HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Comments (73) -

  • Kurt

    11/14/2011 1:46:29 PM |

    I have had a similar result. I eliminated most grains except brown rice, I take one Fisol fish oil capsule with each meal and 1,000 iu of Vitamin D each day. My most recent HDL reading was 79 mg/dl, up from 63 mg/dl about 18 months ago, and 15% higher than my highest reading ever. I was pretty pleased.

  • majkinetor

    11/14/2011 2:49:33 PM |

    What is your opinion on high HDL + high [hs]CRP. Some doctors understand this as marker of inflammation or auto-immune disease.

  • Melissa

    11/14/2011 2:50:04 PM |

    I'll share some (half) of my HDLs with the highest bidder. I worry about mine being too high (they've always been ridiculously high). Is there ever a tipping point where high HDLs are an indication of inflammation? BTW, for the most part, I've been on the regimen you mention above for ages. I've never taken niacin and I don't drink alcohol other than occasional red wine, but I get lots of exercise in the form of yoga, hiking, skiing, etc. I never step foot in a gym. =) I've been GF for a decade.
    Melissa
    Hope all is well with you!

  • Fat Guy Weight Loss

    11/14/2011 3:01:30 PM |

    Sounds like I am doing everything right.  Looking forward to my next cholesterol test to see how high my HDLs are.  So what is your recommendation for Vitamin D supplementation?

  • Linda

    11/14/2011 3:25:04 PM |

    Yup, I am doing all these things recommended by our "esteemed leader" and I am proud to say that my most recent blood work indicated Triglycerides at 49 and HDL's at 90!!!
    Have to see a cardiologist this week due to some weird chest pressure a week ago, no "cardiac event", just weird pressure,  which brought about an angiogram and a stent insertion. I am braced for the inevitable "statin lecture" which I have already endured while still in the hospital. If he persists in pushing this drug, I am going to walk out of his office and look for another doctor.
    With a Tri/HDL ratio of .54, there is no way I am going to swallow statins everyday, destroy my liver and/or muscles, and end up buying more #%*$%  drugs!

  • Kenneth

    11/14/2011 3:41:53 PM |

    Is this fabled HDL effect of Vitamin D somewhat linear over the initial two years or is it some sort of tipping point effect where your HDL jumps up sharply after some sort of saturation point?  Over 8 months or so this year I got my D levels up from about 30 to 60. During that time, my HDL actually dropped from mid to low 30s!  My TG levels are rotten at about 300 even with lots of fish oil and a gram of Niacin.  I've also cut back considerably on carbs, though going wheat free is a real struggle for me.  Is a D-25 level of 60 high enough to see a potential HDL boost? Does one have to wait a full two years to know if you're going to be a responder or not? I've resisted the idea of statins or tricor for years, but I'm not getting a lot of traction with the alternatives. At what point is it reasonable to "throw in the towel"?

  • James Winningham

    11/14/2011 6:42:00 PM |

    Dr. Davis,

    Good information on Omega 3s. I remember reading a lot about the ratio of Omega 3s to 6s, and that Flax oil had that correct ratio. Is there anything to this?

  • Jonathan Carey

    11/14/2011 7:23:06 PM |

    Even with familial hypercholesterolemia, I tripled mine from 34 to 91.  My non-commercial website tells how I did it.

  • Might-o'chondri-AL

    11/14/2011 7:53:41 PM |

    Hi Kenneth,
    If Doc's protocol , & not just recommended supplements but his insistence on carb control, is not producing the anticipated adult trig results then autophagy is likely problematic. Triglyceride (trig) breakdown is less when one's capacity for auto-phagy (cellular self cleaning) is less. The Korean Healthy Twin 2008 study sets trig heritability as +/- 46% but did not parse the genetics.

    Genetics of the autophagy related gene 7 (Atg) means that an individual with low Atg 7 will have less autophagy in the liver and more trigs hanging around in the liver since their liver trigs are not being broken down quickly. And yet, in the young especially,  contrary to linear logic less autophagy "normally" fortuitously trends toward less trigs in the adipose (fat) tissue. So, even a non-obese adult with relatively less adipose mass there can be a genetic quirk inciting high trigs coming out from the liver into circulation that doesn't readily seem related to diet.

    Inside each cell is an auto-phagosome component that is designed with it's own dual membrane to hold lipid "droplets". It is from hydrolysis of trigs in lipid droplets that the liver gets the trigs it sends out from the liver with VLD - this is the trig rich VLDL shuttling which Doc warns us  fosters smLDL.

    The auto-phagosome (cell's self scavenger) is the cellular component that 1st has to be able to pick up the lipid droplet and then move on over to the lyso-some organelle inside that same cell to conjoin. Only then can the un-needed trig, that is now inside the lyso-some, be degraded by the cell's natural lyso-some action. For most aging/old individuals their liver autophagy capability declines and so their livers risk the burden of piling up lipids; &  that can contribute to the age associated progression of the metabolic syndrome's high trigs.

    Doc would know better than me the clinical worth of O'Keefe's  2009 Mayo Clinic symposium contention that  EPA/DHA of 3-4 grams daily is useful to lower trigs, whereas  common 1g/d dose is beneficial against human endothelial/arterial dysfunction. The omega-3 EPA lowers the trigs more than the DHA molecule.

  • Ensues

    11/14/2011 8:32:52 PM |

    I wish I could experience the HDL rise I consistently read about.  I am convinced I have familial hypertriglyeridemia.  I do not eat wheat, supplement aggressively with Vitamin D, and take a significant amount of Pharmx liquid fish oil daily and I cannot achieve an HDL marker above 24.  It ran 23-24 before all of the other actions.  It just does not move despite the interventions.   Starting to titrate up on Niacin now.  Will try everything before I capitulate to a fibrate.  If I lived in WI I would be making an appt with Dr Davis!

  • Bill

    11/14/2011 10:03:33 PM |

    My HDL is off the chart at 159. It's so unusually high that my doc has no idea whether it's good or bad, or what it means.

    He says it's 50% higher than the next highest he's ever seen. He had a hard time thinking of *any* lab result he's seen from any patient that was 50% higher or lower than the max or min he's ever seen in others in his many years of practice. He thinks it definitely means something big, but what?

    He suspects either a genetic oddity (my mother's HDL has always run quite high, too, though not nearly that high), a chronic, latent infection, or ominous autoimmune problems beyond my known Hashimoto's.

    He does not know if my HDL of 159 means my (calculated) LDL of 217 and impressive total cholesterol of 382 are safe or not. My triglycerides are an impeccable 39.

    I plan to do full lipoprotein panel at some point to clarify these strange numbers. I really don't know whether to celebrate or worry. I'm not sure anyone has the answer.

  • Kenneth

    11/14/2011 11:49:40 PM |

    If someone can figure out how to separate out some of your sky-high HDL with plasmaphoresis and preserve it as a blood product for re-infusion, some of us could take some of it off your hands! Smile

  • steve

    11/15/2011 12:14:00 AM |

    Nice to hear about the HDL improvements, but what about particle count? No doubt small LDL particles may decrease, but how high is everyone seeing there Large LDL particles increase to?  It also may be unclear that higher HDL is in and of itself beneficial; many with high HDL have ever increasing calcium scores.

  • Might-o'chondri-AL

    11/15/2011 2:30:30 AM |

    Hi Majknetor,
    CRP (C reative protein) level is more significant regarding the stabiity of plaque (ie: risk of rupture) and less indicative of  the degree of coronary artery calcification.  CRP  can be a marker for other physiological doings in non-cardio vascular pathological processes an individual is undergoing. When adjusted for age and race relying of  CRP as a predictor of heart problems is not precise.

  • Might-o'chondri-AL

    11/15/2011 2:54:23 AM |

    Hi Ensues,
    Lancet's U.K. 2010 meta-analysis ("Effect of fibrate on cardiovascular outcomes: a systemic review & meta-analysis") indicates that fibrates for those with low HDL & high trigs are preventative in the context of  suffering less coronary disease and less re-vascularization surgery  being needed. But,  that  fibrates have no  beneficial effect on strokes  (since strokes, whether hemorhagic or embolism is not "driven" by cholesterol in plaque). And,  in terms of  amount of cardio-vascular fatal events fibrates offer no statistical benefit  vs. not taking fibrates when look at  how many actually die from cardiovascular events.

  • Might-o'chondri-AL

    11/15/2011 4:39:11 AM |

    Unsolicited low HDL primer:
    HDL has protein (ApoA1 & ApoA2) & lipids (cholesterol esters, triglycerides, sphingomyelins & glycerophospholids). "Normally" +/- 70% of  HDL protein is ApoA1 & +/-20% is ApoA2. If your genetics stick you with reduced ApoA1 then that contributes to low HDL levels &  generally ApoA2 is less affected by genetics.

    When % of trig burden in HDL goes up & it  gets to the kidneys that  trig rich HDL's ApoA1 protein undergoes endo-cytosis (engulfing) and the ApoA1 is cleared away by the kidney (whereas ApoA2 is not excreted by the kidney). Then, in this trig dynamic,  HDL levels stay low - since person is repeatedly shy of ApoA1 to build with. If there is genetic low ApoA1 to begin with then this further limits the elaboration of HDL; especially considering ApoA1 is broken down (& eliminated) faster than ApoA2 anyway.

