Heart Scan Blog readers take impressive doses of omega-3s

24. October 2009 William Davis (28)
Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.
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Comments (28) -

  • Mike

    10/24/2009 3:52:01 PM |

    "But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

    So what?

    Wolf, Sears, and Poliquin recommend a high fish oil dose of 0.5g-1.9g EPA/DHA per 10lbs BW; this generally equates to 9-10g range.  All three have had amazing success with sedentary, chronically ill individuals and elite level athletes.

    I believe you yourself have stated in the past that fish oil causes a shift from VLDL and IDL to large particle LDL---a benign, if not beneficial action.

    So is the raising of LDL in high dose fish oil even a concern?  Some clarification on this would be appreciated.

  • Dr. B G

    10/24/2009 4:44:35 PM |

    Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

    Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

    I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

    IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

    Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

    http://drbganimalpharm.blogspot.com/search/label/Evolver

  • Dr. B G

    10/24/2009 4:44:35 PM |

    Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

    Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

    I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

    IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

    Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

    http://drbganimalpharm.blogspot.com/search/label/Evolver

  • TrueDharma

    10/24/2009 5:50:45 PM |

    My EFA results showed an Omega3 index of 11.7% and a Omega 6:3 ratio of 2.3/1. I supplement with 1600mg EPA and 800mg DHA daily. I follow a low carb (high fat) I can't afford to eat "grass fed", but I do avoid processed foods whenever possible and my dietary fats are from coconut oil, lard, beef tallow, butter, olive oil and small amounts sesame oil. The Omega 3 Index test was a bit pricey, but...it did give me some comfort that I am on the right track.

  • Jae

    10/24/2009 5:53:26 PM |

    For those who witnessed an increase in LDL, what was the profile of small, dense VLDL vs large, fluffy VLDL reflected in the increase?

    Also, first-time commenter. Thank you for a great, informative blog.

  • Adam Wilk

    10/24/2009 8:59:52 PM |

    "But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

    I'm hoping (and wondering if...) that while those diligent enough to take that high a dose of omega-3's may have higher measured LDL levels, they indeed have much larger, fluffier particles now than when they began the megadosing.  That would be something marvelous to hear.
    Good stuff here, as usual!
    -Adam

  • Steven Horvitz, D.O.

    10/24/2009 9:35:20 PM |

    If one's LDL's raise dramatically on omega-3's, without the corresponding increase in hdl, or decrease in trigs, is it better to lower the omega 3's?

    Ex:

    pre-omega
    tc 240
    hdl 45
    ldl 165
    tg 70

    during 2000mg omega-3's
    tc 320
    hdl 58
    ldl 240
    tg 90

    Also, the pattern size of the ldl's are type a with a low carb, no grain diet.

  • homertobias

    10/24/2009 11:29:56 PM |

    I'd very much like to know what subfraction of LDL was elevated in the TYP followers on 9,000 plus omega 3's a day.  My experience is that large fluffy LDL increases but not small dense.

  • Kevin

    10/25/2009 8:36:26 AM |

    What about lipid peroxidation on high dose of fish oil?

  • Dr. William Davis

    10/25/2009 2:52:27 PM |

    The form of LDL that increases depends.

    It seems to depend on the genetic basis for small LDL. In other words, if the triggers of small LDL have been removed along with other efforts aimed at reducing small LDL like niacin, and there is no genetic basis for small LDL, then large LDL increases.

    If small LDL is genetically programmed (a lot more common than many think), then small LDL can increase explosively.  

    Having performed many thousands of lipoprotein panels, the latter situation in which small LDL increases is worrisome.

    I am unsure of the implications of the first situation. Sure, we can extrapolate and speculate that it might not be related to increased risk. But I am not willing to gamble someone's health and life on pure speculation with no human data.

  • homertobias

    10/25/2009 5:07:57 PM |

    The only references to an increase in LDLC with fish oil supplementation is from WS Harris who authors 95% of the omega 3 index studies including a 2008 review which concludes that the omega 3 index is superior to omega 3/omega 6 ratio.  When 95% of literature comes from one man who promotes a pricey lab test I can't help but wonder if he gets part of the profits. I have no data to say he does though.

    He has two 1997 publications,one showing that Omnacor given at 4 g epa/dha a day raised ldlc by 10%. 1997 was the predawn era of advanced lipids.  In his second publication individuals with severe hypertriglyceridemia (baseline fasting levels on statins of 500 to 2000) did have a 32% rise in LDLC.  
    Harris has ties to Big Pharma (the maker of Lovasa/Omnacor) and to Monsanto.
    Data that I can easily access ascide from Harris shows effecacy of fish oil supplementation up to 4 grams of epa/dha a day.  5 grams a day for plaque stabilization/ antiinflammatory effect.  9 or 10 grams a day only in obese heart failure patients.  
    My bottom line:  if your baseline tg's are 500-2000, watch out for your ldlp on high dose fish oil.  If you are an obese heart failure patient, lose weight.

