March 15, 2015

Personal

Random finding (plus pi)

The best part of parenting (so far)? Helping your kids overcome things you struggled with. It’s at least in the top 5.

Read Time 6 minutes

The best part of parenting (so far)? Helping your kids overcome things you struggled with. It’s at least in the top 5.

Last Saturday my daughter came home from dance class—something she normally loves—and seemed upset. A bit of prodding led to the cause: a girl in her dance class told her she was “as fat as a hippopotamus.”  My first reaction (note to self: probably not the right one) was to laugh out loud, given that my daughter is probably in the 10th percentile of weight for her age. I’m worried she’s too skinny!

Of course I realized quickly the “facts” were irrelevant in this case. Her body habitus was moot. But her feelings were hurt, and as we all know this wouldn’t be last time someone said something to her—true or untrue—that would hurt her feelings.  I won’t go through the entire discussion we had, as I’m sure those of you with kids have already been through this, and those of you without kids probably aren’t worrying about this type of interaction.

I did, however, decide to tell her about all the people who dislike me and say mean things about me, usually things that aren’t true. She was shocked, “Like what, daddy?” I gave example after example. She was amazed—and relieved, I suspect—to know that she wasn’t alone and that I was able to shrug it off after temporarily being upset by it. I even told her about folks posting videos on YouTube specifically attacking me.

So, when our little talk was over she asked if she could see one of the videos I alluded to. I was a bit hesitant, if only for some of the language used when folks rant against my existence (if she’s going to learn choice 4-letter words in earnest, it should be from me after all), but I figured it was a good idea. She could actually see for herself that people say mean things about her dad and he’s still, more or less, ok.

Which brings me to the point of this quasi-post…

In searching for said YouTube videos, which I eventually found, I stumbled across two talks I gave last year which made their way online, unbeknownst to me.

In keeping with the current spirit of my co-op blog posts, below are links to the two talks.

Talk 1: Evidence for (and against) the dietary guidelines restricting saturated fat

 

 

This talk is an updated version of a talk I gave a few years ago and shared on the blog, in 2012 I think. Even if you watched the earlier version of the talk, if you find this question interesting—what is the case for restricting saturated fat (SFA) intake—it’s worth watching this version. I find this particular topic especially interesting because I think it highlights the challenge we all have, myself included, in setting aside bias when confronted with new information. (My friend Carol’s amazing book, Mistakes Were Made (But Not By Me) cannot be recommend highly enough for people who want to understand how cognitive dissonance wreaks havoc in even otherwise functioning societies.)

And contrary to what some (perhaps many) of you might think, I don’t believe this is a settled debate across the board. What do I mean by that (i.e., “across the board”)? Certainly in this presentation I try to make the case that the continually falling recommendations for SFA—from 12% to 10% to 8% to 5% of total calories—are not supported by convincing science. In fact, such recommendations likely do harm, courtesy of the “substitution effect,” i.e., people end up eating more of other things—namely, sugars and omega-6 polyunsaturated fats (n-6 PUFA)—that likely cause greater metabolic derangement.

However, some readers may interpret the data I present to mean it’s perfectly safe to consume, say, 25% (or more) of total calories from SFA. I realize I may have to turn in my keto-club card, but I am convinced that a subset of the population—I don’t know how large or small, because my “N” is too small—are not better served by mainlining SFA, even in the complete absence of carbohydrates (i.e., nutritional ketosis).  Let me repeat this point: I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA. This leads me to believe some people are not genetically equipped to thrive in prolonged nutritional ketosis.

In one particularly interesting case, a patient in self-prescribed nutritional ketosis presented to me with an LDL-P of more than 3500 nmol/L1i.e., more particles than could be measured by the NMR machine so the report simply said “>3,500 nmol/L”. despite feeling, performing, and looking great. Based on his through-the-roof desmosterol and cholanstanol levels, and a curb-side consult from the Godfather- I mean Dr. Tom Dayspring, I decided to try an experiment. You see, the logical thing to do in this setting would have been to start two drugs immediately (a potent statin to address the hypersynthesis and ezetimibe to address the hyperabsorption) or tell him to abandon ketosis altogether. But this patient was adamant about staying in ketosis given the other benefits, though obviously worried about the long-term coronary implications. So, we agreed that for a 3 month trial period he would reduce SFA to an average of 25 g/day (vs. about 75 to 100 g/day) and make up the difference with monounsaturated fat (MUFA).2We also reduced his omega-3 PUFA given very high RBC EPA and DHA levels.

