Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
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Friday, November 2, 2012

Hacking Jimmy Moore's Latest Lipid Report

So Jimmy Moore has released his latest lipid panels, after losing 50-or-so pounds in 5 or so months of his nutritional ketosis experiment.  Before I comment on these, a huge revelation was made in the post:
Interestingly, before I started on the Atkins diet in January 2004, my highest total cholesterol was only about 230. Of course, my doctor put me on both Lipitor and Crestor to lower that number and it did get down to 130 at some point (don’t know what the breakdown was of HDL and LDL nor do I know what my triglycerides or LDL-P were at the time either).
Ummm ... Jimmy, do you even bother to look back at your own blog? Seems not, which is a darned pity for someone so darned and determined to figure all of this out, but who doesn't even look at his own data.  
Before I started livin’ la vida low-carb, my HDL was a dismal 21 and my triglycerides hovered over 250. My LDL was about 250 which brought my total cholesterol to around 275. It wasn’t a pretty picture.
One of the main "brags" of many low carbers like Jimmy is that after their miraculous transformations on the LC diet, they were able to drop all medications and are in spectacular health.  Jimmy frequently defends low carbers who remain obese, like Andrew DiMino and Laura Dolson, as having spectacular lipids.  Well, that clearly depends on what one considers to be spectacular.  Jimmy Moore is off the statins not because his lipids have normalized, but because he no longer "answers to" mainstream medicine.  Whatever one thinks of the wisdom of that, or of the "conventional", down roughly 110 to 160 lbs from his peak weight, Jimmy's lipids far exceed unmedicated levels circa 2004.  I've taken the liberty of filling in some approximate weights and numbers from earlier years from  here and here.

Forget for a moment who these numbers relate to, and imagine you are a doctor receiving these results for one of your patients from the lab.  Tell me there's a single physician reading this who would encourage this individual to keep doing what they are doing given the results.

Despite all of his transparency, Jimmy never does tell it straight.  Granted, folks memories can fade, but when you have a blog record (and hopefully for his sake he exported/saved the menus blog for his records) one wonders why you wouldn't use it while chasing phantom mysteries.  According to his most recent record,  Jimmy's LDL-C has been higher than it would have ever been at 410 lbs, but the record says it's been around the same as back then with a few blips along the way.    It would be interesting to know if he ran any lipids in 2007 -- either when he started at 220's, gained, lost down to low 2-teens end July, then ballooned back to 260 by Jan 2008.

But just look at those October 2005 numbers where by all indications Jimmy had maintained his 180 lb weight loss in 2004 and was still regularly exercising (the "wrong" way, I might add).  His numbers were *normal*.  Jimmy Moore, with his genetics, remaining excess weight, eating low carb, around 100 g carb/day, and whatever damage his years of obesity had wrought, was metabolically *normal*.  October would have marked 10 months of maintenance and relative weight stability as well, long enough for the prolonged energy deficit "honeymoon" to have worn off.

Then 4-5 months later, things started going south, though still not horribly off the grid.  This was his first particle size determination where he bragged on the large size of his LDL.  His LDL-P, however is high (1724, want < 1000) and small LDL-P is almost 500 (still under 600 ).  ***  I don't know what happened here, HTML got farkled and it doesn't seem to flow,  After 2006 readings, the next set is not until May 2008 ***     These May 2008 readings were taken before Jimmy sought assistance from Dr. Westman, who counseled portion size and increasing percent fat in his diet.  Jimmy mostly took the latter to heart, but seemed to increase the fat more than adjust the percent.  Still, thanks to various experiments, including sweet free challenges, Jimmy was back in the mid 230's by January of 2009, and weighed under 250 through the first six months.  Again ... would have been interesting if the ever curious Jimmy had had his lipids run early in 2009 when he was again near that 230 goal.  There was no mention of lifting weights anymore in 2009, and none of regular exercise either (the occasional refereeing and volleyball game).  The July 2009 numbers are likely in a gain phase (high LDL-P), and October would have been post-Eades 6WCure (small LDL-P).  Nonetheless, the TC continues its march upwards.

Only Jimmy knows the exact differentials between his habits, intake, weight change, etc. that surrounds timepoint-to-timepoint lipid profiles, but the last two are rather horrible!  Despite losing 50 some-odd pounds, his TC remains hovering in the mid-to-high 300's, and his LDL-P is through the roof -- almost 3.5X the maximum normal levels.  He's back-patting that the small LDL-P is quite low at 221, but it's hardly comforting -- especially when compared to the May 2008 numbers.  It's likely because he's been in prolonged calorie deficit.  When one reads Jimmy's blog, and more telling, his responses in comments, he clearly seems concerned, but doesn't want to come off as concerned.

This man has thrown his metabolism completely outta whack!  Genetic component?  Unlikely ... or rather, unlikely one that cannot be managed simply with a more realistic diet, even one that's low carb (see Oct. 2005), and maintaining a reasonably normal weight, even if that weight is still north of ideal for his size/body type.  Prolonged low carbing -- perhaps compounded by weight cycling -- and perhaps further compounded by the "smother everything in butter and CO" habits -- has not been friendly to his personal genetic/physiologic makeup.  It simply hasn't.  

OK ... Now onto some hacking shall we?  I know Jimmy reads here, so perhaps he can put his hatred aside and learn some meaningful things to take with him to discuss with Dr. Dayspring in December.   Oh ... and it's not all about you Jimmy, because I've been thinking about a lot of this stuff ever since the cholesterol discussions in the comments from the Is This Your Paleo Diet? post.  When I started hanging out at PH last year, there were quite a few who were displeased with skyrocketing LDL upon going paleo/primal.  There's lots of great information on cholesterol in this community, and I don't want to leave anyone good out, so I won't even compile a list.  Please feel free to link to what you've found helpful about the net, from any source you deem reputable.  

THERE'S ALSO A HECKUVALOT OF CONFUSION.  I think this stems from the reactionary response to "artery clogging sat fats" and "dietary cholesterol causes high cholesterol" memes that seem to persist to this day.  Folks in this community went from saturated fats not being inherently harmful, to "heart healthy sat fats" and the more the merrier!  As particle size came in vogue, not only were LDL-C's "meaningless" and small dense LDL the "bad guys", but the large fluffy particles were elevated to the undeserved pedestal of "protective".  Higher HDL's are generally considered protective, but nobody bats an eye at HDL's that are wildly high.  Then there's the low triglycerides and the HDL/trig ratio.  On the one hand, folks seem willing to accept that LDL stuff doesn't really apply to them because their HDL/trig ratio or levels or both is highly favorable.  But the thing is, and we ALL need to keep this in mind, just about every large study looking at various biomarkers and risks is looking at large populations that have various lipoprotein levels within certain ranges on an "average" diet -- average being in the 45-50% carb, 15-20% protein, and 35-40% fat ranges.  

All the while, low carbers seem to be terminally tied to the gross misconception on triglycerides.  I do believe I'll construct a Hall of Shame here at the Asylum to collect all in one place as many members of this community as I can that subscribe to the notion that triglycerides (generally fasting VLDL*) that excess carbs are converted to fats by de novo lipogenesis.  If you haven't read my series on "Where Do Triglycerides Come From", may I suggest doing so?  Part I, Part II, Part III.  This is based largely on the work of Marc Hellerstein who has used radioactive labeling to trace the sources of fatty acids packaged up by the liver and exported as VLDL.   The lowered fasting triglycerides in low carbers may be an anomoly, and indicative of the general failure to include the "missing lipoproteins" -- NEFA/FFA.  Even so-called "free" fatty acids are lipoproteins, as they are bound to albumin.  Due to the apparent difficulty to measure these, they are not routinely assessed -- a fact I consider to be a darned shame once someone presents with any sort of lipid profile out of the normal ranges.  With that out of the way ...  


More Smaller VLDL/Fewer NEFA Esterified:   
For starters, whenever I hear of LDL's going up with LC weight loss, I am remind of this post/study:  Failure of LC/HF Diets to Suppress NEFA Release.  This study employed a LCHF (under 20g carb) diet -- controlled with standard LF reducing diet -- in healthy obese patients for 6 weeks weight loss.  They measured triglycerides, LDL and NEFA (among other things) and found that:
  • NEFA levels remained elevated throughout the day in the LCHF group
  • LDL levels increased in the LCHF group, and
  • "The differences in fasting and 24-h FFAs at 6 wk were significantly correlated with the change in LDL cholesterol."
Interestingly changes in fasting triglycerides didn't differ between groups.  VLDL particle size (and volume) can vary widely.  One explanation is that in the carb-restricted state, more and smaller VLDL are created because fewer free fatty acids are esterified to triglycerides and packed into VLDL.  Thus more NEFA remain in circulation, and as the VLDL degrade to LDL losing their triglyceride load, you have more LDL particles.  I think this goes on to some degree in most low carbers.  

Over-Worked Liver Syndrome:  
Our livers are quite the multi-taskers.  With the help of the pancreas secreting insulin and other hormones, the liver works tirelessly to keep "total energy" in circulation relatively constant, as well as ensuring that some minimum glucose is available to meet basic needs at all times.  If anything, the liver works to ensure that fatty acid levels remain in check, moreso than to maintain a minimum level.  In any case, glucose + NEFA is relatively constant except in times of stress when the bloodstream can be flooded with both to ensure adequate energy supplies to sustain activity. On a mixed diet, energy balanced diet, the liver is in its lowest stress state.  It maintains glucose levels fairly effortlessly by breaking down glycogen and gluconeogenesis in the fasted state, and helps clear glucose in the fed state with glycogen synthesis and a bit of de novo lipogenesis.  The liver is constantly mopping up the lipids as well, packaging and repackaging, and plays a critical role in the TAG/FA cycle to keep circulating NEFA appropriate to prevent "overdelivery" to ectopic (non-adipose) tissues.   In its capacity in TAG/FA, the liver is also performing glyceroneogenesis to provide sufficient glycerol-3-phosphate to esterify fatty acids.  Lastly, the liver is always producing some level of ketones, though this is low in this state.
In the VLC state, the liver is stressed and has to work more tirelessly.  Now, as it's glycogen stores are depleted, it is charged with making almost all of the glucose via gluconeogenesis.  It is also making ketones from fatty acids to preserve gluconeogenic substrates and reduce glucose needs by supplying this alternate fuel.  
(1) Glyceroneogenesis suppressed by gluconeogenic demands:  Since glyceroneogenesis is a truncated gluconeogenic pathway, and maintaining minimum glucose levels are top priority for the liver, it is reasonable to assume that the liver may slack off a bit on its glyceroneogenesis duties.  This would reduce esterification and VLDL output.  
(2) Glyceroneogenesis further suppressed by immediate ketogenic demands:    Here is where the coconut oil comes in.  MCT's are rapidly absorbed -- mostly bypassing the chylomicron incorporation and dumped directly into the portal vein where the liver takes them up and oxidizes them.  It does not appear that there are quantitatively significant pathways to elongate MCFA's to LCFA's, thus these fatty acids are thermogenic and act rather "carb-like" in this regard.  However they place a high and immediate demand on the liver to create ketones.  This is a good thing if ketosis is the goal, but the liver may well reduce other things.  
There is plenty of anecdotal evidence for over-working the liver and this organ prioritizing metabolic functions in observations with alcohol.  Alcohol cannot be stored so it is oxidized preferentially, and can dramatically suppress gluconeogenesis.  For those with compromised livers this can be a problem -- search on alcoholic hypoglycemia for example.  

Making LDL Directly?:  
Here's a paper I just came across today ... admittedly I haven't gotten to read it thoroughly.  Although it's rather old (1984), it may well be worth looking into further at some point.  I'd go so far as to put it out there to the audience, that anyone so inclined to do a detailed analysis is welcome to my "floor" here at The Asylum in the form of a guest post (carbsane at gmail dot com), as it would be some time before I would even think about getting to this in any great detail myself.  
One more thing before the relevant findings therein ... this is 80's science and it looks pretty damned good to me.  The scientists get a really bad rap in all of this, and if the LC community ever wants its science and scientists to be taken seriously, it needs to collectively cease and desist on its bashing of other scientists.  
Here's the major thing that surprised me.  The usual progression of lipoproteins is generally that the liver secretes VLDL (large) that degrade to IDL as they lose triglycerides and eventually to LDL which latch onto receptors to deliver cholesterol to cells for use manufacturing hormones and such.   There's a lot there, but:
Kinetic studies in patients with familial hypercholesterolemia have suggested that LDL must arise in part from sources other than VLDL. 
If I'm reading this paper (please correct me if I missed something), one of the things they are saying is that rats fed high cholesterol diets tend to produce more LDL directly from the liver.  They discuss a number of inter-species differences, and this is probably the longest shot amongst my proposals, but the "large fluffy" LDL -- which is characteristic of FH (cite needed please, I recall this from discussions here) -- may be that "missing" LDL source that doesn't come through VLDL degradation.

Danger!  High Fat Load / Low Clearance!  
According to this (1989) abstract:   The principal goal of dietary treatment of familial hypercholesterolemia (FH) is the reduction of the plasma low density lipoprotein (LDL) cholesterol. This is best accomplished by enhancing the number of LDL receptors and, at the same time, depressing liver synthesis of cholesterol. Both cholesterol and saturated fat down-regulate the LDL receptor and inhibit the removal of LDL from the plasma by the liver. Saturated fat down-regulates the LDL receptor, especially when cholesterol is concurrently present in the diet. The total amount of dietary fat is also important. The greater the flux of chylomicron remnants into the liver, the greater is the influx of cholesterol ester.
Now, this is the second time I've evoked FH, and Jimmy mentioned that commenters have suggested he has FH.  I don't believe that he does, as he's has relatively normal and/or not catastrophically high LDL at various times.  However, his lipid profile seems to resemble the FH profile.  Jimmy is "open but coy" about his eating patterns.  He mentions frequently that he  frequently spontaneously fasts for 12-to-24 hours at a time.  Our only glimpse into his menus we've had is this 200g *fat bomb* from his 90 day update.  He's adding in quite a bit of cocoa butter in the form of 2-3 oz chocolate per day (that's quite a lot folks, go look at chocolate bars in the grocery next time you're there if you don't have any leftover Halloween booty for reference or stash on hand)  as well.  Most "high fat meals" in studies are in the 50-75g range for reference.  It is quite possible that even with 12-24 hrs in between "assaults", his LDL receptors can't tell their arses from their elbows if you will

My Suggestions:  (not that he'll listen)

  • Ditch the coconut oil.  For any number of reasons, not the least of which that you are not alone in CO throwing lipids out of whack, just get rid of it.  Replace (partially) with olive oil or macadamia nut oil.  
  • Cut back on all that dairy fat, sorry, those sticks of Kerrygold gotta go.
  • Throw away the ketometer, add carbs in the form of a ton of non-starchy veggies, steamed with a dab of fat for flavor and even eat a chicken breast every once in a while.
  • Eat whole foods and their accompanying fat but lay off the added fats.
  • If you must eat such a high fat diet, eat smaller meals.
  • Exercise regularly like it was 2005.
  • Get your NEFA checked along with your next lipid panel.