  • William Trumbower

    10/25/2009 5:31:50 PM |

    I believe that when people use theraputic levels of fish oil (more than 3gm EPA=DHA)  they should follow their omega profile and lipoprotein analysis closely.  It is possible to push the eicosanoid synthesis pathways toward the arachadonic acid side depending on your diet.   Once you know your optimal dose, then you can adjust it up in certain circumstances.  I attended a football tailgate and found some of the mixed nuts were cooked in soy oil, so I took an extra dose of fishoil when I got home to compensate.

  • Mike

    10/25/2009 5:40:54 PM |

    Thanks for your thoughts on this.  Regarding LDL particle size, how dependable would TG/HDL ratio be?  Sears indicates a ratio less than 2 indicates large benign LDL.  In my own experience over the past few years, as I've increased my fish oil intake (along with a Paleo diet) my HDL has gone up, my LDL has gone up, and my TGs have decreased.

  • Boris

    10/26/2009 1:30:58 AM |

    I have increased my intake of omega-3 since I answered the poll. My problem was that I couldn't take it all at once. Too much fish oil gave me a super upset stomach. Granted, it was the impure Nature Made brand sold at Walmart (34% pure). Now that I am using Omapure, I take one capsule with every meal and then one before bed time. It 6x more expensive than the Nature Made junk but I'm not getting sick from it.

    Does it matter that I break up my intake over the course of the day rather than swallow four capsules all at once?

  • Anonymous

    10/26/2009 1:49:07 AM |

    great information here, thanks all.

    To follow on Dr.BG's note on statin overuse :  there is an interesting presentation of baylor college's lipidsonline.org with discussion of guidelines for statin dosage.  The presenter notes how very little value is obtained from subsequent doubling of a statin dose and the risks for side effects.

    http://www.lipidsonline.org/slides/slide01.cfm?tk=82

    Dr. D.  Thank you for the caution on fish oil. I take 1650mgs EPA/DHA twice per day.  Might be a good idea to cut out a dose if I eat salmon or other oily fish.

    Would love to see more info on MK4/Mk7 K2 and MCFAs like coconut oil.

  • Dr. William Davis

    10/26/2009 1:58:12 AM |

    Hi, Mike--

    While the Triglyceride/HDL ratio can serve as a useful measure of small LDL in a population, it performs poorly when applied to specific individuals. This is because small LDl, while influenced by the situation creating low HDL and high triglycerides, can also behave independently.

    Small LDL is, in my view, best measured specifically.

  • Ross

    10/26/2009 5:52:24 AM |

    It's pretty straightforward to end up in the middle of the pack on that poll.  But don't take gels or you'll be there all day.  One tablespoon of Carlson's Finest has 4800mg O-3's with 2400mg EPA and 1500mg DHA.  One swallow just as I'm sitting down to breakfast makes for a great start to every day.

  • Anonymous

    10/26/2009 1:54:50 PM |

    I was told than an ApoE 4 Patient should not be on therapeutic doses of fish oil (for reasons which you have stated- raising LDL).

  • homertobias

    10/26/2009 2:46:23 PM |

    Dr Davis:

    I would like to know which WS Harris 2008 you referenced and the reference for the females in the Harvard School of Public Health please.
    I also would like to know if there was a correlation between baseline tg levels and those who experienced a more marked elevation of sd LDL on fish oil.

  • homertobias

    10/26/2009 4:14:20 PM |

    I guess that this is my day to ask you questions.
    When you read a MDCT, do you also measure pericardial fat?
    What do you think of Dr. Ding's new MESA findings re pericardial fat.  Thanks in advance.

  • Alan S David

    10/26/2009 6:16:55 PM |

    I take 6000 units daily or more, but I also consume a few tablespoons of ground flax seed daily as well.
    AND still eat fish a few times a week, especially oil rich sardines.

  • jegesq

    10/26/2009 9:28:03 PM |

    Homertobias:

    Lots of interesting work being done on pericardial adipose tissue (PAT) and using CT imaging done in conjunction with CAC scoring to more precisely determine the relationship between PAT and the development of CAD and calcified plaques, i.e., in order to more precisely "score" the level of PAT and to determine association and/or causality with calcific lesions.

    Dr. Lerber at University Hospital in Munich, Germany has observed that PAT accumulation precedes the development of calcified plaques, that increased volume of PAT are associated with reduced levels of  adiponectin and higher CRP.   So the idea is that with more precise measurements and concomittant imaging of both PAT and CAC, we might be able to better detect the presence of disease in an earlier stage.   There is also some push among those doing such research to link PAT thickness assessment with administering routine echo stress testing but this hasn't gained much traction yet other than in a small circle of folks.   The hope though is that PAT can also be used as another surrogate marker for diagnosing preclinical atherosclerosis.