So, on balance, he consumed about the same number of calories and even total quantity of fat, but his distribution of fat intake changed and he heavily swapped out SFA for MUFA.

The result?

His LDL-P fell from >3,500 nmol/L to about 1,300 nmol/L (about 55th percentile), and his CRP fell from 2.9 mg/L to <0.3 mg/L (and for the lipoprotein cognoscenti, both desmosterol and cholanstanol fell).

Pretty cool, huh? So, my point is this: while I believe the population-based guidelines for SFA are not supported by a standard of science I consider acceptable, it does not imply I believe SFA is uniformly safe at all levels for all individuals.

Some of you may be wondering about me. It turns out I’m in the group (recall: I have no idea how large or small this group is) that seems to do well—at least by the tools we have available to assess risk—with large amounts of SFA in my diet, if and when I elect to. Even when I was in ketosis, eating 4,000 kcal/day (literally getting 40 to 45% of my calories from SFA alone) my biomarkers—cardiovascular, insulin resistance, inflammation—were excellent. Better than they ever were or even are today. Though, my point still stands: there are some people who do not appear able to safely consume massive amounts of SFA.

One last point I’ll make on this highly charged topic. I realize there is a contingent within the LCHF community who argue that traditional biomarkers of coronary risk—such as LDL-C or its superior cousin LDL-P—“don’t matter” if one is on a low carb or ketogenic diet. Maybe they are right. I guess time will tell. But I am not convinced, at least not yet.  As a doctor I can’t look a patient in the eye and tell them a sky-high LDL-P is ok because they don’t eat carbohydrates. So if you’re following such a diet, and your LDL-P goes through the roof, I’d urge you to consider a variation of the diet.

(Note: If you post your NMR results, please understand I will not comment on them.)

Talk 2: It was the best of times, it was the worst of times—the tale of the U.S. healthcare system

 

This presentation has nothing to do with nutrition but is, nevertheless, a topic I’m pretty obsessed with: how do we achieve cost containment on healthcare in the United States? (Sorry non-U.S. readers, but we have a bigger problem right now, so I’m focusing on ours over yours!)

This is a pretty controversial topic, so before you jump down my throat, try to sit through the entire talk, especially the parts where I frame the question as one of optimization. Most problems that have been heavily politicized suffer a common problem: they fail to distinguish between what is desirable in a resource unconstrained world (e.g., free health care for everyone that provides perfect care) and what is plausible the real world (e.g., some combination of features, but not 5 starts across the board).

Hope you enjoy the departure from the usual topics.

Pi Day

The math geeks in the audience will appreciate that yesterday, March 14, 2015, represented a very special variant of pi day. Normally, March 14 represents pi to 3 significant digits, namely, 3, 1, and 4 (i.e., 3.14). Yesterday, however, being the pi day in 2015, was especially cute, because it advanced two more significant digits, 1 and 5, via the year (i.e., 3.1415). If you’re a watch geek, in addition to being a math geek–yes, I realize this is not a huge club–the beauty of a perpetual calendar (a type of watch that shows time, month, date, and year inclusive of leap years), made it a really fun day! Why? Because at 9:26 and 54 seconds you found yourself at the following place in time: the 3rd month, 14th day, 15th year (of this century), 9th hour, 26th minute, and 54th second, that is, 3.141592654–pi to 10 significant digits!

After capturing this wonderful moment in time, I sent the picture, below, to my watch mentor (also a math geek; yes I just wrote the words “watch” and “mentor” next to each other). He loved it, but his response was priceless: “Peter, don’t ever show this to any woman you have the slightest interest in….check that, don’t show it to any woman period. Pretty cool though. You are right. I dig it.”

Good thing my days of trying to impress the ladies are far in the rear view mirror.

Parting shot: I did a follow up podcast with Tim Ferriss a few weeks ago. It’s episode #65 which is available on iTunes. This was my first time doing the strange format of just talking by myself. Feedback appreciated if this should morph into something I do quasi-regularly on the blog.