So, there you have it.  My hack.  Jimmy was profoundly normal in terms of insulin function circa the May 2008 tests.  His disturbed metabolism is due to prolonged low carbing with ever increasing extremes of high fat and low carb.  This much is obvious to everyone.    A commenter on his post suggested the following:
You seem to have a very slight blind spot regarding this lipid dilemma, which is certainly understandable because you are very invested in “lo carb, high fat” in several ways.
To which his response was:
I’m not “invested” in anything other than helping people find what will make them optimally healthy.
I'm sure he believes that on some level, but his failure to deal head-on with his disturbing lipid profile, while repeating over and over (and over and over and over) things like healthy_saturated_fats, healthy_ high_fat_moderate_protein_low_carb diet,  "large fluffy protective LDL" and such is disturbing to say the least.  IS HIS LDL-P A MARKER OF TROUBLE TO COME?  The answer is that WE DO NOT KNOW.  We do know this man's metabolism is way out of normal FOR HIM.  And we know he's been anything but optimally healthy for years all the while encouraging others to join him LLVLC.  Wha????  

To deny that a man whose sole income for his family is the LLVLC franchise, makes him "invested" is totally absurd.  Of course he's invested.  There can be no change now to Livin' La Vida AnyOtherWay.   

All I can say is that I'm glad I didn't get sucked into this lower and lower carb trap that is laid out at the door of every LC forum and blog out there.  Jimmy is playing his last LC card ... a ridiculous diet comprised of fat with side orders of protein, where he eats chocolate but claims fruit is off limits for him, and hasn't seen a vegetable in months.  His Hold the Hoax buddy is apparently busy writing a book on her Fat Fasts -- you remember those alternating 1000 cal/day fat fasts Dana Carpender has resorted to after her health deteriorated, right?  I wonder if she'll mention HCG in the book.  Meanwhile I think her venture into snagging paleo market share is due out in December.  

These sorts of high fat diets are not paleo.  They are not traditional/ancestral.  They are in some cases not real food, and in most cases not whole food based.  There's not a species on this planet that could eat this way if it wanted to.  Even the Inuit never ate like this.  But I hear Jimmy will be speaking at PaleoFX.  What a damn shame.  Maybe Paleoista can whip some sense into him with a wet spaghetti squash "noodle".  


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blogblog said...

Our closet relatives bonobos get around 80% of their calories from fruit. They get about ONE PERCENT of their calories from animal sources.

George Henderson said...

I remember from a Krauss paper posted on Hyperlipid that IDL or LDL can be released from liver instead of VLDL in presence of enough SFA and DHA.
This might account for high LDL low VLDL of Jimmy's.

"This SFA loaded particle is exported as an IDL (bad) or a large LDL (good). Luckily the IDL appears, on this diagram, to convert to the large form of LDL. But IDL may only be bad if secreted post prandially, I don't know, life is so complex in the ad hoc world of the lipid hypothesis!

Summary so far: Basic particle plus SFA gives the "good" version of "bad" cholesterol. Don't you just love these terms."

This is the link to the picture:

Hope this helps solve the mystery of Jimmy's metabolism.

Seeing as going VLC pretty much cured my hepatitis a few years ago I find it hard to believe there is anything "stressful" going on hepatically. Drinking half-a-bottle of wine or a high-fructose energy drink; that's stressful. Eggs cooked in tallow; that's relief. I'm not the only person to have noticed this.
Conditions that are not already part of the VLC clinical record are probably not worth worrying about at this late stage of history.

George Henderson said...

BTW, alcohol is a toxin, there is quite a literature on this, Coconut MCTs can prevent alcoholic liver damage:
Alcohol plus MCT is much less toxic than alcohol alone.

A little shonky of you to equate the two!

But I think your advice to Jimmy is completely sound.

Only use CO or MCTs when you DON'T want to eat, not added to meals.

George Henderson said...

We aimed to investigate the relationship between dietary saturated fat on fasting triglyceride (TG) and cholesterol levels, and any mediation of this relationship by dietary carbohydrate intake. Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n = 1036, mean age ± SD = 49 ± 16 y) were included. Mixed linear models were run with saturated fat as a predictor variable and fasting TG, very low density lipoprotein cholesterol (VLDL-C), low density cholesterol (LDL-C) and high density cholesterol (HDL-C) as separate outcome variables. Subsequent models were run which included dietary carbohydrate as a predictor variable, and an interaction term between saturated fat and carbohydrate. All models controlled for age, sex, BMI, blood pressure and dietary covariates. In models that included only saturated fat as a predictor, saturated fat did not show significant associations with fasting lipids. When carbohydrate intake and an interaction term between carbohydrates and saturated fat intake was included, carbohydrate intake did not associate with lipids, but there was an inverse relationship between saturated fat intake and VLDL-C (P = 0.01) with a significant interaction (P = 0.01) between saturated fat and carbohydrate with regard to fasting VLDL-C concentrations. Similar results were observed for fasting TG levels. We conclude that, when controlling for carbohydrate intake, higher saturated fat was associated with lower VLDL-C and TGs. This was not the case at higher intakes of carbohydrate. This has important implications for dietary advice aimed at reducing TG and VLDL-C levels.

Evelyn aka CarbSane said...

I didn't equate CO to alcohol, I'll leave that to the fructophobes. It can have the same effect of monopolizing the liver, however.

Only use CO or MCTs when you DON'T want to eat, not added to meals.

That was my point. Or better yet, eat a piece of coconut.

Evelyn aka CarbSane said...

One thing I don't get vis a vis your hepatitis paragraph, is why is it always an either/or? How LC do you eat? Jimmy's current NK is putting a large burden on the liver. To his detriment? We don't really know, but something's going on there.

Not sure your point of the last sentence.

Chris said...

I am glad you have written this Evelyn. It explains a lot.

Recently more and more I have been feeling disillusioned with so much of the internet "health" and diet subculture, fo lots o reasons, not least all of the drama and marketing of niches and positions.

In exercise, diet and other areas there seems to be this unstated assumption that bloggers know best, while scientists are all either stupid, misinformed, in the pay of big pharma & government. Conventional wisdom we are told is wrong. However in speaking to scientists - some of whom I know as personal friends in the real world - it is obvious that in general this is not true. Yes they can struggle to get this published but usually that is because reviewers are being strict about evidence. However, the scientists do know their stuff. They know the literature and the issues much more than the amateur bloggers.

Yes there are things that need to be put right in conventional wisdom - e.g. the demonisation of saturated fat. But even that is not as simple as it seems. And the scientists and their understanding is usually a lot more nuanced than the newspaper reports.

We really need to look to the scientists and the medical professionals for our health advice, not the bloggers. What is worrying is that he may be doing himself serious harm by his diet because he has rejected mainstream medicine.

In the bodybuilding subculture there is something that they call "bro science" ideas that become common knowledge and practice without and is just what everyone does - e.g. you must eat x grammes of protein within 30 minutes of your workout. Gradually that is changing with the injection of more sound research - that meal timing doesn't really matter for example. We really do not like the science for some reason, we are always looking for some new secret, the gnostic knowledge. Eat real food, exercise sensibly etc is just too boring.

Swede said...

Gotta love the "bro-science!" You could call a lot of the non-sense on health blogs "lo-carb science" or "paleo-science." It's the same thing: stuff gets repeated enough by the right people and it becomes generally accepted as true (see: fluffy LDLs, fat-burning machines, insulin turns you into a fat storage machine, gluten is killing you slowly, etc...).

Reijo said...

Chris, sometimes nutrition bloggers are professionals in health care :-) (but I see and agree on your point about LC community) Evelyn, thanks for all of your efforts putting the facts straight. There are too few nutrition professionals doing the same thing. Most are too tame and blend to take a stand. Such a shame.

Larry Eshelman said...

Excellent post!

Jimmy Moore's lipids have been of some interest to me, since I have seen my lipids follow a similar path. When I was on a moderately low carb diet, I had numbers almost identical to Jimmy's "normal" October 2005 numbers. But as I transitioned to a stricter lowcarb diet, and then to a strict VLC diet, I saw results almost identical to his October 2009 numbers (including a LDL-C of 289 and a NMR LDL-P of 2764). It was only when I started eating a PHD style diet (at the high end for carbs and supplementing with iodine) that I saw my numbers substantially improve. In my case, I can rule out several things. My weight and percentage body fat have been stable for 21 years (150lb, 11.5%). I tried eliminating coconut oil (the only effect was lower HDL-C), eggs (no change), most saturated fat (no change). My improvements came after eating more rice, tubers, vegetables and fruit (and less added fat). My guess is that what caused my lipids to go out of whack was that the VLC was suppressing the functioning of my thyroid.

Jimmy makes a couple of statements which display his "head-in-the-sand" stance:

"There’s still a lot of controversy about whether the LDL-P number (and the parallel marker of Apo B) is as or more important than the LDL particle size. Dr. Dayspring is adamant that it’s all about the LDL-P number and that the size isn’t relevant when it comes to heart health."

Jimmy doesn't want to give up the "large, fluffy LDL particles are protective" in spite of his interview with Dayspring. True, there is a lot of controvery among bloggers, but not much among the scientists doing research in this area. Dayspring's writings represent the point of view of the majority of scientists doing research on lipids. Even Ronald Krauss has pretty much dropped the idea that only small, dense LDL-P are pathological.

JM: "What I want to know is how I can simultaneously have outstanding insulin sensitivity, an A1c score of 4.5, average blood sugars around 81, a heart scan score of zero, undetectable inflammation, 94% of my LDL particles are the large, fluffy kind (Pattern A), a microscopic triglyceride/HDL ratio of 0.7 and active weight/fat loss AND a greater susceptibility for atherosclerosis because of an extremely high LDL-P and Apo B. The answer is out there and I’m bound and determined to uncover it for my book next year."

Jimmy continues to focus on the pathological pattern associated with insulin resistance and the metabolic syndrome (high trigs and a high number of small LDL-P), pretty much ignoring the other pathological pattern of normal trigs and a high number of large LDL-P of which FH is the best known but not only example. In his interview with JM, Dayspring devoted more time on the first pattern, since it is more common, but he does mention the second pattern.

I can only shake my head in amazement at the idea of Jimmy thinking he is qualified to write a book about cholesterol.

I totally agree with Chris's comment about scientists knowing their stuff, except I would distinguish between scientists and medical professionals. Most medical professionals are hopelessly ignorant when it comes to lipids. This a point that Dayspring makes. The main purpose of his website is to educate medical professionals. I doubt if my doctor knows the difference between LDL-P and LDL-C. He dismissed the NMR results (a test which I requested, and paid for, in spite of his protests), but when he saw that my TC and LCL-C was high, he prescribed a statin (which I didn't take). He didn't even ask me about my diet.

Dave said...

Have you read, 'The Great Cholesterol Con' by Anthony Colpo? He pretty compellingly destroys the whole theory that cholesterol has anything to do with heart disease. Personally I think most of this LDL crap is nonsense.

Unknown said...

Regardless of what the ratio of his HDL/HDL transgliceride protogyneme ad hoc prandial inhibitors might tell us, he doesn't look good in his most recent "after" pic, he looks like an unhealthy person who lost some weight but who is still unhealthy.*

If you are going to be an internet diet guru you have to really bring it as far as photos go, Sisson-style.

*He's the one who picked the photo and chose to post it on the internet so the photo is fair game.

ProudDaddy said...

If I understood correctly, Dr Attria says LDL-P is what counts. Somebody else pointed out the actual nanometer diameter range of LDL and compared it to the space between endothelial cells. I'd need to see some real hard evidence before concluding large fluffy LDL can be protective.

My take on the chloresterol theory is that it is the oxidation of LDL in the artery wall that is the main culprit in atherosclerosis. If so, then the LDL-P concentration gradient could be directly proportional to the amount in the wall. What causes the oxidation is the real question.

Larry Eshelman said...

Anthony Colpo's book, The Great Cholesterol Con, demolishes the LDL-C hypothesis, but this is separate from the LDL-P hypothesis. Since Colpo has not said much about LDL-P, it is hard to know for sure what he would say. However, his views do seem close to that of Chris Masterjohn, who focuses on oxidative damage to LDL particles. ProudDaddy is right that according to this view what causes (or prevents) the oxidation is the real question.

In summary, hardly any lipologist believes the LDL-C hypothesis any more. The two main theories are the response-to-retention (LDL-P) hypothesis and the LDL-modification (oxidation) hypothesis, with the former being the majority hypothesis.

Sanjeev said...

each keto adapted true believer's claiming their lipid panel's the best, and each has the other's vice-versa numbers?

Sanjeev said...

> Most medical professionals are hopelessly ignorant when it comes to lipids

I will forever remember the time a nephrologist[1] told me to lower my cholesterol (my lipid numbers are within all the limits but once in a while show up at the high end, sometimes low). He took my blood pressure 8 times (it's been "normal to normal-low" my whole life) before rejecting his personal theory what was wrong with me then looked at my records and fixated on the occasional high cholesterol result.

He must have graduated from the Yosemite Sam medical school - motto on the coat of arms: "extremists are all pikers compared to us".

As bugs bunny might say, "whadda maroon".

I still have NO CLUE - why would a NEPHROLOGIST want to seem my normal cholesterol come down further?

[1] some tests came back badly enough to get a referral but have been normal since then

George Henderson said...

My carb intake is about 75g on average (mostly roots, some fruits honey and sugar). My lipids are pretty normal, around 261 TC, 183 LDL, low TG, good TG/HDL ratio.
On a ketogenic diet my TC (347) and LDL (261) was "HH".
However my HCV viral load was lower on the ketogenic diet, much higher on "normal" mixed diet.
My LFT numbers are equally good on both diets; all normal except slightly elevated ALT.
My ferritin was 251 6 months after ketogenic high-meat diet, but is now 206 and probably trending down still.

Bottom line is I feel more comfortable with some carbs. if I felt better on the ketogenic diet I would stick with it regardless of the whack or otherwise of the lipid numbers. People have lived well for millennia without access to centrifuges.

I blogged about test results here:

George Henderson said...

Here's my cholesterol analogy from my blog:

It’s worth remembering that a crappy diet of cake and biscuits can elevate LDL as surely as a good grain-free diet of eggs, meat and vegetables. We’re not really talking about the same phenomenon at all. Just as, in physics, the phenomenon we call weight can be produced by gravity (on the surface of the earth) or by acceleration (in a centrifuge or rocket), and its meaning and implications may be quite different. Shooting across space in an accelerating rocket ship may well have different long-term consequences compared to standing on the Earth’s surface, even if both sets of scales are reading the same weight at present.

Woodey said...