    Mass spectrometry analysis shows high HDL is most notably associated with  high sphignomyelin levels - since a feature of  high HDL is less trigs  and usually cholesterol esters are only 13 - 27% of the lipid particles on HDL  the it's sphingomyelin carrying capacity goes up . The ApoA2 protein has more affinity for trigs (& cholesterol esters) since ApoA2 limits the other lipids ability to get on the HDL surface; so it is easier to have higher sphignomyelin when there is less Apo2 in one's HDL .  The more ApoA2 , at the expense of ApoA1, the more trigs and more VLDL (fibrates work, in part,  by acting on Apo2's gene regulatory element).

    There are gender differences in HDL levels.  The Dutch Erasmus  Rucphen study puts HDL heritability at 54%  & Caucasians seem more prone to low HDL than some other stock..

  • Might-o'chondri-AL

    11/15/2011 8:52:15 AM |

    cont. (in case some didn't know relevance):
    Having high amounts of HDL means there is lots of sphingomyelin tied up by HDL's ApoA  & thus less freely circulating sphingomyelin to get picked by LDL's ApoB . Blood plasma levels of sphingomyelin are associated with coronary artery disease all by themselves, as a stand alone marker without being referenced to one's cholesterol level.

    This relates to HDL's potential to limit the progression of atherosclerosis &  not HDL's well touted role in reverse cholesterol transport .  When small LDL's ApoB  lipoprotein with a burden of sphingomyelin gets into an artery wall the enzyme sphingomyelinase can hydrolizes  it in a way that leads  to that ApoB's aggregation. Then that lipoprotein can't readily get back out &  it stays there in a form that  adds to the polymerization which occurs when the macrophage foam cell it is in dies and incorporates into plaque.

  • Alexandra

    11/15/2011 11:09:31 AM |

    I haven't ever had complete bloodwork done...well, 18 years ago when I was pregnant with my final child, they took what seemed like a quart of blood from me but those results were never mentioned to me, so I don't know what was done.  If I find a doctor and ask to have bloodwork / a lipid panel, etc. done, what should I ask for? Is there a specific wording required on the prescription so that the lab will check for small vs fluffy?  Vit. D levels, etc.  What else should be checked?  I am 50, have never been ill beyond a cough or cold.. I check my own BP, avg about 118/78. I test my own BS...fasting is in the 80's.  I've been low carb for 4 years (lost 120+lbs) and LC paleo for over 1 year. I feel better than ever so maybe its time for bloodwork to see if things are going as well as I feel they are.
    I appreciate any suggestions.

  • Dr. William Davis

    11/15/2011 1:08:21 PM |

    Hi, Alexandra--

    Ask for lipoprotein analysis. I prefer NMR lipoprotein analysis. However, if your doctor gives you a blank stare, it's not time for asking for labs, but time for a new doctor.

  • Dr. William Davis

    11/15/2011 1:11:42 PM |

    HI, Bill--

    The whole notion of HDL functionality, i.e., separating good from bad effects, is still in its infancy. And, yes, the HDL without doubt increases total cholesterol. Yet another reason why we should completely discard lipid values and only use lipoproteins. My bet is that your measured LDL (e.g., NMR LDL particle number or apo B) are far lower than the calculated value would suggest.

  • Dr. William Davis

    11/15/2011 1:13:47 PM |

    Hi, James-

    Imagine seeing you here!

    Flaxseed is a great source of linolenic acid as an omega-3; it may have modest independent benefits outside of conversion to DHA/EPA. Chia likewise.

  • Dr. William Davis

    11/15/2011 1:14:51 PM |

    Yes, it's likely something close to linear.

    Also, note that, if your diet results in weight loss, there will be a transient DROP in HDL, only to be followed by a long, slow rebound.

  • Dr. William Davis

    11/15/2011 1:15:47 PM |

    Also, Linda, look for other factors, such as Lipoprotein(a), vitamin D deficiency, thyroid dysfunction.

  • Dr. William Davis

    11/15/2011 1:16:16 PM |

    Sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml. Please see the 3 million posts on this blog about this.

  • Dr. William Davis

    11/15/2011 1:18:01 PM |

    Hi, Melissa--

    The data on the potential inflammation and other counterproductive functions on HDL are still too early for prime time. So right now we have measures like total HDL, apo A1, HDL particle number and large vs small HDL. Boston HeartLabs has some additional measures, but I still do not know now valid these measures are. I'd also like to see better corroboration of the French groups indictment of inflammatory HDL before we start to pursue this avenue.

  • Dr. William Davis

    11/15/2011 1:18:49 PM |

    Never heard that.

    I see CRP as a marker of wheat and carbohydrate consumption, along with vitamin D deficiency. Correct those two and CRP almost always drops to zero or close to it.

  • Linda

    11/15/2011 2:35:05 PM |

    Vitamin D3 supplementation?  Check
    Thyroid dysfunction?   Blood test done. TSH was 2.70. Early AM temps are always below 97.8 but my doctor does not see a problem.

    Lipoproteins?  They don't bother to check for that, guess they don't see the importance, at least among the doctors I've seen.

    Oh well..........................

  • berger6696

    11/15/2011 5:05:14 PM |

    I've been wheat free vlc paleo for 6 months.  I've also been supping with 3 1000 mg fish oil and 4000 iu vit D daily for the past 3 months.  My HDL has fluctuated but basically stayed in the mid/low 30's, while my total, LDL and TGs have gone up significantly.  What do you make of this?

  • Alexandra

    11/16/2011 1:20:00 AM |

    Thanks... I don't have a doctor so that will help me weed them out a little.

  • Ensues

    11/16/2011 5:53:30 PM |

    Thanks for the comments Al!  There lies the dilemma I have struggled with.  Do I medicate just to chase a marker?  Looks like some benefit in terms of disease reduction but is that worth any negative consequences from the medication?  I really wish the data was more definitive.

  • Ensues

    11/16/2011 5:54:45 PM |

    No.  BMI hovers around 32-33 after a year of paleo template eating.  (Lost 25ish lbs)

  • Might-o'chondri-AL

    11/16/2011 6:11:56 PM |

    Hi Alexandra ,
    Like you I have no USA doctor , so for NMR twice used (what is now called) iNeedLabs.com : an online service - no prescription required; pay for  tests prior to visiting your local blood draw lab... their doctor authorizes blood draw (not available in N.Y./N.J../Mass./R.I.)

  • Linda

    11/17/2011 12:39:03 AM |

    Dr, some questions for you?
    1. Are statins ever helpful?
    2. Once you take them, are you on them forever?
    3. I now have one stent after an angiogram detected blockage. I also have blockage in two other areas. Is it necessary for me to take a statin even with an excellent HDL/triglyceride ratio, etc?
    4. Dr. tells me if I refuse statins, I WILL have a heart attack!
    5. I am female, over 60, following LC diet, taking D3 5000 IU, etc.

    I have not had a cardiac event, simply chest pressure.

  • Dr. William Davis

    11/17/2011 1:05:10 AM |

    Linda--

    I invite you to read the 1100 posts preceding this one. Note that this blog will not replace your doctor, just help you be better informed.

  • Dr. William Davis

    11/17/2011 1:06:18 AM |

    Insufficient information, Berger.
    If weight loss has occurred, for instance, triglycerides will go up, HDL will go down, LDL can do anything. This all improves when weight plateaus.

  • majkinetor

    11/17/2011 9:54:34 AM |

    There is some info about it here:
    http://perfecthealthdiet.com/?p=3122#comment-21029

  • majkinetor

    11/17/2011 9:58:24 AM |

    Do you think that IF style eating trains autophagy pathways ?

  • berger6696

    11/17/2011 12:58:26 PM |

    Thanks for the reply Doc!  I'm 5'9.5 135lbs.  Vary low body fat and pretty athletic build.  I crossfit.  When I started paleo I was 145 with much more fat around the waist (I swim in my old pants, lost about 2-3" around waist).  I feel really good but my labs are just not working with me (I sent you a copy of my VAP test on Fbook).  I'm just really confused on why my labs are not doing what they should and what to try next?

  • Might-o'chondri-AL

    11/17/2011 9:16:53 PM |

    Hi Majkinetor,
    You're concerned about high HDL & linked to it's relationship with inflammation. Virus (& some bacteria), whether symptomatic or not,  want to use sphingomyelin (HDL carries some) because a series of enzymes converts it into sphingosine-1-phosphate (S1P;  HDL carries some S1P). In some cases super high HDL may be attempt to short out a virus (ie: remove circulating sphingomyelin substrate & clear S1P away)  while the more ancient  viral adaptability tries to take advantage of the situation.  Pathology  worsens when viral proteins "lay" on lipids blocking the micro-somal tri-glyceride transfer protein from promoting key lipoprotein events (beneficial ApoB/VLDL /trig dynamics) in the liver cells' endoplasmic reticulum; & also viral proteins "goop" on to ApoA1 (HDL's main protein) in the golgi apparatus.

