Vitamin D2 vs. vitamin D3

An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.

Comments (21) -

  • Jim Wint

    4/26/2007 1:35:00 PM |

    It's good that you explained how vitamin D3 is better than vitamin D2.

    Your readers should also know that, depending on their skin type, just one or two sessions in a tanning bed will produce all the healthy vitamin D3 a human body can use.

    Moderate tanning is healthy behavior.  Don't sunburn.

  • Anonymous

    4/26/2007 3:36:00 PM |

    Dr. Davis, your blogs on vitamin D are terrific.  I am a colleague of Dr. John Cannell, and am presently coauthoring a book with him.  It will deal with the effect of vitamin D supplementation on athletic performance.  He has also endorsed my current book on the health benefits of sunlight and vitamin D.  If you would like a free copy of that book--Solar Power for Optimal Health--please contact me at megamarc1@aol.com or call me at 435-628-3102.  

    Keep up the good work!

    Marc Sorenson, EdD

  • Darwin

    5/3/2007 9:40:00 PM |

    Re vitamin D consumption, do you have any thoughts re this study?  I'd like to recommend to my parents that they take an oil-based Vit. D supplement (they're in their 70s), but that study gave me pause.

  • Dr. Davis

    5/4/2007 1:09:00 AM |

    Unfortunately, the study was only in abstract form, meaning none of the full details were available.

    Nonetheless, several uncertainties:

    What was the calcium intake? What was the vitamin D intake and what blood level of 25-OH-vitamin D3 was obtained?

    I suspect that few of the participants had even normal vitamin D blood levels. The majority of vitamin D preparations in calcium tablets barely work at all due to poor absorption.

    However, I do worry that, with appropriate D supplementation, the doses of calcium many people take is excessive. The true need for calcium is likely far less when D is fully replenished.

    I would not make any firm judgments based on this preliminary report. Interesting issue, however.

  • Dave Lull

    3/27/2008 3:45:00 AM |

    Hi Dr Davis,

    I'd been persuaded, like you, that D3 is the form of Vitamin D to use for maximum effect.  Now comes this study:

    "Vitamin d2 is as effective as vitamin d3 in maintaining circulating concentrations of 25-hydroxyvitamin d"

    Holick MF, Biancuzzo RM, Chen TC, Klein EK, Young A, Bibuld D, Reitz R, Salameh W, Ameri A, Tannenbaum AD.

    Boston University School of Medicine, 715 Albany Street, M-1013, Boston, Massachusetts 02118. mfholick@bu.edu.

    J Clin Endocrinol Metab. 2008 Mar;93(3):677-81. Epub 2007 Dec 18.

    Dr Holick uses Vitamin d2 in treating his patients.

    He was recently interviewed on the radio program the People's Pharmacy; the interview is available as a podcast.

    Regards,
    Dave

  • Anonymous

    6/24/2008 4:31:00 AM |

    where can I buy vitamin D3 in Gel Caps?  Are they readily available?

  • Anonymous

    7/4/2008 9:36:00 PM |

    http://www.vitacost.com/Carlson-Vitamin-D-Natural

    http://www.vitacost.com/Jarrow-Formulas-Vitamin-D3-1000IU-100-Softgels

    Google "vitamin d2 tablets".  Loog for softgels, or gelcaps.

  • Anonymous

    7/25/2008 4:45:00 PM |

    Buy Vitamin D3 in softgels (oil based form from

    http://www.abacohealth.com/index.php/prodid/NOW113
    or

    http://www.abacohealth.com/index.php/prodid/CAR017

  • Anonymous

    9/21/2008 12:06:00 AM |

    So, if I am buying a supplement that is labeled as Vitamin-D (not D3), but the label says it is 1000 IU of Cholecalciferol, the supplement is really Vitamin D3?

  • Anonymous

    11/18/2008 8:16:00 PM |

    I'm curious why you have no comment on the above story that refutes your entire theory.

  • Anonymous

    12/12/2008 11:56:00 PM |

    Actually your post is very confusing because you say vitamin d3 is 25-oh-d3, actually it's a metabolite of d3, also you say ergocalciferol is inneficient because yields little conversion to 25-oh-d3, but d2 converts ONLY to 25-oh-d2 and very efficiently, and has similar activity to the d3 form(about 2/3 of the potency), the bad about d2 is also that has faster metabolism than d3.
    All in all, d2 is efficient, not like d3, but it's not useless like you say, and d2 has metabolites with potent anticancer activity, similarly to tamoxifen in breast cancer, so d2 has it's own benefits over d3.

  • Alphonzen

    3/19/2009 1:42:00 PM |

    http://www.sciencedaily.com/releases/2008/01/080102122306.htm

    Vitamin D2 Is As Effective As Vitamin D3 In Maintaining Concentrations Of 25-hydroxyvitamin D, Study Suggests

    Sorry blogger, but you have been proven wrong.