 

Pi on abstract background with about 3500 decimal digits by Nicolo Canali De Rossi is licensed under CC by 2.0

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386 Comments

    • OK, OK, technically that’s true Peter, but surely you know what I mean? Let me try to be more punctilious: when I measure Apo-B, in g/L (or mg/dL),
      how can that give me an idea of what my LDL-P is, in nmol/L?

      I got something of an answer in a Varvel, Dayspring et al. article. To be sure, the article looks at cases of discordance between Apo-B and LDL-P (while noting their strong association), so we need to assume that there is no discordance (e.g. not many small particles and not a lot of Lp(a):

      “Although there is no formal standardization program
      for LDL-P,
      it could conceivably conform to the apo B LSP,
      by adding the VLDL particle number to the LDL-P and converting nanomoles per liter (nmol/L) to mass units (mg/dL) based on the molecular weight of apo B (550 000 Da) (49). This conversion recognizes that both total plasma apo B and LDL-P measurements presumably include IDL and Lp(a), in addition to LDL.”
      – Varvel, Dayspring et al.
      http://www.sciencedirect.com/science/article/pii/S1933287414004048

  1. Hi Peter,

    Hope you and your growing family are well.

    I recently started supplementing with Berberine since you mentioned it on your Tim Ferriss interview. And I have a motto that anything Peter Attia is willing to put into his mouth … I’m at least willing to try 🙂 (But seriously, I respect your judgement)

    I’m wondering why you chose Berberine over Metformin for your own personal choice. Being a Doc I assume you could get easily get a prescription for Metformin.

    Metformin would seem to have a much longer history than Berberine for blood sugar control and and has been studied more extensively. (Hence maybe safer?)

    I have concerns over long term use of an Herb which hasn’t been studied that much, but I probably can’t get a script for Metformin since I’m not diabetic.

    Thanks and best regards,
    Eric

  2. Hi Peter,

    I’ve found some interesting information/research on goldenseal and its predominant and most active alkaloid berberine. It looks to me like there is a significant danger of carcinoma/adenoma in the commonly used dosage range for hyperglycemia.

    Let me summarize first. In the 2010/2011 timeframe a long term 2 year rat/mouse study was undertaken by the National Toxicology Program at NIH. They ran 2 week, 3 month and 2 year studies. Liver Hypertrophy was found in both the 2 week and 3 month trials but the 2 year trials showed even more significant damage.

    In the two year study male rats fed 25,000 ppm of goldenseal powder ad libitum showed a 20+% incidence of liver hepatocellular adenoma or carcinoma. This was the most signifcant effect. The concentration of berberine in the goldenseal powder was 3.9% by weight. When all the calculations of converting the amounts taken daily by the rats to a human equivalent dose are done it turns out that the rats with the 20% rate of carcinoma/adenoma were consuming the equivalent of a 100 kg human consuming @880mg/day of berberine. Interestingly there was no carcinoma in the female rats and only 2 with hepatocellular adenoma.

    Jumping from goldenseal powder to berberine as the culprit is a big jump but reading the paper you will see that the researchers, even though avoiding saying it was definitively berberine that was the cause, did talk a lot about berberine in the discussion.
    That first paper is here: http://tpx.sagepub.com/content/39/2/398.long

    Subsequent to the paper and motivated by the paper a second in vitro study was done to try to ascertain how that cancer in the rats might have been caused. In that study the researchers examined 5 alkaloids from goldenseal and found two that were active. Both were topoisomerase I and II interruptors and the researchers felt that this may have been the cause of the cancer in the first experiment. One of those alkaloids palmatine was of much lower concentration and somewhat weaker than that of berberine.
    That paper is here: http://www.sciencedirect.com/science/article/pii/S0378427413008412

    As I said the NTP of the NIH actually ran 3 different trials. A paper containing all the work is here:
    http://ntp.niehs.nih.gov/ntp/htdocs/lt_rpts/tr562.pdf (190 pp)

    There is a summary of the long report immediatley above here:
    http://ntp.niehs.nih.gov/results/pubs/longterm/reports/longterm/tr500580/listedreports/tr562/index.html

    I know it is difficult to get supplements tested but it certainly does seem that another longer term in vivo study of berberine itself is in order. Berberine has become a very popular alternative to metformin and more and more diabetics are taking it. It seems particular risky when considering the fact that the dosage range that appears to have caused cancer in the rats is the same range as many are taking for hyperglycemia on a daily basis.

