Watch your groin

9. March 2007 William Davis (0)
The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.
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It's the score, stupid

It's the score, stupid

14. November 2009 William Davis (4)
Sal has had 3 heart scans. (He was not on the Track Your Plaque program.) His scores:

March, 2006: 439

April, 2007: 573

October, 2009: 799

Presented with the 39% increase from April, 2007 to October, 2009, Sal's doctor responded, "I don't understand. Your LDL cholesterol is fine."

This is the sort of drug-driven, cholesterol-minded thinking that characterizes 90% of primary care and cardiologists' practices: "Cholesterol is fine; therefore, you must be fine, too."

No. Absolutely not.

The data are clear: Heart scan scores that continue to increase at this rate predict high risk for cardiovascular events. Unfortunately, when my colleagues hear this, they respond by scheduling a heart catheterization to prevent heart attack--a practice that has never been shown to be effective and, in my view, constitutes malpractice (i.e., performing heart procedures in people with no symptoms and with either no stress test or a normal stress test).

It's the score, stupid! It's not the LDL cholesterol. Pay attention to the increasing heart scan score and you will know that the disease is progressing at an alarming rate. Accepting this fact will set you and your doctor on the track to ask "Why?"

That's when you start to uncover all the dozens of other reasons that plaque can grow that have nothing to do with LDL cholesterol or statin drugs.
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Comments (4) -

  • Dexter

    11/15/2009 5:43:29 PM |

    Even more evidence that CVD confusion reigns supreme among PCPs.

    http://www.theheart.org/article/1020935.do

  • Roger

    11/15/2009 5:52:16 PM |

    Dr. Davis,

    In June you kindly profiled my "near-miss" CT angiogram, where I had to take charge and make sure I was getting only a CT calcium score scan.

    The good news was that my score was a zero.  I can't really explain that; while I was a vegetarian for many years, I also ate too many refined carbs and until recently was carrying a few too many pounds. There is heart disease in my family.  I am 54 years old.

    Is it genes, luck, or inadvertantly prudent lifestyle?   How often should folks with low scores be re-tested?  I know you probably cover this at TYP but I'm sure the blog readers would also find it informative.  Thanks again for reporting my story.

    Roger

  • Dr. William Davis

    11/15/2009 11:31:13 PM |

    Hi, Roger--

    Genes enter into the equation in a big way. Lifestyle is important, but it is not everything.

    For people starting with a score of zero, I generally suggest waiting 3-5 years before thinking about another scan.

  • Jenny Light

    11/16/2009 5:00:14 PM |

    I'll second the motion about catherizations being malpractice!

    My mom died three years ago in a cath lab!  After having chest pains after a chemical stress test, she was hospitalized overnight and the next day had a catherization with two stents implanted.  

    Something went wrong during the procedure, and an artery was torn. She became unconscious, she stopped breathing, and they were unable to insert a breathing tube.  They did an emergency tracheotomy but it was too late.  No cardiac surgeon was in the facility at the time.

    The cardiologists explination to us was that "she had very small arteries".

    I would think it would be reasonable for a patient to request that a cardiac surgeon be "in the house" during this procedure.

    My dad about hit the roof when he saw the cause of death listed on her death certificate as "myocardial infraction". He requested that the coroner check the circumstances, after which he changed the cause to "cardio-pulmenary arrest due to long term heart disease".  Sorry, but it should have read: "Due to complications during catherization procedure".  

    Not a benign procedure folks!  Ask whether drugs can perhaps be used in lieu of this invasive (and very lucritive for the hospital) action.

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How old are you?

How old are you?

17. October 2009 William Davis (21)
George walks into my office. I ask him his age.

"I'm 21 years old," he declares.

Yet I look at George. He's got gray thinning hair, his posture is slumped forward rather than erect, the flesh on his upper arms hangs loosely, he's got wrinkles on his hands and face, brown spots on the back of his hands and arms. He looks more like 70 years old to me. "I don't think you're 21 years old. I think you're 70."

"Prove it," he says.

Okay. What now? Minus any formal identification like a driver's license, how do I prove that George is really 70-something and not 20-something? Not an easy thing, when you think about it. If George were a tree, I'd cut him down and count his rings. Is there such a phenomenon in humans?

This is actually a fascinating area of research, looking for reliable biomarkers of aging.

Among the most quantitative markers of aging is telomere length. Telomeres were once dismissed as nonsense sequences in DNA. However, more recent thought among geneticists is that telomeres shorten with aging and provide the body's cells a timeline of aging. This way, George's cells act like they are 70, not 13, and don't start producing gobs of growth hormone and testosterone in preparation for puberty.

What can slow or stall the shortening of telomere length? There are two I'm aware of:

1) Caloric deprivation--i.e., taking in fewer calories. This was among the theories explored by Dr. Roy Walford during his Biosphere2 experience, based on his work in mice that showed that caloric deprivation nearly doubled lifespan.