    But as of now, I don't think anyone who does a routine CAC scan, whether with MDCT or EBT is doing any form of assessment of PAT, at least not until there is more data on the reliability of using this as a clinical marker of disease.

    Personally, I think there's a lot of interesting info that can come from this, and the idea of deposition of fat into muscle tissue and necrosis of that tissue, inflammation and the relation to levels of saturated fats consumed from dietary sources is an area that is just begging to be better researched.

    Oh, and by the way, don't believe everything you read here from BG about what foods I consume, how much statin I take, or much else when it comes to me.  In fact, I'd prefer that she simply not make references to me in her writings wherever they appear.  This will obviate the need for me to continue to correct her misstatements about me, my lipids, and drug and supplement usage, as well as the fact that she continues to misrepresent that I have not achieved plaque stability and/or demonstrated regression through serial MDCT CAC scoring over a period of three years despite very low dose use of rosuvastatin.

  • jegesq

    10/27/2009 12:16:24 AM |

    A correction....  My serial scan scores show that I have achieved stability and optimally regression of coronary calcium.   My point is that Dr. BG continues to claim that those taking rosuvastatin at doses of ~10mg daily cannot possibly achieve regression on EBT/MCDT scanning, and that just isn't so.

    I happen to be one of those whom I believe Dr. Davis was referring to with "too much of a good thing" with reference to EPA/DHA dosing.  My dose was upped from ~1-2 grams per day (of EPA/DHA) to ~10 grams based on recommendations from Dr. BG.  This occurred in or around December 2008 and continued until very recently. Based on five consecutive, quarterly NMR's and VAP's, my sdLDL-P remained at >85% of LDL-P, and my trigs went from ~40 to ~75, and, more significantly, my overall LDL-P rose from ~1000 to ~1300.   No other significant impacts were noted, other than CRP dropping to 0.7, which I attribute not to the n-3's, but instead to continued use of rosuvastatin together with combined high dosing of both boswellia and 5-Loxin and large doses of aspirin (taken specifically as an anti-inflammatory due to nerve and muscle pain from a herniated cervical disc in the month immediately prior to the last VAP testing).

    The point though is that in some, excess fish oil can convert to higher trigs and higher LDL, and will not improve the concentration or ratios of sdLDL-P/LDL-P.

    Yes, n=1, but I'm the n, so that's really most important to me, not what Wolf, Sears or anyone else has to say about this.  After all, what we're after is personalized medicine, not epidemiological observations that may be valid in large population studies but which may have no relevance to a particular individual.

  • homertobias

    10/27/2009 4:05:13 PM |

    Hi JEG,
    Thanks for the references.  I am truly upset that you andBG seem to be having a cybertiff.  She has a big heart, alot of enthusiasm, alot of intelligence and makes me laugh. You are a sincere intellectual, very bright, searching for truth in medicine and are doing a good job of it.  I can learn from both of you and want to continue to do so.
    As to omega 3 and dosage.  I can't seem to find any solid benefit to doses over 4g to maybe 5g per day. This seems to max out tg lowering, ldl improvement in particle size, minimal increase in hdl, bp lowering, improvement in tnf alpha, interleukin 6.  Reports on irs effect on HSCRP are conflicting.  One interesting report, Thies F, in Lancet 2003 took 188 patients scheduled for carotid endarterectomy and treated them with either DHA/EPA, sunflower oil, or placebo for an average duration of 42 days prior to surgery.  There was a significant difference in thickness of the fibrous cap over the plaque,the degree of monocyte  infiltration of the fibrous cap, percent DHA etc.  This directly addresses plaque stability.  I love it.

  • Dr. B G

    10/30/2009 5:06:04 AM |

    Homertobias,

    That is a great plaque stablization article -- will have to ck out!



    Jeq,

    I must be correct again as indicated by the length and duration of the post!

    Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

    Gosh... I wonder if the high dose fish oil had anything to do with it?

    EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

    -G

  • Dr. B G

    10/30/2009 5:06:04 AM |

    Homertobias,

    That is a great plaque stablization article -- will have to ck out!



    Jeq,

    I must be correct again as indicated by the length and duration of the post!

    Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

    Gosh... I wonder if the high dose fish oil had anything to do with it?

    EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

    -G

  • Dr. B G

    10/30/2009 5:14:21 AM |

    By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

    Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

    I wonder what the omega-6:3 ratio is now off the fish oil?

  • Dr. B G

    10/30/2009 5:14:21 AM |

    By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

    Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

    I wonder what the omega-6:3 ratio is now off the fish oil?

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Honey: More fructose than high-fructose corn syrup

11. August 2009 William Davis (21)
Honey: It’s natural. Mom probably gave it to you, either straight or in tea for a sore throat when you were a kid. Even today, honey is touted as possessing almost supernatural qualities for promoting health.

