LDL-Cholesterol on the Rise – OMG!

Cardiovascular Health Jeffry Gerber, MD

Cholesterol, or more specifically lipoprotein testing, will remain an important determinant of cardiovascular risk. However, once you or your doctor understands how inflammation and oxidative stress play pivotal roles in the development of atherosclerosis and plaque formation, cholesterol interpretation becomes a whole new ball game!

Listen to the original audio of my one hour interview with Jimmy Moore of Livin La Vida LowCarb Blog, the LLVLC Show (Episode 715) that was used for his upcoming book Cholesterol Clarity: What The HDL Is Wrong With My Numbers?. I am one of 29 expert contributors for the book which will be released to the public next week.

Just as our conversation gets more interesting the audio quality and internet connection deteriorate some. Bear with it, as the key content comes toward the end.

Jimmy is one those rare individuals that, despite doing everything right in terms of lifestyle, nutrition and reducing oxidative stress, his LDL-C as well as other advanced cardiovascular markers like LDL-P and ApoB are on the rise. Most mainstream-minded physicians would consider this unfavorable, but these findings have less significance in Jimmy’s case, especially when considering the complete metabolic picture. Listen to us discuss the results and implications, providing insight into this fascinating topic.

For the full story, don’t forget to order Cholesterol Clarity now available on Amazon.

  • Charles Grashow

    Please explain why high LDL-P (in Jimmy’s case >2700), high small LDL-P (in Jimmy’s case >400) AND high ApoB (238) is a healthy lipid profile? According to Dr. Dayspring LDL-P should be <1000.

    Look at slides 32 & 33

    • Charles,

      You have touched on the heart (no pun intended) of the post and for that matter one of the main reasons Jimmy wrote the book

      Normal values such as LDL-P <1000 also APO-B < 120, LDL-C < 70 and total cholesterol < 200 are based on standard American diets (refined and processed foods as carbs, vegetable oils, salts, etc.), not low carb or paleo. Many of the cholesterol lowering drugs such as Statins mainly lower these numbers and thus these values are heavily influenced by what big pharma has to say is normal.

      Don’t get the impression that I am against Statins and the pharmaceutical industry, modern medicine saves lives. In the right patient, who cannot adhere to proper diet, are sedentary, smoke and drink, have other unfavorable metabolic makers, like insulin resistance, hs-CRP, ox-LDL, myeloperoxidase, genetic markers, heart scans and or C-IMT’s, these standard goals, that Dr. Dayspring and many other quote may be appropriate.

      I find is shortsighted however to base cholesterol therapy only on these numbers and not to consider the big picture, that being underlying oxidative stress and inflammation influenced mainly through appropriate lifestyle.

      The mainstream cholesterol recommendations including, todays guidelines are largely based on ancient hypothesis’ dating back some 60+ years and poorly done feeding trials. There has been very little research looking at cardio-metabloic markers with low-carb and paleo diets until recently. But what is out there looks favorable http://www.awlr.org/carb-restricted-diets.html and we hope to see more outcome studies from groups like http://nusi.org.

      I cannot find any good evidence today that tells me what are specifically normal values for the numbers mentioned above with patients on low carb and paleo lifestyles. There is not enough evidence yet to say with certainty that Jimmys numbers are unfavorable when you look at all of his many other favorable results.

      You can see that Dr. Dayspring (one of the 29 experts interviewed for the book) and I have different opinions on the subject although we both like low carb diets. So without absolute evidence we are left to rely on best evidence and lastly expert opinion. Ultimately we individualize therapy and watch our patients carefully.

      Thanks for asking a tough question!

      Dr. Jeff

      • Charles Grashow

        So – the question that Dr Attia asks cannot be answered today. Why should we then assume that LDL-P >2000 on a low carb diet is somehow better than LDL-P >2000 on a SAD diet?

        Question – are particles somehow different or behave differently on a VLCHF diet?

