'Doc' Describes Me As A 'Dead Man Walking' Because Of My Elevated LDL Cholesterol
One of the risks that I willingly take blogging about health as someone who has not been trained in either medicine or nutrition is the fact that there are a whole lot of people who are much more intelligent than I am about the subjects I write about. It's just a fact of life that I've lived with since day one of my blog more than three years ago. And it doesn't bother me a bit that I don't have all the answers.
The purpose of my blog is for me to share about my experiences livin' la vida low-carb and to hopefully provide some interesting topics for discussion that will enable my readers as well as myself the chance to learn something about their own health that they probably didn't know before. One thing I've found since I started blogging in the health arena is that even the doctors and medical researchers don't always know as much as we think they do. There's a reason they call it "practicing" medicine.
With that said, I recently received a rather challenging e-mail from someone purporting to be a "Doc" according to their e-mail address who wanted to take me to task over the assertions I made in this blog post about my latest cholesterol numbers and specifically the particle size of my LDL as well as my hard-hitting column about the death of the late NBC "Meet The Press" anchorman Tim Russert. It seems the good "Doc" took great exception to my belief that the HDL/triglyceride ratio is a better indicator of heart disease risk than LDL or total cholesterol and that having large LDL particle size is protective against a cardiovascular event.
In a very condescending tone in his e-mail, "Doc" proceeded to berate my gross ignorance of some rather "basic" health concepts that I apparently haven't fully grasped yet (get a load of this guy!):
I nearly fell off my chair reading your well-meaning but very erroneous blog on Tim Russert.
If larger fluffy, buffy LDLs are protective, why is it that people with the highest risk of atherosclerosis and premature death (i.e. familial hypercholesterolemia) have 100% fluffy, buffy, LDLs?? Sure does not protect them! You with an LDL-C greater than 200 likely have large LDLs and are a dead man walking.
If low HDL-C is always bad, why are their several genetic conditions associated with very low HDL-C and longevity? Check out JAMA. 2008;299(21):2524-2532
Why have there been numerous published articles in the last few years describing many patients with myocardial infarctions who have HDL-C > 90 mg/dL?
If low LDL-C is so dangerous, why do people with hypobetalipoproteinemia who go through life with LDL-C between 5 and 40 all have longevity with no ill effects of such low cholesterol levels?
Russert's Lipids: TC = 105 LDL-C = 68 HDL-C = 37
Of course that is impossible: TC = LDL-C + HDL-C + VLDL-C
VLDL-C is derived by dividing TG by 5 thus VLDFL-C = TG/5
Thus using your numbers TG would be zero which is impossible. Of course if you knew anything about lipids, your blog would not contain so many basic errors.
Last bit of advice--Look up apolipoprotein B or LDL-P. Read the newest guidelines: A consensus statement from the ADA and ACC on Lipoprotein Management in Patients with Cardiometabolic Risk (like Russert). They were published in April in Diabetes Care and the Journal of the American College of Cardiology.
Had anyone measured LDL-P on Russert and then treated it aggressively, Russert would still be here. Of course since statins rarely normalize LDL-P, Russert needed additional medication beyond his statin to achieve apoB goal.
Hate to further blow away your statements, but if you read the new ADA/ACC statement you will see that data from three major trials (Framingham, MESA and EPIC Norfolk) have shown that LDL size is no longer considered an independent risk factor for CHD. Only thing that matters is apoB or LDL-P.
Happy reading and please correct your statements on the web site.
Well, I guess he told me, didn't he? It really depends on what research studies you are looking at and he pointed to a few that certainly made sense to him. As I stated before, I'm no expert when it comes to knowing anything and everything about the subjects I write about. I simply share what I do know and have seen applied in real life situations and let those results speak for themselves.
It's a bit presumptuous of this guy to call me a "dead man walking" because of my high "fluffy, buffy LDL" cholesterol. Further belittling my intelligence by attempting to point out my "errors" was also quite unbecoming of someone who alleges to be a professional physician whose goal is to help educate patients and make them healthy. I wouldn't want this fella being my doctor!
Although I didn't have the answers to his remarks, I knew someone who could provide an educated and reasoned response to "Doc." He's a real doctor and avid researcher on low-carb diets--Dr. Eric Westman. The following is Dr. Westman's comments back to "Doc" asking for clarification and presenting some counter-evidence rebutting the original claims made in his e-mail to me:
Thank you for forwarding this email.