    The S1P works both inside and outside cells in "normal" health as a signaling molecule. Viruses (& cancer cells) contrive to hijack this dynamic for those signal effects on cell motility (scoot over), cell's ability to survive challenges, proliferation of cells and in some inflammatory processes. S1P can alter the Calcium 2+ level inside a cell  to put into play enzymes that foster th inflammatory cascades (ex: inside cell cytolsolic phospholipase A2 enzyme being set off makes Arachidonic acid get free to make inflammatory leukotrienes, prostaglandins & thromboxanes - which, many recognize are also unwanted agitators of cardio-vascular inflammation). When the S1P lipase enzyme is around then it breaks down S1P (cancer  blocks S1P lipase enzyme, because without S1P cancer goes apoptotic/dead).

  • Ryan

    11/17/2011 9:35:47 PM |

    US News ranks diets.  Here is what they said about Paelo and no Grains...
    http://health.usnews.com/best-diet/paleo-diet

    "Possibly. By shunning dairy and grains, you’re at risk of missing out on a lot of nutrients. Also, if you’re not careful about making lean meat choices, you’ll quickly ratchet up your risk for heart problems." -- So you are missing out on a lot of nutrients... then they don't name any nutrients you would be missing.  So they are really trying to say if you eat a lot of different veggies and fruit and lean meats and nuts, etc... I would be missing out on something grain offered?  
    Laughable.

    Grains vs other food groups: http://robbwolf.com/book-resources/

  • Kenneth

    11/17/2011 11:50:08 PM |

    Much has been written here about statins and their relative benefits and limitations. Does anyone have any thought/experiences to share about fibrates, specifically fenofibrate? After years of inadequate progress on my triglycerides by other means, I'm going to give generic tricor a shot. My doc doesn't seem to think statins would be of much help with TG, with the possible exception of lipitor, which would be an insurance nightmare.  I can't seem to find a lot of "street wisdom" about Tricor or that class of drugs. It seems to have sort of a nasty reputation for side effects - GI upset and a relatively high incidence of liver trouble.  On the other hand, the potent statins and doses required to really dent TGs would have their own issues too?

      Are there any dosing strategies or nutrients which might mitigate side effects of fibrates  the way Q-10 can with statins?  I'm a bit nervous about taking this plunge into such pharms, but I'm not getting where I need to be with diet, fish oil, niacin and Vitamin D.  I've tried other things touted for this like Sytrinol to no effect. I just don't see a lot of "low-hanging fruit" solutions left. I'm not diabetic, not more than maybe 7 pounds overweight. I'm going to get evaluated for thyroid in a few weeks and that could turn out to be part of it, but in the meantime I've got a script for fenofibrate with my name on it....

  • Linda

    11/18/2011 12:34:00 AM |

    Dr. Davis this information was given on the "Morning Joe" program on MSNBC  11/17/11 what can we get out of it?By Linda Carroll
    msnbc.com contributor
    updated 11/16/2011 3:50:04 PM ET 2011-11-16T20:50:04
    Print Font: +-When it comes to the heart, vitamin D can be a double-edged sword.

    Scientists have long known that low levels of the nutrient can hurt the heart, but new research shows that higher than normal levels can make it beat too fast and out of rhythm, a condition called atrial fibrillation, according to a report presented at the annual meeting of the American Heart Association.

    The study, which followed 132,000 patients at a Utah based medical center, found that the risk of newly developed atrial fibrillation jumped almost three-fold when blood levels of vitamin D were high.

    Most people get at least some of their daily needs of vitamin D from sunlight. But in cold northern climates where everyone bundles up for the winter -- inadvertently blocking rays that raise the body’s vitamin D levels  -- people are often encouraged to take supplements to boost levels of the nutrient to protect the bones and heart, said the study’s lead author, Dr. Jared Bunch, director of electrophysiology research at the Intermountain Medical Center in Murray, Utah.

    However, because everyone absorbs these supplements differently, blood levels need to be tested to make sure they’re in the safe range, Bunch explained.

    High levels of vitamin D only occur when people take supplements, Bunch said. Because consumers assume supplements sold over the counter are safe, they may not realize the danger of taking too much vitamin D, he added.

    “People are looking toward therapies considered to be natural to treat a broad variety of disease states and as a means of prevention,” Bunch said. “We see patients who take a tremendous amount of vitamin supplements.”

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    .Bunch said the normal range for vitamin D was 41 to 80 nanograms per deciliter (ng/dl). Patients in the study were designated as having excessive vitamin D had had readings above 100 ng/dl.

    The recommended daily intake of vitamin D for people from 1 year to age 70 is 600 IUs, or international units a day, based on what is sufficient for bone health, according to the National Institutes of Health. There are few natural food sources of vitamin D, although oily fish such as tuna or salmon are among the best. For example, 3 ounces of cooked salmon contains 447 IUs of vitamin D per serving. Small amounts are also found in cheese and egg yolks. The Department of Agriculture provides a comprehensive list of foods containing vitamin D.

    Bunch advised people who have recently been diagnosed with atrial fibrillation and are taking vitamin D supplements to make sure their doctors check blood levels of the nutrient.

    He suspects that the effects of high vitamin D on heart rhythms are reversible.

    “If the levels are excessive, I would hope that when they’re cut back the arrhythmias would improve as well,” Bunch said.

  • Alexandra

    11/18/2011 1:52:49 AM |

    Thanks,  I happen to be in rural NY...

  • Might-o'chondri-AL

    11/18/2011 2:49:36 AM |

    Again Majkinetor,
    Cell's internal proteo-some takes misread/misfolded/worn out proteins (including nitrated MnSOD) apart  via proteo-lysis for recycling the amino acids, since aminos too "costly" to just ditch & cell wants to control it's  protein concentration in real time. Cell's lyso-some in the old person have less portals to get the damaged mitochondria & lipid droplets in for recycling so usually the aged have 10- 20 %  "cluttered up" cells (ex: neurofibril tangles in Alzheimers uses junked mitochondria membrane segments that collapsed). TFEB is the master protein that switches on our lysosome building gene & thus helps improve autophagy play out.

    A low calorie dieter performs pretty robust  autophagy so is potentially less disease prone & that liver is not burdened with so many defective molecules. However, full-on calorie restriction sees reduced autophagy - probably (?) because most everything molecular is crucially needed right where it is ("if it ain't broke don't fix it" paradigm). Intermittent fasting is like periodic starvation and is a type of full-on calorie restriction; so extended fasting inhibits autophagy.  This it should be pointed out is different (nothings simply linear) than when we normally overnight "fast" (ex: don't eat between dinner & breakfast); which upregulates PPAR & downstream inhibits mTORC1 so that our mTORC1 doesn't dampen down normal nighttime autophagy & cell recuperation .

    If  a fasting thin person's tissue protein gets used to run their metabolism it first has to be de-aminated (amino acids cleaved) so that protein molecule's carbon backbone can be oxidized. If the starvation wasn't too prolonged (like we do overnight) most of that protein molecules carbon will be used to make glucose via gluco-neo-genesis &/or glycogen (via glyco-neo-genesis for back up fuel). Some who lose weight fueling via their protein do so because it takes 7 ATP to turn protein into 1 ATP of useable  energy & then will pee out lots of water to get rid of the ammonia nitrogen byproduct.

      

    If one still has body fat (unlike the emaciated) then the fasting level of  FGF21 (fibroblast growth factor) is what upregulates liver keto-genesis in  period of "starvation".  Since  TypeII diabetics (& many obese) have lots of  FGF21  some diabetics measure ketones in their urine to monitor if their condition is getting potentially perilous. Autophagy goes down when the amount of beta-oxidation being performed goes up;  when there is sparse gene Atg7 activity this down-regulates autophagy  and then there are less trigs building up (ie: autophagy  activity up from more Atg7 activity means more lipid droplets shunted to lyso-some for kicking out of cell to be cobbled into trigs to move around - if not excessive trigs are useful).

    Does intermittent fasting train autophagy to be better? I think in the sense that the yo-yo effect of driving the body to scavenge itself for energy substrate (ideally fatty acids & not protein) means intermittent fasting is an form of conditioning. For most the rising ketogenesis  means there was a drop in circulating insulin. It could be said that fasting/starvation forces the liver to behave insulin intolerant ( when liver autophagy is suppressed there is insulin resistance) & that when resume eating the net affect is beneficial due to hormesis. This hormesis inclines the starved faster person to re-bound with a stronger insulin signaling response. Partly that rebound is due to the exagerated degree insulin signal surges through it's intended cascades when the re-fed person's  liver & skeletal muscle cells' Akt gets phosphorylation anew (sort of a pivotal  "oh yeah/that's it/way to go/do me" phosphorylation event on the waiting serine residue of Akt).

  • Might-o'chondri-AL

    11/18/2011 9:35:59 AM |

    Hi Majkinetor,
    I see Doc's has told you above that IF & autophagy are  " likely something close to linear."  Maybe I am misinterpreting the practice of  intermittent fasting & how it plays into our liver's rhythmic genetic expression. I assume it meant close to 24 hours without food.

