Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Comments (77) -

  • Bill

    9/15/2011 1:13:26 PM |

    But is there any real evidence that small LDL is a *cause* of heart disease? Correlation alone isn't sufficient, of course, and Chris Masterjohn has said that even the correlation largely disappears when traditional "risk factors" such as HDL, LDL, and triglycerides are added to the model.

    I ask in part because I am about to arm wrestle with my primary care doctor about my recent cholesterol panel:

    Total: 382
    HDL: 157
    LDL: 217 (calculated)
    Triglycerides: 39

    He's upset about the LDL, of course, especially since it's progressively risen over time (coinciding with dietary changes pretty compatible with TYP and including quite a bit of sat fat after years as a low-fat vegetarian). Naturally, he wants me to reduce my fat consumption and retest in four months, and I'm sure a statin drug recommendation will follow just as the sunset inevitably follows the sunrise.

    I am thinking of asking for a full lipoprotein panel, with the expectation that it will calm him down by showing 1) much lower real, measured LDL with my rock bottom triglycerides and 2) strong Pattern A LDL with my sky high HDL and low triglycerides.

    But I'm not certain if I can really make a convincing empirical case to him that Pattern A is benign with a high LDL. (I'm also hesitating after hearing Chris Masterjohn say that LDL particle size measurements are hugely dependent on the type of assay used and that as a result it's not clear what, biologically, any given result means until these methodological discrepancies are sorted out.)

  • Peter Silverman

    9/15/2011 2:41:59 PM |

    The article you cite says the number of LDL particles may be more important than the size.  Is that your experience?

  • Howard

    9/15/2011 3:02:31 PM |

    @Bill : Chris Masterjohn also mentioned in a recent podcast that the current measurement technology for LDL particle size is just not sufficiently accurate to be useful.

  • chuck

    9/15/2011 3:48:18 PM |

    what is your feeling on oxidized ldl?

  • chuck

    9/15/2011 3:52:16 PM |

    @howard
    yes, based on the hour to hour, day to day, week to week, and month to month natural fluctuations of lipids in the blood it is difficult to make any real judgements about cholesterol readings without doing multiple panels over a period of time.  the whole medical community seems to be screwed up in this respect.

  • Kathy

    9/15/2011 4:13:20 PM |

    I have no idea what Dr. Davis' response will be, but if you're interested in getting an NMR profile done on your own dime (and if there is a convenient location near you), check out directlabs.com for their September special.  An NMR profile will only set you back $79 (reg $127).  I've been waiting for this "sale" and am getting it done to show my own doctor.  Your health is ultimately in your hands - keep up the good fight!
    Best,
    Kathy

  • edward white

    9/15/2011 5:02:18 PM |

    Dr D,
    I totally agree small LDL is driven by excess carbohydrate intake and postprandial
    triglycerides. However there is a substantial subset of people whose small LDL
    is genetically driven. I believe you are aware of this phenomena.
    Please let these folks know what their options are to address this important issue!
    There can be a good deal of frustration when carbs and triglycerides are addressed but
    with little lowering of small LDL.
    Please help this substantial number of people out by outlining their options...
    Gib

  • Unix-Jedi

    9/15/2011 5:22:13 PM |

    Thanks for that information, Kathy.

  • cancerclasses

    9/15/2011 5:57:26 PM |

    It ain't good,  just ask Wikipedia.   From the Wiki page re 'Chronic endothelial injury hypothesis':
    "Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized.[5] This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.[6]

    Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque[7] Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium.[8] Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis."

  • Bob

    9/15/2011 6:12:21 PM |

    Test reply

  • cancerclasses

    9/15/2011 6:13:54 PM |

    Yes, French cardiologist Guy-Andre Pelouze MD. at the recent Ancestral Health Symposium said in his presentation "Paleodiet and atheroma: A Cardiovascular Surgeon’s Perspective" that:

    1. Native (the reduced form of) LDL cholesterol is NOT atherogenic, only the oxidized form leads to atheroma, atherogenesis & arterial plaque formation.

    2. Without oxidized cholesterol it's very difficult to have arterial plaque formation

    3. Anti-oxidants are ineffective in preventing atheroma.

    4. SDLDL easily enter the subendothelial space because SDLDL are less than 25 nm in diameter and the subendothelial space is 26 nm.

    5. Subendothelial space in humans is very different in humans than other mammals due to the large amount of smooth muscle in the arterial media below the the intima layer.

    And there's much more.  To see a video of Dr. Pelouze's presentation hosted on the Ancestral Health page at Vimeo just google 'vimeo, paleodiet and atheroma', then scroll to video number 33 in the right side box.

  • cancerclasses

    9/15/2011 6:42:38 PM |

    Do you REALLY believe that? We have the ability to measure the distance between the earth and the moon almost down to the millimeter, and certainly down to the centimeter. We have the ability to measure individual atoms with electron and other types of microscopy used in materials engineering and computer chip manufacturing.  Medical, biochemical & physiological textbooks are full of descriptions of the sizes of white and red blood cells, bacteria and viruses, etc. ad infinitum.  Do you REALLY think we lack the ability to measure SDLDL?  Don't be so ready to believe something just because somebody says something about it.  Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion.  

    Furthermore, what's the point of a statement like that?  Should we just give up measuring and trying to understand how SDLDL causes atheroma just because ONE guy says we can't measure them to his degree of satisfaction?  Should we just give up worrying about what we eat, and what we are being sold as foods that are arbitrarily declared to be safe to eat by some anonymous bureaucrat at the FDA?  Should we just ignore the ever increasing incidence rates of cancer, heart disease and atherosclerosis that by all applications of observation and simple logic are known to be entirely due to the modern industrial foods diet in every society and the peoples that subsist on them?  

    I don't think so.  Homey don't play that anymore, at least this one doesn't.