TBH Evelyn I have removed myself from the internet in regards to nutrition, the lone exception being your blogsite. I find you to be very level-headed and use a lot of information to back up your bogs. Common sense tells me the best source to tap into for nutritional help are people with degrees in the field, nutritionists, people with a degree in biology, and doctors. The internet over all is the worst place to get info, simply because any bozo can print something and most likely it is in direct contrast to what someone with 4-8yrs of higher learning would say.

I was listening to the song Lunatic Fringe yesterday and it reminded me of people like Jimmy Moore and any other diet guru on the internet. They are all on the fringe and steeped in lunacy. Its too bad that so many people get caught up in their garbage. I am glad I was able to get away from it and move on. They feed off of people who don't know any better and the one's that think they know, but their knowledge is based on half-assed theories.

I'm doing Weight Watchers, eating less and moving more. Feel better than I did on LC and getting better results, 16.6 lbs after three weeks. All the claims LCers are making from their diet I can make from Weight Watchers. Uh oh, but that shouldn't be. Anyhow I will not recommend WW as the diet to end all diets, I have better things to do with my time, everyone else has to find what is best for them. I'm just glad to be away from the Lunatics.

eulerandothers said...

I looked at Jimmy's lipid results the same way I look at my own results (doesn't everyone enter their blood chemistry results online and refer to them every time they read something in NCBI about lipid levels?) I look at the ratios.

'Greater BMI, higher systolic blood pressure, higher ratio of cholesterol to high-density lipoprotein cholesterol, and presence of DM were all predictive of first CHD events, and all but the presence of DM were predictive of first CeVD events. '

Using the total cholesterol: HDL ratio (this show ups on my doc's chem report as 'coronary risk' with the note that 3.43 is 'below average' risk):

Jimmy had the ratios, starting when he weighed 410 until last month's weight of 255:


About that ratio:

'The total cholesterol-HDL cholesterol ratio is another powerful predictor at all ages in women and is the only lipid predictor independently related to CHD in men 65 to 80 years old. Inspection of the age-specific association of cholesterol with risk in men and women also reveals that the absolute rates of disease worsen with age.'

His current total cholesterol level is his second-highest of all listed, also not good:

'At each index age, lifetime risk of CHD increased with higher cholesterol levels, and time to event decreased. At age 40 years, the lifetime risks of CHD through age 80 years for men with total cholesterol levels less than 200 mg/dL (<5.20 mmol/L), 200 to 239 mg/dL (5.20-6.19 mmol/L), and 240 mg/dL or greater (> or =6.20 mmol/L), respectively, were 31%, 43%, and 57%'

eulerandothers said...

Another ratio is triglyceride:hdl (insulin resistance

' Insulin resistance was defined as the 25% of the population with the highest values for fasting plasma insulin concentration and homeostasis model assessment of insulin resistance. Using TG/HDL concentration ratios >2.5 in women and >3.5 in men identified subgroups of men and women that were comparable in terms of insulin resistance and associated cardiometabolic risk, with significantly higher values for fasting plasma insulin, homeostasis model assessment of insulin resistance, blood pressure, body mass index, waist circumference, and glucose and TG concentrations and lower HDL cholesterol concentrations than in women and men below these cut points.'

Jimmy's ratios (from his highest weight to last month's values) were:

Looks pretty good! Better than mine!

Dr. William Feeman has his CRF (Cholesterol Retention Fraction)which he uses in conjunction with blood pressure and smoking to predict atherothrombotic disease.

'Using a global risk factor graph with the cholesterol retention fraction (CRF, or [low-density lipoprotein cholesterol - high-density lipoprotein cholesterol]/low-density lipoprotein cholesterol) on the vertical axis and systolic blood pressure (SBP) on the horizontal axis, a threshold line can be drawn using CRF-SBP plots (0.74, 100) and (0.49, 140). '

He also explains this in his comment in the look AHEAD trial news on

'The population at risk of ATD is best defined by a ratio between LDL and HDL (I use the Cholestrol Retention fraction, or CRF, defined as [LDL-HDL]/LDL), which is abnormal at 0.70 or higher, borderline at 0.60-0.69, and ideal at 0.59 or less. This works way better than LDL by itself. Lowering the CRF to 0.50 or less (or 0.49 or less if ATD is present) will maximally stabilize/regress plaque, and hence should prevent clinical ATD events. Combine the CRF with systolic blood pressure (SBP) in the form of a graph and stratify by cigarette smoking status and you have all you need to predict the population at risk of ATD. To maximally stabilize/regress plaque lower the CRF to 0.49 or less or lower LDL to 80 mg/dl or less (using the indirect method of HDL measurement, or 70 mg/dl or less using the direct method of HDL measurement). Bob's yur uncle!'

Jimmy's ratios, from at his heaviest weight to last month:


What I notice is the incredible difference losing those first 180 pounds made!

Sanjeev said...

Evelyn and Euler, thanks for your work.

I'm also wondering how Jimmy's thyroid is holding up, and what his cold tolerance is like these days.

Lesley Scott said...

"Only use CO or MCTs when you DON'T want to eat, not added to meals." I started doing this after reading something on Kresser's blog about how fats like coconut milk or coconut oil wouldn't interfere with autophagy in the morning before breakfast, but would stop you from being too hungry or catabolic. We were out of cream & I guess I'm insufficiently Bulletproof when it comes to trying to wrap my head around sticking Kerrygold or ghee in my coffee at 6 am, but I was hungry, so I spied my jar of refined organic coconut oil & added in a Tablespoon (14g). Gingerly, I tried my coffee & was thrilled that you couldn't taste it, plus it did totally take the hunger-edge off. What's weird, though, is what happened later in the day: I could barely look at the dinner I made myself. Having that Tablespoon of fat totally killed my appetite - the whole reward/setpoint thing that Stephan talks about (and Seth Roberts, too), the key being the refined coconut oil added no flavor at all to the mega-rocketfuel espressos which I make for myself in the morning.

I discovered this whole thing by accident. I'm actually still experimenting with this coconut-oil in my coffee thing & its effect on my overall appetite. It brings to mind that post that Stephan wrote about where the volunteers drank that liquid with no flavor from the strange fridge-contraption and because there was no reward in their nourishment, their setpoints dialed way down and they lost weight like crazy.

ProudDaddy said...

I'm wondering about his lean body mass. I'm not sure that serum biomarkers mean much at all when actively losing weight. At some point he'll reach homeostasis and his lipid levels will be more relevant.

Lesley Scott said...

yay Weight Watchers! I'm happily maintaining my weight loss on WW by eating stuff that satiates (and unlike these obese LC'ers doling out diet advice, I'm 5'4" and 109-111 pounds - this at age 47. Counting the Points makes it easy for me to know I'm not going overboard (I truly believe my internal "you're full" meter is dysfunctional). Where I disagree with WW is the idea that you can eat "anything" in moderation, as doing so with some foods makes me binge on sugar like there's no tomorrow.

Sanjeev said...

Have you kept that up?

Roberts' theory predicts that if you keep doing it your brain/body will associate the coffee's taste with the coconut calories and your appetite will no longer be suppressed.

Unless you're crazy-spicing? - adding random spices and mixtures of spices so the coffee's taste varies enough to confuse the sensors in questions into not learning the "coffee = calories" association.

Sanjeev said...

> alternating 1000 cal/day fat fasts Dana Carpender has resorted to ... her venture into snagging paleo market share is due out in December

several interesting things about that ... will she come up with a paleo fat fast ... how to get to 90% fat without industrially processed items, considering ... the Atkins fat fast recommended butter (a chemical extracted from food using machinery) and sour cream (an industrial food) and macadamia nuts (a new world food I believe)

Also interesting will be how they deal with the "no restriction needed", "eat all you want" sales pitch - drop the pitch for the fat fast, and pretend it doesn't conflict? Put it in as some kind of emergency thing (so it doesn't "really" eviscerate the pitch)?

Lesley Scott said...

I did go read what Roberts said & what seems to drive the setpoint first & foremost is the flavor and how strong it is.

So, as long as there's no really "strong" flavor associated with the calories (which need to be the exact same amounts & consumed daily - ie. like your typical fast food), you can go on doing this indefinitely, apparently. I think my "crazy" spicing is accomplished by the fact I have my strong coffee three different ways: the first one of the morning (I get up around 5) is black - so strong espresso-flavor & no calories. The second one has the coconut oil: same strong-espresso flavor but no discernible flavor to the coconut oil but with the 100 or so calories. My third (and final) coffee of the day is after I work later, later in the morning, with almond milk - so a different flavor & completely different calorie count. Roberts mentioned that the reason home-made stuff has less of a flavor-calorie connection is that the calorie count will vary when you make stuff at home, even if it comes out of a box or bag (eg. mashed potatoes or maybe pasta, etc.) which functions to weaken the association, which keeps it from dialing up your fatmass setpoint.

I eat baked potatoes for a snack & have been trying to "crazy spice" those in order for them not to become setpoint-dialing-upping. Roberts mentioned one study where the volunteers were given 2 different spices to use which changed every two months, for a total of 6 months of the study. So I've gone on a serious safari in my spice rack lately.

Lesley Scott said...

here's what Dr Thomas Dayspring said about this JM Lipid Report:

"Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. You also should not say an LDL-C of 285 has no meaning. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I'll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets."

Lerner said...

I had to chuckle a bit on seeing that Dayspring's comments there were voted down. He commits two cardinal sins: 1) saying that SFA can be harmful to some, and 2) saying that statins can be beneficial to some. I don't know how long he can co-exist with Nutzi. He also, btw, disagrees with Attia in saying that that very low LDL is no problem (there are people with genetic beta hypolipoproteinemia who are quite healthy, IIRC). Still, not every comment there is of the rebel-against-the-establishment type, some are very level-headed.

I'd have to agree with Dayspring's suggestions. Since Jimmy didn't get better results from being in weightloss mode, then he is an atypical case. The only thing to do is to try something different and then retest. Though I'd suggest that the high cholesterol intake might be the problem, not high SFA. If so, he might still wrangle having his regular food with the cholesterol somehow removed - or else have only plant SFA and not any SFA from animals.

Another popular canard of LC is that dietary cholesterol has no effect on serum cholesterol. For the "hyper-absorbers", that's not true. After all, the cholesterol absorption-blocking drug ezetimibe works for some people in reducing LDL-C. 2002
"Briefly, most people fed high intakes of
cholesterol in the diet show a modest rise in plasma
cholesterol while a minority shows either a marked rise
or no change... Hence, people with a high serum
cholesterol, and those who show an exaggerated
response to dietary cholesterol, tend to hyper-absorb
dietary cholesterol and have a low rate of cholesterol

Lerner said...

I'd echo Dayspring's claim that when LDL-C is sky high, that can't be good. So actually the LDL-C hypothesis is valid for very high LDL-C. That'd even presumably go for TC, since a very high TC can only result from a very high Apo-B.

But that raises this specter: if any size particle presents the same risk of entry and retention, then seemingly large LDL should be more atherogenic, since they carry a bigger payload into the artery wall.

Sanjeev said...

you need a new tee shirt Jimmy

"my liver's a hater"

blogblog said...

The paleo and low carb bloggers are basically a rabble of self-opinionated and ignorant nobodies. NONE of them could ever be considered an expert in nutrition. Guyenet is basically a lab technician at 32 (he'd be tenured by now if he was any good). Kruse has been deregistered. The Eades are a couple of Arkansas hillbillies flogging cooking appliances. Th rest seem to be nothing more than snake oil salesman.

blogblog said...

I was taught by Professor Jeff Coombes. He is a world authority on cardiovascular and metabolic disorders. He is also President of Exercise and Sport Sciences Australia (the accreditation body for all exercise physioligists, exercise scientits and professional trainers in Australia). Would I take advice from him or some random blogger?

George Henderson said...

Evelyn, there is some really useful stuff in this post of yours.
It helps to explain how the very mechanisms I'm trying to exploit against HCV replication come about from HFLC. low VLDL, low gluconeogenesis, low TG.

You say "it is reasonable to assume that the liver may slack off a bit on its glyceroneogenesis duties. This would reduce esterification and VLDL output."
How does this come about? Reduced glycogen? This could also match a increased need to burn the lipids rather than exporting them. The ketones will be exported and are not competing as a fuel source.

@ Lesley, I have to burst the food reward bubble but I believe coconut oil is especially good at triggering the satiety sensation in the gut. And ketones can also suppress appetite (or long-term fasting would soon become unbearable, whereas they say it gets easier)

I wonder how much fish Jimmy eats. Swapping fish for steaks more often might make a difference.

blogblog said...

Medicine is a trade - not a science. Anyone trained as scientist (like myself)is invariably gobsmacked by the profound ignorance of basic science by the medical profession.

Professor Tim Spector a medical geneticist asked a group of recent medical graduates how many genes humans had. Only 1:20 could give the correct answer (~23,000). Most of these junior doctors thought humans had MILLIONS of genes.

blogblog said...

Colpo is just another blogger with no real qualifications.

Woodey said...

That's great to hear Lesley! Best thing I did was buy an electronic scale. I had no idea how much food I was really taking in until I started measuring and weighing it out. I was shocked by some of the foods I used to eyeball and assume on the amount I was eating. It really does come down to CICO.

Paul N said...

Just because butter and sour cream *can* be industrially processed foods, doesn;t mean they *have* to be.

I sour my own cream by adding (home made) kefir to it -what is industrial about that?

I then make my own butter by shaking said sour cream in a jar - pretty benign I'd say.

Certainly *much* less violent than a blender making veggie smoothies...

There are better and worse ways of preparing almost any foods. The fact that a food *can* be prepared industrially - almost all can - is not a strike in and of itself against that food, it is a strike against industrial preparation. Anyone who takes their food seriously - paleo, LC, vegan, macrobiotic, whatever, knows that.

The butter fast started with Ayurveda thousands of years ago, and worked quite well.

Dave said...

What happened when we listened to people who had "real qualifications"? Yeah, despite eating meat for 2 million years, its actually bad for us because of saturated fat. Right.

Read the book and decide for yourself what the actual scientific literatue says. Certainly doesn't seem to implicate LDL cholesterol.

MM said...

I'm really wondering how Dr. Dayspring managed to get credibility with JM. I've been out of the loop a bit lately, but it seems like suddenly everyone is talking about "what Dayspring recommends." It sounds like he's saying the same thing the conventional wisdom doctors say. For example, "If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet..." Reduce saturated fat?? Isn't that heresy to JM?

Evelyn aka CarbSane said...

Hi George, Glyceroneogenesis is the major path of G3P production in the fasted state in both the liver and adipose tissue. GlyNG is a truncated path of gluconeogenesis, using the same substrates. If the liver is busy using (needing) those substrates to make glucose, it may make less G3P. The unfortunate thing is that IF this is occurring the lipids aren't being burned, they are just essentially passing through the liver and not being recycled back to trigs as they are supposed to be.

Fish? He takes fish oil religiously, but he only actually ate fish like twice a year the whole time he had his menus blog.

Evelyn aka CarbSane said...

