I'm probably living proof that eating or taking calcium does not cause a high heart scan score.  

For around 18 years I suffered from a crippling gut problem.  During that time I was advised to avoid milk products along with high fiber.  Milk was avoided because of lactose intolerance and another effect I noticed it had on the gut.   Calcium rich vegetables were not eaten in much quantity due to fiber causing my gut problem to become worse and more painful.  Early on I tried taking calcium tablets but they caused a great deal of gut problems too so that was stopped.  

Basically my body was calcium deficient for close to 2 decades.        

It was only after I figured out my gut problem was food related - a food allergy - that I began eating fiber calcium rich foods along with cheese again.  It was also around this time that I had a heart scan.  My score is in the top 90% for my age.  From blood testing it appears my plaque build up came from eating a sugar rich / low fiber diet and not eating too much calcium.

Is there a test for K2 deficiency?

What is the best source of K2?

To my knowledge, no clinically available measure of K2 adequacy is yet available. The best source is arguable, but we're gravitating towards supplements that supply the MK-7 form until the data clarify.

Dr Davis,
Thank you for your comments. You state that supplemental calcium does not cause artery calcification, explaining there are different mechanisms in bone vs. arteries, etc. This may not be the case however.  A recent study has shown that calcium supplementation might very well increase vascular events (e.g. heart attack or stroke) in elderly women. According to the studies lead author the findings were surprising and robust.
ref:
1. Bollard MJ, et al. Vascular events in healthy older women receiving calcium supplementation: randomized controlled trial.
2. Medscape CME/CE 1/24/08
ref: British Med. J. 1/15/2008

These calcium concerns can be added to other studies linking excess calcium (esp. calcium citrate) to small vessel calcification in the brain, and others showing increased aluminum levels when co-ingested with sources of aluminum hydroxide, such as antacids. Also noted here is calcium citrate is up to .25 to 2.5 times more absorbed and bioavailable than calcium carbonate. Then a more prudent dose recommendation becomes necessary. Ours is to limit the dosage below the daily value (DV) for most post-menopausal women. The DV is based mostly from lessor absorbed (esp. on an empty stomach) calcium carbonate studies.  
  In our clinic, the following calcium (citrate, or citrate/malate) supplementation guideline is given to postmenopausal women, and especially important for over age 65.
1. Do not take calcium without vitamin D3 and vitamin K2 (MK-7), unless K is contraindicated because of warfarin / coumadin.
2. Limit dosage to 600 mg per day, as unopposed with or without vitamin D. (e.g. a cal+D supplement)
3. Limit dosage to maximum 1200 mg / day with the co-administration of vitamin D (dosage based on 25(OH)D testing) and vitamin K2 (MK-7a) 50-100 mcg /day.  
4. Limit calcium (citrate)intake to 600-1000 mg / day (even with D+K) if known coronary artery disease is present or coronary calcium score elevated, or smoking.  
5. If elevated coronary calcium score is elevated and the risk for CHD is high, individualize the vitamin K2 (MK7) dose upward as high as 300 mcg/day to attempt to reverse the calcification.
6. Do not take aluminum hydroxide antacids, or any other sources of
AH.
7.Related "bone up" caveats: Recognize that bone loss and CHD often co-exist in the same patient. Hip fracture risk is greatly increased with proton pump inhibitors (e.g. reflux meds). Consider natural alternatives to bisphosphonates and calcium+D only supplements.  e.g. The FOOT Plan (Fully Optimized Osteoporosis Therapy) using strontium citrate, potassium (citrate) alkalization,  vitamin D3/K2, omega-3 EPA/DHA, melatonin, and calcium /magnesium citrate. Far greater and faster bone density results occur in both spine and hip, with healthier bone architecture and geometry. And much healthier for the heart too!  

Mark Swanson, ND
drswanson@drswanson.com

Hello,

I was diagnosed with stage III-C uterine cancer about 4 years ago. A recent CT scan of the abdomen and pelvis revealed atherosclerotic disease. However, the same day I took the scan, I also took a Calcium Scoring test which revealed a good score of zero concerning the heart arteries.

I ordered k2 supplements, but I am leery as to whether it would increase estrogen in my body because K2 is generally derived from fermented soy beans. When I was first diagnosed, one oncologist felt soy was ok, another oncologist plus my gynecologist suggested I steer clear of it. I just wonder what your opinion is on this matter. Also, would the fact the scan picked up atherosclerotic disease indicate it is in an advanced stage? Thank you.

Jackie

Thus, bone health and arterial health do indeed intersect via calcium, but not through calcium supplements. Instead, the control exerted by vitamin D connects the seemingly unconnected processes

Chances are the calcium supplement you are taking now is a rock source of calcium. The label will say "calcium carbonate", which is nothing more than limestone. AlgaeCal Plus contains an organic, plant-sourced calcium form derived from a unique South American marine algae called Algas Calcareasâ„¢.