Honey contains B vitamins, minerals, and a handful of antioxidants. It also contains . . . fructose. 60% of honey, in fact, is fructose.

While the average per capita intake of honey is only a modest 1.29 lb per year (National Honey Board; 2008) and therefore contributes only 0.77 lb of fructose per year, there are people who, believing honey to be healthy, use it to excess and use far more than 1.29 lb per year.

How does that compare to table sugar, or sucrose?

Sucrose is 50:50 glucose to fructose. How about high-fructose corn syrup, the sweetener found in virtually all processed foods that has replaced sucrose as the most common sweetener? Depending on the variety, high-fructose corn syrup is generally 42-55% fructose. Many of us (including me) believe that the proliferation of high-fructose corn syrup in processed foods is a big part of the reason Americans are fat and diabetic.

Yes: Judged by its fructose content, honey is worse than high-fructose corn syrup. It is also worse than sucrose.

It means that honey can also contribute to the adverse health effects of fructose, as detailed in this prior Heart Scan Blog post.

Sun, fish, and seaweed

8. August 2009 William Davis (9)
Extraordinary heart health springs from three basic sources in our environment:

Sun, fish, and seaweed.

Sun: Sunlight exposure is nature's intended source of vitamin D. Humans were meant to run naked, or at least scantily clad, in tropical or sub-tropical climates. The large surface area of skin ensured plenty of skin activation of vitamin D, along with long days of intense sun (unlike the seasonal variation of day length and less intense sun further north).

Fish: Fish are the principal source of omega-3 fatty acids, as are, to a lesser degree, wild land animals. Humans as hunter-gatherers tracked, captured, and slaughtered fish and wild game, eaten immediately, since there was no means of storage. Omega-3-rich game was the principal source of fat for primitive cultures.

Seaweed: Seaweed is the world’s most concentrated source of iodine. While seafood like fish and shellfish also contain iodine, seaweed contains, on average, a thousand-fold greater quantity. Seaweed, like plants found on land, are also rich in phytonutrients.

The healthiest cultures on earth follow this simple recipe for health. The unhealthiest population on earth-meaning Americans (i.e., without benefit of bail-out medications and procedures that keep us alive, or vaccinations that protect us from infectious diseases)--neglect all three. Witness the Okinawans, whose daily meals nearly always contain some form of fish and seaweed, and whose sub-tropical climate provides greater sun exposure. It is not unusual for Okinawans to live to 100 years of age, not as an exception, but the rule. Heart disease was virtually unknown except in 90-year olds and older-that is, until the recent adoption of Western practices like fast food and snacks.

It's pretty incredible when you think about it: Simple practices can markedly reduce your likelihood of heart attack and developing heart disease.

Perhaps you’d rather not run naked along a semi-tropical beach, spear fish, and gather seaweed. You could always do the modern equivalents and achieve similar benefits.

Fructose is a coronary risk factor

4. August 2009 William Davis (21)
As discussed in a previous Heart Scan Blog post, Say Goodbye to Fructose, a carefully-conducted University of California study demonstrated that, compared to glucose, fructose induces:

1) Four-fold greater intra-abdominal fat accumulation

2) 13.9% increase in LDL cholesterol, doubled Apoprotein B

3) 44.9% increase in small LDL, 3-fold more than glucose

4) Increased postprandial triglycerides 99.2%.


Other studies have shown that fructose:

--Increases uric acid--No longer is red meat the cause for increased uric acid; fructose has taken its place. Uric acid may act as an independent coronary risk factor and increases high blood pressure and kidney disease.

--Induces insulin resistance, the situation that creates diabetes

--Increases glycation (fructose linked to proteins) and protein cross-linking, processes that underlie atherosclerosis, liver disease, and cataracts.


Make no mistake: Fructose is a powerful coronary risk factor.
There is no doubt whatsoever that a diet rich in fructose from fruit drinks, honey, raisins and other dried fruit like cranberries, sucrose (table sugar), and high-fructose corn syrup is a high-risk path to heart disease.

Also note that many foods labeled "heart healthy" because of low-fat, low saturated fat, addition of sterol esters, or fiber, also contain fructose sources, especially high-fructose corn syrup.

Who lost weight?

1. August 2009 William Davis (30)
The results of the latest Heart Scan Blog poll are in.


I went wheat-free and I . . .


Gained weight 6 (3%)

Lost no weight 41 (21%)

Lost less than 10 lbs 28 (14%)

Lost more than 10 lbs 34 (17%)

Lost more than 20 lbs 22 (11%)

Lost more than 30 lbs 28 (14%)

I'm still losing weight! 30 (15%)

(189 respondents)


This means that, by eliminating wheat:

24% had no success

31% had moderate success (less than 10 lbs or more than 10 lbs)

25% had extravagant results with 20 lbs or more lost

It would be interesting to know where along the weight-loss spectrum the last category, "I'm still losing weight," group falls. (Anyone with a good story please speak up!)

