Value of a zero heart scan score

Margaret is 73. She's a very good 73. She loves children and works full-time in a daycare. She manages her own household, goes to dinner at least once each week with one or more of her adult children. She is slender and has never been in the hospital--until she developed an abnormal heart rhythm called atrial fibrillation.

Most people who develop atrial fibrillation do so with no immediate identifiable cause. However, Margaret has been a widow since her husband died 15 years ago of a heart attack. She was therefore especially frightened of any heart issues in her own health. Her doctor also raised the question of whether atrial fibrillation might represent the first hint of future heart attack.

So we advised a CT heart scan. Score: zero, or no detectable plaque whatsoever. This put Margaret's risk for heart attack as close to zero as humanly possible. (Nobody is truly at zero risk for heart attack for a number of reasons. One reason is that people do irrational things like take cocaine or amphetamines, or they take too much decongestant medication, all of which can trigger heart attack.)

The heart scan settled it. Margaret has the sort of atrial fibrillation which likely simply develops as a result of "wear and tear" on the heart's electrical impulse conducting system and it has nothing to do with coronary heart disease or heart attack.

As that MasterCard commercial goes: Cost of a heart scan: About $200. Peace of mind: priceless.

Comments (1) -

  • Anonymous

    4/19/2009 4:42:00 AM |

    Not entirely true. With all due respect, Dr. Berman, who you have quoted elsewhere in you blog, has stated the following....

      â€œIn symptomatic patients, a calcium score of even zero does not sufficiently rule out the possibility of having an obstructed coronary artery, which was the case here.” Berman suggests that the coronary CTA may become the test of choice in symptomatic patients when the diagnosis is unclear."
    By the way, whatever was the upshot regarding the 'low dose CT angioplasty'? Safe? Revelatory or not?..... Dave in Chicago

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Coronary calcium: Cause or effect?

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Comments (25) -

  • Mike N

    11/28/2010 3:59:05 PM |

    Does this mean we shouldn't be taking calcium supplements? I've been taking 500 mg per day.

  • Richard Laurence

    11/28/2010 5:54:12 PM |

    Hello Dr Davis, I've read recently that calcium supplements are a bad idea - they increase the risk of cardiovascular disease.

    Does dietary calcium have a similar effect? I would value you opinion.

    Thanks,

    Richard

  • Anonymous

    11/28/2010 5:56:34 PM |

    There is a lot of controversy in Canada currently for a treatment of MS; the opening of blocked or restricted neck veins.  Dr. D, you mentioned dementia, which, to my simple understanding, is either nerve damage or vascular dementia due to a series of small strokes. So my reason for this post is to ask the question; Is the tissue type of veins the same as arteries, and if so, would the same inflammation calcification cycle occur?  If the answer is yes, does that imply vitamin D3 /K2 and wheat elimination has potential for MS sufferers and people trying to avoid vascular dementia in old age?
    thanks
    Trev (recovering vegetarian)

    http://www.cbc.ca/health/story/2010/11/18/multiple-sclerosis-vein-death-costa-rica-mostic.html

  • Dr. William Davis

    11/28/2010 6:27:06 PM |

    Mike and Richard--

    I have been advising my patients to take no more than 500 mg calcium per day, given the potential for increased cardiovascular events with higher doses per the studies coming from New Zealand. Also, achieving healthy vitamin D blood levels easily doubles the intestinal absorption of calcium, making supplementation of additional calcium less necessary.

  • Anonymous

    11/28/2010 6:57:46 PM |

    This research was published in 2005.
    Any updates on this?

    Thanks

  • rhc

    11/28/2010 8:20:22 PM |

    Dr. Davis, I hear/read so much about 'inflamation' in the body and 'anti-inflammatory' diets, etc.  So I was wondering if the C-reactive protein test is a reliable way to measure this? If so what is the suggested limit or safe range in YOUR opinion?