  • cancerclasses

    9/15/2011 6:55:16 PM |

    @Bill,  Google and see this study: 'Detection of low density lipoprotein particle fusion by proton nuclear magnetic resonance spectroscopy'.    
    "Abstract: Recent evidence suggests that fusion of low density lipoprotein (LDL) particles is a key process in the initial accumulation of lipid in the arterial intima. In order to gain a better understanding of this early event in the development of atherosclerosis, it would thus be necessary to characterize the process of LDL fusion in detail. Such studies, however, pose severe methodological difficulties, such as differentiation of particle fusion from aggregation. In this paper we describe the use of novel methodology, based on 1H NMR spectroscopy, to study lipoprotein particle fusion."

  • Don

    9/15/2011 7:24:04 PM |

    Bill,
    You have no worry since your triglycerides are quite low and therefore your LDL particles are of healthy size.  Your correctly calculated LDL is only 161 using the Iranian formula (used if triglycerides low).  See LDL calculator here:
    http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

    And never use statins, just cut carbs.
    Don

  • cancerclasses

    9/15/2011 7:34:54 PM |

    "About 80% of cholesterol is composed of fats and oils (Current Atherosclerosis Reports 2004). The
    majority of an arterial clog, 55%, comes from defective cooking oils, containing mainly damaged omega 6. Most of us unknowingly purchase these oils in the cooking oil section of the supermarket. These are the oils we fry with and the oils added to most packaged foods; both fresh and frozen.

    Here’s another shocker. It’s not the saturated fat —it’s the adulterated omega-6 from food processing that clogs arteries! Contrary to what we have heard for decades, it is not the saturated fat you eat that clogs your arteries! How do we know this? A 1994 Lancet article reported investigating the components of arterial plaques. In an aortic artery clog, they found that there are over ten different compounds in arterial plaque, but NO saturated fat. This means the bacon, eggs, cheese, steak, whipped cream, etc. isn’t the reason for a clogged artery. These natural saturated fats are actually good for you. You need them for body structure.

    With the consumption and transport of defective processed oils, LDL cholesterol acts like a “poison delivery system,” bringing deadly transfats and other ruined oils  into the cells. It is primarily the oxidized (adulterated) omega-6 that clogs the arteries, NOT saturated fat!"  

    For more just google 'Brian Peskin saturated fat' and read the day away to your heart's content.

  • Jack Kronk

    9/15/2011 8:37:50 PM |

    "just because somebody says something about it. Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion. "

    lol. you must not know who CMast is.

  • cancerclasses

    9/15/2011 10:27:09 PM |

    Yeah, I do, and that's why I said that.

  • Dr. William Davis

    9/16/2011 2:40:13 AM |

    Hi, Gib--

    The strategies that reduce small LDL are the same whether it's genetically-driven or acquired. However, when (presumptively) genetically-driven, it's just harder and requires a more meticulous effort.

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern.

  • Dr. William Davis

    9/16/2011 2:42:32 AM |

    Big issue. Note that the real culprit in causing plaque may be glycated oxidized LDL.

  • Dr. William Davis

    9/16/2011 2:43:51 AM |

    Hi, Peter--

    No, I think that is wrong. It might be correct if small LDL is regarded in a dichotomous way, i.e., pattern A vs. pattern B. But, when viewed quantitatively, I believe the real culprit is quantity of small LDL.

  • Dr. William Davis

    9/16/2011 2:46:58 AM |

    No question: The various lipoprotein testing companies need to talk and standardize their definitions. But this does not invalidate the concepts.

    Chris Masterjohn is a very bright guy. But on this I disagree. I believe it is wrong to assume that triglycerides and HDL behave in perfect tandem with small LDL. While they do indeed correlate, they do not correlate perfectly and demonstrate independent behavior depending on postprandial phenomena and genetic factors like apo E and apo C.

  • Joyce

    9/16/2011 5:17:54 PM |

    This has nothing to do with LDL, but I don't know where else to ask this, so I'll dive right in.

    I am reading and enjoying your book Wheat Belly, but don't understand why you lump chia seed in with other non-gluten grains to avoid or minimize. .  In my mind it is closer to flax.  Chia is truly an oil-seed and not a grain according to Dr. Coates, the "father" of chia seed research.  I have used it generously, and feel it aids in weight loss.  Chia seed is high in protein and fiber and low in carbs.  Why are you telling us to avoid or limit it?  I feel it is healthier than flax even.

    Please, can you clarify your stance on chia?  I was very disappointed to read that in your book.  Other than that, I really enjoyed Wheat Belly, having avoided gluten for a few years now.

  • Joyce

    9/16/2011 5:33:17 PM |

    P.S.  According to calorieking.com website, 1 oz. raw chia contains 0 carbs and 1 oz. dried chia contains only 1 gram of useable carb.

  • Adriana

    9/17/2011 10:16:37 AM |

    Not everybody who has good HDL, good TG and eats a low carb paleo diet will have low small particle LDL numbers which is why an NMR LipoProfile is important.  People with gut issues, yeast issues,  H. Pylori or an otherwise compromised liver can have unhealthy LDL despite doing everything right on the diet front.  Getting to the root of these issues is critical to resolving it.

  • Dr. William Davis

    9/17/2011 1:23:49 PM |

    Thanks, Joyce. But I don't remember lumping chia with the bad stuff.

    In fact, as you point out, chia belongs with flaxseed as one of the few truly healthy, low-carb foods.

  • Joyce

    9/17/2011 1:45:31 PM |

    Dr. Davies, on p. 212 of your book, chia is lumped in with other non gluten grains.  Maybe in future editions, the publisher can remove that?

    Although I have been gluten free for years, my husband is finally going gluten free..ALL BECAUSE OF YOUR BOOK!  He has some health issues, so for that I humbly thank you.

    Also, his next Toastmasters speech will be on "Wheat Belly"...how about that!

    Thank you so much for a wonderful book.  Your recipes are awesome.  I look forward to a Wheat Belly cookbook!!!!

  • Linda

    9/17/2011 2:57:40 PM |

    There are so many well read and brilliant posters here that I am going to jump in and ask a question totally off topic. This is not Dr. Davis' area of expertise, so I hope others may help.
    I do believe I am dealing with a bone/heel spur. Too much treadmilling, trying to increase speed, etc. I have done research on the condition and I read that turmeric, taken 2-3 times a day, is helpful. I just recently began taking D3 as well, 5000 IU a day. Will the Vit D3 help as well?
    Any thoughts? No, I am choosing not to visit a doctor for a cortisone shot. I am using NSAIDS for the pain and that works very well.