BTW, if the liver doesn't recycle the NEFA, and the adipose tissue isn't recycling it, where does it go? The muscles and other organs that cannot refuse delivery.

Evelyn aka CarbSane said...

Anthony gave me a copy of TGCC, but I never had the opportunity to read it, perhaps over winter break. In reading various debunkings, it seems too many focus on doctor's advice/medical reporting vs. the science. By that I mean that "artery clogging saturated fats" or "dietary cholesterol raises cholesterol", etc.etc. are terms used in "medical news" and by doctors. But there ARE some for whom dietary cholesterol DOES significantly impact LDL levels.

Evelyn aka CarbSane said...

BTW, my impression of AC from his smackdowns of Eades and his Fat Loss Bible is that he is a thorough researcher, and avoids ridiculous cherry picking and mining for anything to support his conclusion no matter how insensible (as in Eades' utterly absurd defense of the metabolic advantage from a few grams differential in insensible water weight!! LOL). This is not to say he's necessarily correct, or that newer evidence might not make him change his mind.

OTOH, we have Taubes who just says TC is meaningless and Jimmy saying LDL-C is irrelevant. Both of those statements are true for some, perhaps a large majority of people. And it has now become "fact" in low carb circles that large "fluffy" LDL is not only not-deleterious, but actually protective! Heck, there's been quite a bit of recent talk about whether or not HDL, long considered to be, is protective after all.

It IS all rather confusing, but one thing I do know, if MY own lipids started changing dramatically and trending worse? I would say SOMETHING's going on and not in a good way. Nobody knows for sure, but I'm sure Jim Fixx would have told the media he "felt great". It's why in many ways CVD is a silent killer.

Charles Grashow said...

"Thomas Dayspring • 4 days ago −
Dr Lipid analysis: Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. You also should not say an LDL-C of 285 has no meaning. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I'll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets."

Here are my latest thoughts on this whole paleo/primal diet

All evolution cares about is the survival of the species - that is that human beings reach reproductive age and that they give birth to enough offspring to continue the growth of the species - that the mothers live long enough to take care of their children until the childre give birth - that's all that evolution cares about - if that occurs and people die in their 50's or 50's so be it

About 50,000 years ago - following a 1,000 year drought in Africa the entire human population was reduced to less than 10,000 - Dr Spencer Wells says the population could have been as low as 2,000 - from this we spread out and basically repopulated the world to the point we are at today

We ate WHATEVER was around.

Humans have multiple copies of the amylase gene - does this mean we are meant to eat starches?

Now that we are at the point where the human species is no longer in danger of dying off sue to low population we can try to determine the optimal diet for longevity

This is where the whole paleo mishigas started

I'm pretty sure of one thing - Jimmy Moore is a heart attack waiting to happen - I'm coming around to the point of view that LDL-C DOES MATTER - that LDL-P DOES MATTER - that an 85% fat diet with loads of added butter, coconut oil, high fat dairy is probably not a good thing

I'm seriously thinking of reducing the saturated fat in my diet and adding 10 mgs of Lipitor on a daily basis

I think the LDL-C should be <100 mgs/dL

Evelyn aka CarbSane said...

There you go again, hating! Didn't you get the memo from Fat Head that we now measure health by not getting heat stroke while playing frisbee golf? LOL.

Evelyn aka CarbSane said...

I'm listening to the Dayspring podcast ( and wondering what was going on in Jimmy's mind throughout it! But Dayspring did a video series with my good buddy Taubes (grin) . He is of the carbs -> triglycerides/VLDL -> high LDL-P. Jimmy's results sure as heck shoot down that notion!

Lesley Scott said...

good move on the kitchen scale. mine lives out on the counter & even though I'm maintaining, whenever I'm in the kitchen, everything passes by the scale. I figure I have so many opportunities eating out to eyeball portions, why not take advantage of the opportunity when I'm home to know for sure. It does come down to CICO, I agree, which to me means a diet primarily of foods that are less processed and more "real". regardless of whether Stone Age or New Age.

Lesley Scott said...

@ George Henderson Interesting about your thoughts that it's the coconut oil rather than the lack of its discernible flavor in the coffee that matter. regardless, it's turned out to be a pretty powerful appetite-regulating weapon for me. And I dunno if it's just me, but even hearing the word "ketones" these days makes me shudder involuntarily, almost as much as the mention of the word...Taubes! Boo! (even worse, as Evelyn once wrote, the phrase: "Gary Taubes teaches us..." Ugh. And Ugh again.)

Funny you should mention fish. That's another one I've discovered through trial & error is really really satiating. It makes a huge difference if I've overdone it earlier in the day & need to eat dinner, but want to really cut back - my goto meal is always fatty fish with a veggie of some sort. Sort of a joyless meal, but it gets the job done - I stay relatively full & the scale stays happy.

Woodey said...

I think the most eye-opening item for me was cheese, it's way heavier than I thought. I used to eat double the amount that I weight out, thinking that I was cutting back. Now that I have the scale I can verify if I really am cutting back or not.

People complain about not losing weight and claim they are eating less then they should, I think they are off on how much they are consuming. This is where I completely agree with Greg Ellis when he tells people they are consuming too much and that is why they aren't losing. When my dad decided to lose weight the only thing he did was cut back on the amount of food he ate, later he started exercising. Looking at him know one could not guess that he was ever overweight.

I like how Weight Watchers is getting me to eat more "real" foods. Processed foods are a waste of points and costly.

Woodey said...

Hello Evelyn,

I was going to email you and ask if you had read the TGCC yet. I'm glad you have a copy and I am dying for you to read it and share your thoughts. That book is one of the few I have kept from my LC/Paleo days, because I thought it had some worth to it. Cheers

MM said...

Yeah, I'm having a hard time finding out much info on Dayspring. The two interviews you mention seem to be it, and I really don't want to torture myself with having to listen to Taubes, or JM. However, if what you say is true, and Dayspring believes carbs cause high LDL-P then JM should be Dayspring's black swan. Or is that whole swan thing passe now?

Charles Grashow said...


I’m currently on a personal quest to find the answers to these questions and more by speaking directly with as many of my expert friends in the medical, nutrition and research fields over the next six months researching and writing my book all about this topic tentatively titled A Patient’s Guide to Understanding Your Cholesterol Test Results (releasing Fall 2013). People are so confused about what to believe about their cholesterol test results that this book is way overdue. Arming people with solid information will help them make a more informed decision about what to do about the current state of their health rather than blindly following some dubious drug therapy promoted by their doctor to treat risk factor numbers. It’s high time we start treating actual DISEASE rather than risk factors anyway.

fiero-flash said...

Context of my comment: Evelyn, I often think you are too harsh on Jimmy. Perhaps this is due to be not knowing everything that went on behind the scenes, but I personally haven't seen enough evidence that he's not a nice guy, that he is much more concerned with making money than helping people at this point, etc. That isn't to say that he isn't financially tied to low-carb, but I still think through denial and wishful thinking he honestly believes he is doling out useful advice and helping people.

Having said that...

How can he not see how it looks to post his extremely alarming lipid results, mention that he's working with a doctor he trusts who thinks said results indicate he is doing tremendous damage to himself, and, IN THE SAME POST, talk about how he's writing a book to help people interpret their own lipid results?

Doesn't listening to Dr. Dayspring (which is a GOOD thing) and considering what he is saying as arguably valid disqualify him from writing such a book? How can someone not sure how to interpret their own results help others?

Now, is possible he could go through this whole experience, learn a lot, and then, if he clearly learned some good information that helped him, end up writing a book about what he'd learned. But that's not what he's doing. He's already has signed to do the book and has a deadline, while he sits there confused by his own results. This is madness.

Chris said...

It is a bit harsh to put Guyenet in the same bracket as Kruse and the Eades. In any case, I wouldn't even call him paleo and he is definitely not low carb.

Chris said...

Reijo - I know, thanks. I was being a bit broad brush there. It is actually a bit scary if we are getting to a position where people are eating in a way that could be very risky. Matt Stone has a book about Paelo Myths which is really good, with a chapter of anecdotes of people who really suffered on a low carb / paleo diet. (Ironic of course is that Matt is another amateur blogger....)

Chris said...

Colpo used to be low carb himself - his forum was "Low Carb Muscle" if I remember correctly. After research and experimentation he rejected it though for a more moderate approach - pretty typical bodybuilding macro counting diet - with carb levels determined by activity. His Fat Loss Bible is a good book too.

Chris said...

Got to agree on the importance of weighing and measuring - even occasionally - if you want to keep control. I've lost a bit of fat this year from paying attention to calories and macros. I am not pursuing low fat as such, but I find I need to limit fat if I am going to get enough protein and carbs without blowing my total calories. A little electronic scale is very valuable

Lerner said...

MM, Dayspring immediately goes to VLC as the panacea. I have never heard him mention eating less or eating low GI or reducing bodyfat. Not a word about benefiting from exercise. So he's in with classical Jimmy and Taubes on that score. He also says somewhere that he himself is 'obviously' IR (or maybe diabetic).

Dayspring also never mentions risk from central adiposity, so I assume that he's gambling on his medications protecting him there.

I don't think at all that Dayspring's views are negated in any way by Jimmy's case. Jimmy seems to be a genetic exception. As Larry has already mentioned, Dayspring also includes as rarer causes the cases of FH and he also mentions hyper cholesterol absorbers.

Dayspring's foundations seem correct, but I disagree with his leap to VLC. Also, Dayspring seems very impressed with Taubes, so Dayspring must have never noticed that the Japanese weren't fat from eating carbs.

There is not much of Jimmy in his two interviews with Dayspring. You just introduce him and he gives his standard talk -- 4,000 times over many years, he says. I think he might be associated with the company that has the patent on that NMR LDL-P test. Somewhere, I *think* he says that "we" just got FDA approval for a smaller machine that will be sold to other practices around the country. Otherwise, why is he spending so much time promoting the NMR test? I don't know. If you find out, please post.

The videos with him and Taubes are very disturbing, I don't blame you for not watching those :) People are judged by the company they keep.

Woodey said...

@Chris - This is my first time doing WW, but not my first time trying to lose weight by measuring. In high school I needed to lose some weight for football and dropped 40lbs by weighing and measuring my food. It seems the best results I have ever had have come from being strict in monitoring my food and knowing exactly how much I have had to eat.

I also have had to limit my fat intake, which is the complete opposite from my LC/paleo days, but with the WW system I can eat more food if I do so. Like I have been telling people, "that scale was the best $40 investment I have made in recent years." :)

bentleyj74 said...

I seem to remember something about lauric acid and satiety/mild nausea [lol] posted on this blog. I agree that coconut has a bit of a different quality to it. I like to use coconut milk in peppermint mocha. Just a tablespoon or two [35ish cals?] is a great afternoon indulgence. The cocoa melts into warm coconut milk perfectly and it has a nice texture. Every bit as good as a calorie dense version of the same thing at 4 bucks a cup.

Sanjeev said...

Always entertaining to watch someone deal with their "issues".

Sanjeev said...

No tribe of 25, two million years ago could do a fat fast using butter and sour cream.

Industry means a lot more than machinery. It includes infrastructure and economies of scale that allow massive amounts of food to be delivered 24x7.

If one consumes a food 24x7 today that was eaten once per month 2 million years ago, that's NOT paleo.

Ayurveda/aryuveda and paleo ... that combo has a "specialness" all its own.

Sanjeev said...

He's been low carb for years and years.

His poison's[0] composition ain't changed much, just the amounts he inflicts upon his hapless body.

And if the usual happens again he'll be overdosing on calories again soon.

Homeostatis? Hold up the jigsaw puzzle piece called homeostasis, and another called "Jimmy Moore" and they don't match. No way, no how, no when

... nope. Ain't happening. UNLESS he gets serious help.

[0] or his preferred substances of abuse

Evelyn aka CarbSane said...

Blogblog, you've managed to get me to defend Kruse! He's a total bullshitter on the internet, science-wise and otherwise, and he's been suspended by his society, but to the best of my knowledge he is still (horrifyingly IMO) licensed to practice. Has anyone in the Nashville area ever checked to see if his practice exists?

As to the Eades, they are the epitome of in-it-for-the-money. Near as I can figure their venture into restaurant ownership came after Protein Power, and what did they invest in? A Mexican fast food joint ... talk about carbfest. The 6WC was a joke and did irreparable damage to their reputations in my book. Eades was just too full of himself changing the world with the sous vide thing. It's not the next microwave! LOL.

As to Stephan, I realize you are influenced by Peter's unrelenting bashing, but your comment doesn't even make sense. For starters, a PhD thesis requires original research. You are guided in this, but it nothing like writing a very long term paper. To my knowledge he is not working in an academic educational position where he is teaching, and even if he was, he is not many years a PhD. Tenure takes a while, and only relates to academics in teaching capacities ... He's been lead author and otherwise othered quite a few peer review papers in major journals in the past year. Lab tech? I think not.

Sanjeev said...

> Only 1:20 could give the correct answer (~23,000).

It would be nice if more had been able to answer correctly.

Personally, If given an either - or choice I would prefer MDs get a course in skeptical thinking, including the logical fallacies and fallacies of memory and cognition than memorize this piece of data.

And as long as we're talking "utopia" I wish all MDs were forced to use Dr. Lawrence Weed's systems or similar, vetted and verified decision systems

rather than the ad hoc expert each MD personally develops through experience.

An excerpt from that interview
LJ: When these medical students trained in medical problem solving graduate, do you envision that the world in which they will practice would be different from today?

In short, the correct diagnosis could have been easily identified in the first 15 minutes of care.

LW: It will be very different. The practice of medicine must become a defined and coordinated system of tasks and reliable performers—just like the airline system is a combination of pilots, mechanics, radar-skilled performers, and others, along with educated consumers who learn their roles from childhood on. The present system of medical schools teaching knowledge and graduating physicians performing as they do now will become an anachronism.

Lerner said...

MM says, "I'm having a hard time finding out much info on Dayspring"

Dayspring thanks Jimmy for introducing him to a whole new audience, viz. the Taubes/Attia followers. Before that, I think Dayspring was only doing talks in person. Plus, he has the lecturepad site, which as Larry mentions is aimed at doctors - though I don't think it is actually accredited CME, you just get some certificate.

Sanjeev said...

> something about lauric acid and satiety/mild nausea [lol] posted on this blog
From the time I was hanging out over @ Seth Roberts' I recall no special consistent satiety attributed to coconut oil over walnut, olive, safflower, canola/rapeseed, or just plain 200 calories sugar sweetened water.

as far as inconsistent satiety, yes ... for each and every material one can name, someone seemed to have gotten good satiety.

Lerner said...

Evelyn, you should appreciate this study (FFT): 1983
"Low-density lipoproteins (LDL) receptor activity, as reflected by LDL degradation, was stimulated by the addition of insulin to cultures of human skin fibroblasts."

bentleyj74 said...