  • Anonymous

    11/28/2010 8:35:58 PM |

    Excellent blog! I eat an almost dairy free diet (grass-fed butter is the exception for vitamins K  and A and butyric acid etc and to add fat to overly lean protein)   that includes almonds, filberts, sardines and salmon with bones and greens for calcium. I also eat lots of very dark chocolate/cocoa.  I supplement with vitamin d.  I recently passed a calcium oxalate kidney stone and doc says my dairy free diet is far too rich in oxalates and phytic acid. I have also been plagued with calf and foot cramps. He suggests adding small amounts of cheese or a calcium supplement to block the oxalates.  Despite my magnesium rich diet -- he also says I need a magnesium supplement. It's only been a few days since I've added 2 calcium/mag tablets at night (only contain about 300mg calcium and 180 mag plus additional mag citrate powder in hot water) and my cramps seem to have subsided.  Anyone else get mineral deficiencies eating paleo style with nuts and bones but no supplements?

  • Lori Miller

    11/28/2010 11:11:37 PM |

    Anonymous, I take Mg supplements, too. I seem to have a hard time absorbing minerals.

    The nuts you're eating contain phytic acid, which blocks mineral absorption. The Weston A. Price Foundation recommends soaking and roasting nuts and seeds to neutralize the phytic acid.

  • john

    11/28/2010 11:50:12 PM |

    This is more complicated than the notion that high calcium intake=high "calcification" ...

    ...Blood Ca and its accumulation in soft tissues can increase (from bones) even though less is eaten. Ca metabolism is far more important than magnitude of intake.  It seems that Ca supplementation actually decreases intracellular amounts.

  • Martin Levac

    11/29/2010 2:26:12 AM |

    If the diet is acidic, calcium will be used to buffer this acid which will ultimately be excreted through the urine. On the other hand, if the diet is alkaline, then no calcium is needed for this purpose. So the question is, where does this un-needed calcium go?

    Maybe an alkaline diet isn't such a good thing after all is all I'm saying.

  • Dr. William Davis

    11/29/2010 2:26:24 AM |

    Anon about MS--

    I would be careful about extrapolating the wheat-dementia connection to MS. It would be deeply concerning if there were a connection, but I am not aware of such a connection.

    The one truly compelling observation being made in MS is the vitamin D discussion. To my knowledge, that clinical trial is still underway in Toronto.

  • nightrite

    11/29/2010 3:08:35 AM |

    I too had lots of trouble with kidney stones but no more.  The only change I made was stopping calcium supplements and starting magnesium.  I take 500 mg of mag at bedtime and have not had a kidney stone pain in almost 2 years.

  • Anonymous

    11/29/2010 5:15:36 AM |

    Dr. Davis,

    Wondering how you explain the paradox that statins seems to significantly increase coronary calcium, but to lower coronary events?


    Thanks,
    David

  • Pat D.

    11/29/2010 6:31:45 AM |

    Regarding magnesium supplementation - I've read that most magnesium supplements have little to no bio-availability, making it pointless to take them.  There are some on the market which address this concern and I've seen good reviews of them - but they do cost more.  I've also read at multiple nutrition sites that our foods have less and less magnesium as our soils are very depleted.  But almonds, pepitas and nut butters are good sources, as are some other foods, like black beans.  There are lists online.  I've also read that Epsom salt baths are a good source of magnesium.  So I take ES baths and I've made myself a magnesium skin lotion with ES.  Instructions for doing this can be found online.

  • Myron

    11/29/2010 7:00:01 PM |

    Basic Ca phosphate crystal deposition disease: Most pathologic calcifications throughout the body contain mixtures of carbonate-substituted hydroxyapatite and octacalcium phosphate. Because these ultramicroscopic crystals are nonacidic Ca phosphates, the term “basic Ca phosphate” (BCP) is much more precise than “apatite.”

    Nutritionally people eat hydroxyapatite not apatite  BCP

    I guessing the moral of the story is to eat acidic calcium, calcium citrate or hydroxyapatite not apatite.

  • Anand Srivastava

    11/29/2010 7:21:51 PM |

    I have read that Vitamin K2 is very helpful in getting rid of the Calcium.