    Since I think the first thing you will want to check is dosage here are my dosage calculations taken from a forum post:

    The weight to weight mg/kg ratio is designed to eliminate the need to take into account the individual weight of the differing subjects. When the number of 54.6 mg/kg (from the research) is cited it means that the animal is consuming his own weight * that amount in berberine as a constituent of the total Goldenseal added to the diet which is 3.9% of the total Goldenseal. If the rat weighed 1kg it would have consumed 54.6mg if it weighed 0.1 kg it would have consumed 0.1 * 54.6mg or 05.46mg.

    Now let’s move to humans. If we had a 1 kg human being they would consume exactly the same as a 1 kg rat or 54.6mg. If we had a 100kg human they would consume 100*54.6mg or 5460mg.

    Because animals have different consumption rates depending on volume:weight ratios experimenters adjust dosages according to those ratios. For rat:human that ratio is 6.2:1 meaning a rat has to consume 6.2 times as much as a human per kg of weight to get the same effect from a drug. Therefore to get the human EQUIVALENT dose the rat dose is divided by 6.2. 5460mg/6.2 = 880mg or slightly less than 2 500mg caps for a 100kg human. 100kg=220pounds.

    Clearly this dose of 880mg is well within what is considered “therapeutic” by the mfgrs and consumers of berberine.

    Peter, I hope you can find the time to read and think about these results. I think a long-term in vivo study is needed for berberine preferably with a large cohort divided as to time of sacrifice into shorter periods to better assess when and how much impact there is. Maybe transgenic or xenografted mice would be an option as well.

    Best regards

    Mike

  3. Your post: “In one particularly interesting case, a patient in self-prescribed nutritional ketosis presented to me with an LDL-P of more than 3500 nmol/L …”

    Had he reached a stable weight for weeks or months? At https://youtu.be/OFD2q5iqevY?t=1h16m40s, Dr. Phinney says adipose tissue floods the blood with stored cholesterol as it loses weight (by shedding cells emptied of TG?), which the liver dumps into bile in the gall bladder, thus into the gut and out of the body with the stool. Once the person’s adipose tissue had “cleansed” itself, the LDL levels reduce markedly.

    Another question: for a person whose prostate is a mass of scar tissue from radiation treatment would a very high LDL-P (2558 nmol/L) indicate that his body is trying to heal itself using the cholesterol? If so, wouldn’t it thwart the body’s efforts by treating the very high LDL-P with statins; or by reducing dietary saturated fat as you propose?

    Related question: does this study say statin use is indicated for post treatment prostate cancer, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384647?? Does it matter that it seems to be funded by industry?

    Thanks,
    -Steve

  4. In your Talk 1 commentary above – what would a diet look like for your experiment patient, higher MUFA, lower PUFA and SFA? More olive oil, avacados, less coconut oil?

  5. Hello, a couple questions Ive had trouble finding information on:
    Why do type two diabetics have higher rates of gluconeogenesis, wouldn’t blood glucose levels (if high due to insulin insensitivity) repress this process?
    Regarding ketosis, ketoacidosis will only rarely take place in other than type 1 diabetics due to the ability for even minimal insulin production in healthy individuals and DM2’s. In ketosis, the body would produce insulin (preventing ketoacidosis) in response to higher ketone levels and thus repress ketone production, or insulin would only be triggered by protein intake? Thanks so much if you have time to respond.

  6. Peter, is there anything going on around Nusi that might be worth sharing?

    I’ve checked the Nusi.org site:
    – the latest News updates date back to August 2015, these are links to an articles by Gary Taubes (not really news) and a mention of Framingham study.
    – under Initiatives, only the Fr. study is mentioned, at the website it says: “This study is currently recruiting participants”.

    Nusi was launched in Sept. 2012. Sure, it takes time to prepare scientific studies well, but how much effort would it cost to publish some regular updates, esp. since none of this were possible without GT’s books winning lots of public (=our) attention & support 🙂

    • Thanks, it is an interesting update.

      I’ve just listened to the latest podcast on Chris Kresser and it seems you’ve moved beyond the war on insuline and simple diet/weight loss issues. On a personal level your new(?) direction makes perfect sense to me!, I’m also no longer interested just in dieting for fat loss or sport performance for this moment, but now that I’ve moved past 40, my goal is to be able to practice my sports (climbing, running, sailing) with my kids in the next 10, 20, 30, … years.