  • Anonymous

    9/24/2009 11:21:46 PM |

    The difference as I've understood - there are actually 5 forms of Vitamin D (D1-D5). Vitamin D2 must be converted to be used, Vitamin D3 is used directly. Vitamin D2 is "relatively ineffective" because it is the  stored form and it's stored in the body's fat- which is why it has certain properties that D3 doesn't possess for fatty tissue health. Eventually D2 effectiveness would equal D3 because the body eventually converts what it needs. However, it has requirements for the conversion, and if taken for anti-inflammatory, anti-cytokine storm, immune modulation, then D3 is the much better form since it can be used immediately. When healthy I take D2 and D3 - D2 fills the body's stores while D3 is consumed. When the immune system is being challenged Vitamin D3 is the better form and will keep the D2 levels in the fat unaffected.

    As far as calcium supplementation - I think it's ludicrous - I can't imagine anyone, other than people that cannot tolerate milk products, not getting enough dietary calcium. I think that's one of the biggest myths propagated today. Hypercalcemia, and even just excessive calcium intake, has been shown to cause brain lesions in elderly, and calcium creates issues when Vitamin D is supplemented.   Magnesium supplementation is MUCH more important for everything from healthful bones, heart rhythm and heart attack protection, to smooth muscle relaxation, and mental acuity. We need a MINIMUM of 400mg and should be taking more.  With everyone drinking bottled water that has next to no magnesium content, we are all susceptible to dangerously low "sudden heart attack" levels of magnesium.

  • Anonymous

    11/16/2009 7:21:58 AM |

    Have you studied people who have had gastric bypass / weight loss surgery? They have completely different calcium citrate and vitamin D requirements than a regular person. Please see the web site www.obesityhelp.com  There are many professionals on this site with articles on supplementation.

    I buy my supplements from http://www.vitalady.com

  • Anonymous

    12/2/2009 6:11:36 PM |

    For vegetarians (where killing of an animal is prohibited) -
    D3 made from lanlolin (sheeps wool) is the only choice, there is no pure plant based D3?

    For Vegans (has to be plant based only)
    Looks like D2 made from yeast is the only choice.
    If any one know best form of D3/D2 suitable for vegetarians/vegans, please post where one can get (Please note, gel capsules are made from animal sources, they would not be suitable). Thank you

  • Steve D'Sa

    2/16/2010 4:27:48 AM |

    I'm taking a vegan calcium supplement, with vitamin D3. Its branded Vitamin Code, RAW CALCIUM, from Garden of Life, its fortified with Magnesium and other things. Its vegan, and RAW. I think the D3 source is algae.

  • Anonymous

    9/8/2010 5:49:49 AM |

    Sorry Steve. The code RAW vitamins you're talking about aren't vegan. They get their D3 "primarily from lanolin" (=occasionally fish?). According to them, since they remove the traces of lanolin during processing, they felt that it was vegan.

    After listening to them go on and on with their justifications of it and why it was vegan, it just felt like a giant marketing scheme. Needless to say, I'm now quite wary of all Garden of Life products.

    Regardless, they're still in the process of changing labels, but in the meantime, nope, not vegan. Frown

  • edegra online

    9/23/2010 6:40:36 AM |

    Thanks for providing the comparison
    between Vitamin D2 and Vitamin D3.


    Best Regards
    Smith Alan

  • buy jeans

    11/3/2010 8:32:37 PM |

    D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

  • Dr Brad

    6/13/2011 5:48:35 AM |

    Case study:  lab result shows Total Vit D, 25-OH 36; D3=6, D2=30.  Person supposedly taking 2000 IU D3 daily.   What is the significance of the D3=6 measurement.  I typically look at total and make recommendation from there but have been told that perhaps I should look at sub-classes. thoughts?

  • Annika Brixner

    5/19/2014 4:34:26 AM |

    Wonderful site. Plenty of useful information here. I am sending it to a few pals ans additionally sharing in delicious. And of course, thank you on your effort!

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Diet is superior to drugs

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Comments (27) -

  • Janknitz

    1/7/2012 6:24:17 PM |

    7 months ago I was dying. I was (still am) morbidly obese. I have GERD, hypertension,  sleep apnea, PCOS/insulin resistance, asthma, chronic back and skeletal pain. I could not walk across the room without severe pain and shortness of breath. I was afraid to do any testing or discuss this with my doctor because I knew that I would be prescribed a bunch of meds (statins, diuretics and BP meds) and sent to kaiser's group nutritional counseling to learn all about how six servings of whole grains and daily exercise would fix everything if I was "compliant".   I am not a compliant person . . .

    I had amazing success with low carb 12 years ago--so successful that I conceived my second child despite PCOS (our first daughter was an in vitro).  But having a baby, working two jobs, and attending a doctoral program at night was a lot to handle, and gradually my diet fell by the wayside.

    Returning to low carb was not as difficult as I imagined. I was still eating wheat and other grains, albeit in very small amounts within my 20 to 30 grams of carbs daily. While I felt better, I was still in a lot of pain and discomfort, still could not exercise.

    I was reading everything I could get my hands on and eventually stumbled upon your blogs and Paleo and primal blogs to.   I decided to cut out grains, even my beloved oats. Even though I love baking bread, I was never a great bread eater, so wheat was actually easier to give up. And since I was already in low carb ketosis, it wasn't physically difficult at all.

    I feel like a 1 ton cement jacket has been removed from my body!  My weightloss has stalled (looks like thyroid or IR is the culprit so I'm working on it) but I feel so energetic that on days I don't have time to exercise I feel restless to get moving. I can walk 2 1/2 miles and all of my chronic pain is gone. GERD is gone, I  haven't had an asthma exacerbation in since last winter, BP is normal. My post prandial blood sugars are good.

