Wednesday, February 15, 2012

I'll Be Live on "Ask the Low-Carb Experts" With Jimmy Moore Tomorrow, Thursday, February 16, 7PM EST -- Call In With Questions!

by Chris Masterjohn
Ahoy mates,

I'll be on "Ask the Low-Carb Experts" with Jimmy Moore live at 7:00 PM Eastern Time tomorrow (Thursday, February 16) to talk about all things pertaining to lipids (aka "Cholesterol 101"). The show will involve a brief introduction to the topic followed by live Q&A with the listeners.  You'll be able to catch the recording of the show after it airs, but if you want your own question answered you'll have to either call in at the appropriate time or submit your question beforehand.  

If you don't live on the East Coast, make sure to adjust the time accordingly.

If you want to give me a heads up about your question in the comments, I may be able to give you a better answer, but I don't anticipate having much time for preparation so this will be a mostly spontaneous affair.  Please note that leaving your question in the comments here will not get it submitted to the show.  To make sure your question makes it on the air, please follow the latest instructions left by Jimmy:

JOIN US ON THE “ASK THE LOW-CARB EXPERTS” PODCAST THIS WEEK: We’re back with another great LIVE interview this week in Episode 6 of “Ask The Low-Carb Experts” coming up on Thursday, February 16, 2012 at 7PM ET addressing the topic “All Things Lipids (Cholesterol 101)” featuring blogger and soon-to-be Nutritional Sciences PhD Chris Masterjohn. If you have questions about cholesterol, HDL, LDL, triglycerides and more that you would like for Chris to address, then feel free to send it to me this week at AskTheLowCarbExperts@gmail.com. Or ask your question LIVE on my show by calling (712) 432-0900 or Skype the show for FREE by calling the username freeconferencing.7124320900. Whether you call or Skype, be sure to use the access code 848908. Listen LIVE and leave us a review at iTunes if you like what you hear. This is your chance to interact with the best nutritional health experts in the world, so don’t be bashful.
 Hope to see you there.  Enjoy! 

Read more about the author, Chris Masterjohn, PhD, here.

33 comments:

  1. As a heads up:
    I have a senior lady that her doctor has recommended her to take statins for a while. She doesn't want to go on them, and her doctor just ran an Lp(a) test and hers was at 80. I seem to recall that statins don't really affect Lp(a) and it's mostly genetic. I'm not sure of her tri:HDL at this time, but should she be worried?
    Seems that Lp(a) is only an issue if you have heart disease or a lot of inflammation.

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  2. Chris,
    I'm a 49 year old, 6',162lb male whose father died at 41 from heart disease (heart attack in 1975). I was taking 40mg of lovastatin for about 4 years. I decided early this year to change my diet to low carb/high fat and started the transition in the spring and was fully engaged (hardly ever any grains, grass fed bison and beef and very little sugar)by the fall. August I cut my statin to 20mg and September to 10mg (October I stopped with statins). In December my doctor did a Lipid profile and ALT (6 months after my physical. Chol-400 (was 215), TRIG-97 (was 95), LDL-309 (was 128), HDL-89 (was 65) and ALT-20 (was 24).

    I am on schedule for another physical/blood test in June again and hope the results have moderated from December. I'm assuming that my liver may have been throwing off alot of cholesterol it had held onto. My weight started dropping fairly rapidly with my diet changes and high intensity training (Mercola's Peak 8) for 21 minutes 3 days a week. My weight is now stable and has been since January. Are there any tests you recommend I get between now and my physical or any other changes in diet or routine?

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    Replies
    1. If your father died of heart disease at age 41, I suspect you have familial hypercholesterolemia (FH). I would seek to get a definitive genetic diagnosis. It's difficult to tell from your story whether your lipids increased because you got rid of your statin or because of your dietary changes.

      Chris

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  3. I'd like some input on how to increase HDL and triglycerides. I've been on a high fat GAPS diet (primarily paleo, really) for 2 years now and my HDL and triglycerides are steadily declining as my LDL and total cholesterol increases. My triglycerides are scarily low in the 20's right now. What's going on here and how can I even things out? I eat plenty of grass-fed and pastured meats and fats and no processed foods or sugars of any kind.

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    Replies
    1. The low triglycerides might not be a problem -- pretty typical of a very low carbohydrate intake. If you are cutting carbs very low, it's probably a thyroid issue.

      Chris

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  4. I've been on a mostly grain free WAP style diet for about 6 months. I just got some blood work done and my total cholesterol was 461 (HDL 99, LDL(calc) 350, TG 61). What could cause this? Should I be worried? My HSCRP was 0.41 and I've been at my proper weight for the last 10 years without much fluctuation.