    +/-6 hours after finishing last meal of the day  there is a rise in lipid droplets shunted for  recycling (a kind of autophagy)  & in the liver these are designed  to be going for ketone making.  Usually our ketone body output lasts +/- 8 hours, but if one is very low carb this might differ . We also should have a  +/- 6 hours cortico-sterone peak that usually  parallels the later part of  a standard overnight ketone cycle . Circadian cortico-sterol levels being up foster the gluco-neogenesis processes we use to build a reserve for when the ketones usually decline. So to hold onto that  reserve (normally for our coming day's get up & go) those cortico-sterols inhibit glucose being taken up into non-liver tissues ( or  used up in the liver). Since insulin signal for glucose to be used is not being acted on I have likened it to being a mimicry of insulin resistance (most people will have insulin in circulation all the time)..

    What do consistently insulin resistant people like Type II diabetics manifest? Lots of muscle protein breakdown (catabolism), protein & ketones  in urine , even before breakfast  lots of trigs (from lipid droplets)  &  plenty of glucose not  being taken up into  tissues. Unfortunately this isn't the way recuperative autophagy is supposed to work, because pathological insulin resistance runs it's program even during the daytime. We are designed to recycle/restore & recuperate while we sleep at night.  Autophagy of our old mitochondria power organelles also ideally happens at night, since you don't want to lose power during an challenge.

    Anyway, so if you had your 8 hours of ketones  +  6 hours of glucose +  2 hours of glycogen filling in  that means after +/- 16 hours of not eating you are into starvation (as opposed to overnight fasting). At this stage your body nutrient sensing is registering the caloric limitation & is trying to hold off doing any cellular house cleaning because that  type of autophagy requires a lot of energy expenditure. If you have some body fat it will go into ketogenesis - but in this instance I don't consider it systemic autophagy, more like catabolism because at that stage you have to bust those fatty acids out to get at them. Calorie restriction is considered to inhibit autophagy, this does not mean no autophagy occurs just minimal autophagy .

  • Roger

    11/19/2011 11:38:14 PM |

    All above is correct, except the 600 IU recommendation, exactly because absorption varies from person to person.  
    The only way to find out if you should be taking more, less, or none st all is with regular blood tests.

  • donna

    11/20/2011 5:23:28 AM |

    Just had mine tested and it is 77.

  • majkinetor

    11/20/2011 11:12:34 AM |

    Thx M-al, for providing me new research points
    I appreciate your detailed response.

  • Dr. William Davis

    11/20/2011 4:02:06 PM |

    Unfortunately, Linda, this will be used as fuel for the "nutritional supplements are dangerous" argument.

    I think the only lesson to learn from this study is that, as we already knew, toxic levels of vitamin D are toxic.

    I advocate testing vitamin D twice per year and I aim for 60-70 ng/ml.

  • Dr. William Davis

    11/20/2011 4:04:52 PM |

    Fenofibrate works to reduce triglycerides, Kenneth, but I have seen almost nobody not respond to the mix you quoted.

    In other words, even if you start with triglycerides of 2000 mg/dl--extremely high--it virtually always drops with wheat elimination and dramatic reduction of carbohydrate and omega-3 fatty acids. While fibrates work to reduce triglycerides, they are almost never necessary.

    So I fear there is something wrong in what you are doing, e.g., insufficient diet change.

  • Dr. William Davis

    11/20/2011 4:05:28 PM |

    Yup, this is the stuff that the dietitians are reading and following.

  • kenneth

    11/20/2011 6:28:36 PM |

    I'll be the first to admit my diet change or at least consistency, is not all that it might be.  Going wheat free/very low carb is a tough deal, especially in light of what you say as far as even one cheat day a week effectively undoing your blood chemistry for a week afterward.  

    I should clarify that fish oil DID help, considerably. My TG was never insane high like 2000, but upper 400s with very low - upper 20s HDL, and God knows what sort of other particle problems, as I haven't done a VAP or NMR.  Just by taking fish oil and eliminating egregious things like lots of pizza and booze, my levels dropped by about a third. Niacin at a gram a day did nothing for TG for me, but did give me a few points on HDL. I have been unable to tolerate a higher dose despite careful titration, and for reasons beyond flushing.  When I was really on top of everything with diet and exercise, it dropped further, but never below 160 and HDL was still unimpressive. I suppose the tricor could work one of two ways, either pharmacologically or  the side effects might turn out to be so intolerable that wheat free discipline doesn't look so bad anymore!

  • fred hoy

    11/20/2011 7:59:46 PM |

    TTHE HEALTHY HEART SONG
    My doctor told me I was plugged, my arteries lined with plaque.
    I need to change my ways today or have a heart attack,
    eat more fish and drink more wine and do more exercise,
    for then you will extend your life, to tell more truths than lies.

    The doctor ordered me some drugs to take each day for sure.
    There is no guarantee of cure, except to make me poor.
    For everywhere both far and near, the rich and poor will die.
    Of heart attack and stroke and in their graves they’ll lie.

    Along came Linus Pauling with his saving protocol.
    He said to drink more orange juice, with a little alcohol.
    The truth that you must know to keep your arteries clear.
    Is not as simple as his words, you must not harbor fear.

    The cure to keep you healthy, is more than vitamin C,
    Amino acids, niacin, and anti-oxidant teas.
    Along with fearsome exercise and cleansing of your gut.
    Remove your mind from prejudice, think thoughts not from your butt.

    It’s been 2 years, since my doctor said my heart is full of fat.
    With Linus Pauling’s protocol, each day I firmly sat.
    My cardio said I should know my calcium score, so he scanned my heart.
    If its under 10 he won’t see me no more.


    The pain is gone, mchest is clear, my pressure’s nice and low.
    When I climb a hill I chug along, my legs just seem to flow.
    My doctor checked my score, he dropped his jaw in awe.
    A zero faced him squarely, thats exactly what he saw.
    yipee yiyay yipee yipee yiyoo learn linus paulings protocol.he song is based on my true experience. for complete story visit "healthyheartfredhoy.com"

  • LindaS

    11/20/2011 8:24:06 PM |

    Thanks for clearifying this Doctor Davis. It seems like everything the  media tells us Re: supplements,  is done in a frightening, alarmist fashion. Except when speaking of pharmaceuticals such  statins or anti-depressants, etc etc. then "all' is good and safe. You can see who holds the money bags!!!!

  • Dr. William Davis

    11/21/2011 1:34:30 PM |

    Yup. Sad, but true.

    Billions of dollars buys plenty of clout and attention. This is why conversations like this count: It is part of our effort to be better armed against it.

  • Dr. William Davis

    11/21/2011 1:35:49 PM |

    Wow, Fred, that's great!

    Now, could you do it in haiku?

  • Dr. William Davis

    11/21/2011 1:37:18 PM |

    Hi, Kenneth--

    HDL will not show its full potential until triglycerides are 60 mg/dl or less. Wheat-free, by the way, is no sacrifice in my mind; it is the most liberating health strategy I know of.

  • Ensues

    11/22/2011 9:24:55 PM |

    Hi Kenneth-

    I am just exactly like you.  Nothing I do budges my tri's or my HDL.  I did Tricor the largest dose possible and together with fish oil, low carb, vitamin d etc I got down to 220.  That's the lowest I have ever seen it.  I personally had no side effects with Tricor.  I quit after a couple of months because I loathed being on a daily medication.  Last reading was 600 and I eat very low carb.  Very frustrating.  Good luck!

  • alfredoe

    11/22/2011 11:22:03 PM |

    Omega 3 from flaxseeds is in a chemical form (ALA) that makes it ineffective for triglycerides control. You need omega 3 in the EPA and DHA chemical form (this kind of omega 3 is ALWAYS from animal origin, never from vegetable origin).

    You should get your omega 3 from fish, cod liver or krill oil. That is the way to lower your triglycerides and raise your HDL cholesterol.

    Please read http://www.omega-3-fish-oil-wonders.com/fish-oil-and-heart-disease.html

  • alfredoe

    11/22/2011 11:35:27 PM |

    I am sorry to contradict no wheat, or low carb, is a BIG sacrifice for many.  I see real carbohydrate addicts every day. I am addict to corn in all its forms, it is a big pain.

  • Kenneth

    11/23/2011 3:41:20 AM |

    Maybe what we need is a strict diet of nothing but iceberg lettuce and a brisk walking program from one end of Australia to the other! Smile I'm going to give the Tricor a shot and see how it does.  In theory it could chop my TG in half from 329 where it last was. Maybe a third is more realistic. IF I get no nasty side effects, the daily drug thing doesn't bother me. I take a handful of supplements twice a day. I suppose I'll keep cracking on the diet and exercise bit too.  I too had hope to do it all without meds but at 41, I figure I don't have a lot of "watch and wait" time left. I got buddies not very much older than me going down with strokes, another who just got home from a five-way bypass. I want no part of that scene!

  • Justin

    11/28/2011 10:25:12 PM |

    Hi Doc,

    Excellent blog. Seriously. You are changing people's lives.

    I'm a firefighter and VERY active, and it's pretty obvious a "low" carbohydrate diet isn't going to work well for me. I've tried it, and the performance hit is significant.

    How would one find a balance between enough "safe" carbohydrates to support activity levels (potatoes, limited rice if no GI issues are evident, tons of vegetables), and keeping those HDL, triglyceride, and particle size distribution numbers looking ideal?

    Thanks a ton,

    Justin Arnold

  • chessguy

    11/30/2011 11:24:34 PM |

    Hi folks,
    I am an unmedicated diabetic and my fasting blood sugar is now around USA 85, uk reading is 4.7,

    my previous hb1ac has always been 5.8 but this time I expect it will be close to 5.0 much better.