    Most of all, LOOK AT THESE LABS!
    Cholesterol  235  
    Triglyceride  71  
    HDL  79  
    Low density lipoprotein calculated  142  

    I know there's more work to be done (I'm going to get those triglycerides below 60!), but this is amazing to me considering I eat all the butter, cream, whole eggs,  animal fat, coconut oil, and olive oil I want.   I eat no grains or sugar, very occasional starchy vegetables, and a small serving of berries daily.  I feel like I have my life back. Thank you, thank you, thank you!

  • Jan

    1/7/2012 6:52:31 PM |

    Very interesting stats and the controlled elements show their significance to the lipid profile. Wondering what the rest of your diet looks like. Are you primal or paleo, vegetarian, vegan? Do you drink fresh green juice daily?  Just curious....one concern I would have, in light of all the great things you are doing, eating out everyday with Asian-style foods leaves freshness, preparation, ingredients to someone else. I have found no matter how careful we are in our choice of a restaurant, eating out means eating off! I couldn't do it everyday.  It will be interesting to follow your diet changes and see what happens!  Happy 2012!

  • Might-o'chondri-AL

    1/7/2012 11:46:08 PM |

    Hi Jan,
    Context first:  my results may not translate to everyone, since weight is never a real problem as the 1st NMR results coincided with laboratory measured fasting serum blood glucose = 83 mg/dL & HbA1c = 5.4 (for comparison after 3rd NMR  HbA1c = 5.3 & then serum glucose = 88 mg/dL, probably a mild side effect from added high dose fish oil).
    Asian restaurant lunch "specials" were chosen for  offering me a variety of affordable places &  menu variation to eat 7 days a week. It was to deliberately try to determine how well my lab results might hold up when have to partly yield responsibility &  dine in the world at large.
    I  arranged all other meals to be one's that were nutritious,  yet  whose regularity could become factored around if the lab results from 1/2 year of  cheap lunches played havoc with my NMR  (or  glycation indicator HbA1c).  I  precisely wanted to avoid trying to micro-manage an unknown assortment of cooks who might be using a  bit of sugar, cheap cooking oil, starch for thickening &  flour to sometimes crust fish. The lunch meal's standard full cup of cooked white/brown rice was eaten to see if it made any difference to my metabolism (ie: fasting serum glucose).
    I stuck with seafood dishes because I haven't eaten meat/chicken in over 40 years & have always had robust fortitude without those proteins. My breakfast & desert/snack protein preference is low/non-fat dairy casein (fermented milk solids with reduced whey - consistency of a pudding I can add anything to).
    To establish a standard evening meal I found a olive oil based brand hummus to measure out as a known portion to make up into a nightly mixed vegetable salad (no additional bread/rice) that didn't whack my post-prandial blood sugar (tested once every 15 min. like Doc suggests & after 1 hour blood sugar just 2 units higher than pre-meal, with just 1 unit higher after 2nd hour of meal).
    Green juice was not a part of these trials , so can't say if would affect NMR results. My budget for lab tests is empty so I am not experimenting to determine any other diet nuances now.

  • Andrew

    1/9/2012 1:04:15 PM |

    While Niacin is not a drug, 500 mg 3 times a day is excessive.

    Recommend reducing Niacin supplementation to reasonable levels taking with everything else taken into consideration.

  • Jim

    1/9/2012 5:54:03 PM |

    Mit:

    So happy for you. I have recently found this site and been reading the info for a couple months now. Is the NMR that you get from ineedlabs the full NMR (beyond standards lipid test from local doctor) or is it a truncated version? Thank you for mentioning the site! Jim

  • Might-o'chondri-AL

    1/9/2012 6:30:07 PM |

    Hi Andrew,
    ? How do  you attribute the rise in HDL those NMR demonstrated ?
    My assessment of my carbohydrate intake during last 1/2 year was certainly not very low carb, but more like moderate . I tried to calculate daily carbs & figure a minimum of  100  to more commonly over 120 gr./day . But ,quite frankly , often as not  more likely at least 150 gr./day since ate couple lunches weekly of spicy asian food that chef's told me they  use some sugar as an ingredient (schechwan fish, 3 flavors fish, half a fortune cookie), starch for  cup of soup thickening& wheat for breading (outer fish crispy)  .
    If I was moderate & not low carb I am at a loss to surmise how  that  made my HDL genetics  now re-programmed to going forward be able to provide me with (say) at least 60 mg/dL  if I cut back to 1,000 mg daily niacin.
    Allow me to recapitulate this data:
    NMR   with  zero (0)  niacin   HDL=45 mg/dL
    next    taking     1,500 mg/d  HDL = 64 mg/dL
    or   lastly           2,000 niacin HDL = 88 mg/dL  ( with no increase in fish oil, nor inc. in vit D supplement)
    You echo Doc in cutting back the niacin & presumably this is to avoid over-taxing the liver - am I correct?
    If  this orientates you opinion after 4 months on 1,500 mg daily Niacin I deliberately tested the standard liver enzymes;  showed  SGOT (AST) =  20 Iu/L & SGPT(ALT) = 17 IU/.  And, let me specify I think liver enzymes should  be checked by anyone regularly taking high  Niacin .
    ? Doesn't it seem that at least 1,500 mg/d Niacin is my individual safe dose ?