Not familiar with Seth Roberts, maybe Evelyn and her magic recall can come to the rescue. Lauric acid, anyone? Something something satiety via nausea? In any case I imagine this isn't a great selling point even if it is true.

Chris said...

A video for Jimmy:

Evelyn aka CarbSane said...

Aww c'mon Paul! How many people are doing this?

George Henderson said...

@ Charles,
low LDL does give reason for concern in some areas.
Rather than taking lipitor, how about adding more fish and nuts? Olive oil? Those are all supposed to lower LDL. It may be necessary to adjust EFA on high SFA diets for some. Also consider whether iodine intake is adequate.

Fructose is preferred over glucose as substrate for glycogen. This, not DNL, might be how fructose elevates triglycerides.

If sugar feeding elevates LDL, and saturated fat elevates LDL, are identical LDL counts from both diets therefore equivalent in CVD risk?

Any interpretation of LDL and risk might be blaming fat for an effect particular to sugar.

This would explain why saturated fat intake doesn't really correlate with CVD risk epidemiologically, yet LDL might (arguably)

Evelyn aka CarbSane said...

He wrote Shangri La diet that suggests eating tasteless oil or sugar water and not eating for several hours before eating a meal. My magic memory remembers Dana Carpender tried this -- waking up to pee at 5am, downing a shotglass of oil, then going back to sleep. I also recall she abandoned this.

Evelyn aka CarbSane said...

BTW, to me, Seth will be best known for this gem of a print interview with Taubes. This was not long after GCBC was published.

Evelyn aka CarbSane said...

George, have you read the Where do Trigs come from series yet? The vast majority of triglycerides secreted from the liver come from repackaging "pre-existing" fatty acids, and NOT from DNL. While a fructose load can transiently increase DNL dramatically, we're still not talking a lot over a 24 hour period. DNL only amounts to a few grams/day.

Gadfly said...

blogblog still repeating the invalid inference about bonobos and chimps, I see. Bloody Kitavans must be suicidal! What with their eating nearly 10 times blogblog's recommended animal protein intake!

Evelyn aka CarbSane said...

@euler -- Thanks for running these numbers! If you have this in a spreadsheet, I'd be curious if you have TC/HDL or LDL/HDL ratios. It has been quite some time since I've had values to worry over -- the last set was in early 2000's when I was quite heavy and my LDL was borderline high. I did my own research back then and because of my high HDL those ratios (and trigs were OK but I have no recollection the exact number) were quite good for goals at the time.

I'd say Jimmy demonstrates Dayspring's almost mockery about how easy the Trig/HDL ratio is to get a handle on things to be waaaaaaaaaay off base.

Evelyn aka CarbSane said...

Thanks Chris! I do believe there's a horrible and unfortunate disconnect between science and medicine. As I listen to Dayspring's podcast I'm cringing here and I'm only halfway through. Some MD's are even worse -- Cate Shanahan who claimed carbs are turned into LDL by the liver comes to mind.

This sort of thing is why it is so important to hold Jimmy Moore accountable too. I am shocked, SHOCKED, he has a book on this in the works.

Evelyn aka CarbSane said...

Sanjeev, which scares you more though? The run-of-the-mill mainstream MD or the "other MD's are so pathetic" types who claim to know the true path? That's partly rhetorical, but also a brain teaser for all here.

Evelyn aka CarbSane said...

Thanks Larry! Yeah, one of these days I'll finish off a rant on scientist vs. doctor vs. wannabes. There are always exceptions, but I do not consider the doctors who run most clinical dietary interventions to be scientists. This is not to say that some docs can't be excellent scientists, but I'm frankly HORRIFIED by some of what passes for "science" that comes out of the mouths of some of these doctors. It wouldn't be quite so annoying if they weren't snidely mocking others in their profession as pathetic (Dayspring uses that word a lot in the first JM podcast, I'm about 3/4 through) know-nothings of divine wisdom.

Charles Grashow said...


I've been corresponding with a doctor at the Cleveland Clinic who specializes in Molecular Cardiology. I e-mailed him the results of my latest blood work and his response was

"The actual percentage of fat is not critical. We suggest limiting saturated fat by restricting meat, milk fat etc.

Avoid trans fats (margarine, commercial cookies, muffins, etc.)

Encourage canola and olive oil, which are high in monounsaturated and polyunsaturated fats.

You are really NOT a high risk patient given your otherwise excellent health and high HDL.

No need to kill a fly with a sledgehammer. Moderate dietary changes and low-dose atorvastatin make the most sense.

I looked further into the “Iranian” method and its really not supported by any good science. Your LDL is probably about 150-160

10 mg of atorvastatin should reduce by about 40%, giving you an LDL of about 100nmg/dL, which is fine for a low risk individual."

Per Jimmy Moore - "My blood work from October 2005 showed my lipid profile as nearly ideal with HDL at 71, triglycerides at 57, VLDL at 11, LDL at 119, and total cholesterol at an acceptable 201. This was what my numbers looked like after livin’ la vida low-carb for about 22 months and I was proud to see them doing so well."

MY question is WHY DID HE CHANGE????

Evelyn aka CarbSane said...

Good to hear WW's working for you Woodey ... hope your semester is going well. The reasons I think Americans didn't on average (NHANES) lower fat are that (a) being "bad" folks would tend more towards underreporting, and (b) it is too darned easy to underestimate amounts, especially in semi-liquid types or things like cheese that don't have markings on the package. Butter and cream cheese are easy to be accurate in estimating if one pays attention to the package, but dressings, mayo, sour cream, or pouring oils?

Too many my age have nightmares of overpriced food scales with postage stamp sized platforms on a spring that were horribly inaccurate. I bought a nice, tablet thin, stainless steel one with tare and all manner of modes (and 3 spare batteries) for $20 off ebay. It measures dead nuts the same for repeated measures of the same thing (something we used to do in any basic measurements lab). Between that and things like WW online or Fitday, etc., it's not your mo/father's CRD!

Evelyn aka CarbSane said...

I think it's the space, but your link didn't work. Here's link to full text
for anyone interested:
(Stephan's PhD alma mater if I'm not mistaken, BTW)

Yes, insulin RESISTANCE, not insulin! T1's have high trigs.

Maybe I should write a book ;-)

Lerner said...

Also wrt Jimmy: what did he do circa 7-13-09 to spike his small LDL to 1261?

wrt to that doc: he just now "looked further into" the Iranian formula? Wouldn't that make him something of a beginner at this?

Also, the doc says "canola and olive oil, which are high in monounsaturated and polyunsaturated fats". Huh? Correct me if I'm wrong: both have in 1st place an equal % of MUFA, but then OO has in 2nd place SFA whereas canola has PUFA. Then they switch for 3rd place. So if you want more PUFA than SFA you'd go for the canola, which also gives some linolenic acid. (Safflower would be mostly PUFA.)

As for myself, I buy EVOO in the 3 liter cans. Plus butter and sometimes cream, and lots of bread and potatoes, etc.

P.S. Didn't you at some recent time post results of directly measured LDL? Which was it closest to, Iranian or Friedwald?

Lerner said...

From the seminal Acheson 1988:
"When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial
de novo lipid synthesis (1 50 g lipid/d using ~475 g CHO/d)
without postabsorptive hyperglycemia." Am JClin Nutr 1988;48:240-7.
"Glycogen storage capacity and de novo lipogenesis during
massive carbohydrate overfeeding in man"

I would take Dayspring's view to mean that an IR person is equivalent to the situation of saturated glycogen stores in a normoglycemic. The glucose has to go somewhere, so it gets DNLed and then packaged into TAG-rich ApoB particles, which btw typically end up as small LDL.

Evelyn aka CarbSane said...

I believe the small LDL-P is directly related to whether he is losing or gaining weight. He had stopped reporting weight by that time in 2009 when it had climbed to mid 240's again. The Oct2009 would have been at least post weight loss if not current, and before significant regains.

Still making it through Dayspring. Sigh ... do I have to watch the Taubes vids? I think I may have to take one for the team!!

Lerner said...

Canola trivia, going from memory: it's essentially called Canada Oil because the grain fields there are ideal for growing huge amounts of it. It started as rapeseed oil, which is unsuitable for humans because the erucic acid in it is toxic - or at least somewhat unpalatable. So the erucic acid was genetically engineered (gasp) out of it. For a time, some trendy websites buzzed that it was dangerous because there was still erucic acid in it, now there are probably some websites warning that it is GMO.

In the story of "Lorenzo's Oil" (which I never actually saw), the parents search for the mystery ingredient that would help their son's rare medical condition. That turned out to be that same MUFA, erucic acid.

Lerner said...

watch the Taubes and Dayspring vids?

WARNING! The following video contains disturbing content, Taubes and Dayspring all chummy:

@5:50, Dayspring rightly says that using wine to increase HDL and therefore have benefit in CAD hasn't been proven in blinded RCTs. However, I'd also ask to see that same level of proof in the whole *LDL-P is atherogenic* approach - and haven't seen it. I don't know if there is any or not. Maybe it's at lecturepad

No, don't watch. But there is the small oddity of Taubes seemingly refusing to even touch the bottle of some alcohol that he's given as a gift.

I'll post a Dayspring-in-a-nutshell a little later, sans any Taubes. Dayspring could be likable without Taubes.

Alex said...

If you're going to argue that we should eat according to what our closest genetic relative ate, an even closer relative than the bonobos was the Neanderthals, and their diet appears to have been significantly meat based.

Lerner said...

Evelyn was right about coconut oil raising LDL. Here we have Brandeis University nutrition scientist K.C. Hayes apparently at the 2010 International Symposium on Saturated Fats:
(55 minutes). The names Phinney and Volek are also associated with the conference.

Hayes talks about how CO (being almost pure SFA) powerfully raises LDL, unless offset by PUFA (as from the dreaded seed oils like Safflower). Mix some safflower with CO and it doesn't raise LDL so much, maybe in a 50/50 mixture IIRC. Studies were in humans and gerbils --- gerbils are chosen because their lipid profiles react a lot to changes in diet.

His talk also gives a nice historical perspective on the research and reasoning through the decades which led to the recommendations to replace SFA with PUFA. Maybe the overall emphasis throughout that time to minimize SFA was ultimately in error, except in exceptional cases of very high LDLs. But anyway Hayes seems to say that you just need to mix the three types to be safer - SFA, PUFA, MUFA. (Co-incidentally, that's what I've been doing myself.)

The official theme of his talk has to do with effects of individual SFAs (rather than just SFA per se), and also their position in 3-legged TAGs.

It starts slowly. CO is first mentioned around 10:00. No mention at all is made of LDL-P, etc. I learned of this researcher because of a commenter named Edmund on Jimmy's site. also hosted the Krauss interview (about beef creating small LDL).

blogblog said...

"A PhD student learns more and more. about less and less. until they eventually know everything about nothing."

Isaac Asimov.

Most senior academics will admit that a PhD is really nothing more than an academic apprenticeship. The topics studied are usually so arcane as to be essentially irrelevant to the real world.

I attacked Guyenet because he doesn't have any humility. He behaves as though he is a world authority on nutrition and has single-handedly solved the entire diet-obesity paradigm. He seems to think his ludicrously simplistic Food Reward hypothesis has all the answers. He relies far too much on reading papers and nowhere near enough on real world experience or communication with experts in other fields.

One of the problems with Food Reward is that mice have a gorge-starve
metabolism totally different to humans. Guyenet has extended mouse behaviour to humans.

Guyenet is totally incapable of accepting alternate arguments. He considers any disagreements with his divine prognostications as being a personal attack.

blogblog said...

humans and our ancestors have been occasionally eating meat for millions of years. That doesn't mean we have evolved to eat large amounts of fatty meat every day.

Contrary to the low carb bloggers claims most traditional human socities have consumed little meat on a regular basis. High meat consumption seems to occur only where palatable fruit and plant matter is relatively scarce (eg deserts and cold climates).

blogblog said...


canoloa came about because early experiments showed erucic acid is toxic to rats. However later experiments showed that dietary fats in general are very poorly tolerated by rats (wild rats only eat about 2-4% fat).

Charles Grashow said...

the Friedewald equation. Through the Friedewald equation, LDL cholesterol is calculated as follows (where TC = total cholesterol, and TG = triglycerides). The inputs and result are in mg/dl.

LDL = TC – HDL – TG / 5

the Iranian equation, LDL is calculated as follows. Again, the inputs and result are in mg/dl.

LDL = TC / 1.19 + TG / 1.9 – HDL / 1.1 – 38

George Henderson said...

@ Charles, the risk (among others) is that statins will increase fasting glucose.

If I was desperate to lower LDL I would use some form of niacin. I quite like niacin. My LFTs actually improved while taking it, so the whole hepatotoxicity thing must be conditional, maybe on hypomethylation.

Sanjeev said...


Sanjeev said...

> the "other MD's are so pathetic" types

All of this type I've come across (in advertising and TV interviews) had something to sell so

Larry Weed could be in that category too but he has a very long track record of proving his points.

Sanjeev said...

had something to sell so

so I'm even more skeptical than usual

George Henderson said...

Rapeseed oil is unpalatable to humans because of the unfortunate name.
Chinese peasants used it for cooking in classical times (nobles used lard).
If you want to eat like a peasant, be my guest.

George Henderson said...

I feed my guests better than that, but you know what I mean.

frank r said...

What I don't understand is the evolutionary basis for the Shangri-La diet, and without an evolutionary explanation, I'm inclined to write the whole thing off as placebo effect. It certainly didn't work for me when I tried it.

There are other ideas for reducing setpoint that do have an evolutionary explanation:
1) Dr Gundry suggests that a diet rich in fruit and grains is interpreted by the boy as autumn-harvest-time-to-fatten-up. Whereas a diet rich in meat is interpreted as winter-time-to-burn-stored-fat. A diet rich in greens is interpreted as spring-summer-time-to-continue-burning-fat-and-become-lean.
2) Cold exposure (Dr Kruse) means winter, and winter is the time to burn stored fat and thus lose weight.
3) Some forms of exercise are difficult when encumbered by excess weight (pull-ups, etc). So performing those exercises may lead to weight loss, especially if diet is adequate enough that the body is reassured that it doesn't need to store energy since plenty more energy will be coming in as food.
4) Most importantly, if you can somehow get weight down and keep it down, then setpoint will eventually be reduced to the new weight. More generally, almost any condition (cold, heat, sleeping on the floor, sleeping in a hammock, sleeping on a rocking boat, sleeping amidst noise, leanness, fatness, bland diet, fatty diet, starchy diet, etc) eventually becomes comfortable if we persist in that condition long enough, regardless of how uncomfortable it was originally. From an evolutionary point of view, it makes no sense for the body to suffer from conditions that are bearable and can't be changed.

Sanjeev said...

the evolutionary basis is this:

1 if your brain & body force you to eat stuff that has not poisoned you before you're less likely to be poisoned

2 Further, flip that around from avoiding poison to something good: evolution would favour your ancestors that found more calories for less work.