  • nina

    9/17/2011 4:48:56 PM |

    I've just spotted this post.  Never tried chia and wonder what you thought.  Have your patients reported similar effects?

    Nina

  • steve

    9/17/2011 7:26:34 PM |

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern

    Could you go in to more depth as to what strict carb reduction menas?  Is it no more than 50grams of starchy carbs such as rice or potatoes, or 100Grams?  I am guessing it is individualized, but some range of restricitons with those who have been successful would be helpful.  
    I have always had a low level of Trigs- never higher tnah 75 even on a hi carb diet, and was surprised to find the NMR showing all small particles!  So Dr. Davis is right to say low Trgs not always indicative of having large LDL.  Switched to elimination of most carbs and totally changed the profile.  Only issue that is while i produced lots of particles with carb diet, i also produce lots of LDL particles with carb restriction.  Genetics i guess!  I am an ApoE 3/3, which was a surprise.  
    Thanks for the good work Dr. D.  Have gotten several to buy Wheat Belly.  It will have an impact!

  • Joyce

    9/17/2011 7:30:40 PM |

    Nina, I am not Dr. Davis (wish I had his knowlege!), and I hope he doesn't mind me jumping in here, but I leaned about chia a few years ago when I read a book by Dr. Wayne Coates on the subject.  Chia has definitely helped me lose weight.  It is very filling.  When mixed with fluids, the chia seeds expand, and they really help to fill you up.  I've found all sorts of wonderful chia recipes on the web - from Chia "Tapioca" to beverages, etc.  I mix  it into many foods.  I think it enhances their taste.  I feel the chia seeds help with weight loss because of their appetite suppressant potential.  I hope this helped, and my apology to the good doctor for hogging the thread.

  • PeteKl

    9/17/2011 10:24:07 PM |

    Your post doesn't provide a lot of info, but if I were to guess I would say your problem is more likely related to walking/running incorrectly than nutritional (assuming you are in reasonable physical condition).  The human foot wasn't designed to be encased in the heavily cushioned shoes we typically wear today.   As a result many of us don't know how to walk or run correctly.

    Some of the better shoe stores will video tape you on a treadmill.  Just seeing the tape may be enough for you to realize what you are doing wrong.  If that doesn't help, there are professionals who should be able to figure out what might be happening.  

    Also consider reading "Born to Run" if you haven't already (it's a good read even for non-runners).  It probably won't give you a direct solution, but it may give you some ideas on where to look.  Good luck.

  • Louise

    9/18/2011 2:10:34 AM |

    Dr. Davis,
       I am 56 and have a strong history of heart disease in my family. I have been eating low carb for a couple of years... ( around 60 gms carb per day average..no pasta, no potato, almost no grain)  My most recent lipid panel showed LDL of 140. HDL 81, Triglycerides 43, CRP 0.2. .  I requested a test to show size of LDL. My doctor declined to order this, saying all LDL is bad.  Instead I was sent for a heart scan  ( paid out of pocket) and my calcium score was 0.  
      So now I'm trying to lower my LDL by lowering saturated fat.  Hard to do when you eat low carb. I wonder if I might be one of those Apo E 4 types that you mention, so thought I should try,.
      Here are my questions:
         Can I test my LDL size myself, through a home test? Or should I try to find out if I have Apo E 4?
          Do I really need to lower LDL if my calcium score is 0?
    Louise

  • Bob Goldstein

    9/18/2011 4:02:36 AM |

    For the last year I have eaten zero fruit, zero grains, zero sugar. Have mostly eaten beef, occasionally eggs cooked in butter. Have done two VAP tests the last year. When I started a year ago, trigs were 115, now 142. HDL was 50, now 46. My LDL did show a change of going from pattern A/B to pattern A.
    Any ideas why a diet for a year devoid of fruit, sugar, grains, would show an increase in trigs, and a slight decrease in HDL. If I have Apo E4 would my ldl go from A/B to A.
    I have lost 25 lbs. in the past year. Could this be a reason my numbers seem to be off?
    Thanks,
    Bob

  • Dr. William Davis

    9/18/2011 3:44:29 PM |

    Hi, Bob--

    Yes, blood drawn in the midst of weight loss can be very misleading.

    Transient effects include increased triglycerides, reduced HDL, even much higher blood sugar. Thankfully, it all gets much better once weight plateaus for a couple of months.

  • Dr. William Davis

    9/18/2011 3:47:39 PM |

    Hi, Louise--

    Sad that you have to educate your doctor.

    I find it unacceptable that a nice person engaged in health is refused a simple, helpful test. Tell your doctor goodbye and find one willing to act as your partner and advocate in health, not an obstruction.

    Yes, you can test it yourself through services like PrivateMDLabs.com. My view is to 1) identify how much, if any small LDL there is, then 2) reduce small LDL with diet. If you have only large LDL, you will absolutely need an LDL particle number by NMR or an apoprotein B to know what the REAL value is.

  • Dr. William Davis

    9/18/2011 3:49:52 PM |

    Thanks, Steve.

    There are a number of posts on this blog that detail how to gauge individual carbohydrate sensitivity. The best way is to check 1-hour after-eating blood sugars. Second best: count carb with the cutoff being determined individually. Just go back over the past 6 months and you will find several discussions.

  • Dr. William Davis

    9/18/2011 3:51:17 PM |

    Hi, Joyce--

    Thank you!

    If chia is listed as among undesirable non-gluten grains, that was my error. Remember what Mark Twain said: "Don't read about health, else you might die of a typo."

  • nina

    9/18/2011 5:13:58 PM |

    Thanks for your response Joyce.  

    The part that fascinated me was the idea that chia triggers a drop in blood sugars without a pre-spike.  I can't find anything on the net about that and wondered if other people had similar experiences.