  • Jacob

    1/9/2012 10:37:21 PM |

    I'm a 38yo white male who experienced a nearly identical change to Mitochondri'Al's without reducing my carbs at all or changing my exercise routine. I'm taking 2,500mg/day of niacin with no side-effects apart from the flush (which I enjoy). My liver enzymes have remained stable and there has been no appreciable increase in homocysteine. Obviously Dr. Davis has infinitely more experience in this realm, but my suggestion would be to continue with the niacin. 1,500 is definitely a safe dose. Intuitively (and I STRESS "intuitively") I feel that it's better for me to take niacin and eat a moderately low-carb diet than to reduce my carb intake to the vanishingly small amount that Dr. Davis recommends. I have cut out wheat though and most grains. Really would love to reincorporate quinoa Smile

    September 2010
    HDL 39
    LDL 135
    Triglycerides 149
    These values had remained stable for 5 years, remaining unchanged in spite of diet and exercise changes. I won't go into all the VAP and NMR nuances (I've had both tests several times), but all the measures improved VERY dramatically...shifted from pattern B -->A LDL, more than quadrupled the "helpful" form of HDL (8 to 35), essentially eliminated IDL. CRP and Fibrinogen were fine to begin with and remained so after a year.

    November 2011
    HDL 87
    LDL 89
    LDL-P 700
    sdLDL <90
    Triglycerdes 40

    My regime included:
    * 2,500 mg/day nicotinic acid
    * Vitamin K2
    * Lovaza, 2 caps/day (I know Dr. Davis hates Lovaza because of the exorbitant price, but my insurance pays for it and I'm not going to shell out $$$ for a nonprescription fish oil of equivalent dosage)
    * Metformin, 500 mg/day (I'm not remotely diabetic. My NMR IR score was 4. However, I wanted to take it as a general antiaging drug and to offset any possible blood sugar increases from the niacin.)
    * D-3, 4000 mcg (or is it IU?)/day
    * Deplin, 7.5 mg/day (to methylate any extra homocysteine from the niacin and metformin and to provide precursors for monoamine neurotransmitters)
    * TMG (same reason as Deplin)
    * Methyl B12 (same as Deplin and TMG; also I'm vegan and don't get much from my diet)
    * 1 tablespoon extra virgin coconut oil / day
    * I purchased a blood glucose meter and test strips. There's more postprandial fluctuation than I would like to see, but my glycated hemoglobin remains at a respectable 5.1. I'd like to get that down to 4.9.
    * Had the battery of cardiovascular-related genetic tests. I'll only mention one: I'm an ApoE 2/3, meaning that moderate fat intake is indicated (versus low fat for 3/4s and 4/4s).

  • Might-o'chondri-AL

    1/9/2012 10:42:21 PM |

    Hi Jim,
    I think  ineedlabs authorized NMR is now sent through the  Labcorp system & so I got whatever Labcorp's NMR details; namely: "LDL-P,  LDL-C,  HDL-P , HDL-C, Triglycerride, Total Cholesterol, small-LDL, LDL size" & also some suggested interpretations Doc says he ignores. Standard old type of lipid test is not  the same as NMR lipo-protein profile , nor  is the  VAP type of lipid test some get.

  • Jacob

    1/9/2012 11:00:15 PM |

    @ Mitochondri'Al

    I had my liver enzymes tested pre-niacin and have repeated the test 7 times. There has been no change. From what I've read it's people taking the extended- and sustained-release formulations who develop liver issues. Immediate-release niacin doesn't seem to affect the liver much.

  • Might-o'chondri-AL

    1/10/2012 1:20:11 AM |

    Hi Jacob,
    I daily eat a good cooked handful  (trying to get beyond need to micro-manage all  portions of ingredients)  of low salt canned red beets into my night time hummus salad.  So, maybe that betaine has been enough to neutralize the homocysteine  you just informed me arises from high dose niacin. I have split niacin in 1,000 mg with morning dairy quark & 1,000mg  with evening meal; flushing has long been minor, aside from reddened face I splash with cold water if think anyone will freak out.

    Since you are the first to suggest blood sugar may elevate from taking high dose niacin this is also intriguingly new to me. My understanding is that it is high dose fish oil that Doc's protocol leads to higher blood sugar. When I introduced high dose EPA/DHA fasting serum glucose went from 1st 83 mg/dL  without fish oil after 4 months on fish oil to 88 mg/dL. Of course I  did start fish oil at the same time as  the niacin, but when I kept fish oil constant and varied upward the niacin (from 1,550 to 2,000 daily) for that last 1/2 year  experimentation my fasting serum glucose stayed at 88 mg/dL. Which  implicates fish oil is the controlled factor provoking 3 mg/dL more fasting blood sugar.

    Doc recently trashed the NMR's derivative chat; but  if  other's have noticed the category "IR score" I'll mention lab 1st gave me an "Insulin Resistance Score " (IR) of 45, 2nd test rated an IR score of 4 and then last NMR put me at 1.  But I am inclined to think many other readers may be more prone to overweight & they  may find it extremely helpful to go with Doc's  "very" low carb to see  lab results he aims for them to achieve if their genetics of blood glucose and lipo-protein are not as favorably responsive as mine seem to be.