2) Vitamin D--Richards et al (2007) found that, the higher the vitamin D, the longer the telomere length. The highest vitamin D levels conferred a 5-year effective difference in telomere length.

So, if I could look inside George's cells and count his telomeres, I could judge with confidence whether he was 21 or 70. Or, he could take vitamin D sufficient to increase blood levels to a healthy range and be more like 65.
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Comments (21) -

  • Ellen

    10/17/2009 11:20:26 AM |

    "gobs"


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

  • LeonRover

    10/17/2009 9:44:35 PM |

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

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

    Y'all have a good day, now.

  • Anonymous

    10/17/2009 11:22:20 PM |

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

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

    Ellie

  • Telephone Triage

    10/18/2009 7:57:18 AM |

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

  • Tim

    10/18/2009 9:26:05 AM |

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

  • Peter

    10/18/2009 2:19:57 PM |

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

  • Peter

    10/18/2009 2:27:49 PM |

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

  • Dr. B G

    10/18/2009 6:41:26 PM |

    Very cool post, Dr. D!!!

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

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

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

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

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

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

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

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

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

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

    -G

  • Dr. B G

    10/18/2009 6:41:26 PM |

    Very cool post, Dr. D!!!

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

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

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

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

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

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

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

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

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

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

    -G

  • Matthew

    10/19/2009 12:54:33 AM |

    Dr. Davis,

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

  • David Throop

    10/19/2009 3:07:30 PM |

    Doc Davis,

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

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

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

  • Michelle

    10/19/2009 7:54:03 PM |

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

    Michelle

  • Dr. William Davis

    10/19/2009 9:58:42 PM |

    Hi, Matthew--

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

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

  • Dr. William Davis

    10/19/2009 10:00:02 PM |

    Hi, G--

    As always, you are full of unique observations.


    Hi, Ellen--

    Perhaps I should have said "oodles."

  • rezzrovv

    10/20/2009 4:21:27 PM |

    Dr. Davis,

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

    Scott Pierce

  • Anonymous

    10/22/2009 5:19:03 AM |

    Hi Dr. Davis,

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

    Thanks,

    David

  • Stan (Heretic)

    10/24/2009 5:06:47 PM |

    Hi Dr. B G,

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

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

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

  • Dr. B G

    10/26/2009 4:44:49 PM |

    Hi Stan,

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

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

    I believe so.

    -G

  • Dr. B G

    10/26/2009 4:44:49 PM |

    Hi Stan,

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

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

    I believe so.

    -G

  • buy jeans

    11/3/2010 2:24:30 PM |

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

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A curious case of regression

A curious case of regression

25. November 2006 William Davis (0)
Randi came to me at age 43. Before I'd met her, she'd undergone two heart scans about one year apart. The initial score was 57--not terribly high, but very high for a 41-year old, pre-menopausal female. Recall that rarely do women have any heart scan score above zero before age 50. Randi's 2nd scan had yielded a score of 72, a 27% increase.

Randi even had her lipoproteins assessed and she had the dreaded Lp(a). So when I met her, we discussed the possible choices in Lp(a) treatment: niacin and estrogens as primary treatment, along with LDL reduction to rock-bottom numbers, along with adjunctive DHEA, almonds, ground flaxseed, and fish oil. Sandi was okay with the adjunctive treatments and was already slender and active (BMI <25), and did not show Lp(a)'s evil partner, small LDL. But Randi had no interest in estrogens, even bio-identical preparations, because of the usual uncertainties associated with estrogen replacement. She also proved to be one of the people truly intolerant to anything but the most minute dose of niacin, experiencing prolonged flushing and abdominal cramps with any dose >250 mg.

Randi even attempted a trial of the Mathias Rath concoction of high-dose vitamin C, lysine, and proline as treatment for Lp(a), but we saw no effect on Lp(a).

Unfortunately, this left Randi's Lp(a) essentially uncorrected. Another scan one year later: 90, another 25% increase. 18 months after that, another scan: 120, a 30% increase.

Now 47-years old, Randi had resigned herself to not being able to control her plaque. We'd run out of options. At that point, I'd started to have everyone's vitamin D blood level assessed and then replaced with vitamin D. I did this with Randi, too.

A year after her last scan, she underwent another. The score: 92, a 23% reduction--substantial reversal following a course of unrelenting progression.

Randi and I, of course, both rejoiced with this unexpected success. But it raised some interesting questions: How important is Lp(a) when vitamin D is normalized and small LDL is not a part of the picture? How consistent with regression be with this strategy over time? Would normalization of vitamin D have stopped plaque from becoming established in the first place?

I hope these issues will clarify over time. For now, I'm thrilled with Randi's success. She remains on her present, "incomplete", though successful program.

Note: I would not ordinarily advise a young woman to undergo serial heart scanning with this frequency. Randi had unusual access to a scan center through a relationship with the staff. I am nonetheless grateful for the lessons her experience have taught us.
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