Panic in the streets

29. November 2006 William Davis (0)
Several days ago, I wrote about a local prominent judge in my neighborhood who was unexpectedly found dead in bed of a heart attack at age 49.

As expected, I've received multiple calls from patients and physicians who want heart catheterizations. For instance, an internist I know called me in a panic. He asked that I perform a heart catheterization in a patient with a heart scan score of 768. I've been seeing this patient for about a year. He's without symptoms, even with strenuous exercise; stress tests (i.e., tests of coronary bloow flow) have been normal.

I remind patients and colleagues every day, day in day out: Having a heart scan score revealing some measure of coronary plaque is not a sufficient reason by itself to proceed with procedures. Fear of suffering a fate like the unfortunate judge is also not a reason to proceed with procedures.

Increased awareness of the gravity of heart disease is a good thing. Some good can come out of a needless tragedy like this. The lesson from the judge's unfortunate experience: he needed a CT heart scan. I'm told that the judge's doctor advised him that a heart scan was a waste of time. I hope that appropriate legal action for negligence is taken by the judge's family against this physician.

Not doing a heart scan is wrong. That's the lesson to learn. The lesson is not that everybody with coronary plaque needs a procedure. Had the judge undergone a simple heart scan, intensified prevention could have been instituted and he'd still be alive with his wife and children today.

The indications for procedures are unchanged by your heart scan. If a stress test is abnormal and indicates poor flow to a part of the heart, that would be a reason. If symptoms like chest discomfort or breathlessness appear, that's an indication. If there's evidence of poor heart muscle contraction, that's a reason to proceed with a procedure. But just having coronary plaque is not a sufficient reason.
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Conventional therapy vs. alternative therapy

Conventional therapy vs. alternative therapy

11. March 2008 William Davis (5)
Rose is a 75-year old woman, mother of four, grandmother of many more.

Rose's story started after a heart attack 18 months ago that resulted in two stents. She was advised to follow an American Heart Association diet and take Lipitor. However, some months later, after her fourth stent, she became disilluioned in the conventional approach to heart disease and sought alternative therapies to help reduce or reverse her heart disease.

She found an alternative health practitioner who advised chelation, antioxidant vitamins for "excessive oxidation," and several homeopathic preparations.

Nothing was said about diet or exercise. Nothing was said about the baked flour products and pastries that occupied at least two meals every day. Nothing was said about the candies she indulged in several times per day, nor the soft drinks. Nothing was said about the wildly fluctuating blood sugars, poorly controlled by an oral diabetes agent. Thirty pounds of weight gain over the past 5 years with no exercise or physical activity? No comment here, too.

In short, Rose was the "graduate" of the conventional approach, as typically offered nationwide thousands of times a week. She was also the recipient of the insight of at least one alternative health practitioner, eager to reject conventional notions of how to achieve heart health.

So I then met her. She was experiencing chest pains every day, several times per day. Blood pressure over 200. At 5 ft, 3 inches, weight: 186 lbs.

Initial laboratory results:

HDL cholesterol 42 mg/dl
LDL 132 mg/dl
Triglycerides 263 mg/dl
Blood sugar 173 mg/dl


You can fill in the rest. In short, Rose was a disaster. Despite the attentions of several professionals from both the conventional as well as alternative camps, she was careening rapidly towards failure. She'd been given various crutches, Band-Aids, and salves, none of which resulted in any possibility of long-term relief from her aggressive disease.

My point: As I've said previously, all we want is truth. We want effective, rational approaches that yield real benefit. A stent? All that provides is temporary restoration of blood flow. Statin agents? They do indeed reduce LDL cholesterol. But what if Rose has 8, 9, or 10 other causes of heart disease unaffected by the statin drug? It will do little or nothing.

Nobody had addressed many of the root causes of Rose's disease: insulin resistance, high triglycerides, inactivity, obesity, hypertension (and identifying the reasons why her blood pressure was so high), vitamin D deficiency (virtually guarantted to be severe), junk foods including the ones known as "whole grains."

My message: Success in heart disease, as well as all aspects of health for that matter, doesn't necessarily have to come from an "alternative" approach, nor a "conventional" approach. It comes from applying what is truly effective, regardless of what label someone applied to it.

I would no sooner trust my health and life to an alternative health practitioner hawking unusual herbs and remedies than I would submit to a heart catheterization, three stents, followed by a statin drug. There's small benefit in both approaches, but none are the best. You've got to look elsewhere for that.


Copyright 2008 William Davis, MD
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Comments (5) -

  • Sue

    3/10/2008 11:19:00 PM |

    I'm really dismayed that the alternative practitioner did not look at diet (most do) but if they did I'm sure they would have recommended the usual low fat. Herbs can be very useful but only if combined with appropriate diet.