I believe we can conclude from this casual exercise that, as a simple strategy, wheat elimination is surprisingly effective.

Why would 3% gain weight? Well, without knowing the details, there are several possible explanations:

1) Weight gain developed through other foods. For instance, I've had people eliminate wheat only to replace it with fattening gluten-free alternatives. Remember: wheat-free is not gluten-free. Others load up on the wrong foods, e.g., Craisins and other dried fruit; overdo dairy; or snack on wheat-free but unhealthy foods like ice cream and chips.

2) Too much alcohol

3) Hypothyroidism--A lot more common than you'd think. In fact, this has been the case with a majority of people who have done everything right, yet either failed to lose weight or gained weight.

Those are the biggies.

I'd like to hear your personal stories of wheat elimination--the ups and downs, your success or failure, how you felt during the process, how easy or difficult, your eventual results. Just post them as a response to this blog post.

A niacin primer

29. July 2009 William Davis (19)
A reader of Life Extension reminded me of a piece I wrote about niacin a couple of years back.

Anyone desiring a primer on how and why to use niacin to correct lipid and lipoprotein patterns might find this useful.

While some people, no matter what they do, cannot tolerate niacin (about 10% of people), many others enjoy spectacular benefits.


Q: I recently had a cholesterol profile blood test and learned that I may be at risk of heart disease because my levels of beneficial HDL (high-density lipoprotein) are too low. I read that niacin could help increase my HDL, but my doctor said niacin is dangerous. Whom should I believe?

A: Your doctor would be right—if we were still living in 1985. Since then, however, we have learned how to use niacin (vitamin B3) safely and effectively. Unfortunately, many physicians have not yet caught up, or are still trapped by the idea that cholesterol-lowering statin drugs are the only way to decrease cardiovascular disease risk. I have personally prescribed niacin for thousands of patients as part of our program to reverse coronary disease. In fact, niacin is the closest thing we have available to a perfect treatment that corrects most of the causes of coronary heart disease.

Continued here.

What would life be like . . . ?

29. July 2009 William Davis (16)
What if coronary heart disease could be prevented--no eliminated--applying methods that were accessible, easy, and cheap?

What if coronary heart disease and, thereby, angina, heart attack, sudden cardiac death, ventricular tachycardia, heart failure, and the cerebrovascular equivalent, stroke, could be eliminated using readily available tools available to virtually everyone in the U.S.? And, over a year, it cost less than a once-a-week latte at Starbucks?

How would the healthcare landscape change? What would become of hospitals, manufacturers of the billions of dollars of hospital equipment necessary to supply the cardiovascular hospital industry (e.g., stent manufacturers, catheter manufacturers, defibrillator and pacemaker manufacturers, pharmaceutical manufacturers who no longer have to produce the volume of antiplatelet agents, inotropic drugs, antiarrhythmic agents, etc.)?

How would our lives change? What would the end of life look like if people stopped dying of heart attack, sudden cardiac death, congestive heart failure at age 55, 65, or 75, but lived out their lives to die of something unrelated?

What if the solution had little or nothing to do with drugs but evolved from simple nutritional strategies, supplements meant to correct the deficiencies that accompany modern lifestyles, and a few unique strategies targeted towards the genetic predispositions that lead to heart disease?

What if all this were possible at a cost of a few hundred dollars per year?

It would certainly be a cataclysmic change. Hospitals would shrink to a small remnant of their current gargantuan, dozens-per-city presence. The need for hospital staff would be slashed by over half. The rare cardiologist would tend to congenital heart disease sufferers and other unusual forms of heart disease and he or she might have a colleague or two in all of a major city.

Healthcare costs would plummet, no longer having to sustain the enormous cardiovascular healthcare machine of hospitals, staff, industry, and long-term care. Health insurance, private or public, would drop by 50%.

It would free up nearly a trillion dollars that could be redirected towards other pursuits, like schools and research. Extraordinary leaps forward in quality of life and science would emerge, given that magnitude of funding.

It's not as grand a thought experiment as Alan Weisman's The World Without Us, in which he imagines what the world would be like without humans altogether.

How long would it take to recover lost ground and restore Eden to the way it must have gleamed and smelled the day before Adam, or Homo habilis, appeared? Could nature ever obliterate all our traces? How would it undo our monumental cities and public works, and reduce our myriad plastics and toxic synthetics back to benign, basic elements?

But I believe this thought experiment--what would life be like without heart disease because it was eliminated using inexpensive tools-- is more plausible, more likely to occur. In fact, it has already begun to occur.

See those vines growing up the side of the hospital?

Are jelly beans heart healthy?