    My plan is very lowcarb , and fairly high fat,circa 20 carbs per day in total.

    I am only about 10 pounds 4 kilo overweight max.

    In the last 4 weeks I have lost 11 pounds circa 5 kilo on the very low carb high fat diet/ with ligh exercise too.

    My aim is to lower my cholesterol without statins if possible, and to loose a few kilos, And reduce my Hb1ac.

    My energy levels are fantastic , my vit D was around 40 a year ago it is 70 now as I have been on a few sunny holidays and supplements of circa 2000iu vit d daily.And fish high in omega  3 times a week.

    The question is the big rise in LDL normal, or any ideas I can reflect on.????

    Did I take the test too early ?? ##
    Has any one else experienced this.??

    Has any one taken crestor or some statin for a while til this levels out hopefully,

    Any one taking a statin while on a low carb high fat diet and why , did the low carb high fat not work ??

    MY total cholesterol and HDL have gone "beserk" , but triglycerides have lowered.

    Total Cholesterol: << this was taken two weeks ago it was only the third week into my very low carb high fat diet,#
    9.8 mmol/L = 382.2 mg/dL

    LDL Cholesterol:
    7.6 mmol/L = 296.4 mg/dL ~ My ldl has basically doubled here ###

    HDL Cholesterol:
    1.46 mmol/L = 56.94 mg/dL slight improvement here

    triglycerides:
    1.54 mmol/L = 137.06 mg/dL big improvement here THEY HAVE NEVER BEEN SO LOW

    Test taken on 29/07/2011 <<<< Before the very low carb high fat diet.

    " THE UK & USA MEASUREMENTS ARE SHOWN side by side ".

    Total Cholesterol:
    5.8 mmol/L = 226.2 mg/dL

    LDL Cholesterol:
    3.4 mmol/L = 132.6 mg/dL

    HDL Cholesterol:
    1.37 mmol/L = 53.43 mg/dL

    triglycerides:
    2.25 mmol/L = 200.25 mg/dL
    Goodluck
    chessguy

  • Dr. William Davis

    12/1/2011 4:18:21 AM |

    Hi, Chess--

    Recall that LDL is a calculated value and thereby an incredibly unreliable value. The fact that triglycerides have dropped so precipitously suggests that LDL has converted to large and will overestimate true LDL.

    What you need is a genuine lipoprotein panel, e.g., NMR, once weight has plateaued for about 2 months.

  • Dr. William Davis

    12/1/2011 4:24:10 AM |

    Thanks, Justin.

    The "performance hit" is likely temporary and tends to diminish or disappear within a few days to weeks, as your body converts to a fat burning metabolism.

    The only time you need to actually supplement carbohydrates is during an exceptional long-distance or long-duration effort.

  • Kenneth

    12/2/2011 10:28:54 PM |

    What's your sense of the prospects of the CETP inhibitors now in the pipleline? It seems like they managed to engineer out the blood pressure problems caused by aldosterone or whatever it was, and they show phenomenal increases in HDL. IF any of these pan out and the HDL produces is actually functional, I'd be all over that.....

  • JLMK

    12/6/2011 4:31:53 AM |

    Linda,
    For more info on statins, please see Stephanie Seneff's take. She recently presented at the Weston A Price conference in Dallas.

    http://people.csail.mit.edu/seneff/statins_think_twice.html

    Best wishes,

  • Dr. William Davis

    12/6/2011 5:25:39 PM |

    Stilll much to learn about those agents.

    However, in the meantime, I am witnessing HDL values of 80 mg/dl and near-complete or complete elimination of small LDL with the diet. By the time the CETP inhibitors come out on the market, I don't think we will need them.

  • Bob

    5/2/2012 7:42:59 PM |

    Hi Dr Davis,

    I am striving to approach the 80 marker, although my HDL has not been that high. In 2008 it was 53 with a total cholesterol level of 194. Trigylcerides were 46. Glucose was 93. I am a 6 foot tall, 55 year old guy and 178 lbs.

    With the help from a Naturopath, I have added 750mg of Nicotinic Acid (Slo niacin) per day to lower a slightly elevated level of LPa of 16mg. and I have large buoyant LDL. The results of a few months on the slo Niacin is that my Total Cholesterol is 175, Trigylcerides are 22, HDL is 75, and LDL is 96. My glucose tested at 96.Liver tested normal, slightly elevated kidney function.

    My question is on the Niacin and glucose levels- I understand that Niacin will increase glucose, but how do I go about lowering it? I try to eat low gylcemic, try to eat low carb- certainly no refined carbs, (about 100 grams a day)and I excercise regularly.

    What else can I do to get my glucose down and move the HDL up? Thank you, Sir.

  • Charles

    7/7/2014 1:14:51 PM |

    500 mg of otc niacin gives me trigs of about 49, HDL of about 69 and Iranian LDL of about 62. 750 mg gave me trigs of 34, Iranian LDL of 34 and HDL of 57.

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CRP and Jupiter

CRP and Jupiter

What is C-reactive protein (CRP)?

It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6.

What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

In other words, many, many conditions, from trivial to serious, trigger increased inflammatory markers like CRP.

A recent analysis (Genetically elevated C-reactive protein and ischemic vascular disease of persons with genetically elevated levels of CRP) suggests that CRP does not, by itself, cause atherosclerotic disease. CRP is therefore simply a marker for conditions that heighten inflammatory responses.

The AstraZeneca people sponsored the enormous JUPITER study of the statin drug, Crestor, that has been causing a stir, mostly glowing pronouncements of how the world would be a better place if everyone took Crestor.

In JUPITER, nealry 18,000 people (men 50 years and over, women 60 years and over) took 20 mg per day Crestor for two years. Participants all had starting LDL cholesterols in the "normal" range of no higher than 130 mg/dl and elevated CRP of 2 mg/dl or greater.

Crestor treatment resulted in 44% reduction in nonfatal heart attack, nonfatal stroke, hospitalization for unstable angina, revascularization (bypass surgery, stents) and death from cardiovascular causes. The reduction in nonfatal heart attack was most marked at 55%.

Admittedly, these are impressive results. Benefits held true for both males and females. At the very least, JUPITER should put to rest some of the fringe arguments that statins do not reduce cardiovascular events. They do. There is no sense in arguing against that. While we might argue about the value of statins in various subsets of people, there is no doubt that they do indeed exert a significant effect.

However, contrary to the hype and broad pronouncements of my colleagues, my concerns are:

1) Rather than shotgun the inflammatory response with a statin drug regardless of cause, doesn't it make more sense to ask why a specific individual has an increased CRP in the first place? For instance, if the answer is vitamin D deficiency, doesn't correction of the deficiency make more sense? (Vitamin D by itself reduces CRP around 60%--more than statin drugs.) Not to mention you obtain all the extraordinary benefits of vitamin D restoration, such as reduced cancer risk, increased bone density, relief from winter "blues," rise in HDL, etc. How about junk foods, obesity, and unrelated inflammatory conditions? Would we therefore indirectly be treating obesity with Crestor?

2) Crestor 20 mg per day, contrary to the study and to many statin studies, will not be tolerated for long by the majority. Muscles aches are not common--they are inevitable, sometimes incapacitating. While JUPITER showed 15% of both treatment and placebo groups experienced muscle effects--no different--this is wildly contrary to real life.

3) While there was a 55% reduction in the number of heart attacks, there continued to be a substantial number of heart attacks in the Crestor treatment arm. Clearly, reduction of CRP with Crestor, while helpful, is not a cure.

I view studies like JUPITER as simply an interesting piece of semi-scientific evidence, tainted to an unknown degree by commercial interests (including those of Dr. Paul Ridker, one of the principal investigators). It is not a mandate to use Crestor carte blanche in people with elevations of CRP.

My interpretation of these data in a practical sense is that Crestor 20 mg per day as sole therapy is useful in a disinterested, non-compliant patient who is unwilling to make substantial changes in lifestyle and nutrition. Helpful? Yes, but hardly an invitation for the world to take Crestor.

I believe that doesn't include any of the readers of this blog.

Comments (15) -

  • e4e

    11/11/2008 9:28:00 PM |

    Typo alert. You said, "3) 45% of the people on the Crestor treatment arm of the trial did experience heart attack. Clearly, reduction of CRP with Crestor, while helpful, is not a cure."

    That does not seem correct.

  • Anonymous

    11/11/2008 11:05:00 PM |

    Dr. Davis,
    This is interesting that you mention that vitamin D can reduce CRP.
    Statin researcher Dr.Beatrice Golomb,MD said that statins BLOCK the formation of vitamin D. (her comment can be heard on her
    YouTube video) Is it possible that blocking of vitamin D could be responsible for the statin side effects?

  • Dr. William Davis

    11/12/2008 1:03:00 AM |

    e4e--

    Thanks for catching that.

    Now corrected.

  • Anonymous

    11/12/2008 1:50:00 AM |

    I'm glad you did a post concerning the JUPITER study, Dr. Davis.

    I saw this news story on NBC Nightly News last night extolling Crestor even for people with low CV risk factors. And, I said to myself, I bet Dr. Davis will soon have something to say about this study.