  • Jacob

    1/10/2012 3:33:50 AM |

    @Mitochondri'Al...

    The hyperglycemic effect of high-dose niacin is very well documented, though in my case I don't think it had much of an effect. Even in diabetics, the consensus seems to be that the benefits of niacin outweight any associated blood sugar increase. Like you, I didn't go into this with a weight issue. I'm ~5 pounds lighter than when I began this regimen (5'10'' 152 pounds now), a change attributable entirely to the Metformin.

    The rise in homocysteine from high-dose niacin has something to with niacin's action depleting the available methyl donors. I don't think beets will provide anything approaching the amount of TMG necessary to methylate excess homocysteine back to methionine (which is a SAM-E precursor...oh happy day). I take about 3,000 mg/day of TMG. It's an inexpensive supplement, and I'd rather be safe than sorry, as homocysteine can make some major mischief over time in the vascular endothelium.

    I didn't know about the fish oil / blood sugar connection.

    FYI, I don't know if you're familiar with the study in which participants taking vitamins A and C with niacin showed a much-reduced--in fact, practically negated--effect of niacin on blood lipis versus those not taking A and C. No further investigation took place, and the mechanism (assuming this finding is valid) remains unknown. As a precautionary measure, I drink my vitamin A - rich green juices and take my C supplements at least a few hours before or after taking niacin.

    BTW, I've read in several places that effects of niacin can become MORE robust over time, which squares with the steady increase in HDL and the HDL-2 subfraction I've observed over the last year, as well as a decreasing LDL value and increase in mean LDL size.

    One anomalous thing I've noticed is that my lp(a) reading on VAP tests has increased from 4 to 17, but the test for lp(a) alone has remained at the minimum value. I had a VAP today and will be getting the lp(a) monoassay on Wednesday. If this strange discrepancy shows up again, I'm going to call Atherotech and LabCorp and ask them what's up. I did recently read a study in which blood samples from one or more patients were sent to Atherotech, Liposcience, Berkeley Heartlab, and one other company; there were striking discrepancies among the reported results from the four labs. Interestingly, of the four, Atherotech's VAP test was the least likely to characterize a patient as having Pattern A LDL; although, now that I think about it, Liposcience (NMR) doesn't even use the Pattern A, AB, B terminology, do they? Anyway, it's fun to share these observations with a group that actually is thinking about this stuff! I've posted all my blood panels to my facebook account along with what I did to achieve the dramatic changes reflected in the data. My friends found it all very interesting but only one has initiated a similar experiment.

  • Jacob

    1/10/2012 3:34:45 AM |

    outweight = outweigh

  • Might-o'chondri-AL

    1/10/2012 7:59:56 AM |

    Why Doc's low carb may be more important for some more than others is these after meal events. He's pointed out that high after meal (post-prandial) blood sugar (glucose) are a problem because the liver will make that excess glucose into triglycerides (trigs). Some of us may also trend toward low trigs, despite any  post-prandial  glucose spikes, because of our constellation of genetic quirks in how the sequential triglyceride synthesizing enzymes play out their essential esterifying and hydrolyzing ( enzymes = glycerol-3 phosphate acyl-transferase1, 1-acyl-glycerol-3-phosphate-O-acyl-transfe​rase5 & 9, plus di-acyl-glycerol acyl-transferase2). I should stress that my non-low carb lunches were always followed by me walking around extensively on errands - so any contradiction inferred from my lab results (above)  with Doc's low carb preference may be explained by my immediate use of the post-prandial glucose in real time skeletal muscle activity  & not just my genetics.

    Doc insists excess post-prandial trigs should be avoided because those trigs get cobbled into VLDL cholesterol and sent out from the liver. It is when the VLDL comes back to the liver without giving up most of it's trigs that confuses many people. This is because, in the specific context of post-prandial  VLDL, the molecule that brokers recycling entry into the  liver of that VLDL (whatever it's residual trig load) does so in accord with ApoE. (note: it is  not the same type of dynamic that happens with clearing our LDL.)

    Curiously, it is the isoform variant of ApoE4 which can help get the most VLDL quickest into the liver cells; so ApoE4 individuals are shunting plenty of  VLDL in, for recycling, but at the same time plenty of  ApoE4 is also coming into that liver cell. Conversely, ApoE3 will be relatively slower clearing VLDL out of circulation & ApoE2 conformation is slowest in helping get returning VLDL into liver cells; which means, for ApoE2 there's more of a backlog going on in the blood stream of VLDL (& any of those post-prandial trigs our skeletal muscles didn't take up when trigs circulated by).

    Once an individual VLDL complex is inside a liver cell it is subjected to an initial processing in a specialized compartment  (endo-some) of the cell that naturally lowers the pH in that intra-cellular compartment to break the VLDL complex apart for recycling. In response to that normal processing pH drop the ApoE4 molecule (as opposed to other ApoE isoforms) becomes more fickle; basicly  it's (ApoE4) molecular configuration is vulnerable to undergo changes like become globular gel, truncated in some sectors and open up it's hydro-phobic surfaces. In simple terms this means that re-cycling truncated ApoE4 won't move well in the liver cell's interior fluid matrix and hug the lipids it finds closest there more so than recylcled ApoE3 & ApoE2 does.