27. July 2009 William Davis (0)
Total Fat

3 g or less

Less than 6.5 g





Saturated Fat



1 g or less

1 g or less





Cholesterol

20 mg or less

20 mg or less





Sodium

480 mg or less per RACC* & labeled serving

480 mg or less per RACC* & labeled serving





Nutrients

Contain 10 percent or more of the daily value of 1 of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber



Contain 10 percent or more of the daily value of 1of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber





Trans fat

Less than 0.5 g per RACC* and labeled serving



Less than 0.5 g per RACC* and labeled serving





Whole Grain

N/A



51 percent by weight/RACC*







Minimum Dietary Fiber



N/A

1.7 g/RACC of 30 g

2.5 g/RACC of 45 g

2.8 g/RACC of 50 g

3.0 g/RACC of 55 g





(RACC=Reference Amount Customarily Consumed)

Thyroid correction: The woeful prevailing standard

27. July 2009 William Davis (16)
Rich has been taking Synthroid or levothyroxine for many years.

When Rich came to my office for continuing management 10 years after his bypass surgery, I checked his thyroid panel:

TSH 7.44 uIU/L

Free T4 1.88 ng/dl (Ref range 0.80-1.90 ng/dl)

Free T3 2.0 pg/ml (Ref range 2.3-4.2 pg/ml)


Rich's thyroid hormone distortions--high TSH, low T3--are sufficient to account for a tripling of heart attack risk long-term.

As Richs' thyroid was being managed by his primary care physician, I notified this doctor of Rich's panel. He therefore increased Rich's levothyroxine from 75 mcg per day to 100 mcg per day. Another thyroid panel several months later showed:

TSH 0.98 uIU/L

Free T4 2.38 ng/dl

Free T3 2.0 pg/ml


As you would expect, increasing the intake of the T4 hormone (levothyroxine) increased free T4 and suppressed TSH.

But what about T3? It's unchanged.

Indeed, Rich says that he feels no better and, in fact, wakes up in the morning foggy and requires a nap in the afternoon.

In my experience, the majority (approximately 70%, but not 100%) experience subjective improvement when T3 is added in some form and the free T3 level is increased. While the data (summarized here) are conflicted on whether there is objective benefit to T3 management and supplementation, there seems to be a poorly-quantified subjective improvement.

Rich's increased levothyroxine dose decreased (calculated) LDL cholesterol by 10 mg/dl. Based on my experience, I'll bet that his lipid panel would likely be further improved with T3 correction.

What I find incredible is the absolutely rabid resistance waged by primary care physicians and endocrinologists against this notion of T3, mostly due to fears of the remote likelihood of inducing atrial fibrillation and osteoporosis, while they are ready to prescribe lifelong statin drugs without a moment's hesitation.

Launch of new Track Your Plaque newsletter: Cardiac Confidential

27. July 2009 William Davis (3)
Track Your Plaque has just launched a new version of our newsletter. We call it Cardiac Confidential.

Cardiac Confidential is meant to be a no-holds-barred, go-for-the-throat exposé of the world of heart disease. We will expose the dishonest, reveal what we view as the underlying truth. We'll even have an occasional "undercover" report of what goes on in hospitals and the go-for-the-money world of heart procedures.

Read the first issue here (open to everyone) in which "Laurie" describes her encounter with a sleazy, profiteering cardiologist. She survives, but not without paying a dear price.
All posts by william-davis

More catheterizations would make me happy!

11. October 2006 William Davis (0)
I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

9. October 2006 William Davis (1)
I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

6. October 2006 William Davis (0)
A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!

6. October 2006 William Davis (0)


Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.

Fish oil in the news

3. October 2006 William Davis (2)


Hooray for the New York Times. They ran an article pointing out the miserable and inexcusable failure of American physicians to use fish oil after heart attack.

“It is clearly recommended in international guidelines,” said Dr. Massimo Santini, the hospital’s chief of cardiology, who added that it would be considered tantamount to malpractice in Italy to omit the drug.

...in the United States, heart attack victims are not generally given omega-3 fatty acids, even as they are routinely offered more expensive and invasive treatments, like pills to lower cholesterol or implantable defibrillators. Prescription fish oil, sold under the brand name Omacor, is not even approved by the Food and Drug Administration for use in heart patients."

The article focuses on the use of fish oil only after heart attack and doesn't tackle the larger issue of how fish oil is crucial for coronary disease in general. Of course, the article doesn't address the extraordinary effects of fish oil on lipoproteins, particularly triglyceride-containing varieties like VLDL and the postprandial (after-eating) intermediate-density lipoprotein (IDL).

It also talks about prescription fish oil and just glosses over fish oil as a nutritional supplement. I know of few reasons to use the prescription form. More than 90% of the time, nutritional sources of fish oil do the trick. (That is, fish oil capsule supplements, not just eating fish which doesn't provide enough for coronary plaque reduction or control.)