    The next time I see my GP, I can pretty much count on him pushing Crestor on me.  He is very, very pro-statin drug and dislikes that I don't take "something" as a 48 y.o. M.  This, even though I only have a 104LDL/51HDL/54TG lipid profile.

    I keep telling him I do take something, 1g Niacin, 4gs EPA/DHA's, 5000IU vitamin D3, and 90mcgs vitamin K2 daily.  His answer is always; Zocor is much more effective in reducing CV risk than just taking vitamin pills.

    *sigh*

  • Sue

    11/12/2008 10:28:00 AM |

    There is a lot of blogging about the Jupiter study:

    http://high-fat-nutrition.blogspot.com/2008/11/cholesterol-heart-attacks-and-jupiter.html

    http://junkfoodscience.blogspot.com/2008/11/when-news-sounds-too-good-statins-new.html

    http://www.proteinpower.com/drmike/cardiovascular-disease/1853/

  • Anonymous

    11/13/2008 2:05:00 PM |

    What are we to believe when experts so often disagree with each other?
    I remain curious about the statement statin researcher, Dr.Beatrice Golomb made about statins blocking the formation of vitamin D.  
    A web search of "statins and Vitamin D" show results of other medical studies. They indicate that statins actually INCREASE vitamin D.
    What is the reality here?

  • Anonymous

    11/14/2008 7:41:00 PM |

    Dr Davis,

    Generally I think your blog is very informative and interesting.
    On this occasion I think you ahve been more than a little generous to Astra Zenaca in particular and to statins in general.

    Others have coevered this in more detail elsewhere so I'll just list a few facts that I feel are relevant:

    (i)  The selection criteria for the study is highly selective, an far from normal. I gather that the presence of high CRP and low or normal cholesterol is very rare.

    (ii) Those taking crestor had a developed diabetes at a high er rate than those in the placebo group.

    (iii)  Whereas there were in fact a higher proportion of people with metabolic syndrome in the placebo group.  Quite a big turnaround equally deserving of headlines.  "statins cause diabetes, even in nealthy people..."  There were also a higher proportion of people with a family history of CVD in the placebo group.

    (iv)  One of the lead people on the reseach panelhas recently patented a test for measuring CRP levels - "coincidence"

    (v)  More fatal attacks in the crestor group than in the placebo group.

    (vi)  Absoute number not having (non fatal) heart attacks very small.

    (vii)  Number to treat very high.

    (viii)  Maybe the test was ended early because of the fear of the small trend of benefits reversing and greater levels of cancer, etc showing up.  Presumably if you believe all the hype continuing the trial would have benefitted those in the crestor group whilst no harm came to the placebo group.  

    (ix)  1 in 4 stop taking crestor yet side effects were the same in the placebo and crestor taking groups.

    (x) 28% more deaths from non CVD causes in the Crestor group.  It quite reasoneble to assume that deaths arising as a side effect of taking these drugs would increase over time.

    I could go on, but I think the above makes my point.

    Of course another interpretation of the data is that high cholesterol doesn't cause heart disease, someting else does - inflamation?  

    - in the same way that high blood sugar doesn't cause type 1 diabetes - its a consequence of a failing pancreas.

    Paul Anderson.

  • Anna

    11/15/2008 2:56:00 PM |

    Anonymous said:  What are we to believe when experts so often disagree with each other?

    We don't want experts to agree, for the most part.  When they agree too much, that means little is begin done to push the bounderies of knowledge.  

    I think too many non-experts want to be told what to think, and abdicate their own responsibility to at least try to understand the factors involved and be part of the decision.  

    I realize life is (too) complicated today and we can't know how to do everything ourselves, so we farm out a lot of the "improve and repair" work to experts (car mechanics, electricians, plumbers, and yes, physicians).  But we still need to know enough to know if the proposed work is good or not.  It's not much different with health and/or medicine, in fact it's more important.  Cars or electrical wiring can be replaced after shoddy work; health is more challenging.

    Dr. Davis, I hope you don't take offense to my comparison of physicians and medical experts to trade jobs (nor do I mean any offense to tradesmen).  I merely mean to say we rely all the time on people who have more specialized knowledge and skills than we do.  We still need to understand what's going on.

  • Anonymous

    11/17/2008 4:07:00 AM |

    Anna said, "We don't want experts to agree, for the most part. When they agree too much, that means little is begin done to push the bounderies of knowledge."

    You make a good point, Anna.  
    Regarding the question about disagreement among medical professionals,I would expect that well done unbiased studies would result in clear irrefutable facts. The question was does a statin block vitamin D production or does it enhance it? Doctors disagree on this issue. Why?  There is no way we can know this on our own.
    Regardless of how self-reliant we are, we can only make intelligent health care decisions when we have clear and accurate information.
    When the pharmaceutical industry has so much control of medical education, we definitely have a challenge.

  • Weight Loss

    4/10/2009 2:33:00 AM |

    your article is great. Also CRP does not cause atherosclerotic disease, I too find this after a long study. Thanks for your suggestions.

  • Anonymous

    5/5/2009 8:17:00 PM |

    Another probable typo, and a common one throughout the medical literature, is the use of mg/dL units rather than mg/L.  The correct cutoff value for eligibity in the Jupiter study was 10 times lower at 2 mg/L.

  • Anonymous

    11/12/2009 4:53:53 AM |

    >>>>> Vitamin D by itself reduces CRP around 60%--more than statin drugs <<<<

    Could I have a good source for this statement.  I find it fascinating.

    /a family doc in Canada.
    Thanks !

  • Erick

    6/30/2010 5:36:08 PM |

    I've been looking for info on CRP and Jupiter and luckily I ran into your blog, it has great info on what I'm looking and is going to be quite useful for the paper I'm working on.
    BTW is crazy how many viagra online blogs I manage to dodge in order to get the right site and the right information.
    Thanks for the post and have a nice day.

  • Green Parks

    10/14/2010 6:09:03 PM |

    Hello.. Firstly I would like to send greetings to all readers. After this, I recognize the content so interesting about this article. For me personally I liked all the information. I would like to know of cases like this more often. In my personal experience I might mention a book called Green Parks Costa Rica in this book that I mentioned have very interesting topics, and also you have much to do with the main theme of this article.

  • buy jeans

    11/2/2010 8:14:13 PM |

    You make a good point, Anna.
    Regarding the question about disagreement among medical professionals,I would expect that well done unbiased studies would result in clear irrefutable facts. The question was does a statin block vitamin D production or does it enhance it? Doctors disagree on this issue

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A Track Your Plaque failure

A Track Your Plaque failure

We recently had a man suffer a heart attack after beginning the program. Let me tell you the details.

Jerry's heart scan score 781, age 53. Multiple lipoprotein abnormalities: HDL 32 mg/dl, triglycerides 279 mg/dl, nearly all of his LDL was in small particles with an "effective" LDL (LDL particle number), and very high IDL. So Jerry added fish oil 6000 mg per day, niacin, and vitamin D to the statin drug prescribed by his primary physician. Jerry added oat bran, ground flaxseed, and tried to eat fish at least once per week.

However, Jerry continued to smoke. He'd smoked for 40 years (!), up to 2 packs per day, and just reasoned that it was too late to quit. He also continued to indulge in the packaged, processed foods that were part of his convenience story business.

Jerry's stress test was normal--no chest pain, normal EKG, normal images of blood flow, though he was somewhat breathless, likely from his lung disease from smoking.

Two months into his program, he abruptly experienced severe crushing pain in his chest. Because he was traveling, he ended up in a small local hospital. A failed angioplasty led to urgent coronary bypass surgery.

Jerry's alive. Now he's a non-smoker. He's got the pursed lips and peculiar breathing pattern that smokers get, but he's breathing.

Lesson: In the face of the most powerful program for heart disease known, it can still be overpowered by Twinkies, Hoho's, pretzels, chips--and cigarettes.

The new year is approaching. Be grateful for another year of healthy life and commit to a new year of even greater health. If you're a smoker, there's no choice: you've got to quit.
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Normal cholesterol panel . . . no heart disease?

Normal cholesterol panel . . . no heart disease?

I often hear this comment: "I have a normal cholesterol panel. So I have low risk for heart disease, right?"

While there's a germ of truth in the statement, there are many exceptions. Having "normal" cholesterol values is far from a guarantee that you won't drop over at your daughter's wedding or find yourself lying on a gurney at your nearest profit-center-for-health, aka hospital, heading for the cath lab.

Statistically, large populations do indeed show fewer heart attacks at the lower end of the curve for low total and  LDL cholesterol and the higher end of HDL. But that's on a population basis. When applied to a specific individual, population observations can fall apart. Heart attack can occur at the low risk end of the curve; no heart attack can occur at the high risk end of the curve.

First of all, to me a "normal" lipid panel is not adhering to the lax notion of "normal" specified in the lab's "reference range" drawn from population observations. Most labs, for instance, specify that an HDL cholesterol of 40 mg/dl or more and triglycerides of 150 mg/dl or less are in the normal ranges. However, heart disease can readily occur with normal values of, say, an HDL of 48 mg/dl and triglycerides of 125 mg/dl, both of which allow substantial small oxidation-prone LDL particles to develop. So "normal" may not be ideal or desirable. Look at any study comparing people with heart disease vs. those without, for instance: Typical HDLs in people with heart attacks are around 46 mg/dl, while HDLs in people without heart attacks typically average 48 mg/dl--there is nearly perfect overlap in the distribution curves.