Calcium supplements helps strengthen your bones. You should always take them to maintain your strong bones.

Lorna Vanderhaeghe products

"gobs"


Hahaha... I can so tell you are from Milwaukee. That is such a Wisconsin expression.  

Another take on the Greek philosophical question: what is time? Even tho' they could count days and years, their answer was: "time is the measure of change". But perhaps that should be reversed to: "change is the measure of time".

Doc, it seems to me the burden of proof was on the guy. You simply say: you only left high school three years ago? Gosh, there are no reports that any male has undergone the developmental changes I can see, in such a short time!
Another point, the number of telomeres at the end of cells has to be calibrated against other measures, such as the sun going round the earth. All any particular individual has to claim is: my telomeres are lost 10 times faster than any one else's, now YOU prove otherwise.

Y'all have a good day, now.

"If George were a tree, I'd cut him down and count his rings"
Too funny, Dr Davis.

George's telomere's....reduced to T-stumps.

Ellie

Lovely blog...it is scary the way we are being attacked by the diseases at very early ages also.

Al Sears says that high homocystein levels shortens telemores three times faster.

I take vitamin D and I want to live longer.  I believe it will help because you said so,and I believe everything you say, including when you say you're not sure.

Regarding "gobs", this is a popular expression in Oregon, too, and I'm not sure how you tell where an expression originated.

Very cool post, Dr. D!!!

I've been into telomeres for awhile!!  Mag-deficiency is associated with reduced telomeres in vivo in rats(and reduced glutathione). HERE

NAC can ameliorate some of the Mag-deficiency oxidative stress in vitro. NAC is the precursor for one of the most potent antioxidants, glutathione. HERE

Glutathione peroxidases which generate more protective glutathione are selenium-containing enzymes. Selenium was correlated to longer telomeres and lower BP. Selenium.

Glutathione strongly and positively affects telomere lengthening and telomerase activity. Role of nuclear glutathione as a key regulator of cell proliferation

Curiously, (?via epigenetics and X-related telomere genetics?) maternal diet can shorten telomeres in rats. Epigenetics: maternal diet shortens aortic telomeres.

Precursors of glutathione are:
--NAC (sulfur proteins)
--undenatured whey protein (sulfur proteins, like glutamine, arginine, taurine)
--SAMe

(PO suppl w/ GSH apparently doesn't work well)

Of course there are many other ways to increase glutathione... Like the TYP program -- flavonoids, fish oil, alpha lipoic acid, MELATONIN, silymarin (WCCA's fave), selenium, magnesium, zinc, etc.

I believe the omega-6:3 index is one of the best biomarkers for aging, at least until we can count our 'tree rings'! In post-MI rats, n-3 PUFAS increased glutathione and was incredibly protective. HERE

The traditional 1960s rural Cretans shared the same low CAD rate as Japan with a high fat diet. To me,  the Cretan diet is  associated with high glutathione, selenium, low n-6, high high  n-3 ALA EPA DHA, 41% fat (like TYP Diet 3), intermittent fasting (Greek Orthodox practice), pastured-raised eggs, chicken, goat, mutton, wild seafood/snails, and very fatty sheep/goat yogurt and cheeses (rich in taurine and saturated fatty acids). HERE and HERE. And Simopoulus.

-G

Very cool post, Dr. D!!!

I've been into telomeres for awhile!!  Mag-deficiency is associated with reduced telomeres in vivo in rats(and reduced glutathione). HERE

NAC can ameliorate some of the Mag-deficiency oxidative stress in vitro. NAC is the precursor for one of the most potent antioxidants, glutathione. HERE

Glutathione peroxidases which generate more protective glutathione are selenium-containing enzymes. Selenium was correlated to longer telomeres and lower BP. Selenium.

Glutathione strongly and positively affects telomere lengthening and telomerase activity. Role of nuclear glutathione as a key regulator of cell proliferation

Curiously, (?via epigenetics and X-related telomere genetics?) maternal diet can shorten telomeres in rats. Epigenetics: maternal diet shortens aortic telomeres.

Precursors of glutathione are:
--NAC (sulfur proteins)
--undenatured whey protein (sulfur proteins, like glutamine, arginine, taurine)
--SAMe

(PO suppl w/ GSH apparently doesn't work well)

Of course there are many other ways to increase glutathione... Like the TYP program -- flavonoids, fish oil, alpha lipoic acid, MELATONIN, silymarin (WCCA's fave), selenium, magnesium, zinc, etc.