That's not exactly how SR puts it but evolutionarily it's solid

> if you can somehow get weight down and keep it down, then setpoint will eventually be reduced to the new weight

That's rare.

Few can put go completely on auto pilot after a large weight loss. Success stories invariably have some active monitoring, with many folks having to do a lot of work to maintain their loss.

I suspect that a reward-system-damping/quieting/suppressing diet would let one eventually go completely auto pilot (with some effort still needed to stay on a damping diet)

> sleeping in a hammock, sleeping on a rocking boat, sleeping amidst noise,

You just cited some analogies to how Roberts' proposed mechanisms could evolve

> without an evolutionary explanation, I'm inclined to write the whole thing off

having plausible evolutionary mechanisms in hand is a plus but discarding ideas if they have no current evolutionary path is dubious ... that's part of the path Michael Behe & Philip Johnson traveled.

Sanjeev said...

> but evolutionarily it's solid

while being pretty loose and non rigorous

Sanjeev said...

> reward-system-damping/quieting/suppressing diet would let one eventually go completely auto pilot
needs to be tested, preferably several randomized controlled trials,

Larry Eshelman said...

Although I find it disconcerting that Dayspring has become such a buddy with Taubes, I don't expect this to last. As Charles's quote indicates, low carb isn't a dogma for Dayspring -- lowering one's LDL-P is what is important, even if this means giving up eating truck loads of saturated fat.

blogblog said...

I have never claimed that we shouild eat the same diet as bonobos. I have stated that we evolved from frugivores and have very few (if any) specific adaptations to a high fat meat-based diet.

True carnivores such as dogs and cats have a vastly different digestive anatomy and physiology to humans.
eg Cats:
- have no taste receptors for sweetness.
- have a very limited ability to synthesise proteins.
- are mostly unable to assmiliate vitamins and minerals from plant sources.
- have extremely limited tolerance to plant phytochemicals. eg caffeine and aspirin are fatal to cats in very low doses.

The Neanderthals were simply one of the many failed hominid experiments. Last time I checked they were extinct.

Neanderthals had no choice but to be carnivores. They inhabited an environment very similar to the modern Arctic where edible plant foods were in extremely limited supply .

blogblog said...

Humans don't need monosaturates. We can readily synthesise them.

Coconut oil is nothing like tallow or lard. MCTs found in CO are metabolised quite differently to the LCTs in animal fats.

blogblog said...

This is the type of event you need to attend to learn from REAL experts:

International Conference on The Science of Nutrition in Medicine and Healthcare.

Larry Eshelman said...

By the "LDL-C hypothesis" I was referring to the mechanism for causing CVD. I totally agree that "when LDL-C is sky high, that can't be good." TC is correlated with LDL-C which is correlated with LDL-P. The question is: when they are disconcordant, which is the better predictor? The evidence indicates that if one has low LDL-C but relatively high LDL-P (like presumeably Tim Russert had) one should worry. On the other hand, if one has moderately high LDL-C but low LDL-P, one needn't worry.

Among the scientists studying lipids there is not much debate about this. However, there is a debate about whether these discordant cases occur often enough to justify testing for LDL-P (or ApoB). Interestingly, the debate isn't only about the additional cost. One argument used against additional testing is that after years of educating doctors about the dangers of high TC and LDL-C, switching to LDL-P will cause confusion.

I should add that high LDL-P can be caused either by producing a lot of LDL particles, or by reduced clearance (reduced number LDL receptors). Chris Masterjohn argues that the problem mainly lies with the latter, because the longer the LDL particles hang around, the more likely they are to oxidize. So one can add two more correlations: high LDL-P is correlated with long LDL-P half life and higher oxidation. Dayspring doesn't address any of this.

blogblog said...


"If one consumes a food 24x7 today that was eaten once per month 2 million years ago, that's NOT paleo."

A bit like the alleged Masai practice of eating vast quantities of meat in one sitting. They do - a couple of times per year.

blogblog said...

@Frank R

"Dr Gundry suggests that a diet rich in fruit and grains is interpreted by the boy as autumn-harvest-time-to-fatten-up. Whereas a diet rich in meat is interpreted as winter-time-to-burn-stored-fat. A diet rich in greens is interpreted as spring-summer-time-to-continue-burning-fat-and-become-lean."

Complete nonsense. Hibernation is controlled primarily by day length and temperature. Animals that normally hibernate don't eat more or hibernate if you move them to a more tempearte climate.

2) Cold exposure (Dr Kruse) means winter, and winter is the time to burn stored fat and thus lose weight.

Everything that Jack Kruse says is unscientific BS. Humans evolved in the tropics where there is NO Winter.

blogblog said...


How am I wrong?

Guyenet relies far too much on "book learning" and rarely discusses his views with real experts. He simply don't understand the deeper context of his statements and so makes many very obvious mistakes. eg If he knew more about REAL food science (not the BS published in'Nourishing Traditions) he would be far better informed.

Guyenet and his followers are bunch of fundamentalists. If you point out to Guyenet that he is wrong (which happens to be very often) he becomes very defensive and starts telling you that are completely ignorant. His rabid followers then mention that he has a PhD in nutrition (wrong - it's neuroscience) and is infallible.

I will give two examples of Guyenet's idiocy and arrogance. [I'll give these two examples because I originally trained as food scientist and am familiar with many traditional food processing methods.]

1. Guyenet claimed that modern flour is much more refined than in the past. He then proceeded to supply some dubious information. his claimes are technically true but completely false in practice. Flour was less refined in the past but it was always sifted before use to remove any fibre. I pointed out this fact but I was informed I was wrong.

2. He claims that sugar consumption has risen dramtically and is a major cause of the obesity epidemic. When I corrected him by saying that overall sugar consumption had FALLEN dramatically in Australia over the past century he said I was wrong. When I showed him the irrefutable evidence - CSR sugar records (CSR was Australia's monopoly producer of sugar until the 1990s. There were zero sugar imports for over 120 years.) Guyenet then claimed the records were wrong. The guy is a total fucking idiot.

Gadfly said...

blogblog's Unproven Assumption #1: we require specific adaptations like those of felines to be able to eat a diet based on fat and meat.

blogblog's Unproven Assumption #2: Neanderthal extinction had anything at all to do with their diet.

Alex said...

If you compare humans to other apes, it's easy to see that our digestive tract actually is adapted to eating a higher nutritional density diet that includes meat. As a whole, the gut is much smaller, the small intestine is very long, and the large intestine is quite short. And, we produce enzymes to digest all three macronutrients.

Evelyn aka CarbSane said...

OK Blogblog, I've let you have your say and should probably delete this for the last sentence. But I'll leave it up, and serve the warning now. If you have a problem with Stephan, take it up with him and if he dismisses your arguments, I suppose you can always start your own blog. I won't let you turn my comments into a food (reward) fight that isn't even relevant to the topic of discussion here.

Lesley and George were discussing the hows and whys that CO might be satiating/assist in weight management. Let's leave it at that, shall we?

Evelyn aka CarbSane said...

So far I'm not having my usual problems listening to the first Dayspring interview, Jimmy mostly let's him go on.

Lesley, Thanks for copying that here for posterity! I'm amazed he let it through. Having listened to most of the interview, I really wonder WTF was going on in Jimmy's mind as he heard Dayspring go on and on and use phrases like "single most predictive", "lethal", "nightmare", etc. talking about LDL-P, something for which he knew his lipid profile has been heading way out there for a good long time now.

I'm surprised he let Dayspring's comment through, though I suppose this is a decision he figures he stood more to lose if he censored it. I predict that like many older posts, comments will be turned off and hidden a few months down the line.

Here's a discussion from LLVLC Disco board in 2009, when LDL-P was 2130:

In response to numbers going in wrong direction, Jimmy: "THANK YOU for your comments, Paula. However, with all due respect, my numbers are fantastic according to Dr. Westman and my small LDL-P is still pretty amazing."

and then "Excellent info guys! THANKS! For the record, I am not at all worried about my numbers. They are stellar in my book and Dr. Westman was not fazed a bit when he saw them."

Dayspring would call them a nightmare. Jimmy called them stellar. I'm hoping he's bluffing that he was approached to write a book on this stuff to bolster his clout. Who would buy such a book??

Evelyn aka CarbSane said...

Yep Alex, we're omnivores.

Evelyn aka CarbSane said...

Dayspring seems quite wedded to carbs -> high trigs/VLDL hypothesis, however. He's not a eat-a-crapload-of-sat-fats guy, clearly, but he seems pretty convinced it's the evil carbs putting all that fat into our artery walls.

I'm having a hard time with the penetrating the artery wall mechanism. Sounds very mechanically based the way it comes off in that first podcast. But then he goes on (I'm trying to get the vision of VLDL-HDL sex out of my head - grin) about the triglyceride load carried by various particles and how that seems to be the problem.

If I were Jimmy, I'd be worried, and no years-old heart scan score of zero would make me feel much better.

Larry Eshelman said...

It is my understanding that the response-to-retention hypothesis, which is the most prominent theory, is very mechanical: particles under 70nm can sometimes pass through the endothelial wall. The more LDL particles that one has, the more likely some will penetrate, and the more that penetrate, the more likely some will be retained. The alternative theory, the LDL-modification theory, holds that only LDL particles that are oxidized are likely to be retained and cause problems.

With regard to triglyceride load: the more triglycerides one produces in the liver (mainly from NEFA), the more VLDL-P, IDL-P, and LDL-P one will need produce to transport the triglycerides.

Evelyn aka CarbSane said...

I'm not here convince anyone of what kind of guy Jimmy is, I just provide the facts in one place and let people decide for themselves. He made a decision sometime in 2007 (?) to leave his full time job to pursue this full time, and since his wife has not worked outside the home (did she ever?) since all of this began, that decision involved even more risk. He is FAR too invested in all of this to write any sort of book on the science, which includes any sort of "layman's guide" to nutrition, lipids, etc.

The big problem for him is he jumped headlong at Dayspring's blaming of carbs and is now being faced with some very ugly realities. Low carbers have emphatically and sanctimoniously been "shouting" for years that the entire lipid hypothesis (like there's some single unifying one anyway) is bunk. Jimmy is heavily invested in "healthy" sat fats and "protective" large fluffy LDL. I'm quite surprised, really, he had him on another podcast.

OTOH, I believe he deliberately left out the pre-2008 numbers that show just how badly his numbers have gone off the rail. It shows his is not a genetic issue per se.

A normal LC diet, a few more carbs, and regular exercise had him doing rather well.

Evelyn aka CarbSane said...

Well, I've finished Dayspring's first podcast with Jimmy. He ended it with "if you're insulin resistant, read Taubes' book". SIGH!

LOL!!! Around the 6:45-ish mark, Taubes says preggo women get fat below the waist because if they get fat above, they'd fall over. Isn't evolution grand!!!!

Evelyn aka CarbSane said...

@Charles: "MY question is WHY DID HE CHANGE????"

He started regaining. Likely for one reason and one reason only -- he started moving less. As he worked more and more at a desk at home blogging, instead of outside the home, and according to his Jan 2007 NYrs Resolutions was also slacking off his cardio, and likely pushing the limits a bit with too many LC "candy cigarettes", he was putting back on a few pounds.

In 2007 he was pushing 250 when he did Kimkins. That was a disaster, because KK was unsustainable crash diet, but also for his credibility as he was trying to grow his business. And then along came Gary Taubes telling him everything he always wanted to hear about carbs and exercise etc.etc. He blamed creatine for his weight gains that really were post KK rebound. He's been chasing mysteries ever since, beginning with Westman in mid-2008.

The better question is why he doesn't go back to what worked for him in 2004-5? It was (1) LLVLC, (2) had him healthy by most measures, (3) relatively easily maintaining by his accounts, (4) insulin sensitive, etc.etc.

Instead he's forging forward with ever more extreme(ly ridiculous) approaches. I'm surprised he didn't see SOME improvement accompanying the weight loss, but that only drives the point home even further. Jimmy is, if they exist, the person who should NOT eat a ton of saturated fat on top of saturated fat and whatnot.

If I lost 50 lbs and my lipids went more haywire, I'd abort what I was doing!!

an3drew said...

I've simply started taking 1200 mg of red yeast rice/day. My LDL is now around 120, where before it was 200-ish. I'm not going to sit around and let everyone's online debates dictate entirely where I go/what I do with regard to my diet and health.

I eat real food to my very, very honest best and supplement with red yeast rice, CoQ10 and fish oil to hopefully give myself a healthy cardiovascular system.

ProudDaddy said...

Googling ldl size and endothelial space got me a 26-page PDF. Turned out, it is by Thomas Dayspring. Haven't studied it yet as it's time for my volunteer work at my daughter's school. Anyhow, Google showed the phrase "particles under 70nm can sometimes penetrate", so I wonder if it is Larry's source.

A carefully constructed paper with illustrations might better represent Dayspring's views than an interview. Let me know if you're interested in it and can't find it.

Larry Eshelman said...

Yes, that is my source. Dayspring is not an original lipid researcher, but rather an educator. I have read many of the articles by prominent lipid researches whom he cites, such as Sniderman, Mora, Otvos, Cromwell, and as far as I can tell he does a good job of representing the current views of these researchers. On the other hand, he ignores the alternative hypothesis -- the modified (oxidized) LDL hypothesis.

Lerner said...

Larry says "low carb isn't a dogma for Dayspring".

I haven't personally heard anything from Dayspring that wasn't VLC (for IR people). I interpreted his advice to Jimmy on reducing SFA to mean switching from SFA to other fats. Come to think of it, I haven't heard of any VLCers who concentrated on getting MUFA or PUFA. Vegan VLCers?

At the end of atlcx29, IIRC he says that lo carb is the 'only' way to both reduce LDL-P and increase HLD-P. He also ignores HDL oxidation which might make it useless or even harmful. As with all gurus, he does focus on his own view as the be-all / end-all. Speaking of which:
"Declining fitness over a decade doubles risks of AMI, death"
November 4, 2012

Here's a prediction from me: some years in the future, registry studies at ERs will show that ~40% of MI patients will have 'normal' LDL-P.

Lerner said...

Evelyn says, "no years-old heart scan score of zero..."

Aha, he didn't mention that "years old" part. He does, however, refer to some HF-VLC GP named Rocky with a similar score. The thing is, having zero calcium doesn't mean there is zero plaque. In fact, calcified plaque might be more stable - less likely to rupture, which might be why the body calcifies it. Having 'hardened' arteries would be better than Sudden Cardiac Death.

Besides, if any VLCer has a currect CAC test, then that'd presumably reflect also the years of SAD eating. They can't say "I've been VLC for 2 years and have a great CAC" and attribute that to VLC.

Lerner said...

I had some memory of rapeseed oil being bitter, so looking now I see this:
"It was less useful as food for animals or humans because it has a bitter taste due to high levels of glucosinolates. Varieties have now, however, been bred to reduce the content of glucosinolates, yielding a more palatable oil. This has had the side effect that the oil contains much less erucic acid.[citation needed]

Also, I've never been pretentious about food and would have no problem with "peasant food". Are you claiming that food gets healthier as it gets costlier?

