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 C
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.