    Martin Levac also raises a good point. I would think as long as the diet is balanced, then calcium will not stay in the arteries.

    It could be that too alkaline diets might cause this problem. In India several very strict vegetarian (not vegan) societies do not eat onions and garlic. Both are very highly alkaline.

    While Non-vegetarian societies eat a lot of them. I guess the difference may be due to the acid base theory. The over all diet should be very slightly alkaline to be best.

  • Anonymous

    11/30/2010 1:16:14 AM |

    This ACID/BASE diet argument is a little odd sounding to me but even a quick Google leads to the simple explanation that it is the influence of minerals in the diet on blood pH

    "The consumption of animal protein, grain, and high amounts of milk increases the acidity of the body, whereas foods rich in minerals such as green vegetables and fruit increase the alkalinity. Generally, the Western diet induces a chronic, low-grade metabolic acidosis.  This relates to the loss of calcium through excretion in urine.  Here is the link:-
    http://jn.nutrition.org/content/136/9/2374.full#BIB7

    cool, but is there any link to heart heath?

  • Monique Hawkins

    11/30/2010 2:33:24 AM |

    I see that some readers asked the same question I was thinking related to calcium supplements. For instance, I hear quite a bit how much coral calcium is good for people. I would assume based on what you have said to take no more than 500 mg of that as well per day?

  • Dr. William Davis

    11/30/2010 3:20:33 AM |

    HI, David--

    While statins do not have much effect on slowing the progression of coronary calcium, I know of no data suggesting that they increase coronary calcium.


    Hi, Pat--

    While absorption of magnesium products varies widely, magnesium "salts" like the malate and glycinate are absorbed quite well.

  • Might-o'chondri-AL

    11/30/2010 4:52:20 AM |

    Basicly, calcium concentrated outside a cell has a safe bio-chemical role to perform & magnesium inside that same cell has it's major bio-chemical role. They both have vital cellular functions.

    When calcium "lingers" inside a cell it keeps over-stimulating things; building up in there is even worse. This inflammatory mechanism occurs in many tissues, not just blood vessels.


    Dietary deficiencies of calcium & magnesium naturally trigger a para-thyroid hormone activation. This hormone signal is for getting more calcium available to the body's tissue cells.

    As you get older there is commonly more para-thyroid hormone circulating in your blood. It can form a negative feedback loop with pro-inflammatory factors (like cytokines); as the inflammation keeps calcium inside the cell.

    Cause or effect of calcium being where it's not supposed to be may involve a vicious circle. Rare youngsters with coronary calcium would suggest uncommon genetics.

  • PY

    11/30/2010 9:20:02 PM |

    The preceding paragraph to the above-quoted passage is probably also very relevant to this discussion:

    "It is not clear how or why the claims for high vitamin D levels started, medical experts say. First there were two studies, which turned out to be incorrect, that said people needed 30 nanograms of vitamin D per milliliter of blood, the upper end of what the committee says is a normal range. They were followed by articles and claims and books saying much higher levels — 40 to 50 nanograms or even higher — were needed."

    Can you point us to other studies that point to the efficacy of 30 ng+ concentrations?  

    I am not attempting to be adversarial at all to your views -- I have been following them closely following my own research.  But given that I havea  data-driven bent, this report has given me a reason to reconsider, and I would love your guidance.

  • Anonymous

    12/2/2010 12:01:13 AM |

    I doubt anyone needs calcium or magnesium supplementation. Calcium and magnesium are virtually impossible to avoid - I believe they're in every plant food. I'll stick with D3, MK-7 and hormones.

  • Dr Matti Tolonen

    12/4/2010 1:39:56 PM |

    "Less calcium, less plaque to rupture, less risk."
    It is well known that ethylesterized omega-3 fatty acids, e.g., E-EPA, stabilize arterial plaques. This explains at least partly how these omega-3´s protect the heart and arteries. See for instance J Atheroscler Thromb. Epub ahead of print 2010 Nov 17

    http://www.jstage.jst.go.jp/article/jat/advpub/0/1011160316/_pdf

  • Leo

    12/5/2010 12:56:06 PM |

    Minä suosittelen K2-vitam.  Se poistaa kalkkia ja ehkäiseen sen kertymistä verisuoniin !!!