    Nina

  • Bob Goldstein

    9/18/2011 7:08:22 PM |

    Thanks for the reply Dr. Davis. I have a blood test scheduled six months from now, and hopefully I will see better numbers. My LDL shows pattern A so at least I did see one positive change.
    Love your blog. Have learned a lot and it was the reason I gave up grains and sugar. 1 full year, no cheats.

  • Annlee

    9/18/2011 10:41:56 PM |

    Consider also going barefoot as much as possible - around the house, etc. You don't necessarily have to run barefoot (unless you work into it *gradually* and choose to continue it). I've recovered from heel spurs with stretching my achilles, with emphasis on stretching the soleus, and letting my feet bear my weight without any props underneath. For stretches, Anderson & Anderson have a very good book - Stretching - available on amazon.com. You didn't develop the spurs overnight, and they won't clear that quickly, either. Be patient and work with your body.

    You may also wish to consider vitamin K2, very good for ensuring calcium deposition occurs in the correct locations.

  • Kira

    9/19/2011 6:52:43 AM |

    Hi Doctor Davis, I talked to your about a year ago and you were kind enough then to comment on my blood results saying there was nothing to worry about - according to the Iranian formula.  I would greatly appreciate if you looked at my new results, they scared my whole family, I certainly am not going to show to the family physician, and I don't even want to think about changing from paleo style of eating to some kind of low fat cholesterol lowering diet, and taking any drugs/supplements. But may be I have to? I am 36 y.o., 5'4 and weigh 104lb.
    Glucose 85
    VAP TEST:
    Lipids
    LDL Cholesterol 149!
    HDL 130
    VLDL 14
    CHOLESTEROL, Total 293!
    Triglycerides 48
    Non HDL Col (LDL+VLDL) 163!
    apoB100-calc 96
    IDL Cholest 4
    Remnant Lipo. (IDL+VLDL3) 12
    Sub-Class Information:
    HDL-2  35
    HDL-3  95
    VLDL-3  8
    LDL1 Pattern A 3.1
    LDL2 Pattern A 26.0
    LDL3 Pattern B  71.0
    LDL 4 Pattern B  31.4

    The ordinary, non-VAP Lipid panel shows:
    Cholest TOTAL 279 !
    Triglycerides 48
    HDL Cholest 144
    VLDL Cholest Cal 10
    LDL Cholest Calc 125 !

    Also, I can't understand how my vit. D can be so low - 29.0, when I have been sun tanning all summer here in Orange County, California, at peak hours. Is there anything that you know of that may inhibit the vit. D conversion from the sun?
    Again, I greatly appreciate any insight that you can give me on this situation...

  • Louise

    9/19/2011 4:52:38 PM |

    Dr Davis,
      Thank you for your reply.  For now, I found a lab I can go to and get myself tested. Two hours away.. (Oddly, I must leave NY state to get this done due to billing law.). I'm going to do this! Do you agree that my best choice is the NMR?

  • otterotter

    9/19/2011 5:43:51 PM |

    Hi Gib,

    Option 1 will be cutting the saturated fat and cholesterol from the diet in addition to cutting the carbs. I tried eliminating eggs and cheese and my total cholesterol down from 400 to 260. By adding back "one egg a day", it went back to 320 (that's the impact of the dietary cholesterol on me, confirmed twice). I am currrently trying to replacing all saturated fat with mono unsaturated fat (olive+canola), just want to see how big the impact is. I am also going to test coconut oil separately, it is a cholesterol-free plant based medium-chain saturated fat, there is a chance I might respond to it differently.

    Option 2 will be taking Statin drugs. I know it has side effects, but that's better than small dense LDL. Based on Dr Davis's previous response, for apoE, sometimes we have to go to Statin for the rescue. (My doc was pushing statin really hard on me, and I have been resisting that for the last year)

    otter

  • Joyce

    9/19/2011 5:50:45 PM |

    Dr. Davis, you are so funny.  We'll take your book....typos and all!  Now...how about a cookbook to compliment Wheat Belly/  PLEASE????

  • nina

    9/19/2011 7:41:34 PM |

    Sorry I missed the link:

    http://suzanneloomscreativity.blogspot.com/2011/09/lowering-blood-sugar.html

    Nina

  • PeteKl

    9/19/2011 9:24:31 PM |

    Hi Kira,

    Just out of curiosity, could you summarize your "paleo style of eating".  I have a good friend of mine who has similar numbers (low trigs, high HDL, high LDL).  I would describe her diet as "low-carb (no sugar, no grains), low-veggie (under 15%), high meat, high sat-fat (particularly cheese, eggs and coconut)".  Is your diet somewhat similar?  I would be interested to know how the two of you compare.

  • Dr. William Davis

    9/20/2011 12:36:46 PM |

    NMR is my preferred method, since it yields the LDL particle number, what I believe should be the gold standard.

  • Dr. William Davis

    9/20/2011 12:38:12 PM |

    Thanks for asking, Joyce! I've had very preliminary conversations with my editor, but nothing firm yet.

    In the meantime, in addition to the discussion on this blog, see the Wheat Belly Blog, where I will publish recipes one by one.

  • Dr. William Davis

    9/20/2011 12:41:39 PM |

    Hi, Kira--

    You have a surprising dominance of small LDL particles, despite your slender build and lifestyle (LDL 3+4 divided by "real" LDL). This is likely genetically-determined. The means of correcting this is beyond the scope of this blog, unfortunately. You might consider joining the discussion in the Track Your Plaque website.

    The vitamin D issue is common, an impaired or lost ability to activate vit D in the skin. It means doing it orally.

  • Adam

    9/20/2011 6:40:19 PM |

    Dr. Davis. I'm a type 1 diabetic who is on a low carb diet (mostly primal-esque) with only meat and veg. No fruit, no grains, no legumes. I lost 14 kgs in the first three months, then stabalized at around 89 kgs. Granted my fat is going down a wee bit as muscle mass increases (doing the slow burn exercises, plus HIIT training and martial arts). That is the background.

