threw out the chocolate, did not eat sugar, flour (except a little as a binder in muffins), corn syrup, or any processed foods.  I quickly dropped the fifty pounds I'd been trying to lose over the previous two decades.  

The strong meds sent me down to the 60's in glucose scores.  This made my doctor and her nurse angry -- they are 80 miles from me and I made contact on the phone.   Figuring I was on my own, I dropped all meds, then added back one metformin in the morning.  This has given me an a1c of 6.1.  The doctor refused to believe my reports.  There is no diabetes specialist for hundreds of miles, not even a nurse/counselor -- yet rates are very high.  My experience is shared by at least three other women in this village of 300.

It appears that diabetes is one of the political diseases.  To say nothing of deliberate corporate evil.

Prairie Mary

Wow, Prairie!

What an interesting experience. I love hearing about non-pharmaceutical successes!

Dr Davis, I have been reading your blog with interest since we first "met" in cyberspace. You may remember that I heartily agree with your views on the ADA and it's dietary advice. I wrote on it a while ago: http://loraldiabetes.blogspot.com/2006/11/diabetes-authorities.html

You post some very valuable advice. However, I do find it hard to accept "He is now clearly, solidly, and confidently NON-diabetic."

To the best of my knowledge, there is no cure presently. I would not apply this to you, but my usual advice to any diabetic dealing with a doctor who claims to cure diabetes would be to find a new doctor. To me, until a complete cure is discovered, it is a four-letter word in that context.

"Russ" may now be a very well-controlled type 2 diabetic, but he would still be a diabetic. As a diabetic in a similar position of good control I only have to test my blood glucose after an unwise high-carb meal to remind myself that I am not cured, just well-controlled.

Hi, Alan--

I agree that there is tremendous variation in insulin and glucose responses.

However, I have seen many people who exhibit entirely normal after-eating responses when diet has been modified and after weight loss. Of course, not everybody achieves this, but many do.

Wow, Dr. D -- that was the most superfabulous exposition!!!

you hit it right on the nail!again!!

We all exist somewhere on the 'Metabolic spectrum' -- having the ability to convert glucose energy from any food source (ie, tree bark, vegetation stems & leaves, etc, the quintessential Paleo diet) was actually a survival mechanism. Most races are hard wired that way, and some more especially so (perhaps they lived in more rigorously harsh environments like the Pima American Indians which have the highest rates of T2DM).
I believe you are curing people -- if they maintain non-diabetic glucose levels (without meds) for some time then I believe that is a cure in my book. The corporate world is not ready to lose profits, and therefore they will always be hardpressed to acknowledge 'cures'.  But we're ready for cures!  keep bringin 'em on!!!!

Non-Diabetic Glucose Ranges:
Pre-meal = and < 99
1-2h post meal < 120-130
I h-a-t-e that pyramid... as you are aware... it should be flipped around w/ veggies on the BOTTOM, then raw nuts, fish oils.

That was entirely lovely...THANK YOU!

Ok, I cannot refrain in sharing these older studies which relevantly showed that either high carb was bad or that low carb was VERY GOOD for lowering TGs and raising HDLs and lower small atherogenic LDLs... (i apologize if the links get chopped up)