I believe the omega-6:3 index is one of the best biomarkers for aging, at least until we can count our 'tree rings'! In post-MI rats, n-3 PUFAS increased glutathione and was incredibly protective. HERE

The traditional 1960s rural Cretans shared the same low CAD rate as Japan with a high fat diet. To me,  the Cretan diet is  associated with high glutathione, selenium, low n-6, high high  n-3 ALA EPA DHA, 41% fat (like TYP Diet 3), intermittent fasting (Greek Orthodox practice), pastured-raised eggs, chicken, goat, mutton, wild seafood/snails, and very fatty sheep/goat yogurt and cheeses (rich in taurine and saturated fatty acids). HERE and HERE. And Simopoulus.

-G

Dr. Davis,

Have you heard about ELC (earlobe crease) as a possible key sign of aging? It seems that tons of studies show a very strong positive connection between younger people with an earlobe crease and CVD. What do you think?

3) The Ornish diet.

http://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(08)70234-1/fulltext

Doc Davis,

Last week, the U.S. Preventive Services Task Force came out with a review and with recommendations about using emerging risk factors for predicting and managing heart disease.  I think there's a lot in there that you'll agree with.  But they were negative about calcium scoring.

Sandy Swarz, whose scholarship is pretty sharp, gives a summary.

I'd really like to see your response to all this.

It is scary how many young people are getting elderly diseases. I know someone who died of a massive MI at the age of 26. I am also proof of that. I have CAD, hypothyriodism, Low Vitamin D, Low B12, gastritis, and valve disease and I am only 35. I am looking forward to being able to reverse some of these diseases naturally.

Michelle

Hi, Matthew--

I believe there's some evidence that ear lobe creases are associated with increased coronary risk, but I don't know of any data relating them in younger people specifically.

I have one myself, and it's been there for as long as I can remember and does indeed correlate with my family's aggressive heart disease pattern.

Hi, G--

As always, you are full of unique observations.


Hi, Ellen--

Perhaps I should have said "oodles."

Dr. Davis,

See David Throop's comment above.  I actually came looking to see if you might have commented on this yet.  Curious your take.

Scott Pierce

Hi Dr. Davis,

Have you observed a correlation between earlobe creases and coronary calcification among your patients?

Thanks,

David

Hi Dr. B G,

Interesting.  Magnesium deficiency vs telomeres length could also be explained as a secondary effect caused by the excessive metabolism of carbohydrates as the primary factor.  High magnesium intake is required for glucose metabolism, see for example Implications of oxidative stress in high sucrose low magnesium diet fed rats

Similar situation may exist with glutathione, high glutatione may be a secondary marker for a diet high in dairy and (thus automatically) lower in carbohydrates.  This paper you linked Maternal diet influences DNA damage, aortic telomere length, oxidative stress, and antioxidant defense capacity in rats seems to be pointing to a high carb diet as one of the factors that may cause accelerated growth of low birth weight babies (the paper discusses human studies as well), which then is correlated with higher CVD risk, shorter telomeres and worsens other markers (bones abnormality etc).

   In contrast to this, high fat low carb nutrition seems to slow down babies and infants growth and slows the onset of puberty, which according to the logic presented by the papers discussed above, ought to reduce oxidative stress, slow down the shortnening of telomeres and reduce the CVD risk later in life.
Regards,
Stan

Hi Stan,

Yes -- there are many implications to such data and other epi-genetic data. Low protein maternal  diets increase Met Syn for 2 generations in rat pups.

Low Sat Fat maternal diets?  High carb, low protein, allergenic wheat maternal diets?  I believe we are epi-genetically affecting many future generations and their metabolism, growth hormone, thyroid hormone, leptin/ adiponectin and perhaps even vitamin D hormone pathways... This may explain why right now CAD and diabetes is rampant compared to just 1-2 generations ago. I have 80-90s year old patients how are 20x more healthier than my 30-40 year olds! Have we genetically predisposed ourselves to the 'over summer' mode that Dr. T at Nephropal has talked about by our mother's diets and her lack of sunlight, rich fatty foods, omega-3, and excess omega-6 in utero??

I believe so.

-G

Hi Stan,

Yes -- there are many implications to such data and other epi-genetic data. Low protein maternal  diets increase Met Syn for 2 generations in rat pups.

Low Sat Fat maternal diets?  High carb, low protein, allergenic wheat maternal diets?  I believe we are epi-genetically affecting many future generations and their metabolism, growth hormone, thyroid hormone, leptin/ adiponectin and perhaps even vitamin D hormone pathways... This may explain why right now CAD and diabetes is rampant compared to just 1-2 generations ago. I have 80-90s year old patients how are 20x more healthier than my 30-40 year olds! Have we genetically predisposed ourselves to the 'over summer' mode that Dr. T at Nephropal has talked about by our mother's diets and her lack of sunlight, rich fatty foods, omega-3, and excess omega-6 in utero??

I believe so.

-G

However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.