There are also causes for heart disease that are not revealed by the lipid values. Lipoprotein(a), or Lp(a), is among the most important exceptions: You can have a heart attack, stroke, three stents or bypass surgery at age 40 even with spectacular lipid values if you have this genetically-determined condition. And it's not rare, since 11% of the population express it. How about people with the apo E2 genetic variation? These people tend to have normal fasting cholesterol values (if they have only one copy of E2, not two) but have extravagant abnormalities after they eat that contribute to risk. You won't know this from a standard cholesterol panel.

Vitamin D deficiency can be suggested by low HDL and omega-3 fatty acid deficiency suggested by higher triglycerides, but deficiencies of both can exist in severe degrees even with reasonably favorable ranges for both lipid values. Despite the recent inane comments by the Institute of Medicine committee, from what I've witnessed from replacing vitamin D to achieve serum 25-hydroxy vitamin D levels of 60-70 ng/ml, vitamin D deficiency is among the most powerful and correctable causes of heart disease I've ever seen. And, while greater quantities of omega-3 fatty acids from fish oil are associated with lower triglycerides, they are even better at reducing postprandial phenomena, i.e., the after-eating flood of lipoproteins like VLDL and chylomicron remnants, that underlie formation of much atherosclerotic plaque--but not revealed by fasting lipids.

I view standard cholesterol panels as the 1963 version of heart disease prediction. We've come a long way since then and we now have far better tools for prediction of heart attack. Yet the majority of physicians and the public still follow the outdated notion that a cholesterol panel is sufficient to predict your heart's future. Nostalgic, quaint perhaps, but as outdated as transistor radios and prime time acts on the Ed Sullivan show.

 

Comments (19) -

  • Might-o'chondri-AL

    6/15/2011 4:14:41 PM |

    I  was surprised that in order to get my  vitamin D25 level to 58.3 ng/mL  this winter in southern California I had to take 6,000 IU daily  of vitamin D3;  as was outside in short sleeves a fair spell every day.   This was first time where could test,  and my first time supplementing as well;  now am using at least 7,000 IU daily of vitamin D3 and it's summer months.

    Set my blind trial dose,   as a precaution, on low side based on info read here (from T. Hutchinson) suggesting 1,000 IU D3 for every 25 pounds body weight;  I had no clue what my baseline D3 was . Used  glycerin drops from Vitality Works out of New Mexico,  where 5 drops = 2,000 IU D3 ;  I've no financial interest in this.

    All males on my paternal side died from heart related problems before their late 50's so went ahead and tested my Lp(a) a while back;  I got clued in to Lp(a) by reading Doc's posts here . Was pleased and relieved to see a Lp(a) reading of just 2 , since lab gives less than 20 Lp(a) as normal.

  • Jimmy

    6/16/2011 12:07:56 AM |

    Then how is Lp(a) best treated?
    I am 36 and have had high Lp(a) for 16 years now. It sits near 100. That with low HDL and high LDL I feel like a walking time bomb. My father passed at 44 and mom at 46 and all uncles on mom's side dead prior to 50 of heart disease. Father was adopted, so do not know his side. What is worse, is that I have just relocated to Toronto, Canada (from the US) and I cannot find a doctor who even acknowledges what Lp(a) is. Nor can I find one (and I have been searching for 2 years) who thinks my cholesterol is high enough to "worry about".  It's even worse here than in my small town back in the US as far as getting decent lipid testing and advice Frown     Sorry to rant.

  • Lora

    6/16/2011 1:33:58 AM |

    I'm glad that you are warning people with normal cholesterol panels not to be complacent about their arterial status. My  cholesterol totals from age 40 to 52  ranged between 114 and 132.  My HDLs in my late 40s/early 50s were 64, 58, 53; LDLs 55, 56, 48; triglycerides 66, 49, 70.  The cholesterol totals on the latter two panels were below the normal range, which I've read can be problematic, though that's a topic that it is very difficult to find info about. What a surprise to get an severely infected blister on my foot, complicated by poor circulation, and to subsequently be found to have "mild arteriosclerotic changes" in my lower extremities.  I wonder about the mildness b/c now I perceive the dramatically decreased amount of hair on my legs as an indicator of poor circulation.

  • Dr. William Davis

    6/16/2011 11:54:41 AM |

    Jimmy-

    Please do not accept the advice offered by many of my colleagues that there is no treatment for Lp(a), or that the only treatment is to reduce LDL to less than 80 mg/dl with statins. All nonsense.

    Undoubtedly, the science behind Lp(a) is still unfolding and is proving to be more complex than initially thought. For instance, newer observations are suggesting that the atherogenic (plaque-causing) potential of Lp(a) may be largely due to its oxidized phospholipid and phospholipase A2 content.

    Nonetheless, I urge you  to participate in our discussions on the Track Your Plaque website, where you will find extensive reports and discussions on what to do with Lp(a). Our current first treatment of choice is high-dose fish oil, i.e., 6000 mg per day EPA + DHA.

  • Dr. William Davis

    6/16/2011 11:56:51 AM |

    Hi, Lora--

    Clearly, your answers won't be found in cholesterol values. This is far more common than often thought.

    Look for Lp(a), small LDL, vitamin D deficiency, and consider omega-3 fatty acid supplementation. Consider unappreciated hypertension and endogenous glycation, i. e, high HbA1c.

  • James

    6/16/2011 8:22:33 PM |

    When I got my in-office lipid panel results, my doctor was pleased by the results (I was too):

    Trigs: 50
    Total Chol: 198
    HDL-C: 70
    LDL-C: 118 (slightly elevated)

    That gives me a TC/H of 2.8, which I assume is excellent.

    BUT, I also got a NMR LipoProfile test, and here were those results:
    LDL-P: 1410 (High)
    Small LDL-P: 613 (High)
    Vit D: 31.4 (Low)

    I was surprised that the NMR test revealed some risk, while my standard panel did not. My doctor now wants to test me again in 4 months.

  • kenneth

    6/17/2011 1:39:19 PM |

    I've never been able to get my HDL above 36 (it's as low as 25). Triglycerides in me and my brother run 400-500 uncontrolled (neither of us is at all obese). I'm at 8 grams of fish oil now, 1 g of IR niacin and I've bumped up my Vitamin D to 8,000 a day, and I'm hoping that makes a difference at least with the HDL. My LDL and total cholesterol numbers are "normal" although god knows what a VAP or NMR would reveal. Would I be crazy to think about adding a bit of statin to this mix, ie 10 mg/day of atorvastatin or simvistatin? Has anyone had any luck with sytrinol or anything else? I'm not wheat free I know, but I have cut way down.

  • Anand

    6/17/2011 4:23:50 PM |

    Dr. Davis,
    What is your take on the AIM-HIGH trial ?
    My Lpa, measured at Berkeley is extremely elevated at 190 mg/ dl. Their assay is supposed to be isoform insensitive. I am on 20 mg crestor and 2 g niaspan along with 2g carnitine, 2500 IU vitamin d (level is 36) and 3 g EPA plus DHA.
    I do follow a low carb diet.
    I also have FH. Untreated my TC was 300 with LDL over 200.  I already have one stent in mid LAD despite being thin (BMI 23).
    I am wondering how to monitor my coronary arteries besides the standard stress test.

    An and

  • Lora

    6/17/2011 8:32:43 PM |

    Thank you for the information. My HbA1c when checked was 5.6. I had already started cutting back significantly on carbs a couple of weeks before that. I think endogenous glycation has been a significant factor for me. I've avoided white sugar for many years, but I used to quite frequently eat beans and whole grains, including whole grain oatmeal every morning. I discovered with a OneTouch UltraMini glucose monitor that my BG went into the 170s after eating that!  I haven't found any other food that sends my BG so high.  (And  I used to frequently eat the oatmeal along with fruit!) An hour after the drink in a glucose tolerance test my BG was 138 (then went to 79 an hour later).  My vitamin D when checked was 43.6 so not terrible, but showing room for improvement. I'ave been taking Member's Mark fish oil (which I read about on this web site) for quite awhile, but I’d been somewhat erratic with it before realizing my problem. I have a variant of "white coat" hypertension, which I've read is probably more harmful than it was once thought to be. Normally my BP is on the low side but stressful situations sometimes cause it to spike dramatically. My BMI has been 20 for years, used to be lower. I've never smoked. I wonder about carnitine b/c my diet has been largely, though not entirely, vegetarian for years. I definitely haven’t been getting enough exercise. Also, I've come across journal articles about Type D personality traits and think they may be a factor.  I have to get Lp(a), small LDL, and other sub-elements checked.    

    Thanks again! I have learned a lot from this web site.

  • Helen

    6/20/2011 7:11:33 PM |

    Lora -

    Yikes!  You sound almost exactly like me.  I don't really know what to do about the glucose spikes.  Low carb didn't help me.  I'm not trying to burst Dr. Davis' bubble or anything, just saying what was true for me.  Fish oil and niacin make my blood sugar spike more.  My blood pressure and resting heart rate are low, though.  Only occasionally do I get the white coat hypertension thing.  But otherwise, my cholesterol panel and blood sugar experiences mirror yours pretty well.