Am J Med. 1987 Feb;82(2):213-20. Links
Deleterious metabolic effects of high-carbohydrate, sucrose-containing diets in patients with non-insulin-dependent diabetes mellitus.
Coulston AM, Hollenbeck CB, Swislocki AL, Chen YD, Reaven GM.
The effects of variations in dietary carbohydrate and fat intake on various aspects of carbohydrate and lipid metabolism were studied in patients with non-insulin-dependent diabetes mellitus (NIDDM). Two test diets were utilized, and they were consumed in random order over two 15-day periods. One diet was low in fat and high in carbohydrate, and corresponded closely to recent recommendations made by the American Diabetes Association (ADA), containing (as percent of total calories) 20 percent protein, 20 percent fat, and 60 percent carbohydrate, with 10 percent of total calories as sucrose. The other diet contained 20 percent protein, 40 percent fat, and 40 percent carbohydrate, with sucrose accounting for 3 percent of total calories. Although plasma fasting glucose and insulin concentrations were similar with both diets, incremental glucose and insulin responses from 8 a.m. to 4 p.m. were higher (p less than 0.01), and mean (+/- SEM) 24-hour urine glucose excretion was significantly greater (55 +/- 16 versus 26 +/- 4 g/24 hours p less than 0.02) in response to the low-fat, high-carbohydrate diet. In addition, fasting and postprandial triglyceride levels were increased (p less than 0.001 and p less than 0.05, respectively) and high-density lipoprotein (HDL) cholesterol concentrations were reduced (p less than 0.02) when patients with NIDDM ate the low-fat, high-carbohydrate diet. Finally, since low-density lipoprotein (LDL) concentrations did not change with diet, the HDL/LDL cholesterol ratio fell in response to the low-fat, high-carbohydrate diet. These results document that low-fat, high-carbohydrate diets, containing moderate amounts of sucrose, similar in composition to the recommendations of the ADA, have deleterious metabolic effects when consumed by patients with NIDDM for 15 days. Until it can be shown that these untoward effects are evanescent, and that long-term ingestion of similar diets will result in beneficial metabolic changes, it seems prudent to avoid the use of low-fat, high-carbohydrate diets containing moderate amounts of sucrose in patients with NIDDM.
PMID: 3544839 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=3544839&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs1

Am J Hypertens. 1990 Jul;3(7):527-32.
Links Effect of low fat-high carbohydrate diets in hypertensive patients with non-insulin-dependent diabetes mellitus.
Fuh MM, Lee MM, Jeng CY, Ma F, Chen YD, Reaven GM.
Department of Medicine, Tri-Service General Hospital, Taipei, Republic of China.
Effects of variations in dietary fat and carbohydrate content on various aspects of glucose, insulin, and lipoprotein metabolism were evaluated in 11 patients with hypertension, who also had non-insulin-dependent diabetes mellitus (NIDDM). All of these patients were being treated with sulfonylureas, thiazides, and beta-adrenergic receptor antagonists. The comparison diets contained either 40 or 60% of total calories as carbohydrate, with reciprocal changes in fat content from 40 to 20%. The diets were consumed in a random order for 15 days in a crossover experimental design. The ratio of polyunsaturated to saturated fat and total cholesterol intake were held constant in the two diets. Plasma glucose and insulin concentrations were significantly (P less than .001) elevated throughout the day when patients consumed the 60% carbohydrate diet. Fasting plasma total and very-low-density lipoprotein (VLDL) and triglyceride (TG) concentrations increased by 30% (P less than .001) after 15 days on the 60% carbohydrate diet. Total plasma cholesterol concentrations were similar on both diets, as were low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol concentrations.
PMID: 2194509 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=2194509&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs1

JAMA. 1994 May 11;271(18):1421-8.
Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus.
Garg A, Bantle JP, Henry RR, Coulston AM, Griver KA, Raatz SK, Brinkley L, Chen YD, Grundy SM, Huet BA, et al.
Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas 75235-9052.
OBJECTIVE--To study effects of variation in carbohydrate content of diet on glycemia and plasma lipoproteins in patients with non-insulin-dependent diabetes mellitus (NIDDM). DESIGN--A four-center randomized crossover trial. SETTING--Outpatient and inpatient evaluation in metabolic units. PATIENTS--Forty-two NIDDM patients receiving glipizide therapy. INTERVENTIONS--A high-carbohydrate diet containing 55% of the total energy as carbohydrates and 30% as fats was compared with a high-monounsaturated-fat diet containing 40% carbohydrates and 45% fats. The amounts of saturated fats, polyunsaturated fats, cholesterol, sucrose, and protein were similar. The study diets, prepared in metabolic kitchens, were provided as the sole nutrients to subjects for 6 weeks each. To assess longer-term effects, a subgroup of 21 patients continued the diet they received second for an additional 8 weeks. MAIN OUTCOME MEASURES--Fasting plasma glucose, insulin, lipoproteins, and glycosylated hemoglobin concentrations. Twenty-four-hour profiles of glucose, insulin, and triglyceride levels. RESULTS--The site of study as well as the diet order did not affect the results. Compared with the high-monounsaturated-fat diet, the high-carbohydrate diet increased fasting plasma triglyceride levels and very low-density lipoprotein cholesterol levels by 24% (P < .0001) and 23% (P = .0001), respectively, and increased daylong plasma triglyceride, glucose, and insulin values by 10% (P = .03), 12% (P < .0001), and 9% (P = .02), respectively. Plasma total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels remained unchanged. The effects of both diets on plasma glucose, insulin, and triglyceride levels persisted for 14 weeks. CONCLUSIONS--In NIDDM patients, high-carbohydrate diets compared with high-monounsaturated-fat diets caused persistent deterioration of glycemic control and accentuation of hyperinsulinemia, as well as increased plasma triglyceride and very-low-density lipoprotein cholesterol levels, which may not be desirable.
PMID: 7848401 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=7848401&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs1