Lerner said...

I regard MUFA as a source of calories that is probably not harmful (when not too excess), and the many phytonutrients in EVOO just might be helpful. Switching from canola to EVOO is a small and easy measure to take, so it doesn't require a lot of evidence to justify it. OTOH making a radical switch, such as to VLC or veganism, would be a bigger and riskier step that should require very convincing evidence. That's my approach, anyway.

Lerner said...

Even worse, he says, "PLEASE read Taubes book". Like in an infomercial. Or a link exchange.

It's important to restate that Dayspring is always generally talking about people with IR. He says, "who isn't these days?" What is the prevalence of IR anyway?

I think nothing of having half a loaf of bread at a time, plus lots of other carbs throughout any given day. I just had a standard panel in mid-October, and my trigs are at 55.

Charles Grashow said...

Didn't Dayspring tell Jimmy that if his LDL-P numbers didn't improve he would recommend that he take a statin drug?

Charles Grashow said...

Dr Dayspring's comment to Jimmy

"You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I'll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets."

Jimmy's question to Dr. Dayspring

"Thanks for your input Dr. Dayspring. My comment about no meaning was that it didn't tell the whole story. So if I'm not supposed to consume saturated fat, then what sources of fat should I eat?"

I suggested this

"This is a very low carb diet—20 to 40 grams of digestible carbohydrate daily—designed for loss of excess
body fat.
Here’s what you’ll eat:
1) Unlimited fish, meat, chicken, turkey, eggs, shrimp, lobster, pork skins
2) Fish, at least 4 oz (115 g) daily; ideally half of all animal protein
3) Olive oil, virgin or extra-virgin, at least 2–3 tbsp (30–45 ml) daily
4) Nuts and seeds, 1 oz (28 g) daily
5) Vegetables, up to 14 oz (400 g) daily
6) Wine, 6–12 fl oz (180–360 ml) daily (see alternatives in Miscellaneous Comments)
7) Cheese, up to 3 oz (85 g) daily, optional
8) Daily supplements:
 1 or 2 plain Centrum multivitamin/multimineral supplements (two if over 250 lb or 114 kg)
 Magnesium oxide 250 mg
 Calcium carbonate 500 mg elemental calcium (500 mg twice daily if over 250 lb or 114
 Extra vitamin D to reach total of 1,000–1,200 IU (each Centrum has 400 IU)
 Potassium gluconate 2,750 mg (450 mg elemental potassium) or Morton Salt Substitute
(potassium chloride) ¼ tsp (1.2 g)
 If prone to constipation: sugar-free Metamucil powder 1–2 rounded tsp (5.8–11.6 g) in
 At least three quarts or liters of water"

Lerner said...

Lest anyone think that Dayspring's presentations are without error, here are a couple of them:

---- in his first Jimmy interview, he's talking (roughly at 30 minutes) about how everyone needs particle-number testing. He says something about "world class athletes" dropping from SCD. That's very misleading, since most of such cases are caused #1 by congenital heart defects (structurally, especially HCM and HOCM, plus faulty valves or even aortic dissections), not atherothrombosis.
"Shocking Heart Deaths: Why They Happen"

The #2 cause might be myocarditis, wherein a heart infection leads to electrical disturbance and VFib. In many school sports programs these days, players cannot return to the field after a bad cold until several weeks have passed - especially if they'd also had tachycardia.

Testing LDL-P has nothing to do with that.

----- Next, Dayspring's lecturepad images show ApoB as being like a spaghetti strand. In reality, it's more like a wide belt, though misshapen.

This is done from electron microscopy:
and lists the underlying PLOSOne paper.

That's not necessarily insignificant because the heavy-duty nature of ApoB might give some clue... to something. Maybe it's akin to a jet fighter being snagged on an aircraft carrier deck - the equipment has to be very rugged. But OTOH some other less-rugged apolipoproteins (e.g. on VLDL) besides ApoB are grabbed by receptors in the liver.

Larry Eshelman said...

Let me clarify what I meant by "low carb isn't a dogma for Dayspring". Dayspring has been taken in by Taubes (and a lot of other smart people were initially), but I don't believe that low-carb is something that he is wedded to. Unlike Moore or Taubes it is not a belief that defines him intellectually. He is much more tied to the LDL-P hypothesis. I expect that when the evidence starts piling up that low carb is compatible with and may even cause high LDL-P, he will abandone the low carb hypothesis.

frank r said...

There's a substantial difference in night-time temperatures between seasons in places like Tanzania, and in the cool season nights drop to 50 deg Fahrenheit. That's cold for sleeping under the stars with no blanket. You can make a fire (and humnans surely did to keep the lions away), but only heats one side of the body and heats that side so much that you tend to keep a distance. I'm speaking from experience camping. Fur blankets are too heavy for hunter-gatherers to carry around with them.

frank r said...

@Sanjeev: Obviously, humans tend to seek out food that give lots of calorie for little work. The question is why eating healthy calories with little taste to them causes the setpoint to go down. Why would evolution produce that?

Now if the Shangri-La diet involved putting poison into foods we had previously enjoyed, so that we came to associate those foods with nausea (aversion therapy), that would make plenty of sense. But then that name Shangri-La wouldn't make sense because this is a hard way to lose weight.

frank r said...

@blogblog: Humans may be different from animals with respect to hibernation. In any case, the theory cannot be proved/disproved by clinical tests because it is impossible to make these double-blind with humans. This is the problem with everything to do with diet. With enough willpower, virtually anyone can lose weight and keep it off. But willpower and placebo effect go hand in hand.

Gundry's more profound theory is that humans have a killer gene which is activated by eating an excessively rich diet. The idea is that older humans who eat a rich diet and get fat and don't execise are stealing from their grandchildren and not doing any work to help those grandchildren survive, so inclusive fitness is raised by activating the killer gene in those olde humans. Whereas older humans who eat only the minimum to stay alive, and eat mostly poor foods (especially greens), and do some light work each day, are probably providing a net benefit to their grandchildren and so should be kept alive.

Lerner said...

Okay, Larry, I got it. Now, would you care to say a sentence or two on what, if anything, you've decided to do regarding raising HDL-P?

an3drew said...

I've been taking red yeast rice for a few months and my fasting glucose just tested at 82. I think that's okay, but then again I don't have a pre-red yeast rice test to compare it to.

Lowered the hell out of my LDL, though.

Lerner said...

wrt to niacin for raising HDL-P (or other lipid altering uses), lots of people get very turned off by the flush (many Pts don't comply with the their niaspan prescription because of it). I happen to kind of like the flush. But for those who don't, a very effective preventive measure is taking quercetin. That almost completely abolishes the flush for me. It works as a mast cell stabilizer, and works much better than aspirin (which is a COX inhibitor).

The MD/researcher to look up on this is Theoharides. Another flavonoid to use is luteolin, e.g. from olive oil, though it's not so commonly available.

Larry Eshelman said...

I haven't listened to the interview. (I hate listening to interviews, and prefer writings.) But from reading his writings on HDL, many of which may have been written before he discovered Taubes, my impression was that the workings of HDL is so complicated (a lot of HDL-remodeling) that HDL-C and HDL-P are very difficult to interpret. Certainly, in those writings Dayspring was calling into question the great faith that many VLC-ers and Paleos put in their high HDL-C numbers.

Larry Eshelman said...

Here is a quote from Dayspring on HDL in an article titled "High density lipoprotein trafficking of cholesterol": "If one looks at the overall efficient flux process of peripheral cholesterol transport, where HDL particles are formed, lipidated, exchange lipids, and then delipidated one can understand that the overall process will not affect the total HDLC level in a predictable fashion, as there is constant remodeling or shifting of HDL particle size and cholesterol content. Despite what has been taught for decades, a serum HDL-C has no relationship to the apoA-I lipid trafficking process... . Indeed there is no real-world available blood test (e.g. HDL sizes, HDL-P, HDL subfraction-cholesterol) that a clinician can use to assay exactly what HDLs are doing in a given individual."

Larry Eshelman said...

I just found another articles that I have that references the < 70nm number:

Role of Oxidative Modifications in Atherosclerosis

"It is estimated that ~85% of subendothelia lipoprotein delivery is the result of transcytosis, and this process is restricted to particles < 70nm in diameter."

The author cites: Simionescu M and Simionescu N. Proatherosclerotic events: pathobiochemical changes occurring in the arterial wall before monocyte migration. FASEB J 7: 1359–1366, 1993.

Lerner said...

Do ducks float? That's another way of saying: does Dayspring recommend lipid modifying drugs?

I could kick myself for not spotting it from the beginning, but I guess I was lulled because I'd only heard of Dayspring via Paleo/AHS Jimmy; plus, Dayspring wasn't giving any disclosures.

His close ties with Pharma don't bother me a bit. I have never taken a statin; but there are people who have to, despite their best efforts at lifestyle modification. Besides, there are tons of people who just won't do ELMM, so the simple matter is that they need drugs. C'est la vie.

On top of it all, Dayspring has been putting out some good articles, which give insight I think into non-drug approaches that a person can take.

Okay, time for a quick quiz... who said the following: 'For those who do not know, I am a consultant and National Speaker for both Abbott Labs and Merck (Schering Plough). I educate professionals all the time about aggressive use of lipid drugs to achieve goals.

I believe Niaspan, Zetia, fenofibrate, Trilipix, and Lovaza are grossly under prescribed. They are all potential “statin-helper” drugs.'

Okay, you guessed it, it was Tom Dayspring. 2009

I don't know if he still gets speaking fees from Pharma. I myself don't mind that at all, but I suspect that Paleos and others might.

With that said, on to the informative part: "My guess is also that niacin improved apoA-I and total HDL-P..."

(which is how I'd stumbled in a websearch on that article)

Earlier, he said, "Furthermore, the morons in the press are running around telling people they can take an over the counter vitamin for CHD. Niacin at 2000 mg or more mg per day is way beyond the vitamin dosage: it is a major pharmacological dose of a vitamin B3 and cannot be considered a vitamin at that dose and certainly has issues that must be followed."

I've only taken niacin maybe once every 3 or 4 weeks, for various reasons. Usually 500 mg. I don't think I actually need HDL raising, but it'd be a kick to get super high - so perhaps I'll take it more often for a brief period.

Maybe Dayspring will pop in here some day, post Taubes era.

Lerner said...

Transcytosis? That changes things and is the opposite of what I'd been thinking about intercellular endothelial spaces. That fits, then, with the 'crashing' - and maybe also with the role of hypertension. Thanks.

"Transcytosis is the process by which various macromolecules are transported across the interior of a cell. Macromolecules are captured in vesicles on one side of the cell, drawn across the cell, and ejected on the other side." --- from wikipedia

ProudDaddy said...

I'm not certain that it has been noted here that LDL diameters are about 19-23nm. Not sure JM knows this, or he would have dropped the large fluffy protective idea by now.

Larry Eshelman said...

Since the volume is proportional to the cube of the radius, a 19-23mn diameter range means that a large particle can hold about 1.77 time more core lipids than a small particle.

Charles Grashow said...

won’t be writing an actual post tonight because I’ll be spending all day defending my Fat Head Open title against Jimmy Moore, who has been threatening to kick my tail for weeks now. He was a raw beginner when I got him addicted to the game in July, but he’s been playing regularly at home ever since. He bought a basket for his yard and plays from different street locations for different par lengths. He warned me he’s much improved. He’ll be here all week trying to prove it. So it’s on …

Larry Eshelman said...


I now realize that we are seeing Dayspring from the opposite perspective. I discovered his website several years ago and saw him as being pretty mainstream but knowledgeable of the current lipid research. Since I expected him to be anti-low-carb and anti-paleo, I was recently quite taken aback to learn that Peter Attia was relying upon him, and even more so when I later learned that he had appeared on a Jimmy Moore podcast and was sympathetic to Taubes. Nothing in his earlier writings prepared me for this. I consider his pre-Taubes writings to be a fairly reliable statement of the mainstream lipid research, and I recommend him to those who want to understand the thinking of the majority of lipid researchers.

Lerner said...

Note Dayspring's synopsis of plaque progression/regression versus events, which are generally two separate processes. E.g. pointedly, "Pravachol reduces outcomes in its trials but was associated with plaque progression in an IVUS study (REVERSAL)." So that presumably brings in the anti-inflammatory aspect of statins, which might possibly be mimicked somewhat with turmeric, quercetin, etc. But also what foods should be avoided? Which foods sought out? You start to get into the tricky realms of the naturopaths.


IVUS is IntraVascular UltraSound, the sono tip goes right inside the artery to get the best look.

Unknown said...

There are courses in public parks where you have to walk a mile or so to finish the round, that would be the way to go.

It's hard to argue against walking.

Evelyn aka CarbSane said...

Hi Larry, I too have only learned of Dayspring through his podcasts with Jimmy (currently trying to listen to that video series in the background). He does seem to have been commercially involved for quite some time, but I'd agree with Lerner, this does not necessarily tarnish what he had to say. I wonder if he has fallen into a common trap of rebel/groundbreaker/visionary. To me, the particle theory seems to stand up pretty well against the data/observations we have. But then he wanders into the realm of schtick mining and trying to explain the dietary causes.

Here's where, after listening to his first podcast with Jimmy, I think he's gone off the rails a bit. It is almost painful at times to listen to one doctor bash others for being "pathetic" and his intonation is clearly mocking of others at times. It is quite a turn-off. He is also pretty darned committed to the carbs being the culprit -- as in the carbs making for huge triglyceride-rich VLDL because they make the liver fatty and the liver needs to get rid of all that fat. I would love to have a look inside his head when he got a load of Jimmy's lipid profile (and I'm curious if he had a clue what he was dealing with there). I note that I've added 3 rather telling data points to the mix that Jimmy leaves out. Without those one might presume there's an underlying genetic thing going on there, and perhaps Jimmy was just misremembering his pre-Atkins lipids.

I imagine Dayspring thinks Jimmy is an anomaly, and he may well be to some degree, but there's that 2005 data in there that says otherwise. Genetic dyslipidemia shows up before age 35, especially when someone has gotten as morbidly obese as Jimmy did.

I HOPE this will have him looking deeper into the role of IR, and Gary Taubes' take on it, and that Jimmy will be honest with him on that as well. Jimmy had the "OGTT" done shortly after those May 08 readings with Dr. Westman, and his fasting insulin and glucose would have made for an excellent HOMA-IR score, and he wasn't hyperinsulinemic either. Now it would have been nice to see his insulin response to carbs, but he certainly didn't become IR then obese.

In any case, I hope Dayspring will take a step back from his newfound fame with LLVLC and examine his beliefs vis a vis carbs. He is adamant -- basically a "good luck with that if you don't cut the carbs" attitude -- that the only way to lower LDL-P is to cut carbs. Jimmy has done so as much as possible and lost 50 lbs and still he is awash in circulating lipids. It seems Dayspring would consider Jimmy's HDL numbers nothing to write home about.