1. The definition of "cardiometabolic risk" is changing, and its relationship to cardiovascular disease is imperfect. In spite of this, many medical authorities want you to do what they recommend. There are many exceptions to the recommendations, and I believe the authorities will acknowledge this readily.
2. Please teach me, "Doc." You wrote that people with "familial hypercholesterolemia have 100% fluffy, buffy, LDLs." Can you provide a reference for this statement (even case studies are fine)? Here is a recent article and it suggests otherwise...but the abstract doesn't really give enough information until I can read the full study. J Pediatr. 2008 Jun;152(6):873-8. Epub 2008 Feb 8
3. You wrote: "If low HDL-C is always bad, why are their several genetic conditions associated with very low HDL-C and longevity?"
I think that this just points out again how imperfect these markers are.
4. You wrote: "LDL size is no longer considered an independent risk factor for CHD. Only thing that matters is apoB or LDL-P."
"Doc" let me just take a moment to explain what "independent risk factor" means statistically--it is a common source of confusion. "Independent risk factor" means that, after accounting for some information, the addition of a new factor (variable) adds no more information (the association is no longer statistically significant).
My understanding is that LDL size and LDL-P are highly intercorrelated ("track together"), so that after accounting for one, the other is no longer statistically significant in its association with cardiovascular disease. It does NOT mean that LDL size is not important--it just means that you get no more additional information about the presence of cardiovascular disease from knowing LDL size when you already know LDL-P.
I look forward to learning more from you. Thanks.
Eric C. Westman, MD MHS
Associate Professor of Medicine
Director, Lifestyle Medicine Clinic
Excellent job, Dr. Westman! You took each of the points made by "Doc" and offered him the opportunity to see other data that he may not have considered otherwise. I appreciated you taking time out of your busy schedule to write back to "Doc" and give him a chance to learn something new himself. Unfortunately, that's the last we've heard of good ole "Doc." There's been nary a word out of him since Dr. Westman's reply.
Am I fallible? Yes, more than I'd like to admit. Do I know everything there is about diet, health, and nutrition? Anyone who tells you they do should be avoided because they are lying. Do I enjoy inciting an open discussion and debate of ideas? You bet your sweet bippy I do which is why I don't mind hearing from people who necessarily disagree with my viewpoints and wish to correct me. If I'm wrong and evidence is presented to me proving it, then I'm the first to make the corrections and admit the error of my ways.
But in this case, "Doc," I won't be changing a thing! By the way, where'd ya go? I'd love to hear what you have to say about what Dr. Westman said.
The purpose of my blog is for me to share about my experiences livin' la vida low-carb and to hopefully provide some interesting topics for discussion that will enable my readers as well as myself the chance to learn something about their own health that they probably didn't know before. One thing I've found since I started blogging in the health arena is that even the doctors and medical researchers don't always know as much as we think they do. There's a reason they call it "practicing" medicine.
With that said, I recently received a rather challenging e-mail from someone purporting to be a "Doc" according to their e-mail address who wanted to take me to task over the assertions I made in this blog post about my latest cholesterol numbers and specifically the particle size of my LDL as well as my hard-hitting column about the death of the late NBC "Meet The Press" anchorman Tim Russert. It seems the good "Doc" took great exception to my belief that the HDL/triglyceride ratio is a better indicator of heart disease risk than LDL or total cholesterol and that having large LDL particle size is protective against a cardiovascular event.
In a very condescending tone in his e-mail, "Doc" proceeded to berate my gross ignorance of some rather "basic" health concepts that I apparently haven't fully grasped yet (get a load of this guy!):
I nearly fell off my chair reading your well-meaning but very erroneous blog on Tim Russert.
If larger fluffy, buffy LDLs are protective, why is it that people with the highest risk of atherosclerosis and premature death (i.e. familial hypercholesterolemia) have 100% fluffy, buffy, LDLs?? Sure does not protect them! You with an LDL-C greater than 200 likely have large LDLs and are a dead man walking.
If low HDL-C is always bad, why are their several genetic conditions associated with very low HDL-C and longevity? Check out JAMA. 2008;299(21):2524-2532
Why have there been numerous published articles in the last few years describing many patients with myocardial infarctions who have HDL-C > 90 mg/dL?