N Engl J Med. 1988 Sep 29;319(13):829-34.
Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus.
Garg A, Bonanome A, Grundy SM, Zhang ZJ, Unger RH.
Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas 75235-9052.
We compared a high-carbohydrate diet with a high-fat diet (specifically, a diet high in monounsaturated fatty acids) for effects on glycemic control and plasma lipoproteins in 10 patients with non-insulin-dependent diabetes mellitus (NIDDM) receiving insulin therapy. The patients were randomly assigned to receive first one diet and then the other, each for 28 days, in a metabolic ward. In the high-carbohydrate diet, 25 percent of the energy was in the form of fat and 60 percent in the form of carbohydrates (47 percent of the total energy was in the form of complex carbohydrates); the high-monounsaturated-fat diet was 50 percent fat (33 percent of the total energy in the form of monounsaturated fatty acids) and 35 percent carbohydrates. The two diets had the same amounts of simple carbohydrates and fiber. As compared with the high-carbohydrate diet, the high-monounsaturated-fat diet resulted in lower mean plasma glucose levels and reduced insulin requirements, lower levels of plasma triglycerides and very-low-density lipoprotein cholesterol (lower by 25 and 35 percent, respectively; P less than 0.01), and higher levels of high-density lipoprotein (HDL) cholesterol (higher by 13 percent; P less than 0.005). Levels of total cholesterol and low-density lipoprotein (LDL) cholesterol did not differ significantly in patients on the two diets. These preliminary results suggest that partial replacement of complex carbohydrates with monounsaturated fatty acids in the diets of patients with NIDDM does not increase the level of LDL cholesterol and may improve glycemic control and the levels of plasma triglycerides and HDL cholesterol.
PMID: 3045553 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=3045553&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlusDrugs1

Hi, G--

Thanks for all the wonderful references.

Interestingly, the "low carbohydrate" arm in all the studies were actually high-carbohydrate by some standards. I suspect that even more pronounced differences would have been seen with a stricter reduction of carbohydrates.

Is it any wonder that we now have a nation full of obese pre-diabetics and diabetics? All with accelerated heart disease and cancer risk?

Yet the offical organizations cling to the old notions.

Dr. Davis,
This isn't related to this post, but I am wondering about fish oil supplementation for people on Warfarin.  There's an "ask your healthcare professional" notice on our bottle of fish oil.  What does this mean?

Dr. Davis, you said... "However, I have seen many people who exhibit entirely normal after-eating responses when diet has been modified and after weight loss. Of course, not everybody achieves this, but many do."

This remains as long as they stick to the diet that achieved this for them; however, if they eat crap again, their postprandials rise to diabetic levels again which is *not* the case for nondiabetics.  Thus they are a very well-controlled diabetic, not a cured diabetic.

I am diabetic, but my husband is not.  I have tested his postprandial bg after eating 1/8th of a double layer chocolate cake and it is in the 70s.  Not that chocolate cake is healthy for him either, but no matter how long I am well-controlled or how much weight I lose, I will never be able to eat that without my postprandial bg going to diabetic levels.