    VLDL, thus will shed it's ApoE  and that ApoE will ideally move to another compartment inside the same liver cell to tag up with an HDL that has been taken up by that liver cell. One of the things this does for us is hold that ApoE molecule nearby, but where pH isn't going to drop. In this phase until the ApoE gets incorporated, as a component, into on of two cholesterol components. One is to put the recycled ApoE into fledgeling HDL that then becomes "mature" HDL sent out of the liver into circulation.. The other, less understood function (and purpose of this long explanation) is of stashing our VLDL recycled ApoE temporarily bound close by to an HDL (inside the liver cell) is to take & re-use it  (ApoE) reformulated with a VLDL molecule when the liver needs to send out any post-prandial trigs.

    Doc's paradigm is preventative, meaning avoid lingering high blood glucose (hyper-glycemia) due to excessive single meal carbs and thus put less demand for ApoE to be cycled into trig loaded VLDL that might just come back again & again demanding the liver engage in futility. For those with degrees of ApoE4 variants there is slower teaming up of it to that helpful HDL inside the liver cell that normally pulls ApoE away from the cell's low pH compartment. Explicitly it is HDL itself that activates this key stage; it is an additional specialized function of HDL. I don't know if one aspect of having low blood level's of HDL is from when a person's stuck with high trigs driving them to cobble it (trigs) into VLDL  with ApoE and this stalls too much HDL inside liver cells performing an HDL function in there & not out as circulating.HDL.

    Some theorize that by diverting so much ApoE  into post-prandial trig loaded  VLDL there is then going to be "mature" HDL going out of the liver that doesn't carry the ideal amount of  ApoE  to fully perform a cholesterol pick-up function for the HDL molecule while HDL is out in circulation. And  if one has ApoE4 being recycled, which is relatively slower to get over to any HDL in the liver cell, then the "mature" HDL will also go out with less ApoE to snatch back cholesterol.

    Lost? ....We essentially don't want "fat" (lipid, like trigs) we may have made to build up in the liver. So,  if we can't get all the "fat" lipids we made out of our excess blood sugar (glucose) get sent out  of the liver as trigs tied to VLDL there is a backlog of trigs always hanging around in the liver . And then, because the process of  us making trigs potentially stalls at a transitional molecule involved called di-acyl-glycerol (please note, don't let this long word make you confused now: this is just being two "fats", since "di" =2 in a formation that is one step short of the well known  tri =3 "fats"  formation  of tri-acyl-glycerol , that everybody  calls tri-glyceride for short & I  lazily type as  "trigs" ). Anyway ending simply,  it is this intermediate "fat" lipid of di-acyl-glycerol  subsequently building up in the liver that triggers a cascade  (for geeks: protein kinase C ), which ends up involving  the receptor for insulin in that liver cell. This unwanted downstream phase of bonding to that insulin receptor blunts the next cascade (4 geeks: tyrosine kinase) and  then that step is more directly what contributes to liver insulin resistance over time (ie: insulin comes to liver cell but more & more insulin receptors being kept too busy) . This is the problem played out by  our "fat" lipids in a chain of events that individuals with excessive trigs risk getting stuck with. Doc warns us to  beware of carbs making you synthesize lots of after meal trigs from prolonged high blood glucose which then forces you to put out VLDL (ie: to try to reliably take trig load off your liver). Elsewhere he stated, in accord with current science, that it is post-prandial trigs that are the most insidious trigs.

  • Jacob

    1/10/2012 8:58:03 AM |

    Interesting about the postprandial trigs. I was unaware of their significance. Makes sense, though, given the relatively greater importance of the magnitude of postprandial blood glucose excursions versus fasting levels.

    Your post conjured up images from long-ago courses on enzyme mechanisms, except without the fun electron pushing.

  • Might-o'chondri-AL

    1/11/2012 3:44:15 AM |

    2011 Post-prandial trigs relation to cardio-vascular details at the link below will give abstract but click at box where says "The full text is free" in pdf. if inclined.
    http://www.ingentaconnect.com/content/ben/cvp/2011/00000009/00000003/art00001
    (titled) "Free Content Assessment and Clinical Relevance of Non-Fasting and Postprandial Triglycerides: An Expert Panel Statement"
    Current Vascular Pharmacology, Volume 9, Number 3, May 2011 , pp. 258-270(13)

  • Taking Charge

    1/11/2012 3:55:46 PM |

    While not directly related to this thread I wanted to get this request out there. I am hoping that  some one can help me find a doctor that is following a similar or the same protocol wtih vitamin K2 etc. and diet as Dr. Davis'.
    I was recently diagnosed with aortic stenosis and am looking for an alternative to valve replacement. I am looking for a cardiologist in the Greater Toronto ON  - Buffalo NY area.
    Thanks in advance for any suggestions given.

  • Galina L.