    The reason I'm posting here is confusion about cholesterol. I just got my latest results back from the lab, and they are the same. While my HbA1C is 5.3 (not bad), my cholesterol numbers don't look hot. Tryglicerides are fine (as I've stopped losing weight quickly), but HDL is low at 39, and LDL (doctor forgot to put in particle size check, but it cna't be that good as I'm a diabetic) was 150 on the spot. This was measured, not calculated.

    I take ~7k miligrams (or whatever the measurement is) of fish oil a day. Well, 7k of EHA/DHA, more in total quanity including inert substances. With my exercise, low carb diet, and fish oil supplements, how is it that my HDL are sti

    A fictional tale of medical economics in heart disease

    Dr. Robert Connors is the hospital’s most prized cardiologist.

    Practically a fixture in the cath lab, he generates more revenues for the hospital than any of his colleagues. Last year alone, he performed over 1500 procedures, bringing in $18 million dollars to the cath lab, $27 million to the hospital. Dr. Connors is very good at what he does: 55-years old, he has been involved in high-tech heart care since the “early days,” 25 years ago, when hospital procedures really began to take off.

    Over his career, he has personally performed over 25,000 heart procedures and has built a reputation as a skilled operator of complex coronary procedures. Because of his skills, he enjoys a vigorous flow of referrals for procedures from dozens of primary care physicians. His skill has also earned him referrals from cardiologist colleagues who seek his abilities for difficult cases.

    On any day, Dr. Connors typically schedules up to 12 procedures. His entire day is spent in the cath lab, usually from 7 am until 6 pm. He meets many patients for the first time on the catheterization laboratory table as staff shave their groin, preparing for the procedure. Much of the procedure itself is not even performed by Dr. Connors, but by one or another cardiologists-in-training, a “fellow,” or member of the fellowship the hospital proudly maintains as a clinical teaching institution. Nor will Dr. Connors talk to most patients at the close of the procedure. He leaves that to either the fellow or a nurse. Dr. Connors views himself as a procedural specialist, not someone who has to take care of patients. He gave up seeing patients in his office over 10 years ago.

    Dr. Connors’ procedural enthusiasm gained him the attention of drug and medical device manufacturers. Because Dr. Connors lectures widely and advises colleagues, his comments can dramatically alter perceptions of the value of a technology. He has, on many occasions, catapulted an unpopular device to most-asked-for among colleagues, bringing millions of dollars in revenues to the manufacturer. One particularly lucrative arrangement he made around 10 years ago involved a “closure” device, a $400 single-use plug used to close the access site made during heart catheterizations. By swaying his colleagues at _______ Hospital, 50 orders per day (one per procedure) tallied $20,000 every day, $7.1 million dollars per year for the manufacturer. Although he’d used other devices on the market, the 5,000 shares of stock he was offered encouraged him to issue glowing comments to colleagues on the superiority of this specific brand of closure device. Now over 90% of all catheterizations at _______ Hospital conclude with the device manufactured by the company in which Dr. Connors maintains partial ownership.

    Negative comments, on the other hand, topple other products when Dr. Connors sees fit to pan them. For this reason, device and drug manufacturers run straight to Dr. Connors to gain his good graces as soon as possible after a product is released into the market. Because the competition is just as likely to do the same, it has often come down to a bidding war, the company providing the most lucrative arrangement most likely to win.

    Thus, Dr. Connors proudly boasts of how many times he has flown to Hawaii, Europe, and other exotic locations at industry expense. He also boasts of how, for $100,000 paid to him for a “consulting fee,” he can overturn the choice of products lining hospital shelves. As the hospital’s annual budget for coronary devices will top $84,000,000 this year, device manufacturers regard the sum paid Connors as a profitable investment.

    Despite his lofty status in the hospital, Dr. Connors has long expressed a love-hate relationship with ________ Hospital. While he enjoys his work and has made a more than comfortable income, he has long felt that the hospital administration didn’t truly appreciate his contributions. Five years ago, he therefore demanded that he be made “Director of Research.” After all, he had hired a nurse to help him coordinate enrollment of patients into several device trials brought to him by medical device manufacturers. When he encountered an initial lukewarm response from hospital administrators, he threatened to take his “business” elsewhere to a competing hospital. Hospital administrators gave in. They provided him with the title he wanted, along with $100,000 annual “stipend.”

    Just fiction? Make no bones about it: Cardiac care is business, big business. And there's money to be made, lots of it.


    Copyright 2008 William Davis, MD

    Disease engineering

    Imagine you catch pneumonia.

    You have a fever of 103, you’re coughing up thick, yellow sputum. Breathing is getting difficult. You hobble to the doctor, who then fails to prescribe you antibiotics. You get some kind of explanation about unnecessary exposure to antibiotics to avoid creating resistant organisms, yadda yadda. So you make do with some Tylenol®, cough syrup, and resign yourself to a few lousy days of suffering.

    Five days into your illness, you’ve not shown up for work, you’re having trouble breathing, and you’re getting delirious. An emergency trip to the hospital follows, where a bronchoscopy is performed (an imaging scope threaded down your airway) and organisms recovered for diagnosis. You’re put on a ventilator through a tube in your throat to support your breathing and treated with intravenous antibiotics. Delayed treatment permits infection to escape into the fluid around your lungs, creating an “empyema,” an extension of the infection that requires insertion of a tube into your chest through an incision to drain the infection. You require feeding through a tube in your nose, since the ventilator prevents you from eating through your mouth. After 10 days, several healing incisions, and a hospital bill totaling $75,000, you’re discharged only to be face eights weeks of rehabilitation because of the extreme toll your illness extracted. Your doctor also advises you that, given the damage incurred to your lungs and airways, you will be prone to more lung infections in the future, and similar situations could recur whenever a cold or virus comes long.

    A disease treatable by taking a 10-day, $20 course of oral antibiotics at home was converted into a lengthy hospital stay that generated extravagant professional fees, testing, and costly supportive care. You’ve lost several weeks of income. You’re weak and demoralized, frightened that the next flu or virus could mean another trip to the hospital. You are susceptible to repeated bouts of such episodes in future.

    Such a scenario would be unimaginable with a common infection like pneumonia, or it would be grounds for filing a malpractice lawsuit. But, as horrific as it sounds in another sphere of health care, it is, in effect, analogous to how heart disease is managed in current medical practice.