If low LDL-C is so dangerous, why do people with hypobetalipoproteinemia who go through life with LDL-C between 5 and 40 all have longevity with no ill effects of such low cholesterol levels?
Russert's Lipids: TC = 105 LDL-C = 68 HDL-C = 37
Of course that is impossible: TC = LDL-C + HDL-C + VLDL-C
VLDL-C is derived by dividing TG by 5 thus VLDFL-C = TG/5
Thus using your numbers TG would be zero which is impossible. Of course if you knew anything about lipids, your blog would not contain so many basic errors.
Last bit of advice--Look up apolipoprotein B or LDL-P. Read the newest guidelines: A consensus statement from the ADA and ACC on Lipoprotein Management in Patients with Cardiometabolic Risk (like Russert). They were published in April in Diabetes Care and the Journal of the American College of Cardiology.
Had anyone measured LDL-P on Russert and then treated it aggressively, Russert would still be here. Of course since statins rarely normalize LDL-P, Russert needed additional medication beyond his statin to achieve apoB goal.
Hate to further blow away your statements, but if you read the new ADA/ACC statement you will see that data from three major trials (Framingham, MESA and EPIC Norfolk) have shown that LDL size is no longer considered an independent risk factor for CHD. Only thing that matters is apoB or LDL-P.
Happy reading and please correct your statements on the web site.
Well, I guess he told me, didn't he? It really depends on what research studies you are looking at and he pointed to a few that certainly made sense to him. As I stated before, I'm no expert when it comes to knowing anything and everything about the subjects I write about. I simply share what I do know and have seen applied in real life situations and let those results speak for themselves.
It's a bit presumptuous of this guy to call me a "dead man walking" because of my high "fluffy, buffy LDL" cholesterol. Further belittling my intelligence by attempting to point out my "errors" was also quite unbecoming of someone who alleges to be a professional physician whose goal is to help educate patients and make them healthy. I wouldn't want this fella being my doctor!
Although I didn't have the answers to his remarks, I knew someone who could provide an educated and reasoned response to "Doc." He's a real doctor and avid researcher on low-carb diets--Dr. Eric Westman. The following is Dr. Westman's comments back to "Doc" asking for clarification and presenting some counter-evidence rebutting the original claims made in his e-mail to me:
Thank you for forwarding this email.
1. The definition of "cardiometabolic risk" is changing, and its relationship to cardiovascular disease is imperfect. In spite of this, many medical authorities want you to do what they recommend. There are many exceptions to the recommendations, and I believe the authorities will acknowledge this readily.
2. Please teach me, "Doc." You wrote that people with "familial hypercholesterolemia have 100% fluffy, buffy, LDLs." Can you provide a reference for this statement (even case studies are fine)? Here is a recent article and it suggests otherwise...but the abstract doesn't really give enough information until I can read the full study. J Pediatr. 2008 Jun;152(6):873-8. Epub 2008 Feb 8
3. You wrote: "If low HDL-C is always bad, why are their several genetic conditions associated with very low HDL-C and longevity?"
I think that this just points out again how imperfect these markers are.
4. You wrote: "LDL size is no longer considered an independent risk factor for CHD. Only thing that matters is apoB or LDL-P."
"Doc" let me just take a moment to explain what "independent risk factor" means statistically--it is a common source of confusion. "Independent risk factor" means that, after accounting for some information, the addition of a new factor (variable) adds no more information (the association is no longer statistically significant).
My understanding is that LDL size and LDL-P are highly intercorrelated ("track together"), so that after accounting for one, the other is no longer statistically significant in its association with cardiovascular disease. It does NOT mean that LDL size is not important--it just means that you get no more additional information about the presence of cardiovascular disease from knowing LDL size when you already know LDL-P.
I look forward to learning more from you. Thanks.
Eric C. Westman, MD MHS
Associate Professor of Medicine
Director, Lifestyle Medicine Clinic
Excellent job, Dr. Westman! You took each of the points made by "Doc" and offered him the opportunity to see other data that he may not have considered otherwise. I appreciated you taking time out of your busy schedule to write back to "Doc" and give him a chance to learn something new himself. Unfortunately, that's the last we've heard of good ole "Doc." There's been nary a word out of him since Dr. Westman's reply.