  • mike V

    3/10/2008 11:53:00 PM |

    Re: Rose

    Please follow up on Rose's TYP progress from time to time.
    We can find all kinds of studies and other info. Only your blog provides us with real world practical feedback on results with real patients.

    Thanks
    MikeV

  • Danimal

    3/11/2008 12:45:00 AM |

    I hear ya, Dr. Davis. My dad just had his 2nd bypass during an aortic pseudo-aneurism operation. He had a rock the size of my thumb knuckle removed from his aorta, his chest cracked, and still has massive occlusion of his arteries. Still, my RN-having stepmadre insists on him pursuing an AHA-approved low-fat, high-carb diet, and won't even consider putting him on Vitamin D and Niacin. How can you fight against the experts of the AHA?

  • Sravana

    3/11/2008 6:51:00 PM |

    As an alternative healthcare provider (acupuncturist/herbalist), you can BET that I would be talking to her about diet and exercise. I would've taken her BP, and probably sent her to an MD immediately to get that taken care of.

    Now, given that she was a wreck, what kind of exercise program would you put her on? I'm thinking a 20 minute walk every day, at whatever pace she could manage without chest pain - but she's already *having* chest pain! I'm curious how you handle that.

  • Anonymous

    8/31/2008 12:09:00 AM |

    "There is a clear need for a rapid, simple, safe, and sensitive method of determining the type and intensity of inflammation in the gut mucosa in clinical practice. In this study, we have evaluated the potential of a new method, the mucosal patch technique, in patients with and without apparent gut inflammation, as assessed by conventional diagnostic procedures.

    http://www.ncbi.nlm.nih.gov/pubmed/15542519

    "In 18 of 20 patients gluten challenge induced neutrophil activation defined as increased [myeloperoxidase] MPO release and increased NO synthesis. Ten of these 20 patients showed a similarly strong inflammatory reaction to CM challenge."

    http://www.ncbi.nlm.nih.gov/pubmed/17302893

    "Molecular chlorine generated by the myeloperoxidase-hydrogen peroxide-chloride system of phagocytes converts low density lipoprotein cholesterol into a family of chlorinated sterols."

    Myeloperoxidase, a heme protein secreted by phagocytes, is a potent catalyst for LDL oxidation in vitro, and active enzyme is present in human atherosclerotic lesions. ... Our observations suggest that Cl2 generation in acidic compartments may constitute one pathway for oxidation of LDL cholesterol in the artery wall.

    http://www.ncbi.nlm.nih.gov/pubmed/8798498

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Statin buster?

Statin buster?

19. November 2010 William Davis (20)
Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.
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Comments (20) -

  • Anonymous

    11/19/2010 1:42:54 PM |

    dr. davis whats your take on brown rice? is it a good replacement for wheat? a cup full at mealtimes?

  • steve

    11/19/2010 5:09:16 PM |

    Dr Davis:  As you well know, not all of us can lower small LDL through carb restriction and wheat elimination to a level where small LDL is only say 30% of total LDL, a number low enough to perhaps get plaque regression. I have elimated all wheat, and eat low carb,have achieved HDL of 59, LDL of 45, NMR particle of 609, 57% of which remain small. Take Crestor and Zetia. Vitamin d measures at 60 and no thyroid issues.   My TRG's are only 28.  So, i think i am one that may have a CETP issue not responsive wholly to diet; if this drug works, it would most likely be of help to me and many others. The only way my particle count comes down is with drugs.  Not sure how i can go lower on the carb front given my only carbs now are veggies; no fruit or starch except teaspoon of Metamcuceil.  Any other natural ways to lower small LDL?

  • Jim

    11/19/2010 6:20:15 PM |

    OK, I'm confused.  It sounds like this drug will increase the number of small LDL:

    "This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S."

    But then, maybe not:

    "CETP inhibition is really a strategy to reduce small LDL particles"

  • Anonymous

    11/19/2010 6:30:19 PM |

    Dear Dr Davis,
    what is your commentary about this new investigation which represents decreasing properties of whole grain food to ldl levels
    http://jn.nutrition.org/content/140/12/2153.short?rss=1
    Thank you in advance for your opinion
    George

  • Anonymous

    11/19/2010 6:36:08 PM |

    Dr. D.

    I love your Blog. Keep up the good work.

    A few years ago I would have been very excited about this new class of drugs. I am however not so sure this drug will be the super star people think it will be (despite being able to raise HDL so much).