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  5. i am going to disagree with your comments on Jimmy Moore. Most who I have spoken with have found that they have been Pattern A on VAP and Pattern B on NMR. You said it the other way. As a matter of fact I was found to be A on VAP and B on NMR. Moreover many are discordant; they have far more LDL particles than you would expect given their LDL number. As an example I had an LDL of 72, and particle count of LDL of 1,800. Since you are concerned with oxidation and degradation of particles, it would stand to reason that you would find in discordant cases cause for concern. Note my total cholesterol was only 175, trgs 72, and normal thyroid and weight and A1C.
    The work of Dayspring and other lipidologists shows many cases where FH does not exist, but particles being totally discordant with LDL concentration

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    Replies
    1. Hi Steve,

      In this paper...

      http://circ.ahajournals.org/content/119/17/2396.full#_jmp0_

      ... in samples taken from 40 people, tube gel electrophoresis was most likely to give pattern A and least likely to give pattern B. VAP was the opposite, and NMR was intermediate. So in this set of people, NMR was more likely to give pattern A than VAP, and vice versa. However, I think your examples, while different, support my point that the different methods disagree and there is not standardized criteria for assessing particle size.

      I don't understand your point about the discordance between LDL-C and LDL particle number. My point was that there is no strong evidence that particle size is an independent predictor of CHD, independent of the total-to-HDL-C ratio. The fact that variation exists does not mean that it tells us anything about heart disease risk, so I don't understand how you can use the existence of this variation to disagree with me.

      Chris

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  6. Hi there,

    I'm am just starting a series on my real food blog entitled 'Lets put Cholesterol under the Microscope'. I'll be sure to reference your work, as I will be gathering evidence from all over the globe.

    Thank you for your hard work. I am finding it hard to find information upon the different between blood Cholesterol and dietary Cholesterol? I this an important point to mention?

    Many Thanks,

    Natasha from www.thenourishingroad.co.uk

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    Replies
    1. Natasha,

      Please see here:

      https://www.cholesterol-and-health.com/Cholesterol-Rich-Foods-Raise-Blood-Cholesterol.html

      Chris

      Delete
  7. Hi Chris:
    I may have been unclear. There are many who have an LDL profile that would appear to be normal, or in a normal range, but when their particles are analyzed they may exhibit discordance, ie having particle count of 1,500 or more when LDL is only around 100. For many of these people who are not FH since their cholesterol is under 250, they appear to have CAD, or profile that fits with a family history of CAD.
    Have these many particles floating around in the blood stream would seem to fit with your view of CAD being the result of particles hanging around in the blood stream to long even with good functioning thyroid. Pattern A vs. Pattern B not as important as the total number of particles floating around in the blood stream(see Atvos and Dayspring work).
    Short of statin use, I have not heard of any means to provide either the best anti inflammatory environment or clearance from upregulating LDL receptors if thyroid is functioning adequately. Would be interested in your thoughts on this. Would also guess that maybe producing lots of particles when LDL appears to be normal which increases the probability of particle degradation is a variant of FH

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    Replies
    1. Hi Steve,

      I still don't follow you very well. First, you seem to be making a direct comparison between LDL particle number and "LDL," even though by the former you are referring to the number of LDL particles and by the latter you are referring to the mass of cholesterol contained in them, and you haven't attached units to either of them. An LDL particle number of 1500 is normal if the units are nanomoles per liter (nmol/L), and is consistent with lack of heart disease according to this study, for example:

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720529/

      (See table 1, where men without CVD at follow-up had a mean particle number of 1509 nmol/L.)

      I agree with you that you that many small particles MAY indicate a metabolic backup. However, as I have said and written in the past, there are many other reasons one could develop small dense LDL, and just because there is a correlation between this and heart disease risk does not mean that every cause of small dense LDL is also a cause of heart disease, particularly if we see small dense LDL as a non-specific metabolic marker rather than a cause of heart disease itself.

      The balance of studies thus far conducted suggest that particle size and number are not independent predictors of heart disease once adjusted for the total-to-HDL-C ratio. We need more research, and we need standardized criteria for measuring particle size and number, before we can form firm conclusions, but the present state of the data suggests to me that small dense LDL (i.e. more LDL particles per mass of LDL-C) does not convey any information that is not already conveyed by the total-to-HDL-C ratio.

      I think you would have to assess why the LDL receptor activity is not functioning adequately, if indeed that is the cause, before developing strategies to fix it. But I do not think you can conclude that this activity is low based on a high LDL particle number alone.

      Hope that helps,
      Chris

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  8. Hi Chris,

    Just wanted to thank you for your inspirational work. I have started my little series on cholesterol here:

    http://www.thenourishingroad.co.uk/2012/02/lets-put-cholesterol-under-microscope_20.html

    I wonder what you think? Happy for real constructive criticism, as I am simply a passionate mum on a mission (I am hopeless at science!!)...

    I'm turning my attention to how Cholesterol improves / prevents deterioration of the brain / memory...any pointers?

    Many thanks from your new English fan,

    Natasha :)

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