    First, you’re permitted to develop the condition. It may require years of ignoring telltale signs, it may require your unwitting participation in unhealthy lifestyle practices, like low-fat diets, "eat more whole grains," and "know your numbers."

    It then eventuates in some catastrophe like heart attack or similar unstable heart situation, at which point you no longer have a choice but to submit to major heart procedures. That’s when you receive your heart catheterization, coronary stents, bypass, defibrillators, etc.

    Of course, none of these procedural treatments cures the disease, no more than a Band Aid® heals the gash in your leg. The conditions that were present that created heart disease continue, allowing a progressive disease to worsen. At some point, you will need to return to the hospital for yet more procedures when trouble recurs, which it inevitably does.

    A coronary bypass operation costs, on average $67,823. That includes the cost for the heart catheterization performed by a cardiologist to provide the surgical roadmap of your coronary arteries, the surgeon’s fees, the hospital charges. If there are any complications of your procedure, then your hospital bill may total a substantially higher figure.

    $67,823 is just the upfront financial pay-off. Over the long run, your life is actually worth far more to the cardiovascular health care system because no heart procedure yields a permanent fix. In fact, repeated reliance on the system is the rule.

    In fact, over 90% of people who enter the American cardiovascular health care system do so through a revolving door of multiple procedures over several years. It is truly a rare person, for instance, who undergoes a coronary bypass operation, never to be seen again the wards of the hospital because he remains healthy and free of catastrophe. A much more familiar scenario is the man or woman who undergoes two or three heart catheterizations, receives 3,4, or 6 stents, followed a few years later by a heart bypass, pacemaker, defibrillator, as well as the tests performed for catastrophe management, such as nuclear stress test, echocardiogram, laboratory blood analysis, and consultation with several specialists. The total revenue opportunity is many-fold higher than the initial 60-some thousand dollars, but instead totals hundreds of thousands of dollars per person.

    A heart attack alone is a $100,000 revenue opportunity (Agency for Healthcare Research and Quality, 2004).

    Of all coronary bypass procedures performed, 25% are “re-do’s”, or bypasses in people who’ve had a previous one, two, or three bypass procedures.

    Perhaps it's excessively cynical to label it "disease engineering." But, whether from benign neglect or purposeful failure to diagnose, the fact remains: Heart disease is, all too often by the standard path, undiagnosed and neglected for years until the procedural payoff strikes.


    Copyright 2008 William Davis, MD

    Free checking, auto shows, low-cost hotel rooms, and bypass surgery

    Of the three major highways that lace the city of Milwaukee, there are at least five, and sometimes as many as ten, billboards that prominently feature one hospital heart program or another.

    The passing of former First Lady, Ladybird Johnson in July, 2007, reminds us that, just 30 years ago, billboards were a far more common feature (many called them eyesores), proliferating like a dense forest of trees competing for a sliver of sunlight. Ladybird Johnson played a pivotal role in helping to dramatically reduce the number of billboards permissible on the nation’s highways. Of the relative few that remain today, a premium must be paid to post an advertisement. It costs several thousands dollars every month to maintain these highway commercials. But it’s not just an expense; it’s an investment.

    The tens of thousands of eyes that view these billboards every day are potential customers, insured Milwaukeeans who carry health insurance and represent a major heart procedure just waiting to happen. They “need” to be directed to the right place. The billboards don’t feature health and wellness, heart disease prevention, or nutritional advice. They feature surgeons proudly wearing scrubs and masks, nurses, and declarations of the advantages of each hospital program. In effect, they invite you to have your heart attack, heart catheterization, bypass surgery, or other major heart procedure at their hospital. High-tech, high-ticket hospital heart care has become the subject of mainstream marketing, the stuff of flyers, brochures, and billboards.

    The excesses of “big heart disease” have created a system that makes procedural heart disease “repair” far more profitable than heart disease prevention. Unfortunately, “repair” has disastrous financial, physical, and emotional consequences for everyone save the “repairman.”

    While great good has been achieved by the American health care system, this gargantuan and inefficient system has also cultivated a culture of excess that has made many of its participants—physicians, hospitals, drug and device manufacturers—rich. And at our expense.

    This approach was, to a degree, justifiable at a time when nothing better was available. But that's no longer true.


    Copyright 2008 William Davis, MD

    No-flush niacin kills

    Gwen was miserable and defeated.

    No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor).

    No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small.

    Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

    I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events.

    Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about.

    When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended.

    What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed.

    So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague.

    No-flush niacin does not work. Period.


    Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin.


    Copyright 2008 William Davis, MD

    Breakfast comments

    I received some wonderful comments to the What's for breakfast blog post.

    Even though comments are viewable by clicking on them, I wanted to be sure these were readily visible, since they were so helpful and augmented the few suggestions I made. I'm impressed with the variety of foods people are willing to introduce into breakfast, particularly foods not traditionally thought to be part of standard American breakfast choices.




    I normally eat a handful of almonds, some raw cashews, and occasionally an orange for breakfast. I used to eat cheese with breakfast also, but found once I began eating cheese it was hard for me to stop at one or two pieces.

    Anonymous



    My favorite breakfast is often left over Thai curry. I omit the rice. I also like making a thai omelet which is simply 2 eggs and some fish sauce and water and serving it with Sirachi sauce or Thai peanut sauce. It is street vendor food in Thailand I hear. Here's a recipe.

    I find left over dinners are quite wonderful for breakfast. You just have to get past this notion that you have to eat certain foods at certain times in the day. Where'd that idea come from anyway?