Occasionally, I'll meet someone who has a severe hypertriglyceridemia (very high triglycerides), or is a Apo E 2/2 homozygote (very rare). These special instances may, indeed, do better using prescription fish oil, since it is more concentrated--one prescription capsule providing the same omega-3 fatty acid content as three conventional capsules (1000 mg fish oil, 300 mg EPA+DHA).


But for most of us, the standard fish oil supplement you buy at the health food store or department store does just fine. If you read about the impurity of fish oil supplements (likely prompted by the manufacturer of Omacor, prescription fish oil), refer to the studies by Consumer Reports and Consumer Labs, both of which found no mercury or pesticide residues in dozens of fish oil preparations tested.

Look on the bright side. The conversation is growing. Fish oil, whether prescription or my favorite, Sam's Club Members' Mark brand, is a fabulously effective supplement with benefits that, in nearly all cases, exceeds the benefits of drugs.

Fish oil is an absolute requirement for your Track Your Plaque program and for you to hope to achieve control or reduction of your heart scan score.

Nutritional approaches to homocysteine reduction

3. October 2006 William Davis (0)

For an in-depth discussion of nutritional approaches to homocysteine reduction, see my new article, Nutritional Therapies for Managing Homocysteine , in the most recent issue of Life Extension magazine. You'll find it at:

http://www.lef.org/magazine/mag2006/oct2006_report_homocysteine_01.htm

The report contains a detailed discussion of how to use foods to control homocysteine levels. Though I'm not a homocysteine-crazed fanatic like Life Extension publisher, William Falloon, I still there's some interesting aspects of homocysteine metabolism that need to be explored. I also think there's some genuine benefit to reducing homocystine, preferably with foods, secondarily with supplements.

Also see our recent update on homocysteine on the www.cureality.com website at:
http://www.cureality.com/library/fl_01-006homocysteine.asp

In the update, we tried to make sense of what the new studies on homocysteine treatment, NORVIT and HOPE-2, tell us in light of all the other studies on homocysteine that preceded them.

The American Heart Association diet guarantees you get heart disease!

2. October 2006 William Davis (1)
Perhaps I stated that too strongly.

But the fact remains: the diet advocated by the American Heart Association is awful. The foods endorsed by their approach have no place on a list of healthy foods. Yes, you will find vegetables and fruits, etc.. But you will also find that the 2006 American Heart Association Diet and Lifestyle Recommendations dance around the issue of what foods to avoid. There's no explicit mention of how, for instance, common foods like Shredded Wheat cereal, ketchup, low-fat salad dressings, etc, among thousands of others, should be avoided.

No matter how you time your meals, mix them, combine proteins, fats, and carbohydrates, etc., you simply cannot squeeze health out of products like breakfast cereals, instant mashed potatoes, dried soup mixes, wheat crackers, etc. Yet these are the sorts of foods that are implicitly allowable in the Heart Association's diet program.

You can obtain a little insight into the motivations behind the diet design by looking at the Heart Association's Annual Report list of major supporters:

--ACH Food Companies--maker of Mazola margarine and corn oil. A contributor of between $500,000 and $999,000 to the Heart Association.

--ConAgra Foods--You know them as Chef BoyArdee, Peter Pan peanut butter, Kid Cuisine (pizza, macaroni and cheese). ConAgra contributed between $500,000 and $999,000 to the Heart Association.

--Archer Daniels Midland--Huge worldwide supplier of wheat flours, high-fructose corn syrup, and basic ingredients for manufacture of soft drinks, candies, and baked foods. ADM contributed between $1-4.9 million dollars to the American Heart Association.

Of course, the Heart Association provides many hugely positive services like funding research. But, on many official statements, you need to read between the lines. The Heart Association is funded by industry: medical device makers, drug makers, food manufacturers. Yes, some is contributed in the interest of health. But you can be sure that lots of money is also contributed in the hope of protecting specific commercial interests. Many of those decisions are made behind closed doors or on the golf course.

Be skeptical. Just because the Heart Association diet is a Casper Milquetoast version of a health program, it does not mean that you have to subscribe to their watered-down, politically correct, and downright useless nutrition recommendations.

I'm just right!

2. October 2006 William Davis (1)
Ben is an energetic 45-year old entrepreneur. He started his own security alarm company and has, with tremendous hard work and long hours, built it into a successful local business. Despite his long hours, he found time to coach his son's football team and help with raising his 3 kids.

Ben's life took a detour when he had urgent bypass surgery at age 39. Just three years later, the chest pains and fatigue he'd experienced before bypass returned. Another heart catheterization revealed that all of his bypass grafts except one had closed. Three stents were implanted to salvage his original coronary arteries.