    According to Chris Masterjohn @ The Daily Lipid Blog, he believes that much of the benefit of HDL is because HDL transfers vitamin E to the endothelial cells and that CETP inhibitors actually decrease the transfer of vitamin E from other lipoproteins to HDL by about half.   Frown

    http://blog.cholesterol-and-health.com/2009/03/wherefore-art-thy-protection-o-hdl.html

  • O Primitivo

    11/19/2010 7:49:50 PM |

    Another recent statin study, with null results: http://www.ncbi.nlm.nih.gov/pubmed/21067805

  • j. Carey

    11/20/2010 12:29:06 AM |

    My experience on the Paleo diet plus psyllium plus guar gum equals this drug.  My HDLs went from 35 to 91.

  • Chris

    11/20/2010 12:40:34 AM |

    @ JCarey:

    Paleo diet + psyllium + guar gum raises HDL?
    Glad you hdl's are up..got any references or links for this?

  • Paul

    11/20/2010 3:52:46 AM |

    This is my take Chris.

    Paleo diet = increases HDL as a result of an increase of dietary fats.

    Psyllium husk = lowers LDL by stimulating the conversion of cholesterol into bile acid.  It may also lower small LDL by controlling glucose levels by slowing digestion.

    Guar gum = lowers small LDL by controlling glucose levels by slowing digestion.

  • Anonymous

    11/20/2010 3:54:43 AM |

    It amazes me to no end that people have forgotten what the longest long term study has shown us about LDL.  1998 final Framingham data.  Those with the lowest LDL levels died the soonest and those with the highest levels lived the longest and yet we are still trying to lower LDL small large or medium sized.  Its the oxLDL that matter. Dr. Davis keep fighting the battle.  

    Dr. K

  • Anonymous

    11/20/2010 12:03:14 PM |

    I notice from the Merck statement that this drug did not reduce CRP like most statins.

  • Dr. William Davis

    11/20/2010 12:57:58 PM |

    A few responses:

    Anonymous--It depends on individual carb sensitivity. Most people can tolerate small quantities, e.g., 1/2 per serving. Others (like me) cannot even tolerate this much without triggering a surge in blood glucose and small LDL.

    Steve--You likely have what I call "genetic" small LDL, meaning a CETP variant. Niacin can help. Beyond this, we struggle. I've seen variable effects with more fats, phosphatidylcholine, medium-chain triglycerides, and milk thistle. We also lack endpoint data to tell us what a desirable level is. I believe, however, it is somewhere around 300 nmol/L.

    Jim--In the first paragraph, I was referring to the small LDL-yielding effects of CETP and triglyceride exchange. Blocking CETP prevents this exchange from occurring.

  • Anonymous

    11/20/2010 7:54:02 PM |

    thanks for the response dr. davis.

  • escee

    11/21/2010 6:16:19 AM |

    What I saw from the study was no real difference after 76 weeks in mortality or cardiovascular events. In fact there were 11 deaths in the anacetrapib group and 8 deaths in the control group.

    I don't find that encouraging, but maybe it was too short term.

  • steve

    11/21/2010 6:13:36 PM |

    thank you Dr Davis for your recommendations.  I have tried Slo-Niacin and had great difficulty tolerating it at 1500/1000 mg doses. Felt much better when not on it.  Have tightened up my diet even more, eliminating fruit and cheese and Greek Yogurt.  Will see what next NMR brings.  Might add Niacin at low dose to existing regime.  My small LDL particle size at 20.6 is type A and small particles not to far off from the 300 you suggest despite the proportion of small LDL to total LDL being larger than optimal

  • Randy

    11/22/2010 3:14:45 PM |

    Dr. Davis - can you comment on an article that Shane Ellison has written entitled "Hidden Truth About Cholesterol-Lowering Drugs"?

    Within the article, Mr. Ellison provides the statement that low cholesterol is a bad thing, not a good thing and people with higher cholesterol are living longer.

    Can you place this in context with regard to small LDL particles?

  • Tyson

    11/23/2010 2:26:21 AM |

    Steve,
    I'm not Dr. Davis, but I also have difficulty with Niacin.  I also have high homocysteine.  These 2 things can go hand in hand.  For me, it's a methylation problem.  I'm an undermethylator, which means I have to supplement with TMG and a few other things.  You should get your Homocysteine checked, and if it is elevated, be very careful with Niacin, since Niacin can make it worse unless you supplement with TMG etc...

  • steve

    11/23/2010 3:30:35 PM |

    thanks Tyson:  Homocysteine level is in normal range,but near the high end, ie 10 vs. 12 being top of the range.  My understanding is that it elevates with age and i am pushing 60.  I also hear that a B complex vitamin might make sense.

    Perhaps Dr. Davis may weigh in on the homocysteine issue with regards to treatment and Niacin use.