Type 2 diabetes is primarily about insulin resistance (IR).  Diet, exercise and weight loss can greatly improve insulin sensitivity and thus improve the disease condition so that bg control is easier and postprandial excursions less extreme.  One can improve the disease to the degree that one can achieve nondiabetic numbers, and if IR improves, do so even while eating more carb than could be handled while gaining control.  Diabetes can *certainly* be improved; it does not *have* to be a progressive disease.

But by the time one is diagnosed with T2, there have usually been very high serum insulin levels for years as well as pancreatic damage reducing if not entirely eliminating the phase 1 insulin response.  Being in good control does not heal the pancreas, reduce serum insulin to normal levels, nor remove IAPP plaques, etc. And it does not mean you can have nondiabetic postprandial response to eating crap.

I completely agree with your post overall.  These types of results are great and good patients achieve them.  I only disagree in the same place Alan disagreed; the word "cure" implies something more than can currently be achieved.  Diabetics can have good control, even very good control and nondiabetic numbers, but we are not cured.  

But you absolutely have the right approach as opposed to the ADA; to them I say, "let them eat cake."

I see what your trying to say. Yes, I would agree that's true for the majority of former pre-diabetics and diabetics.

I too am a type II who was "cured" by doing Atkins. I was on tons of insulin, metphormin, cozaar,lipitor and within 32 hr of starting Atkins had to quit insulin. I have low carbed for 4 yrs and fell off the wagon a yr ago.Back on now after a hard lesson learned.

My A1C were 5.5 without insulin or meds and eating Atkins.I allowed my doc to persuade me I needed grains and fiber and I went on some and it completely threw me off and the cravings were like a drug addict wanting more drugs.

I lost control of my appetite, my cravings and my blood glucose levels.

I asked my doc why they pushed grains and was told the CDA is sponsored by the Cdn wheat board.
Duh...it made me angry but it motivated me to go back on insulin to get bg down again and go low carb and within 2 weeks I no longer needed insulin once again.

I was so good with bg control for several yrs I thought I was "cured", but would have some healthy grians like cooked oat bran with large old fashioned oatmeal flakes and whamoooooo
and my bg would bounce right back up there.

However, I am not on insulin anymore, I use some Glucophage(and only use brand name Glucophage as yes it does work better than metphormin for me and for almost all of Dr Bernstein's patients it works better as well....go figure...).
All druggists and Dr told me its exactly the same but it is not and once you learn how the FDA allows for differences in brand and generic names it will blow your sox off.

I am skeptical of all who tell me now I need wheat, starch and grains and can have some sugars....they don't live in my body, they don't know the demons of craving I suffer when I go off my low carb program and if I follow their advice I wont live to be an old lady.

I will never be "cured", the beast will rear its ugly head and harm me every time I eat something with grains, wheat, starch or yes crap.....but even when I eat "good grains"...my body just cant do it anymore.

I am 57 and had yrs of overloading, I am in better shape now than ever in my life and I wish I was "cured" but I am not.

I am aiming for an A1C of a non diabetic of 4.2 to 4.5 and slowly will get there.

But in doing so I butt heads with all of the medical community yet they see me and exclaim how wonderful I look, how much weight I have lost, thnx to people who think outside the box like Dr. Atkins,( he made some boos boos in his new stuff which I think was from peer pressure, he should never have encouraged grains, fruits back into the prgram as it made bg go up for diabetics,causing cravings and high bg, he changed his original program) Dr. Bernstien,( he is strciter than Atkins and says you are diabetic, your body no longer tolerates grains, starches, sugars so get over it, if you want to live long)Dr. Davis and Dr.Blancehtt( from what I read here)are now treating the other side of evil us diabetics live with....heart disease.

Now I know there are some well educated medical people who are looking outside the box, listening to their patients stories and treating us like we have some gray matter between our ears and trying to find out how to diagnsoe and treat us, I finally feel some element of security and safety.