      I’d still have one more question if you don’t mind: do you still consider your goal to affect the public policy, to potentially help people like those your mentioned in your TedTalk? Or have you got disappointed/disillusioned with the system and see little chances of changing it? I have really no clue on the actual state of NuSi, but it seems the progress hasn’t been dramatic. I might be wrong, I hope I’m wring.

  7. Re-updated –
    Evidence for (and against) the dietary guidelines restricting saturated fat.

    Very interesting read thank you for sharing your update, I have long followed you and your self-experimentation. As an avid cyclist who I’ve always appreciated your posts, especially when it involves performance and low carb. I would really like to get your thoughts (maybe another blog topic) on your 20/20/60 diet and its relationship to your performance. I’ve cycled in and out of ketosis over the years riding up to 600km some weeks in ketosis. I’ve been considering carb cycling or timing based on energy my needs. Any people or resources you’d recommend on this.

    Thank you again

  8. I’ve enjoyed your blog and learned much along the way. Would consuming exogenous ketones allow one to undertake a multiple day activity like hiking and consume substantially less calories while maintaining body mass? (I hesitate to use the term weight since you have explained well the ebb and flow of hydration). It seemed from your cycling tests that this could be the case?

    Thanks,
    Scott

  9. I’ve recently just started reading your writings and listening to your lectures (podcasts you are in, too), Peter. I must say: Congrats on the self-experimentation and determination to get the results you desired.

    I won’t ask for medical advice, as I know the professional obligations you have elsewhere. However, I was hoping you could point me into the right direction, as it regards to research and self-experimentation. Right now, I am using PubMed through my university and possess no formal background in biochemistry, nutrition, etc. (I’m an ECON major).

    I’m currently 21, but at the age of 15 lost about 120 lbs (272 to 150 lbs) in a span of 9 months. Through that time period, I was diagnosed with an eating disorder and suffered through depression. No sympathy wanted; I am a product of my own decisions.

    Today, I am 21 and have reverted back to the low end of things (am at 143 lbs, roughly 6’1” and got a body fat % at Complete Nutrition that read 4% — unsure how accurate; probably not much). Right now, I am experiencing fatigue and have very dry, red hands. My most recent blood pressure reading was 97/66 and a heart beat/minute of 45. Right now, my morning glucose reading after an overnight fasting period is in the 80-85 mg/dL range. In a sense, I believe I am fairly insulin sensitive.

    My source of carbs right now are oats in the morning, beans/lentils for lunch and sweet potato/quinoa for dinner. No variation from those. I eat berries with breakfast and an apple for dinner. Three meals, one snack before bed. I’ve lost about 15 lbs since September of 2015, but am unsure how much food I actually need to eat just to maintain weight. Right now, I eat roughly 2,000 kcal a day.

    My goal is to gain about 30 lbs of muscle, but don’t know where to start. I understand I have a shaky past with food, but am trying to face my demons and overcome my fears.

    I know you can’t really help, but wanted to get this out there (even if it is very informal). Perhaps one of your other readers can help guide me in the right direction.

    Most articles/blog posts are directed towards individuals on the opposite spectrum. It is quite frustrating trying to find reliable information to help me regain the life I lost.

    I’m on a mission right now. Again, I know you can’t help, but anything would be helpful. No matter what, I am determined not to fail.

    Keep up the good work, and I look forward to keep reading your work in the future.

    Best,

    JA

  10. Hello Dr. Attia,
    Thank you so much for all the web content. I remember on your TedTalk that you said there are other metabolic disorders other than diabetes Type II that are more “sinister”. Can you elaborate? Thanks!

  11. Peter:

    This comment is a propos of nothing except a gut reaction of needing to respond to your outpouring of obvious affection for your daughter. She is greatly blessed, and so are you. I recall the raw emotions that were ignited in me by the birth of my daughter 31 years ago, and the many, many interactions that I have tried to have, on an emotional, intellectual and moral level since. Somehow, I managed not to spoil her rotten, but that’s largely my wife’s doing, as she was strict, with very firm boundaries, beyond me at the time, but what I realise in hindsight was essential to hour children’s growth. My daughter realised early on that she could not tolerate the icky biology things that she encountered in school, but which her Daddy insisted on discussing ad nauseum, so rather than pursue the biological sciences, she followed her own path of finding things out by becoming an electrical engineer. So now she is a secure, intelligent, funny, caring, athletic, capable human being who I have no problem leaving in charge of the world she will live in. She just had a baby 3 weeks ago, just at the time when I thought, maybe she’s not her Daddy’s little girl any more. (Please forgive the rather sexist slant here — I have a younger child, an equally capable, compassionate and funny son, whom I love equally fiercely, but, you know, it’s different). From a logical viewpoint, parenthood is the most sacred mission. But it’s the emotional intensity that was the most unexpected for me. Peter, you have absolutely no idea what’s ahead!!