    1/11/2012 7:14:38 PM |

    @ Might
    Sorry, it my comment is out of tangent, but as a long-time fan of you, I want to share a Russian recipe of a beet salad with you. It contains cooked (or canned) chopped beets, chopped raw onion, chopped  fermented pickles or sauerkraut, some potatoes cooked and cut in small cubes (it is possible to skip), salad is seasoned with mix of brine and olive oil (in Russia an unrefined sunflower oil is used).  Other things may be added like cooked cubed or shredded raw carrots, fresh cucumber ,celery, some herbs, maybe garlic.  It is often consumed instead of a potatoes salad, especially at winter time..

  • Jacob

    1/13/2012 4:50:46 AM |

    The lp(a)  measurement truly puzzles me. When I get the lp(a) monoassay it always comes back <2 (the minimum measurable) , but the VAP is all over the place (up to 17).

  • Might-o'chondri-AL

    1/13/2012 3:31:55 PM |

    Hi GalinaL,
    Thank you. Beets' nitrate are converted into nitrite in us to do all kinds of good things, as medical news reports.

  • Gene K

    1/13/2012 6:15:53 PM |

    Galina,
    How about a Russian borscht (a beet soup, for those who are not familiar with it)? We had it at home recently, but I neglected to take my BG after eating, so will do it next time. It is hard to give up beets, but Might's comment about it is encouraging. I also surprised Dr Davis that such dish existed, when I saw him not long ago.

  • Galina L

    1/14/2012 3:32:19 AM |

    Borscht is a cabbage soup , with two main features - first of all it contains beets(obviously), second, very important  secret difference,  that it is seasoned , when it is almost ready,  with the bacon (fatty part) crashed together with some salt and couple garlic gloves. I use mortar and pestle, but it is possible to do crashing between wax paper sheets, plastic sheets, just make sure it looks more or less like a paste. There several recipes,
    here is an example - use broth or  water, may be 3 - 4 cups, bring it to a boil, while water is getting into a  boiling, make sauteed veggies , fist put on a pan chopped carrots (1 big or 2 small) and parsley , then bell pepper, then chopped onions, when onions are ready - add  1 -2 tomatoes. Prepare garlic+bacon paste. Put 1/2 head of shredded cabbage into boiling salted water, when cabbage is almost ready, add sauteed veggies, let is quickly boil, add  the chopped content of one can of beets(beets must be added only after sour ingredient - tomato in that recipe) with the liquid and the paste, then  take it  from the heat, close with a lid.. Taste is better next day. I didn't mention herbs, possible vegetables to add, when to put salt. It taste very good with sour cream, chopped chives, even slice of a lemon in your plate..

    There many variations, important thing - don't let it boil again after it  isready - it will change color and flavor.

  • Might-o'chondri-AL

    1/14/2012 4:39:38 AM |

    Hi Jacob,
    Lp(a) is a molecule with an Apo-lipo-protein B100 core like an LDL with protein ApoA bonded on it. The gene LPA encodes for the Apo-lipo-protein A & there are many genetic variations of LPA.

    When the LPA copy # if greater the amount of gene driven expression going on is less. This is apart from  any SNP (polymorphism) of LPA & involves the number of reating domain(s), called  "kringles" (kringle IV domain). Basicly the more kringles the less genetic induced protein to build up into a full Apo-lipo-protein A. In Europeans +/- 60% of the variation in circulating Lp(a) is due to the peculiarity of kringle copy #.

    The SNP variants (of LPA) have more relationship to the way that particular conformation of  Lp(a) might uniquely degrade and give off metabolic by-products that potentially can act against organ tissue promoting enough new blood supply (angio-genesis). If the heart can readily make new blood supply routes that is ideal & thus a specific genetic Lp(a) variant that doesn't stymie angio-genesis is not a cardio-vascular problem  - irregardless of that Lp(a) level.

    You take supplements to restore homocysteine back into methionine. There is a specific LPA polymorphism giving one a SNP allele 4399 methionine (in substitution for the standard isoleucine amino) inclining those people to make +/- 6 times more Lp(a) than otherwise. I don't know if you carry that particular SNP, but if your rise in Lp(a) coincides with your protocol against homocysteine you may (?) be feeding  into
    the LPA4399Met hand . Admittedly far fetched, yet methionine boosting is not always benign for longevity according to some investigators.

    Vitamin A converts to retinoic acid in the body & this may ( ?) be more relevant. The Retinoic acid-related orphan receptor alpha (RORalpha) has 4 different variant iso-forms. It (RORalpha) is found in the nucleus of liver cells and responds to melatonin if you supplement with  melatonin as well.

    Your RORalpha iso-form may also be prone to receiving activation when there is  excess vitamin A's retinoic acid reaching the liver. RORalpha activation gets it's  nuclear response element ( Rev-erba) to bind to DNA & this engages several genes. In other words liver RORalpha up-regulation greatly influences Apo-lipo-proteins A, as well as A"V"(5), & C"III" (3) put out by the liver - among other things (ex: carb processes).

    Which, coincidentally, leads back to heart as per 3rd paragraph above....Hypoxia (oxygen low) also activates RORalpha, and thus Lp(a);  but one's LPA variant iso-form can give an Lp(a) degradation that acts anti(against)-angio-geneic. Then that heart's ability to get alternate blood supply  of oxygen to fall back on is limited; meaning the degree of  hypoxia damage done to any of that heart's cells becomes more problematic. Hypoxia isn't an all at once state of an all over or nothing organ-wide event.