My blood tests don't lie although I have been treated by many Dr as though I am lying when I say what my blood meter shows and then they see their own lab results and are wowed.

One other aspect I ahve noticed here, if anyone writes a differeing of opinion than Dr D he doesnt shut us up and hears us and often comments that is somethign frutehr he will explore or look into.

I appreciate that we have your intelligent brain, yrs of medical practices and ability to think without getting defensive,

Dr like you should have a Nobel prize as in a few decades this will hopefully all be commonplace treatment for heart issues and diabetes.

Thanks for sharing your insightful experience, Chickadee.

I personally have a similar pattern to yours, but have managed to keep off all meds once I dropped all wheat, along with processed carbohydrates. While we have to be careful in too broadly generalizing our experiences, I would estimate that this pattern is shared by 70% of people to various degrees.

I just want to add I agree with Chickadee.  It's Dr. D's blog, he doesn't have post comments from those who disagree; but part of why I participate here is because I saw that he did that.  

I also personally appreciate that he changes his mind (the info on this blog is different in some aspects than the info in the TYP book).  It's obvious he is still learning; too many people are dogmatic about their opinions.  

Research progresses; so what we know changes.  I want my own choices to be based on the best current knowledge, not someone's near-religious beliefs.

Yes patti, metoo!!!

Chickadee (vlm and Praire Mary), Your experience is truly amazing.  You're preservering by faithfully following what you know to be true, in the face of the current medical establishment. You must be a beacon of motivation for a lot of  your friends and family (and you must appear hot and amazing as well!)...  I have to check out IAPP plaque -- luv learning stuff here!! I believe T2 parallels other chronic conditions like CAD -- if the destruction of cells is not irreparable (like CAD, if imminent myocardium death from obstruction and oxygen deprivation exists, then stents/bypasses are crucial and life-preserving), then a 'cure' is possible because our body has the capacity to repair and recover.  However as you discussed, if enough destruction of beta-islet pancreatic cells has already occurred, then recovery may not be possible to maintain normal 1 to 2h-pp glucose after a large glycemic load.  Unfortunately, 50% of islet cells are usually GONE at diagnosis for most T2DMs and progressively decline annually unless dramatic changes happen. Imperative changes like those encouraged and emphasized by the TYP plan. Even more important is to stop the destruction before we become older. I believe TYP should be taught to all children. as soon as possible.
Pregnancy (progesterone-dominant) and certain drugs (prednisone) cause transient diabetes -- however when the triggers are gone (ie, give birth and resume exercise or stop the offending agent Prednisone) -- normal glycemic indices will often resume.
My children only get 2 hrs of physical ed now per week in school, as a result (my understanding) of Bush's 'leave no child behind policy' which they claim is to bolster academics. Most unfortunate for the physical and endocrin/cardiovasc health of all Americans (hopefully Canadians are better off! well, you are... you don't have Bush... and soon neither will we). Remember, as kids we had ONE HOUR of PE e-v-e-r-y-d-a-y? Plus, playing outdoors until the sun went down!? Gone are those days esp in the decade of video games (and internet *sigh* -- look at me what a hypocrit)... surburban concrete and indoor malls...
Most clinical studies are suspect because only the drug companies can afford them.  Big companies have lobbyists and choke-holds on all the major 'public health' sources (including ALL the major med schools and universities also... JAMA and most publications).
Only vigilant far-reaching visionaries like Dr. D go far and beyond the call of duty to do the thankless job of educating and propagating  solutions for the #1 killer of women and men -- heart disease (AND #2 killer cancer arguably as well, and obesity and T2DM and most autoimmune disorders too).  THANK YOU DR. D!!!!
Many of the strategies for CAD reversal are applicable to T2DM glycemic control optimization (I've personally lived it b4 I read the book/blog and see it in the diab patients that follow it). Getting enough vitamin D (esp you're Canadian and get absolutely no UVB above the 37th latitude) is key. In fact Vit D is more effective at insulin sensitization than metformin and other drugs (again, if there are enough remaining beta islet cells to sensitize).
Exercising and therefore consuming minimum 350 calories daily (or 5,000 to 10,000 steps) via a pedometer as Dr. D prescribes in the TYP plan is imperative for insulin sensitization. Use it or lose it.
'Bad' carb elimination, good carb restriction. Sufficient protein and good oils.
Keeping your estrogen levels 'normal' arguable > 50 for most women (pre- or post menopausal -- if you have no breast CA in your family history)... Testosterone, in men, the corollary (and women too).
Strength training -- lifting 3 x week all the major muscle groups -- 3 sets of 10 reps -- will achieve significantly improved IR as well (and a higher sense of mood and prevent spinal osteoporosis). Lean body mass, or MUSCLE, effectively metabolizes even at rest (for example, when our b**tts are atrophying in front of the computer). The more muscle, the more metabolism!
Stress reduction, lowering cortisol through yoga/tai chi, being 'happy', optimizing your vitamin 'O' (the intangible optimism -- as Dr. D  puts it!!)...  the more love we give, the more we get! Lovingkindness -- it all works! The added benefit with less cortisol is less visceral fat deposition on the belly... as well as the liver, heart, coronary vasculature -- don't need those love-handles to LOVE!