    • Su-Chong, I know the feeling. Daddy-daughter-date-nights are the highlight of my month. I hope you’re right (re: what’s ahead). Seems like it can’t get better than this!

  12. Peter:

    I just have to warn you, one Dad to another, of one terrible thing that will come. Despite your best intentions and all your heads ups, there will come a day when you will fail her. And you will feel worse than at any other time in your whole life, worse than after your worst clinical misjudgements, worse than…just anything. For me, it was when I joined the parents class at my daughter’s tap lessons. It was quite good at first; I had never danced before, and after a while I even looked as though my kicks weren’t meant to be lethal. At the end of the year there was a recital, and the final number had the whole ensemble, with the whole parent section joining in the back row, with the climax having the parents doing “wings”, except I didn’t realise at the time that what we were doing with our feet was not really the standard stuff (my daughter only disclosed this to me later, to spare my feelings). It was wonderful. There were 2 performances, so we went to grab a quick snack and come back for the 2nd performance. Except I had heard the time wrong, and, cut to the chase, we missed our parts in the finale. I was just devastated. But she forgave me. And that just made me feel lower than dirt. Just letting you know. It’s going to happen to you too, someday, somehow. And there’s nothing you can do to prevent it.

    But, you’ll survive, and next morning, somehow, the world will still be there, and life will restart, after a fashion, and be ok again. Just a heads up, Buddy.

    BTW I also have a nickname for Grandson (it must be a mechanism for veiling our overflowing emotions). They took the longest time finding names that they liked. As her husband is of Scandinavian stock, I decided on Gunnar, and threatened that that would be it, boy or girl. Well, after he was born, they took so long to name him I just kept on calling him Gunnar. So I understand Michael Jackson.

  13. I’m one of the “lucky” few that apparently are in this situation. My LDL-P came in at a whopping 3,341 with HDL at 7733 and Tris at 67. As per what was described here I cut back drastically on my SFA and upped MUFA big time. I have some doctors appointments lined up and I’m looking forward to seeing what the results are but, in addition to that my HGBA1C level showed that I was prediabetic too! I was wondering if you observed that behavior in any of your patients… my diet is pretty strictly limited to broccoli, butter, and beef, with the occasional indulgences being low-sugar as well (100% dark choloate, coocnut manna, and So Delicious Unsweetened Coconut ice cream).

    Thanks for this post- it was pretty reassuring to know that I’m not the only one.

  14. First, let me confess to anyone reading this that I am a bona fide Libertarian Socialist.

    Dr. Attia, I am sure you are probably already aware of the defamation blog posted by Michael Suede (Libertarian blogger – also has a YouTube channel) back in March. Have you had a chance to respond to it? While there are certainly holes in several of the arguments made (and there isn’t much you can do about conspiracy theories, unfortunately), he did cite a lot of research publications, many in which you are probably already well versed.

    https://www.libertariannews.org/2016/03/07/dr-peter-attia-readdressing-dietary-guidelines/

    I don’t wish to see any unfounded barriers to your research efforts that are inspired by such. Your work is vital work. You promised years ago to “go where the data takes me” and we have faith in you. Please, do not ignore any valid criticisms that may have been addressed here, and do not turn a cheek to slander. You should respond, and do so publicly.

    • The title of his post is “Dr. Peter Attia: Hack, Liar and All Round Disgusting Individual.” Really? Wow, tell me how you really feel. When last I checked someone who opens with an ad hominem attack isn’t worth the ether they occupy.

  15. Any quick thoughts on Desmosterol vs Lathosterol to get a snapshot of synthesis status? Also, wouldn’t using Beta-Sitosterol and Campesterol as markers for intestinal absorption be highly dependent on how much plant material is in someones current diet?

    Thanks!

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