That's when I met Ben. Shockingly (perhaps I should know by now!), Ben was taking Lipitor and had been advised to follow a low-fat diet. That was the full extent of his heart disease prevention program. The burning question that I wanted answered was "Why did a 39-year old man have heart disease?".

Our analysis uncovered a smorgasbord of hidden patterns. You name it, Ben had it: postprandial (after-eating) patterns like IDL, low HDL, and, most notably, small LDL and lipoprotein(a). That's why Ben had heart disease as a 39-year old man--plain and simple.

We proceeded to correct all of his patterns. But the one aspect of his program that he struggled with: weight. At 5 ft 9 inches, Ben started at 285 lbs before bypass. He did manage to get to 270 after his surgery. I told him that, if he was going to get full control of his small LDL pattern, he needed to get to <210 lbs, perhaps even lower. Without substantial weight loss, he would never seize full control over coronary plaque.

Ben was satisfied that we had identified the hidden causes of his heart disease. But he remained skeptical that that magnitude of weight loss was necessary. Built like a football player, he looked stocky but not outright fat. He got down to 240 lbs but then he decided that he looked too skinny and just went right back up to 250-260 in weight.

At a weight of 250, this puts Ben's BMI (body mass index) at around 37, way over the cut-off of 30 for obesity. Now, the BMI can be misleading in people with larger frames and more muscle. But Ben undeniably had a generous abdomen, encasing the visceral fat that drives small LDL.

Unfortunately, Ben remained skeptical until I put three more stents into his right coronary artery last evening.

Small LDL is a powerful activator of lipoprotein(a). In other words, there's something peculiarly evil about the combination of small LDL and lipoprotein(a) that brings out the worst in both. You can't correct just one or the other. You've got to correct both. Don't learn this lesson the hard way.

I think (hope) that Ben is on track to get to around 200 lbs.

Prevention: Bad news in bits and pieces

30. September 2006 William Davis (1)
Jan clearly did not want to talk about her heart scan. Her score of 502 came as a shock to her. After all, she'd survived breast cancer just a year earlier, having been through dozens of radiation treatments, chemotherapy, not the mention the emotional upheaval.

Now I was telling Jan that she had a very high heart scan score with a heart attack risk of 5% per year. Then we got to her lipoprotein patterns: Jan had several striking abnormalities, including a misleading LDL cholesterol that underestimated her true LDL by nearly 100% (LDL particle number), small LDL, and the dreaded lipoprotein(a).

"I can't handle this! Why did I get the stupid scan in the first place?!"

Giving her a chance to collect her emotions, I discussed how, even though this business can be frightening, it's far--FAR--better than the alternative: heart attack at 3 am, rush to the hospital, stents, bypass surgery, etc. Or, death for the >30% of people who don't make it to the hospital in time.

That's why I often tell people that prevention of disease is bad news in bits and pieces. But it's a lot more manageable this way. Coronary plaque is a controllable process. You don't have much control in the midst of a heart attack.

A second chance

29. September 2006 William Davis (1)
Stewart had a CT heart scan in 2004. Score: 475.

As always in the Track Your Plaque program, Stewart had his lipoproteins assessed. Among his patterns were LDL 157 mg/dl, severe small LDL, and the (post-prandial, or after-eating) IDL. Stewart was also "pre-diabetic" with a blood sugar of 123 mg/dl. Blood pressure was also a major issue. Although initially concerned, life and distractions got in the way, and Stewart's attentions drifted away.

Two years of a lackadaisical effort and Stewart's heart scan score was 600, a 26% increase. Not as bad as it could have been doing nothing (i.e., 30% per year), but still far from great. But, even with the increase in score, we still really didn't get Stewart's attention. He went about his business with a very lax dietary program, overindulging in breads, crackers, goodies, hot dogs, etc., and following a virtually non-existent exercise program except for playing golf once or twice a week.

Unfortunately, Stewart started having pains in his chest with very minimal efforts like climbing a single flight of stairs. His stress test proved abnormal. Stewart then received a stent in his left anterior descending coronary and another in his circumflex. His right coronary artery had a 40-50% blockage, close to requiring a stent.

I stressed to Stewart that this had been preventable. Should motivation remain unchanged, the next step would be bypass surgery.

I think I finally succeeded in getting Stewart's attention. He found the prospect of a bypass operation a lot more concrete than the idea of progression or regression of coronary plaque. So Stewart is being given a second chance. Unfortunately, we will no longer be able to track Stewart's plaque very effectively, since two of three arteries now contain stents, and only the right coronary remains scorable.

I hope Stewart succeeds. But I sure wish he had done this earlier. He had realistic hopes of never requiring stents or bypass surgery.

Learn from Stewart's mistakes. Attention to your program requires vigilance. You can't ignore the causes of your coronary plaque for any length of time without it catching up to you. But seize your first and best chance.