You're awesome -- keep it up!

btw, make sure the TSH is 0.2 to 3.0! adequate thyroid function affects IR, lipoprotein patterns, heart hypertrophic changes, etc. guess what yoga poses do? cobra-pose for instance helps 'massage' the thyroid and parathyroid glands to remove toxins and allow an influx of fresh oxygenated blood! the deep nasal breathing allows the adrenal nervous system to shut off (which shunts blood from vital organs like the liver/kidney in order to oxygenate the muscles for 'fight-flight'), yoga turns on the cholinergic NS to promote rejuvenation and restoration including improved blood flow to the heart, kidneys/adrenals, and liver, etc.

Thanks, as always, G, for your delightful commentary.

I love your "vitamin O" idea!

Thnx for encouragement g as sometimes it feels like I do my health program in isolation if I didn’t have access to these forums etc.

When I ask for tests I am often treated like I am “neurotic” for one Dr told me I am a double double Type A for being so careful with my diabetes as only 50% of diabetics can achieve an A1C of under 8.

I thought oh great, glad I am or I would still be 80 pounds overweight if I kept eating the Cdn Diabetic program and still  injecting about 150 units of insulin a day!!!
Bring on the Type A,,,, is that kind of like the Vitamin O…lol.

I told him I believed diabetics couldn’t achieve under an 8 for A1c was due in part that they were told to eat low fat, high carbs. Diabetics feel great shame in following a program yet gaining weight and still having a high A1C. This shame is left in a shroud and never dealt with.

I wish I had this info a few decades ago when I used to have GP’s refer me their diabetic patients to learn coping strategies and we taught relaxation techniques etc and behavior mod, if only I understood how hungry a diabetic is with BG dropping and rising. My hunger has not been an issue since I started low carb, it did when I fell off the wagon. I now use duct tape and stay securely in!!!

I believe I still have some beta cells as there are days I can go without using glucophage at all, particularly on a very physically active day. …or if I am at a wedding or a dance and I have a few glasses of wine, my BG drops a lot and I don’t use meds. I only drink a few times a year though and have tried to learn to drink red wine nightly but don’t enjoy it and would end up with another bad habit I am sure.

In winter when I am more sedentary I can see right away I need to use 500mg of Gluco TID.Man I will be happy if high doses of Vit D 3 help me with my A1C’s!!!!



See Dr Bernstein and Atkins both said as soon as a type II is diagnosed they should go on small amts of fast acting insulin and preserve what beta cells they have left. Yet it is used as a last resort.

I wish more Dr would read Dr Bernstein and Davis. Bernstein is offering a cruise for Dr to go on and get educational hours and he will train them his technique, its all a business write off but last I heard he had trouble filling the 100 needed for the cruise.
Info is at www.diabetesincontrol.com

In my mind I believe for me that eating low carb meant I only ate nutrient dense foods thus my body healed itself and began to slowly allow the beta cells to resurface and do their work. Grains are not nutrient dense for me.