  • Anonymous

    12/13/2010 5:23:31 PM |

    Are all OTC omega 3 products ethylesterized? If not, which ones are?

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Medicine ain't what it used to be

Medicine ain't what it used to be

The practice of medicine ain't what it used to be.

For instance:

White coats are out-of-date--Not only do they serve as filthy reservoirs of microorganisms (since they hang unwashed after repeated use week after week), they only serve to distance the practitioner from the patient, an outdated notion that should join electroshock therapy to treat homosexuality and other "disorders" in the museum of outdated medical practices.
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Menopause unleashes lipoprotein(a)

Menopause unleashes lipoprotein(a)

Faye was clearly frustrated.

At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever.

"Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."

She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling.

But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.

A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:

--Lp(a) levels rise dramatically.

--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s.

--Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a).

All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease.

If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.
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Equal calories, different effects

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Comments (15) -

  • MAC

    1/9/2008 1:55:00 AM |

    Dr. Davis,
        You have to check out Dr. Eades blog on the same study. You both had different takes but came to the same conclusion. http://www.proteinpower.com/drmike/

  • Dr. Davis

    1/9/2008 3:22:00 AM |

    Hi, MAC--

    Thanks for pointing out Dr. Eades post.

    I've lately come to read his posts regularly, as I have been thoroughly impressed with his insights.

    It's good to know there's some real thinkers out there!

  • rick

    1/9/2008 4:37:00 AM |

    Had the HCLF group enjoyed the same nearly 50% drop in TG as the VLCHF group, their calculated LDL would have dropped to 117 rather than 108.  So part of their comparative advantage is not a benefit at all.

  • Anonymous

    1/9/2008 5:33:00 AM |

    Hello,

    Dr. Davis, what is your viewpoint on saturated fat intake and arterial damage? Although perhaps saturated fat doesn't affect lipid values too negatively (in fact, it seems to raise HDL), maybe it can eventually lead to heart disease by other means -- inflammation/damage to arteries, leading to plaque build-up?

    There is a reference to a study here, which you've probably seen:

    http://www.sciencedaily.com/releases/2006/08/060808091635.htm

    I'm curious on your viewpoints, as we know not all fats are bad, but it seems a little muddy as to if certain saturated fats are bad or not.

  • chcikadeenorth

    1/9/2008 5:37:00 AM |

    Hi, you commented once on my high hdl..68...it happened after I low carbed, high calories( plus 1800 a day) and hi fat but under 20 gr of sat fat a day.My Ldl went up but lipoprotein(a) was still within the norm not for TYP but for lab values,
    I hear nothing but good results  with LC going back to Atkins,Bernsteins, Eades, Westman and you Dr D so keep plodding along. Soon everyone will know what a wheat belly is and rather than plod you'll be galloping writing another book SmileThnx for all.

  • Dr. Davis

    1/9/2008 1:33:00 PM |

    Most of the feeding studies like the one you cited are flawed in that they claim to have isolated the effect of saturated fat on some measure, brachial forearm dilatation, in this instance. Unfortunately, they did no such thing. They did not control well for carbohydrate effects. Gary Taubes would point out that they presumed that carbohydrates are good and therefore all adverse effects must be from the saturated fat component.

    We are planning a thorough review of the issue in future.

  • g

    1/9/2008 4:50:00 PM |

    You know... I'd love to see the CAC scores (or even IMT if possible?) for people on Protein Power?  Has that ever been studied?  Mac, have you ever had an EBT/CT scan? (are you > 40 yr?)