    Zute



    I’ve tried eating oatmeal throughout my life, really wanting to like it. Until now the mere taste or smell of it made my stomach queasy. The key for me was toasting the oatmeal. Here’s what I generally do:

    For Steel-cut oatmeal with the taste and texture of rice pudding-

    In a frypan:
    Toss 1 TBS of butter or so into a hot pan.
    Add 1 cup of steel-cut oatmeal until toasted.
    --few minutes
    In a saucepan:
    Boil 2-1/2 cups water
    Add 1 cinnamon stick (or equivalent)
    Add toasted Steel-cut oatmeal and cook for 15-20 minutes or so

    Add 1-1/2 cups of low-fat milk, yogurt, or some combination, etc…
    -Optional- Wisk an egg yolk into the milk.
    -Optional- Add ¼ tsp salt.
    -Optional- 2 TBS honey or Brown sugar. I use one 1 TBS of each.
    Add some lemon or orange zest

    Return to a boil for 10-15 minutes and then chill before eating. The oatmeal will congeal, resembling rice pudding.
    Sprinkle more cinnamon/sugar on top
    Add what you like: raisins, nuts, etc...

    Use the cinnamon stick if you can, it really makes the difference. I’m constantly refining this recipe.


    Anonymous



    Once I decided to give up my (former) love affair with breakfast cereals, I was in a quandary about what to do for breakfast. I don't have much time in the morning to get creative and don't have the inclination at that time of the day to do so either.

    I've settled on a routine of 2 hard-boiled (organic free-range) eggs (I boil them up a week in advance and leave them, shells-on, in the fridge), and a home-made protein-berry smoothie (frozen organic unsweetened berries, water-based).

    This 8 am combo is easy, fast and tasty (I vary the berries and sometimes add natural flavour extracts for variety). It keeps my blood sugar flat and me full until my 1pm lunchtime. And I don't miss the cereals one bit!


    Anonymous



    I met an out-of-town friend for breakfast the other morning at a French-style bakery cafe. I ordered the goat cheese and herb omelet, but said I didn't want the potatoes or bread with it. They offered extra fruit or a salad instead. I chose the salad, with olive oil and vinegar. My friend wondered how I could eat a salad so early. Why not?

    At home I usually eat 2 or 3 eggs over easy cooked in butter for breakfast most mornings and I am comfortably hungry for lunch about 3-4 hours later. But after my nicely filling cheese omelet and generous romaine salad (with a tiny bit of fruit - I ate the berries/melon and left the super-sweet pineapple), I wasn't hungry again until very late in the afternoon so had a small snack (cheese and half an apple) to hold me off and ate my next meal at dinner time. And it was a slow-developing comfortable hunger, not the powerful, "gotta eat something, anything" hunger that follows carb-heavy food.

    Breakfast food, indeed!


    Anna



    You are absolutely right - breakfast is the most difficult meal to change. When I gave up wheat, I started using brown rice or potatoes mixed with anything interesting - nuts or meat or veges. I have now learned that these carbs make my blood glucose skyrocket. I have dropped the rice and potatoes and my BG has dropped nicely.

    My favorite breakfast is sauteed veggies with some leftover meat or even an omelette. Soups are great in the AM. Nuts are for the days I am in a hurry.

    Would be a little easier if I were not dairy intolerant.


    Anne



    Here in South India,it is 'Idli' - steam-cooked Lentil-rice (predominantly lentil) droppings, and 'Dosa' - lentil-rice pancakes. We have altered it a bit by increasing lentil ratio and dropping the rice to a minimum. Tastes good and fills you nice, for 4-5 hours.

    Neelesh



    I have two or three eggs, usually scrambled, but sunny-side-up and over-easy get thrown in for variety. I cook them using butter made from grass-fed cows. I also make my scrambled eggs using whipping cream instead of the more typical water or milk. I'll put a spoonful of fresh-made salsa over the top for some zing, some sliced cheese on the side and a cup of whole, organic milk to drink.

    I'm completely sold on the "high-fat, moderate-protein, low-carb" diet and especially the admonition to start the day with a strong breakfast. My overall energy levels are fantastic, running performance is as good as high-school, and my belly hasn't looked this tight in decades.


    Ross

    What's for breakfast?

    Breakfast, for some reason, seems to be the toughest meal of the day for many people.

    I think it's because the quest for sweet has dominated the American breakfast for so long, with its half-century legacy of cartoon character-festooned breakfast cereals; baked flour products like pancakes, waffles, and English muffins; more recently, "healthy" alternatives like bran muffins and oat waffles.

    This breakfast lifestyle has also contributed to the obesity and diabetes ("diabesity") epidemic. Breakfasts of wheat- or corn-based cereals, even those labeled "heart healthy," fruit, and whole grain breads are guaranteed paths to low HDL cholesterol, high triglycerides, flagrant small LDL, increased inflammatory responses, high blood pressure, and higher blood sugar. Such foods also make you tired, make your abdominal fat grow (wheat belly), and increase appetite so that you want more.

    So what can you eat for breakfast that doesn't provoke these patterns?

    I will never pretend to be terribly clever in creating meal menus, but I can tell you what has worked for me and many of my patients. Be warned: It may require you to suspend your previous notions of what "should" be included in a list of breakfast foods.

    Here are some examples that you may find helpful:

    --Raw nuts--one or several handfuls of raw almonds, walnuts, pecans, pistachios
    --Cheeses--the real, traditional sorts like gouda, goat, Swiss, edam, etc. (not Velveeta, Cheez Whiz, etc.)
    --Eggs, Egg Beaters--and "spice" them up with sun-dried tomatoes, salsa, olives, tapenades, olive oil, onions, green peppers, etc.
    --Yogurt (real, of course), cottage cheese
    --Ground flaxseed, oat bran--as hot cereals or added to yogurt, cottage, or other foods. Esp. helpful for reducing both total LDL and the proportion of small LDL.
    --Oatmeal--slow-cooked, not the instant nonsense.
    --Soups--great for winter.
    --Dinner foods--chicken, beef, fish, green beans, asparagus, tomatoes, etc., most easily added by saving left-overs from dinner. You'll be surprised how filling dinner foods eaten at breakfast can be.

    It's really not that tough. It just means selecting from an entirely different list of foods than you might be accustomed to.


    Copyright 2008 William Davis, MD

    The first lawsuit?