Am I fallible? Yes, more than I'd like to admit. Do I know everything there is about diet, health, and nutrition? Anyone who tells you they do should be avoided because they are lying. Do I enjoy inciting an open discussion and debate of ideas? You bet your sweet bippy I do which is why I don't mind hearing from people who necessarily disagree with my viewpoints and wish to correct me. If I'm wrong and evidence is presented to me proving it, then I'm the first to make the corrections and admit the error of my ways.
But in this case, "Doc," I won't be changing a thing! By the way, where'd ya go? I'd love to hear what you have to say about what Dr. Westman said.
Labels: cholesterol, diet, Doc, Eric Westman, fluffy, HDL, health, Jimmy Moore, LDL, low-carb, nutrition, particle size, Tim Russert
posted by Jimmy Moore at
7/13/2008 09:09:00 PM
8 Comments:
Okay, I took up "Doc"'s challenge to read up on apolipoprotein B. and I think he has comprehension issues. Following the link, I thought this quote was telling:
"Most relevant information regarding mouse APOB homologue, mApoB, has come from mouse studies. Mice overexpressing mApoB have increased levels of LDL "bad cholesterol" and decreased levels of HDL 'good cholesterol'"
I know humans don't always respond the same way as mice, but I couldn't help but notice the part about the decreased levels of HDL. So, I'm thinking that apoB is not the "only thing that matters." And is apoB/LDL-P associated with the particle size of LDL (does it perhaps correlate with the smaller, denser size?).
Well, here is the summary from the "newest" guidelines that "Doc" urges Jimmy to read (and it's really not all that new; didn't "Doc" see the "small particle" references and the "low HDL references?)
"Patients with cardiometabolic risk factors represent a group at high lifetime risk for CVD. These patients frequently have dyslipoproteinemia (low HDL cholesterol, increased triglycerides, and/or an increased number of small LDL particles). We recommend an assessment of global risk followed by a multifactorial risk reduction strategy for such individuals targeting each risk factor and emphasizing both lifestyle and pharmacologic therapy. In terms of dyslipoproteinemia, we recommend the following:
• Statin therapy for the majority of dyslipoproteinemic adult patients with CMR
• For patients with CMR on statin therapy, guiding therapy with measurements of apoB and treatment to apoB goals in addition to LDL cholesterol and non-HDL cholesterol assessments
• Treatment goals, summarized in Table 1, that address the high lifetime risk of patients with dyslipoproteinemia and CMR.
• Clinical trials to determine whether the pharmacologic therapy required to achieve very low levels of atherogenic lipoproteins is safe and cost-effective
• A concerted, multifaceted, public health effort, focused on lifestyle modification, to reduce mean population levels of atherogenic lipoproteins to values well below current ones."
Seems that "Doc" is in favor of statins and other drugs (surprised?), but is totally blind to how low-carb would reduce many of the risk factors mentioned in these guidelines, such as obesity, hypertension, diabetes, high insulin levels, high triglycerides, and low HDL.
Didirina
Statistical associations do not prove causality. If LDL-P is associated with CHD, it could be that LDL-P causes CHD, or that whatever else causes CHD also elevated LDL-P. Perhaps "Doc" could take the time to fill us in on the mechanism by which LDL-P causes CHD?
"Doc", if any kind of doctor, is probably an osteopath, if s/he is a "doctor" at all. A "real" doctor would have signed his/her full name for further contact. This person is a medical "wanna-be."
"Doc"'s challenge question, "If low HDL-C is always bad, why are their several genetic conditions associated with very low HDL-C and longevity?" also sort of misses the mark. The key word here is "genetic." We've heard of folks who've smoked all their lives and lived to be 100; scientists suspect that they are genetically protected from developing cancer. Policy is not generated by the exceptions to the rule. Also, I don't believe that anyone has necessarily stated that "low LDL-C is so dangerous," but that high LDL-C levels are not dangerous when triglycerides are lowered and HDL-C levels are high because then the LDL-C type is most likely the "fluffy, buffy" type. Sheesh.
Didirina
Whoa, Kitty, I take exception to your putdown of "osteopaths!"
I worked for many years as a Medical Staff Coordinator in major hospitals. Part of that job is reviewing credentials for physicians when they first apply to be on staff, as well as monitoring current medical staff's current medical education, to make sure they keep up with it every year.