    I think that would be very very COOL data Smile   Thanks for sharing -- I've checked DR. Eades out since you started posting...  His wife does a nice 'tablescape' like Sandra Lee!  
    I loved his post on foie gras!  That's what I tell my elevated liver test patients -- they are making their fatty livers into FOIE GRAS (and good think I'm not Hannibal... but I like chianti *ha ahaaa*).

    g

  • andyj

    1/9/2008 5:53:00 PM |

    While I would dearly love to try this myself, I am still (as always) having a mental problem with the high-fat part.  I am currently trying to fine tune a plan to do a calorie-restricted diet (about 1600 calories) but I'm not sure how low I can get the carbohydrate segment to go  -- certainly not under 10%.   Most of the fat will be from nuts and chocolate (and salmon and sardines) and I will certainly do a NMR after the fact.  The biggest problem is crafting something you can actually live with for an extended period of time, not just a couple of months.  Therein lies the real problem.  Maybe we should just stop eating altogether!  I have plans for a blog entry on just this subject --  what if we ate only when we truly had to?  Some days I'd have no problem dropping down to about 1000 calories a day, but of course then exercise would be out of the question.  Yeah, this plan still needs some tinkering before I attempt it.  
              andysheart.blogspot.com

  • MAC

    1/9/2008 8:01:00 PM |

    Dr. Davis,
       New paper on Vitamin D and heart diseases. Paper says they cannot recommend testing for Vit D nor recommend supplementaion for those with a known deficiency.
    http://www.sciencedaily.com/releases
    /2008/01/080107181600.htm

    To g: I am over 40 and only low carbing recently. Previous to that used vegan diet to lose weight successfully. Have not had a heart scan yet but seriously thinking of it as my father was diagnosed with Type 2 at 65 and had quadruple bypass.

    P.S. Went to doc the other day and we decided to do some blood work since it had been while and unbeknownst to me until I looked at the paper work he had ordered a Vit D 25OH test and I got him to order a lipoprotein analysis for the lipid part. No discussion, he agreed. I think he keeps up on  latest research.

  • Dr. Davis

    1/9/2008 8:25:00 PM |

    Hi, MAC--

    Progress!

  • MAC

    1/9/2008 11:18:00 PM |

    FYI.

    Posted by me on Dr. Eades site:

    "You and Dr. Davis both reviewed the same study in your respective blogs on the same day. Bit of different takes but same conclusion. http://heartscanblog.blogspot.com/

    Hi MAC–

    I’m a reader of Dr. Davis’ blog from time to time. I guess today that great minds thought alike.

  • g

    1/10/2008 4:20:00 AM |

    MAC -- it sounds like you have a biochem background too?  Yes, I agree many great thinkers are coming up with vastly similar conclusions!  I think that the best balance betw being fed and 'fasting' maybe key (didn't u discuss earlier?). Where is that? maybe being mildly ketotic? at 5-10? or 0-20?  for CAD who knows yet?

    Here's an example of industry looking for a single drug ligand/target (a $325 million one)...  The answer has already been discovered.  you've found it, dude!  I'm not sure about the relationship betw protein and plaque and CAD yet...  do you have some insights?

    http://blogs.wsj.com/health/2008/01/08/rna-mania-genzyme-drops-325-million-on-cholesterol-shot/#comment-60086

    THANKS!! g

  • MAC

    1/10/2008 3:24:00 PM |

    To g: I think you have me confused with another poster. Sorry don't think that was me. Maybe Peter? Minor in chemistry and lots of science courses but no biochem.

    BTW, the great mind in this case was Dr. Davis, and that was Dr. Eades paying him the compliment.

  • g

    1/10/2008 8:49:00 PM |

    Sorry for the confusion -- so many quality post-ers here!  It's great that you're considering starting on vit D -- it improved insulin sensivity in a small trial 60% (that's more than any drug out there like metformin or Actos).

  • chickadeenorth

    1/11/2008 7:45:00 PM |

    g et al  do you have some reading material about Vit D improving insulin resistance I could take to my doc. I am on 4000 units a day, haven't noticed any difference but it is only about 2 weeks now.

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