        Question – what if they’re the same Then wouldn’t the risk factor be the same

        • Charles – The particles might be the same but are they floating is a sea of high oxidative stress or not is the question. Daysrping and Attia hardly discuss oxidative stress and I pointed this out to Attia both online and in person. Have you ever looked at the work of Chris Masterjohn on the topic of oxidative stress: http://www.cholesterol-and-health.com/about-cholesterol-and-health.html

          • Charles Grashow

            What are your thoughts on this. “are they floating is a sea of high oxidative stress or not.”

          • Charles Grashow

            Doctor Gerber

            What are your thoughts on this test




            Cholesterol-Absorber Status Modifies the LDL Cholesterol–Lowering Effect of a Mediterranean-Type Diet in Adults with Moderate
            Cardiovascular Risk Factor

            Cholesterol synthesis/absorption status was not markedly altered by diet, but the decrease in plasma LDL-C due to the Mediterranean-type diet occurred only in low absorbers of cholesterol. This should be considered during further dietary interventions.

            Our second key finding was that the response of plasma biochemical
            variables to a given diet was modulated by the cholesterol absorption status of the participants determined at entry. Plasma total cholesterol and LDL-C tended to decrease in low and high absorbers of both sexes, but, very interestingly, the reduction in LDL-C was marked only in low absorbers (−8.6%, P < 0.03 in low absorbers vs. −3.6%, 0.09 ≤ P < 0.24 in high absorbers). In contrast, no noticeable changes in plasma TG or TRL-TG concentrations were observed at that time, indicating that the reduction in dietary intakes of cholesterol and SFA had a unique effect on plasma cholesterol and LDL-C concentrations. This finding suggests that a low intake of dietary cholesterol (i.e., ~175 mg/d) and SFA (i.e., ~10% energy), as occurred with the LFCMD, caused a greater reduction in the LDL-C concentrations in participants with a low cholesterol
            absorption efficiency. Conversely, participants with a high absorption status elicited a negligible beneficiary LDL-C lowering after 3 mo of consuming a LFCMD with reduced dietary cholesterol intake.

            In conclusion, the present study of 125 men and women at moderate
            cardiovascular risk provides 2 important pieces of information. First, the synthesis/absorption balance for cholesterol, the key for cholesterol homeostasis, is likely an intrinsic trait of the participants that is not noticeably altered by changing the diet. This applies to both men and women; thus, there is no apparent sex specificity. Second, we showed that
            the cholesterol absorption status of both men and women is a clear determinant of responsiveness to a healthy dietary challenge by
            predicting a significant lowering of LDL-C in participants with a low-cholesterol absorption status. If this observation is confirmed by other studies, it may be possible to measure the serum surrogate markers
            in men and women at CVD risk to determine the cholesterol absorption status and thus to predict whether a given individual may be able to lower LDL-C with dietary modification.

          • Interesting!

          • charles grashow

            Any other comment besides “interesting”?

            Also – your thoughts


            Is there “evidence to support the contention that “large fluffy” cholesterol (or
            the metabolic milieu underlying it) is benign or, as sometimes claimed,


          • Charles – Large LDL particles might be less prone to oxidation compared to sd-LDL.

          • charles grashow

            Any published studies that might prove this theory.

          • Charles – Lots of theory and opinion as to why plaque forms, mostly based on scientific observation when the pathologists look at what comprises plaque: inflammatory factors, foam cells and predominately oxidized sd-LDL just to name a few. Does this prove that sd-LDL is more prone to oxidation, maybe not, just a theory!

            I agree with Dr. Dayspring that the LDL particle size alone might not be the best predictor of risk but then again I do not think that LDL-P (particle count) alone is a best predictor. lifestyle, diet and the entire metabolic picture including cholesterol absorption, production and clearance need to be considered.

            Again, your questions are insightful but I am not sure where our conversation is headed. In 2013 there are lots of opinions on the topic of cholesterol, heart disease and diet because it will take lots of time and money to due outcome studies. In the meantime best evidence and expert opinion is all we have to fall back on. For me, big pharma has overemphasized medications to lower cholesterol and that can’t be the only approach to heart disease prevention.

            Keep reading – Dr Jeff.

  • Pingback: [Fan Club] LCHF Lifestyle - Part 2 - Page 319 - www.hardwarezone.com.sg()