Low carbing offered me this:
-I got off $1000 a yr of Imitrax as my migraines stopped.
-My hot flushes stopped.
- I had severe arthritis and used a ton of vioxx, my arthritis went away a few weeks after low carbing and I have not had treatment for it since 03. I have no pain at all.
-My blood pressure dropped but I take cozzaar still as want an Ace inhibitor to protect my kidneys as well but BP is normally about 111/62, I am 57 and am still overweight about 20 pounds but have lost 80 pounds.

So see I did this basically all against medical advice but once my long term GP( she moved after 21 yrs) saw the blood work she began to soften in her approach and support me and did allot of blood work as I was scared starting to eat more protein and using some fats.
I had been so brain washed.
Its hard to eat much protein after decades of eating protein to the size of a deck of cards and using heart smart margarines instead of butter but I watched my blood work carefully and all my lipids came way down, especially my trig. Broccolli is even better with a tad of butter. A cup of coffee with a bit of cream doesn’t make my BG go up, but using the skim milk in coffee made my BG rise.

I didn’t know about the Vit D until TYP blog and forum and am gonna flood this new young doc I have with all this info but have only seen her once and don’t want to turn her off. So will slowly plod along.

She is a real smart wise young woman, I can tell, and she is very open minded. She has already read Bernstein’s book and I am going to buy her TYP as a gift. She kind of wondered about me going for another calcium score and didn’t know anything about the advanced lipid profiling but she ordered it anyhow.

I know doc have allot of reading and work to do and its impossible to be the expert on everything but I see she is wise and confident enough to have an open mind.

One more tidbit you doc's here may be interested in knowing about.

Dr Westman from the Duke did a project up in a Native reservation in northern Canada called Alert Bay. It was rampant with diabetics. He trained a Dr from Edtmn and his wife who was a nurse pract and Health Canada sponsored them. The whole village was taught to go back to their way of living from before they were influenced by white man and to eat more fish, meat, seeds, berries, basically almost an Atkins type program and it was a huge success.


Dr Westman is very approachable and if you wanted I would ask him if I could give you his email in a private email as he has a head full of great ideas too about treating type II diabetes.

In some ways to me it seems like all you wise docs are working in isolation around the world and you need a forum or a gathering place to host all these wonderful ideas so you can educate your colleagues

How could we make this happen.???

A conference in the Canadian Rockies!!!.

I'll help organize it, not in winter though as the suns rays are so low and it is minus 29 degrees as I sit and type, but oh so pretty with all the snow covered mtns.

This blog is more informative to me than anything I have had access to on the net and I have read and researched for ys to help my health improve.

I feel so privileged to have found you folks and have learned so much in the past few weeks.

I only wish the muscles I have built in my fingers typing could be transplanted into the lazy parts of my body.

Hi, Chickadee--

Thanks always for telling us your fascinating story. It's wonderful to know that we are having such an impact on lives, even in the "wilderness."

We can always be reached through the contact@trackyourplaque.com e-mail, of course, or through our Forum (when repaired--I believe it's almost there). I'd love to start a conversation with Dr. Westman. I didn't know that such a real-world "experiment" had been conducted. It would provide priceless information.

We have some ideas in the works for better delivery of this message to the broader public, but it all takes time. But it will be fun and yield some interesting opportunities!