    The closing arguments in actor John Ritter's wrongful death lawsuit are over and the two doctors charged with negligence cleared, five years after his death from a dissection (tear of the inner lining) of the thoracic aorta. The family sought $67 million in damages, claiming that the aortic dissection was misdiagnosed as a heart attack and that the enlarged aorta should have been reported to Mr. Ritter two years earlier during a full body scan.

    The AP story can be viewed at http://ap.google.com/article/ALeqM5gmv6HnJJPBee2gWgEYResT5m6YkAD8VDF9CO0


    Well, perhaps this is the start of a trend. Up until now, it has been commonplace for doctors to ignore many of the important findings on heart scans, full body scans, and similar direct-to-the-public imaging services. For instance, similar to John Ritter's case, enlarged thoracic aortas are commonly ignored. I'd even say that as a rule they are ignored. I have seen many patients in consultation who have had large aortas identified on heart scans, yet nothing--not a thing--was done about it. While the doctors escaped a lawsuit this time, it might not happen a second time.

    I truly hope that Mr. Ritter's unfortunate experience and the consequent lawsuit do not trigger the usual defensive medicine response of resorting to major procedural "solutions."

    A better response would be to 1) identify the problem--enlarged aorta in this case, 2) identify the causes, then 3) correct the causes. It does not necessarily mean that a major procedure like replacing the aorta (a horrendous surgery, by the way) needs to be pursued each and every time.

    It is possible that Mr. Ritter's lawsuit is just the first. Over the next several years, it could trigger an avalanche of lawsuits for all the neglected findings on tests like heart scans, body scans, and other imaging methods that are gaining expanded direct-to-consumer access.


    Images courtesy Wikipedia.

    The origins of heart catheterization: Part II

    On the afternoon of October 30th, 1958, nearly 30 years after Werner Forssmann’s fumbling attempts, Dr. Mason Sones, a 5 foot 5 inch, plain-talking, cuss-every-few-words, cigarette-wielding radiologist at the Cleveland Clinic, was performing a routine angiogram of a patient’s aorta (the large vessel emerging from the heart) in a dark basement laboratory. (In Sones’ day, imaging methods remained primitive, disease diagnosis relying more than anything else on the physician’s powers of observation and crude diagnostic procedures. Abdominal pain was assessed with exploratory laparotomy, headaches with air injected into the brain and nervous system (“pneumoencephalography”), an excruciatingly painful ordeal. Being able to track the course of x-ray dye injected into specific internal organs, whether liver, biliary tree, aorta, lungs, or coronary arteries, represented a huge advance in diagnostic tools for human disease.)

    In 1958, no one had yet injected dye directly into the coronary artery of a living human.


    Just as the dye injector was triggered, Dr. Sones’ eyes widened in horror when the black and white monitor showed that the catheter had inadvertently jumped into the right coronary artery. The injection pump, already triggered to release its load, proceeded to pump 30 cc of X-ray dye straight into the artery. (Modern techniques usually require only 5–10 cc of dye.) Dr. Sones recounts the incident:

    “It was late in the day and we were tired. I hit the switch to rev up the x-ray generator so I could see. As the picture came on, I could see that the damn catheter was in the guy’s right coronary artery. And there I was, down in the hole [a recess to shield him from radiation]. I yelled, “Pull it out! Pull it out!”*? By that time, about 30 cc of the dye had gone into the coronary artery. I climbed out of the hole and I grabbed a knife. I thought that his heart would fibrillate and I would have to open his chest and shock his heart. [In Sones’ day, modern CPR hadn’t yet been developed as a method of resuscitation.] But he didn’t fibrillate—his heart stopped. I demanded he cough. He coughed three times and his heart began to beat again. I knew at once that if the heart could tolerate 30 cc of dye, we would be able to safely inject small amounts directly into the coronary artery. I knew that night that we would have a tool to define the anatomic nature of coronary disease.”


    *An observer, Dr. Julio Sosa, reported that Dr. Sones, in his shock, also blurted, “We’ve killed him!” After all, conventional wisdom of that era, based on observations from dye injections into the coronary arteries of dogs, was that injecting x-ray dye into human coronary arteries would result in immediate death from the electrical imbalance provoked in heart muscle momentarily deprived of oxygen-carrying blood.

    Thus it was established that it was indeed possible to directly inject x-ray dye into human coronary arteries and reveal its internal contours. That’s not to say that the x-ray dyes of 1958 were innocuous. Far from it. In addition to briefly interrupting heart rhythm, as happened with Sones’ first accidental attempt, the dyes used then typically caused dizziness and the sudden urge to vomit. During the first 30 years of direct coronary catheterizations, it was common for hospital staff to run to the patient’s side, bucket in hand to catch the inevitable vomit, once the heart was jump-started by coughing.

    Not surprisingly, Dr. Sones’ discovery set off both an avalanche of criticism and bold predictions of how the new technique might change the course of diagnosis in heart disease.

    Over the subsequent weeks and months, Dr. Sones proceeded to purposefully insert catheters into coronary arteries and create angiograms that revealed the extent of coronary atherosclerosis. He learned how to fashion new catheter shapes to facilitate access to the arteries. Sones developed an impressive experience in the new technique. For the first time, clear images of the coronary arteries were routinely obtainable for the confident diagnosis of coronary atherosclerosis before death. Dr. Sones became an unlikely celebrity in Cleveland, entertaining physicians from around the world eager to learn about his methods, politicians and celebrities, even Middle Eastern nobility complete with bodyguards and food testers.

    Dr. Sones continued to work in Cleveland, furthering the techniques of heart catheterization after his fortuitous error. He died of lung cancer in 1985, 17 years after his discovery.

    Thus was born the modern age of heart catheterization.

    Today, over 10,000 heart procedures are performed in the U.S. every day, 365 days a year, the vast majority of which involve heart catheterization or begin with a heart catheterization. Dr. Sones' fortuitous blunder was followed by 30 years of productive refinement and development before the blatant excesses of this technique really began to be exploited.


    Copyright 2008 William Davis, MD

    The origins of heart catheterization: Part I

    The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

    The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

    Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.

    One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.



    Thus, the very first catheterization of the heart was performed.



    An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

    Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

    Strange, but true.


    Copyright 2008 William Davis, MD