  • Lora

    6/22/2011 7:43:10 PM |

    Helen,

    Fortunately, decreasing or avoiding certain carbs does help me control my blood glucose. I bought a glucose monitor, as suggested by Dr. Davis. Ironically, I have discovered that some of the foods I used to make it a point to eat for health reasons (oatmeal, apple) spike my blood sugar the most.

  • SK

    6/25/2011 2:27:20 PM |

    We are big fans of fish oil.

    BUT, now we read this: "our findings are disconcerting as they suggest that ω-3 fatty acids, considered beneficial for coronary artery disease prevention, may increase high-grade prostate cancer risk, whereas trans-fatty acids, considered harmful, may reduce high-grade prostate cancer risk. " ???
    http://aje.oxfordjournals.org/content/173/12/1429.full

    thoughts???

  • SK

    6/25/2011 2:31:28 PM |

    OOopps,

    my mistake. let me post this at the right blog topic....

  • Gregory

    6/27/2011 1:34:08 AM |

    Lora,

    I too: a cup of muesli and fruit for breakfast for years. One day I tested: 179 after 1 hour. I now try to aim for 1 hr post prandial 110. No more muesli and fruit for breakfast!

  • Dr. Hasitha Dissanayake

    7/1/2011 5:02:37 PM |

    Dr. Davis, you have nicely described the high lipid levels and its impact on heart disease. Yes, as you have described the hight lipid level is not the only cause for heart diseases. Other major risk factors include smoking, hypertension and  diabetes. Further there are also number of minor risk factors for heart diseases as well, such as family history, sedentary life style, male gender etc.

    We should not make our minds by looking only at normal cholesterol panel. As you have described already vitamin D in important to produce more HDL and Omega-3 fatty acids. Any way vitamin A, C and E act as anti oxidants and also reduce the cancer risk. Visit http://agelag.blogspot.com

    Nice blog Dr. Davis... Keep on writing...

  • John

    7/21/2011 6:16:28 PM |

    WOW! all these numbers/letters and i've not a clue what most of them mean! i'm aware of the hdl/ldl numbers/levels , though not of the others. i happened across this site/blog from another nd/md's blog and i find this stuff to be mind-boggling! my health challenge: Late Nov. 2010, i had a stent placed in a major artery that i'm told was 90-95% blocked. while recovering in cath lab, i almost bled to death with a hemotopa ( ? ) the size of an orange, i was told upon my discharge by the nurse who saw it and literally saved my life. i've since been on plavix 75mg, 1x/day in which i've chosen to cut these in half and now take 1/2 pill at 12+ hours intervals or when i suddenly feel tired, pains and get scared. i should also tell you i've been diagnosed w/ peripheral neuropathy and experience many different types of stinging/pinching pain in various parts of by body. doing alot of computer work ( i work from home on the internety ) with one=finger hunt-n-pek typing also causes numbness and pain in my right hand. the very first day after the procedure,  i was given 7 - yes, 7! - plavix75mg. needless to say, the ensuing 4 weeks was hell for me and out of fear, i was back and forth to a heart hospital about 4 different ocassions. my entire right leg, groin, testacles and penis was purple/bluish and bruised. Now, i have not felt good since this stent was put in. i feel that the other type stent could have been used instead of the drug-alluding stent. I was also prescibed a statin of which I've NOT taken since finding out how ineffective and dangerous they are and that we actually need cholesterol especially for prpoer brain functioning. as i type now, i'm in discomfort. i recently started drinking a organic magnesium supplement called Natural Calm but aside from it cleaning me out, i feel no better at this point. I NEED HELP! i'm depressed and very irritable over the smallest things, at times. I have attempted to follow Dr. D'adamo's Eat right For your Blood type diet, but, since these supplements can be quite expensive ( i'm on a S.S. disability for Tourettes Syndrome ) i don't take them as often as i should so i really can't say whether or not they help. i've eaten breads my entire life and pizza as and still is my favorite ( i'm italian of course-Smile basically, i've been eating all foods my entire life that i shouldn't have been. i'm driving my wife and myself crazy and she does return the "favor' quite often. so now i read all this info. about vit. D and fish oils and i'm more confused than ever. being in NY, i'm aware of the vit. d ( lack of ) in relation to depression or SAD, etc.  i'm praying i find some nd/md who is willing and able to work with me to get me off this plavix and gabapentin 300mg ( 3 caps, 2x per day or as i feel they are needed ). my cardi says that after 1 year he'll be able to take me off the plavix, but, honestly, i feel this drug is killing me. oh...i also have the beginnings of Barretts Esophagus ( very small, i'm told ) and my gastro and cardi feel the combination of Plavix 75mg, Protonix 40mg, enteric coated Reg. strength aspirin ( of which i take 1-2  Baby aspirin instead, very rarely ),
    gabapentin 300mg is safe for me and outweighs the 30% or so possibility of having a blood clot at the stent. I've also thin blood to begin with ( type 0+ ) and i'm just feeling miserable! i do have a good day here and there, but mostly my days are spent very uncomfortable, irratable, depressed, tired and angry. I used to be healthy and exercised but now if i get out to walk a while, that's about it. i've never weighed in at more than 185 with much of my life weighing between 155-170. i am 5'7" and had always been considered to have broad shoulders and was husky as a young child. i'm hoping to get some relief and my good health back. i thank you for reading this and letting me vent. i apologize for any typos and the inconsistencies.

  • Lawrence

    9/30/2011 12:38:03 PM |

    Dear Dr William Davis
    In May of 2009 my wife had a brain aneurism and stroke.  (Then 52)
    Two years on she is extremely well due to a very skilled neurosurgeon. It has come to light that my wife has type 2 diabetes, high blood pressure and high cholesterol.
    Her medications are 1000mg of Metformin twice daily with meals.
    160mg of Diovan  mornings.
    25 mg HCTZ mornings.
    We are supplementing her meds with 1000mg of fish oil and now 2000iu of Vitamin D.
    A month ago we started using the Heart Technology Heart Tech formula two scoops  a day.
    Approx one month after starting the Heart Tech Formula my wife has had some blood work done.
    The results are as follows:
    A1C 7.1
    Lipoprotein A 23 nmol/L
    Vitamin D, 25 Hydroxy (vd25)  33ng/ml.
    C-reactive Protein HS 0.80 mg/dl.
    Cholesterol 236 md/dl.
    HDL 48 mg/dl.
    Triglyceride  181 mg/dl.
    VLDL  36 mg/dl.
    LDL 152 mg/dl.
    Non –HDL  188
    LDL/HDL ratio 3.17.
    My wife was originally taking Simvastain 25mg per day but our PCP stopped this due to some nasty side effects, he has since suggested we start  Lipitor, but after reading so many worrying articles regarding Lipitor and other statin usage  we are very reluctant to start using the Lipitor.
    I wonder if you would mind discussing our options and what you would consider my wife’s risk of Heart Attack and stroke are and if you feel the use of vitamin C, lysine etc in the Heart Tech will help with her risk.  I am new to the site so have not found my way around yet.
    Thank you.
    Lawrence

  • Dr. William Davis

    10/1/2011 2:04:52 PM |

    Hi, Lawrence--

    I would strongly urge you and your wife to 1) read the many posts on this blog about the exact situation your wife is experiencing and, 2) if interested in more information, consider going to the Track Your Plaque website, where many discussions are conducted on these issues every day.

    Your wife's pattern is a clear-cut example of carbohydrate excess and/or genetic susceptibility and vitamin D deficiency. All of this is readily, easily, and safety correctable with no drugs.

  • Lawrence

    10/1/2011 9:33:03 PM |

    Dear Dr William Davis
    I suppose in some ways being diagnosed with type 2 has been a good thing, in spite of my wife mild brain damage she is starting to realize that she has to cut out all the rapid acting carbohydrates that she used to exist on. It has taken me some time to find the right approach to helping control her BG, but she is now starting to see the better BG reading so is responding to the good feedback. We are increasing our dose of Vitamin D3 to 10000 IU.  We plan to continue with the Heart Tech, my feeling is her LPa would have been much higher if she had not had a month of the Heart Tech formula prior to her blood draw.
    I will certainly log in to Track Your Plague, thank you for taking the time to respond to my questions, it’s very reassuring that you feel she will respond to the Track Your Plaque.
    Lawrence

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The Framingham Crap Shoot

The Framingham Crap Shoot

The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.


Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

Comments (2) -

  • katherine

    11/24/2008 3:31:00 PM |

    just came across this...thoughts?

    http://thegearjunkie.com/the-runners-heart

  • John

    11/29/2008 3:33:00 AM |

    Good article. One of the most common mistakes made by health conscious individuals is the idea that if study X says A is bad or good then one should adjust one's lifestyle accordingly.

    If only it were that simple. A statistical analysis of a group is applicable to that group, not necessarily the specific individuals within that group; let alone those outside the studied group. We cannot determine individual risk on the basis of such studies yet time and again these studies are mentioned as "evidence" that we must accept. Sadly, too many health promoters, who should know better, tend to make the same logical error.

    Very pleased to see that this error is highlighted here.

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