  • Daniel A. Clinton, RN, BSN

    11/28/2010 6:10:04 PM |

    Don't get your hopes up for anacetrapib. Despite the researchers best attempts to hide it, the anacetrapib group had higher cardiac mortality, and higher overall mortality. So, do you care that some numbers changed, or that the drug increases the risk of death? I wrote an article on the subject on my blog: http://clintoncpr.blogspot.com/2010/11/anacetrapib-scam-improve-your.html

  • Sifter

    11/28/2010 11:36:04 PM |

    Considering alledged 400% increase in cardiovascular mortality rate....

    http://high-fat-nutrition.blogspot.com/2010/11/anacetrapib-giggle.html

    ...I think I'll pass on this new wonder drug.

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Factory hospitals

Factory hospitals

8. November 2008 William Davis (8)
Twenty years ago, the American farming industry experienced a dilemma: How to grow more soybeans, corn, or wheat from a limited amount of farmland, raise more cattle and hogs in a shorter period of time, fatter and ready for slaughter within months rather than years?













(Image courtesy Wikipedia)

The solution: Synthetically fertilize farmland for greater crop yield; “factory farms” for livestock in which chickens or pigs are crammed into tiny cages that leave no room to turn, cattle packed tightly into manure-filled paddocks. As author Michael Pollan put it in his candid look at American health and eating, The Omnivore’s Dilemma:


“To visit a modern Concentrated Animal Feeding Operation (CAFO) is to enter a world that for all its technological sophistication is still designed on seventeenth-century Cartesian principles: Animals are treated as machines—“production units”—incapable of feeling pain. Since no thinking person can possibly believe this anymore, industrial animal agriculture depends on a suspension of disbelief on the part of the people who operate it and a willingness to avert one’s eyes on the part of everyone else. . .”


Pollan goes on to argue that the cultural distance inserted between the brutal factory farm existence of livestock and your dinner table permits this to continue:


“. . .the life of the pig has moved out of view; when’s the last time you saw a pig in person? Meat comes from the grocery store, where it is cut and packaged to look as little like parts of animals as possible. The disappearance of animals from our lives has opened a space in which there’s no reality check on the sentiment or the brutality . . .”


The same disconnect has occurred in healthcare for the heart. The emotional distance thrust between the hospital-employed primary care physician, the procedure-driven cardiologist, the crammed-into-a-niche electrophysiologist (heart rhythm specialist) or cardiothoracic surgeon whose principal concerns are procedures—with an eye always towards litigation risk—mimics factory farms that now litter the landscape of the Midwest. The hospitals and doctors who deliver the process see us less as human beings and more as the next profit opportunity.

The “factory hospital” has allowed the subjugation of humans into the service of procedural volume, all in the name of fattening revenues. Never mind that people are not (usually) killed outright but subjected to a succession of life-disrupting procedures over many years. But whether livestock in a factory farm or humans in a factory hospital, the net result to the people controlling the process is identical: increased profits.

The system doesn’t grow to meet market demand, but to grow profits. The myth that allows this growth is perpetuated by the participants who stand to gain from that growth.

See hospitals for what they are: businesses. Despite most hospitals retaining "Saint" in their name, there is no longer anything saintly or charitable about these commercial operations. They are ever bit as profit-seeking as GE, Enron, or Mobil.
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Comments (8) -

  • Jenny

    11/9/2008 2:48:00 PM |

    Dr. Davis,

    Have you read the book, Hippocrates' Shadow? You have a lot in common with the physician who wrote it and I think it would be very productive for you to contact him and discuss strategies together.

    I blogged about the book in detail at my Diabetes Update Blog a few days ago.

    We patients can't do much about this, but physicians working together could.

  • Zbigniew

    11/9/2008 8:43:00 PM |

    adequate analogy Smile, but what we get here is a gloomy picture with little hope - while thanks to blogs like yours we may be more lucky than those poor animals.

    So the punchline should be something like "educate, read, b/c if everyone takes care of themselves then everyone will be taken care of"

    best regards,

  • steve

    11/10/2008 2:35:00 PM |

    would be interested in your views of Crestor study, and statins in general: when should they be used, etc?

    thank you

  • Anonymous

    11/11/2008 12:31:00 AM |

    Thanks Jenny, for mentioning the book, Hippocrates'Shadow. This sounds very interesting and I can hardly wait to find a copy.  
    Another great book is "How Doctor's Think, by Jerome Groopman,M.D.
    Dr. Davis, I appreciate this wonderful blog and your excellent advice. You restore some of my lost confidence in the medical profession.

  • puddle

    11/11/2008 3:30:00 AM |

    Thank you, again.  And again.

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