This just came through one of my shared links sites: How low-carb diets help metabolize fats better: http://www.healthcentral.com/diabetes/c/17/17226/eat-fat-grow-thin/pf/

"The beta oxidation (or “burning”) of fat by the body requires the action of an enzyme called insulin-sensitive lipase. This enzyme is turned off by insulin. Eating carbohydrate obliges the body of a nondiabetic to make insulin in proportion to the amount consumed and obliges many diabetics to inject insulin to prevent blood sugar elevation. When insulin levels go up, fat oxidation therefore goes down, and since insulin is also the fat-storage hormone, dietary fat is stored. Furthermore, insulin signals the liver to convert the carbon backbone of carbohydrates (glucose) to saturated fat, which then appears in the blood as triglycerides, which are subsequently stored. So calories of fat are handled much differently on a low-carbohydrate diet than on a high-carbohydrate diet. Recent studies on humans eating equivalent amounts of fat show that those eating more carbs store more fat."
- Dr. Bernstein

S

I'm not sure if I could survive the Rockies... but that cruise sure sounds enticing!!  thanks for all your info Chickadee -- I'm so grateful for forums like this!  You are doing a stupendous job on your body! Man, a1c < 5%!  So you teach mind body philosophies, eh?  Your MH is definitely strong. I consult on migraines and T2DM issues. It's funny how all these conditions are linked... along with IBS, Alzheim, UC, Crohn's, and other inflammatory conditions (even colon CA)...
I do really believe that our bodies have the capacity to heal and be whole (mentally and physically) but we really need to be educated...  and have the proper tools at our disposal... that's so hard! you're totally right!  And now people no longer need to experiment and fool around.. the solutions already EXIST!!!

I'd echo your same concerns -- after Dr. D receives a Nobel prize (which is just a matter of time) -- will he lack the time for the plebs and peons on the blog?  *chuckle* maybe he'll have trained enough protege's like yourself to outsource... *ha haaa haa*

Perhaps Dr. Barry Marshall (who discovered HP as causing ulcers and gastric cancer) would've received a Nobel 10-20 yrs sooner if he had a blog and layman-oriented publications!  ;)

Yes the net certainly makes us all closer and wiser and ideas catch on quicker, it is actually amazing. Bill Gates didn't know what he did for health when he developed some of his software ey.

I never knew back when I was in the field about diabetes, OCPD, migraines, belly fat,hunger, all those dynamics that now make me get red flags.I had them all, many of us did,thought it was from the work we did not the starch and sugar we ate really as we were all low low fat eating people.

Man I can walk thru Wal Mart and tell who is diabetic or pre diabetic if there is such thing...you know like being pre pregnant...LOL


You could survive the Rockies, our winters can be harsh, cold and beautiful( I went north two weeks ago to see the polar bears in Churchill....amazing) but our summers are awesome. I live right by Jasper national park and it is one of the Seven Wonders of the World.

You know.... about Dr Eric Westman, he has done low carb Atkins like program for diabetes since about 2002 or so. He sent me tons of scientific research about chol studies and ldl numbers not being all what they are cracked up to be and to watch for lipo (a) etc way back ys ago.Thats why I had mine tested and it always came back low under the range but I didn't know much else about it until I read TYP.



Anyhow Westman has been onto low carb and diabetes and obesity and the Duke is known all over as being experts in field of obesity and diabetes.


I think cause the media slammed Atkins so bad and there were allot of mytths surrounding him some of these doc's hung low.

Recall the history of Freud, when he first heard about incest he got boo'd as he was going to present it at an international conference and his peers jeered him so he changed it all and we ended up with these anal and odephial(sp) complexes and it took a hundred plus ys to remove those myths.

Well I think it is the same with low carb, even sat fats not being the devil. In 1oo yr it will be the norm, like in Taubes research he demonstrates that in 1862 Dr were telling diabetics and obese people to eat meat, dairy and a bit of fruit and veg and it worked.No starch, no sugars.

Oh well, someday, this will be common place, we will get a heart scan like we line up for the flu shot and we'll all know our numbers and talk about it as we play bridge.

It will beocme a household word, in the mean time I am trying to learn so much lately my mind and body feels overwhwlmd but I feel joyous at knowing I can do something about my plague.I only wish I knew about Vit d and fish oil sooner.

We are all so fortunate we can read and share and ask questions here and it is not open for just medical doctors as I think we can all learn from each other.

Why isn't this common practice? If pre-diabetes and diabetes can be cured by such a simple approach, why isn't it more widely embraced? After all, what other devastating diseases can claim to have such a simple, straightforward way to achieve cure?