    Cardio-vascular problems are said to be an "inflammation" problem & the more pro-inflammatory Il-6 (interleukin 6) the greater upregulation of Lp(a) going into circulation. Doc expounds his low carb protocol cuts down inflammation marker CRP (C-reactive protein) & Il-6 is a big part of CRP dynamic.  By blunting  Il-6 (or if  fortunately genetically don't make or even receptor  much) there is less Apo-lipo-protein B being made that is an important part of  liver's VLDL formation. Consider, as an example,  that the drug "Mipomersin" acts to block ApoB synthesis with a side effect of lowering Lp(a).

    Unfortunately too, high Il-6 is associated with lots of  triglycerides being made in the liver .  Having high Il-6 instigating lots of ApoB to cobble the excess trigs it (Il-6) provoked into VLDL  favors getting those Il-6 hyped trigs get sent out into circulation. Then too high Il-6 makes for lower rates of liver trig clearance from the trigs brought back by various lipo-proteins. D ue to the inflammatory  settting when the VLDL (with it's remaining load of trigs) comes back to a liver cell for VLDL re-cycling (detailed in earlier comment here)  it can't unload  & clear it's trigs  due to the co-existing high levels of Lp(a).

    In other words,  induced to make lots of Lp(a) overactivated LPA gene means excessive ApoA. Since ApoA can also go where ApoE  can , the  molecule of ApoE that is normally designed to get free from the VLDL risks getting out-competed. Then HDL inside that liver cell doesn't mediate the movement of  stale VLDL's  ApoE as much (because busy with ApoA),  which creates a backlog of  freed ApoE in that  cell's endosome  forcing other returning VLDL ( with it's trigs & ApoE) stalled in a traffic jam.  And that HDL doesn't rush to leave the liver cell because it isn't getting normal ApoE chain of events making it a "mature" HDL; so circulating HDL level is paradoxically lessened despite plenty of  ApoA  around.

  • Might-o'chondri-AL

    1/14/2012 6:23:11 AM |

    IL-6 meant by Il-6 (among other proof reading  mistakes )

  • Gene K

    1/14/2012 9:32:24 PM |

    Galina,
    Thank you for this extensive recipe. I am tempted to continue, but it is not my blog. Maybe Dr Davis will find these Russian recipes good for the TYP program...

  • Jacob

    1/16/2012 1:52:02 AM |

    ". There is a specific LPA polymorphism giving one a SNP allele 4399 methionine (in substitution for the standard isoleucine amino) inclining those people to make +/- 6 times more Lp(a) than otherwise. I don’t know if you carry that particular SNP..."

    I don't. I'm 4399 Ile/Ile homozygous.

  • Jacob

    1/16/2012 1:58:50 AM |

    Also LPA-Intron 25: tt homozygous.
    KIF6: 719 Trp/Arg heterozygous :-(  [[I don't want to take statins though]]
    9p21: ag heterozygous at rs10757278 and gc heterozygous at rs1222049 [[I read a recent study indicating that a diet primarily composed of vegetables and fruits (and maybe nuts) almost negates the associated risk here, and that's how I eat. So, fingers crossed.]]

  • Dennis

    1/23/2012 6:47:58 PM |

    While Dr. Davis' website & blogs got me started on the path of getting off the statins, etc (thank you 1000 times!!!)...I believe we are over-thinking this and making it way too complicated.
    Look at it from an evolutionary biology perspective (I just finished Food and Western Disease by Staffan Lindeberg, http://www.amazon.com/Food-Western-Disease-evolutionary-perspective/dp/1405197714) Our metabolic processes developed over the course of millions of years, being optimized by evolution all along the way. We ate meat, eggs, fruit, veges, nuts and did just fine. Then about 10,000 years ago we figured out we could stay put, not follow the wild herds and dig up food as much, and grow our food where we lived. Big problem...the food we decided to grow makes us sick (wheat, corn, rice). Not falling down, vomiting sick, but just a little at a time sick. We get fat, have strokes, heartattacks, high BP, diabetes, cancer, etc... aka Western Disease. But don't all the experts tell us to eat whole grain, and drink milk, and eat cheese, and use olive oil??? That's where the next problem arises...we don't know what we don't know. All the "science" behind good nutrition today is based on studies with many, many flaws. And, our metabolic systems are so enourmously complex, that we don't really understand how it works. If you look at people today, who still maintain a paleolithic diet (hunter / gatherer) you find that they do not suffer from Western Diseases. When they move from their ancestral ways to "modern" diets, they suffer like we do.
    I've gone from a Mediterranean diet to a Paleo diet, lost 15 lbs in 7 wks without changing my exercise routine, stopped taking my statin, am eating less, sleeping better, and feel really good. And this coming from a lifelong semi-hardcore athlete, who at 45 got a stent in a coronary artery, and prescriptions for Plavix and Simvastatin. Two years later i felt like crap and decided it was time to do something different. First stop was DR. Davis' sites, then others. The blood work is coming in mid Feb to establish the first real data points.
    Bottom line...eat what the cave man ate, get plenty of sleep, go outside in the sun, do some strenuous excercise, and quit letting your doctor feed you the Big Pharma line of BS. It's not easy. Nothing worth while is. But, as your body changes, so will your resolve to save your own life!
    //DM9

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