Being well acquainted with the medical education and background of both M.D.s and D.O.s, I can assure you that D.O.s have as much as, and often more, education as M.D.s do! They go to medical schools which are accredited by the very same agency, plus they also do a one-year rotating internship after graduation from medical school, no matter what specialty they are going into. It is required of all D.O.s to do that internship.
M.D.s more often do no internship at all, but go straight into residency for their specialty right out of medical school (which gives D.O.s one more year of schooling and a more well-rounded experience, in my opinion).
When osteopathic physicians specialize, they learn in the same teaching hospitals, side by side with M.D. graduates. Do NOT put osteopathic physicians down as non-physicians! That just shows your ignorance.
I consider D.O.s superior to the average M.D. because, in osteopathic medical schools, their students are taught to take the "whole patient" into consideration...including physical, mental, and psychological health...plus they learn about spinal manipulation and how an aligned spine contributes to the overall health of the patient.
I consider D.O.s to be similar to an M.D. and a chiropractor rolled in one. Two docs rolled into one, so to speak. I personally always seek out D.O.s for my personal physicians. I find them to have much more interest in me as a patient and have a much better bedside manner, as well as to be usually more well-read medically and better informed as to newer treatment options.
My current PCP is an osteopathic physician who wants me, as a Type 2 diabetic, on a very low carb diet! I take no diabetic meds at all and my blood sugars are stable...my blood pressure is on the low side. (I've been on low carb since 1997.) My doc knows the latest about EVERYTHING! No matter what I read about to take in to her, she's already read it and can discuss it with me in knowledgeable and usually positive terms.
I would be utterly surprised if this "Doc" who wrote to Jimmy is an "osteopath," as you so callously and in ignorance suggested. He sounds to me like a know-it-all medical student still, not yet a doctor at all.
Carol
I have lost 145 pounds eating only dogfood. My blood markers are excellent, though I have developed a special interest in tennis balls, which I can smell at 20 yards. I want my friends to throw them for me constantly, and this has cost me a few friends, but maybe how good a friend were they anyway. I can't seem to get any dogfood company to sponser me, I suppose they are worried about legal issues, like if I get heartworm or hip displasia, but dogfood is pretty cheap compared to some of the alternatives, which are starting to sound better and better lately. Peter
And your point is, Peter? By the way, dog food is VERY high in carbs. NOT HEALTHY! :P
Since "Doc" wanted to get personal with Jimmy's lifestyle, claiming him to be a "dead man walking," let's see how the guidelines stack up against Jimmy's stats:
"Patients with cardiometabolic risk factors represent a group at high lifetime risk for CVD. These patients frequently have dyslipoproteinemia (low HDL cholesterol, increased triglycerides, and/or an increased number of small LDL particles)(WHICH JIMMY DOES NOT HAVE!). We recommend an assessment of global risk followed by a multifactorial risk reduction strategy for such individuals targeting each risk factor and emphasizing both lifestyle (SUCH AS LLVLC?) and pharmacologic therapy. In terms of dyslipoproteinemia (WHICH JIMMY DOESN'T HAVE!), we recommend the following:
• Statin therapy for the majority of dyslipoproteinemic adult patients with CMR (JIMMY DOESN'T REQUIRE STATIN THERAPY BECAUSE HE DOESN'T HAVE DYSLIPOPROTEINEMIA)
• For patients with CMR on statin therapy, guiding therapy with measurements of apoB and treatment to apoB goals in addition to LDL cholesterol and non-HDL cholesterol assessments (NOT APPLICABLE TO JIMMY)
• Treatment goals, summarized in Table 1, that address the high lifetime risk of patients with dyslipoproteinemia and CMR. (NOT APPLICABLE!)
• Clinical trials to determine whether the pharmacologic therapy required to achieve very low levels of atherogenic lipoproteins is safe and cost-effective (NOTICE THAT AFTER RECOMMENDING AND GIVING PEOPLE PHARMACOLOGIC THERAPY, THEY THEN WANT TO TEST IT TO SEE WHETHER IT'S SAFE!!
• A concerted, multifaceted, public health effort, focused on lifestyle modification (LLVLC??), to reduce mean population levels of atherogenic lipoproteins to values well below current ones."
So, since none of these recommendations would apply to Jimmy, and seeing how even they don't know how safe their plan is, exactly HOW is Jimmy a "dead man walking"?
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