There's definitely somthing more to his "where there are a lot of fathers, there are a lot of children" theory of LDL as spawn of VLDL, because Jimmy's VLDL is infinitessimal.

Evelyn aka CarbSane said...

Anything that gets Jimmy up and around is good for him. Hard to argue with it I agree. But he's probably over-estimating his activity.

ProudDaddy said...

I noted the diameter range to put it into perspective with regard to the 70nm upper limit on getting through the endothelial space. It wouldn't seem to me to be that much different.

BTW! Larry, my Dayspring PDF does mention LDL reacting with ROS. Although he doesn't use the term oxidation, that's what it sounds like to this layman. Any ideas about what attracts the macrophages?

Unknown said...

This lipid stuff always leaves me bewildered, 155 posts arguing over I don't know what.

Debating what you should eat is an industry in itself, so I can see why there is disagreement over EL but the MM part is pretty clear. I enjoyed virtually all of my weight loss while I was doing nothing more strenuous than walking at a comfortable pace, no idea what my lipid report looks like.*

I would be more impressed with "I walked a 5k!" than whatever the lipid report signifies.

*That is actually not quite true, I recently had my lipids tested for the first time in many years and the result was that I have the lipids of an amphibian reptile, which as anyone versed in the science knows is the best of all possible lipids. My lipids are so good that technically I am not even human.

Charles Grashow said...

"Charles Grashow • 8 hours ago

Jimmy - you said "My blood work from October 2005 showed my lipid profile as nearly ideal with HDL at 71, triglycerides at 57, VLDL at 11, LDL at 119, and total cholesterol at an acceptable 201. This was what my numbers looked like after livin’ la vida low-carb for about 22 months and I was proud to see them doing so well."

What have you changed since then and why don't you go back to what you were doing then??

LLVLCBlog Mod Charles Grashow • 7 hours ago −
What was working then doesn't work for me now 7 yeas later. Thus, I adjust."

My question - why did he change what WAS WORKING??

blogblog said...

Rapeseed oil is indeed quite bitter. It's traditional use was for lubricants.

blogblog said...

Lobsters, oysters and caviar were all cheap peasant foods 200 years ago. They only become desirable when they became rare (and more expensive).

Lobsters were once so despised that servants frequently had clauses in their employment contracts demanding that they were not to be fed lobsters more than once a week.

Apocryphon said...

No, Evelyn was not right about coconut oil raising LDL. "Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation." -

paleotwopointoh said...

Blogblog, you are just repeating food myths.

Larry Eshelman said...


A agree that Dayspring has "gone off the rails a bit." Reading Dayspring, prior to his pairing with Taubes, I don't remember him saying anything about (other than perhaps the usual bromides) diet. In one of his podcasts with Jimmy, Dayspring notes that his medical expertise is on lipids and not other areas. Too bad he doesn't apply this to carb metabolism.

You might be on to something about the "rebel" mentality. I've noticed that those arguing for the LDL-P retention hypothesis fall into two camps. Those who see this as a natural evolution of the old LDL-C hypothesis and those who see this as a refutation of the old LDL-C hypothesis. (They hold the same theory -- it is a matter of presentation.) Dayspring tend to fall into the latter camp.

Larry Eshelman said...


I believe both the response-to-retention hypothesis and the oxidative modification hypothesis involve oxidation. It is a question of when it occurs in the process (late or early). In the article, "Role of Oxidative Modifications in Atherosclerosis" that I referenced earlier, the author says that the apoliproprotein B-100 lysine groups on oxidized LDL particles are modified so that the "net negative charge of the lipoprotein particle increases. This modification of apoliprotein B-100 renders LDL susceptible to macrophage uptake".

Since for the oxidation-modificaiton hypothesis oxidation is a precipitating event, preventing oxidation should prevent atherosclerosis. And in particular, taking anti-oxidants should help prevent atherosclerosis. The oxidation-modification hypothesis has been called into question since in clinical trials, taking anti-oxidants has not been helpful. The counter-argument is that the wrong anti-oxidant supplements were used.

Evelyn aka CarbSane said...

After listening to the Taubes/Dayspring videos, and Dayspring LLVLC podcast, I'm somewhat confused regarding an inconsistency I'm picking up on. If I can summarize:
1. plaque made of cholesterol
2. circulating cholesterol irrelevant, it's only if it gets into your artery wall that causes a problem
3. more particles = higher likelihood of this happening
4. more VLDL (fathers) -> more LDL (children) & more LDL carrying more triglycerides they aren't supposed to carry
5. HDL & VLDL collide (have sex) and transfer bodily lipids and HDL now carry triglycerides too
6. like with LDL, HDL-P is important not HDL-C
7. HDL-C is lower when they are promiscuous with the VLDL so they are carrying more trigs per particle, but we want a high number of HDL cholesterol only transporting particles

Here's my confusion. What are the dump trucks dropping off in the artery wall? Why is high LDL-P deleterious vs. high HDL-P? If particles contain more trigs and less cholesterol, and we don't want the dump trucks dropping off too much cholesterol, wouldn't this be contrary to the infiltration theory?

On a side note, I found parts of the Dayspring/Taubes videos to be downright hilarious. Get a load of the looks Taubes shoots this guy who reminds me of some bizarre cross between Grandpa Munster, Alfonse D'Amato and Ed Koch. It makes me wish I had read his works as Larry did, as one cannot undo the impressions he's left with me now.

Lerner said...

I would be very skeptical of any recommendations that Dayspring makes for Niaspan (prescription, timed release) over ordinary niacin. His patron, Abbott, makes Niaspan.

Larry Eshelman said...

Here is my understanding of the LDL dump truck analogy. The dump trucks mainly deliver triglycerides -- to muscles and fat cells. The various lipases are used to empty the triglyceride content of the LDL particles. (I believe this can be done without the LDL particle passing through the endothelium.) The problem is that the LDL-P dump trucks can get stuck in the arterial wall. On the other hand, the HDL-P dump trucks don't get stuck in the arterial wall. In fact, these can sometimes remove some of the cholesterol from the LDL particles stuck in the arterial wall.

Most of the cholesterol in the LDL-P dump trucks is returned to the liver. Some of it is first passed to HDL-P, and then most of that is returned to the liver. However, some of the HDL-C is delivered to stereoidogenic tissue when needed.

Larry Eshelman said...

An addendum: In fact, I'm pretty sure that the LDL-P can deliver their triglycerides to cells without passing through the endothelium. Large VLDL (those above 70nm) can't pass through the endothelium, but there purpose is to deliver triglycerides to cells. According to the LDL-P retention hypothesis, the LDL-P passing through the endothelium isn't a good thing.

Lerner said...

-- What are the dump trucks dropping off in the artery wall?

The LDL particles stay there (mechanism being unknown for sure, AFAIK - it might be due to Lp(a) or might not, or electrical charges). A macrophage, in it's role as scavenger, detects oxidized entities. That might usually indicate a senescent blood cell, e.g., that needs to be terminated. A macrophage/monocyte wouldn't interfere with a non-oxidized cell or lipoprotein (leaving aside TLRs and so on). Then, an HDL might dock with the macrophage (which is itself within the artery wall), take some 0f the HDL's cholesterol, and exit back to circulation.

--- Why is high LDL-P deleterious vs. high HDL-P?

HDL is conducting "reverse transport" of cholesterol, out of the artery wall

---- If particles contain more trigs and less cholesterol, and we don't want the dump trucks dropping off too much cholesterol, wouldn't this be contrary to the infiltration theory?

If HDL-C is low and HDL-TAG is high, that's not bad in and of itself, but does signal that the VLDLs have had too much TAG upon their creation. So low HDL along with high trigs is a marker for high LDL-P, while isolated low-HDL can be from causes other than high trigs (smoking lowers HDL, low SFA does, high TFA does) and therefore might not be marker for high LDL-P. The actual TAG content of HDL should not be too relevant.

Lerner said...

--- more VLDL (fathers) -> more LDL (children)

I'm not a fan of Dayspring's analogies, since one parent can have more than one child.

Also, note that some IDLs get reclaimed by the liver (roughly 50%, if I remember his lecturepad correctly), so IDL recycling can conceivably be a critical step in lowering LDL numbers... but I haven't heard Dayspring discuss that as an alternative to lowering LDL-P.

Larry Eshelman said...

I got the direction of the cholesterol between LDL-P and HDL-P backwards. Cholesterol usually passes from HDL-P to LDL-P via CETP.

I agree with Lerner, above, but want to add that there are two kinds of reverse cholesterol transport. (1) Direct: from HDL-P to the liver. (2) Indirect: from HDL-P to LDL-P to the liver. A small part of reverse transport is of cholesterol from the macrophage.

Lerner said...

---- The various lipases are used to empty the triglyceride content of the LDL particles. (I believe this can be done without the LDL particle passing through the endothelium.)

The ApoB particles typically dock with target cells, and do not get endocytosed; the CE gets converted to C which enters the target cell since it can pass through the cell membrane. The TAG gets converted to FAs which also enter the target cell.

So the trancytosis of whole LDLs through the endothelium seems as if it is done deliberately by endothelial cells. My guess is that it's because of an out-of-fashion theory: cholesterol is used by the body in the same way that mortar is used to repair cracks. Artery paths are non-idential from person to person. So the stress points from systolic pressure (at turns or bifurcations) will be different. Deposition of cholesterol is a natural process to reinforce damaged areas (as 'rip-rap' stone is used to reinforce a river dike at bends). But the process gets carried away and becomes pathological.


Everything I'm saying here should be prefaced by "it's my current understanding that so-and-so takes place..." I'm not arguing or claiming expertise.

Lerner said...

---- A small part of reverse transport is of cholesterol from the macrophage.

I lerned my version mainly from the animations put out by the APOLLO program on CVD research:
which are also on youtube now. APOLLO includes the trials like JUPITER, SATURN, ASTEROID.

My thinking is that LDLs are meant to get under the endothelium, leave off some cholesterol and then depart. But when cytokines from inflammation are present, a monocyte extravasates into the artery wall, becomes a scavenging macrophage, then overeats on too many oxidized LDLs and becomes a bloated foam cell. HDLs are meanwhile taking away cholesterol from the sub-endothelial macrophages, but with high LDL-P more cholesterol is being deposited than is being taken away - so plaque grows. Some foam cells die, and you have the lipid core.

Evelyn aka CarbSane said...

Thank you Larry & Lerner! Here's where I'm going with this -- it's the mechanical aspect of this that doesn't make much sense to me. Going back to the particle size thing (I understand this isn't the issue with the dumptrucks) the "vision" is of these small dense LDL being able to borough like chiggers into the artery wall. But HDL are smaller still. Thus the "collision theories" seem misguided to me, there has to be signalling (surface proteins, not an area of controversy) governing all of this. And that is why the "reverse transport" by HDL vs. LDL.

Even the great Malcolm Kendrick oversimplifies the process VLDL->IDL->LDL ~~>HDL. It is so mind-bogglingly more complicated than all of that, and yet that simplification is not all that bad a basis to explain the majority of what's going on.

Larry Eshelman said...

Evelyn, here is a short, technical summary of the "response-to-retention hypothesis" that I copied from "Role of Oxidative Modifications in Atherosclerosis"

The response-to-retention hypothesis

This hypothesis submits that the lipoprotein retention is the inciting event for atherosclerosis (Fig. 4). Within 2 h of injecting LDL into rabbits, arterial retention of LDL and its microaggregates can be observed (667). The underlying mechanisms involved in this process are just now coming to light. It is estimated that ~85% of subendothelial lipoprotein delivery is the result of transcytosis, and this process is restricted to particles <70 nm in diameter (852). This size restriction is important as it suggests that lipoprotein lipase activity is needed for tri-acylgycerol-rich lipoproteins to reach the subendothelial space (1110). The retention of lipoproteins within the arterial wall, however, appears tightly linked to components of the extracellular matrix. Apolipoprotein B-100, the single protein associated with LDL, is retained within the arterial wall in close association with arterial proteoglycans (118, 1091). This interaction is mediated by specific residues (3359–3369) (71) that, when mutated, protect experimental animals against the development of atherosclerosis (71, 857). Apolipoprotein B-48, which appears to be equally atherogenic as apolipoprotein B-100 in mice (990), also binds avidly to proteoglycans, and this interaction is mediated by residues 84–94 of apolipoprotein B-48 (250). Thus these data support an important role for proteoglycan binding in the retention of apolipoprotein B-containing lipoproteins in the early stages of atherosclerosis.

In addition to proteoglycan binding, lipolytic and lysosomal enzymes in the extracellular matrix also appear to play a role. For example, lipoprotein lipase enhances the adherence of LDL in vitro (1035), and this effect is independent of enzymatic activity (1034). Once retained(667, 931), perhaps through the action of secretory sphingomyelinase (1074), an enzyme that also generates ceramides that mediate apoptosis and mitogenesis (357, 455), as well as lysosomal enzymes such as cathepsin D and lysosomal acid lipase (350). Most importantly, aggregated LDL is avidly taken up by macrophages and smooth muscle cells (440) and thus can support foam cell formation (991). Thus many features of atherosclerosis can be attributed to enhanced retention of LDL within the arterial wall and its association with proteoglycans.

Larry Eshelman said...

And here is a description of the oxidative modification hypothesis from the same source:

The oxidative modification hypothesis ... focuses on the concept that LDL in its native state is not atherogenic. However, LDL modified chemically is readily internalized by macrophages through a so-called “scavenger receptor” pathway (317). Exposure to vascular cells in medium that contains transition metals also results in modification of LDL such that it serves as a ligand for the scavenger receptor pathway (395). It is now clear that one mechanism whereby cells in vitro render LDL a substrate for the scavenger receptor pathway is via oxidation of LDL lipids and the resulting modification of apolipoprotein B-100 (886). These observations form the basis for the oxidative modification hypothesis of atherosclerosis (Fig. 5), in which LDL traverses the subendothelial space of lesion-prone arterial sites. During this process, LDL lipids are subject to oxidation and, as a consequence, apolipoprotein B-100 lysine groups are modified so that the net negative charge of the lipoprotein particle increases (347). This modification of apolipoprotein B-100 renders LDL susceptible to macrophage uptake via a number of scavenger receptor pathways producing cholesterol ester-laden foam cells (349). It is this accumulation of foam cells that forms the nidus of a developing atherosclerotic lesion.

The process of LDL oxidation is associated with a number of other potentially proatherogenic events. For example, during the initial stages of in vitro LDL oxidation, modification of LDL lipids can occur in the absence of any changes to apolipoprotein B-100. Such modified LDL has been termed “minimally modified LDL” and shown in vitro to induce the synthesis of monocyte chemotactic protein-1 in both smooth muscle and endothelial cells (171, 754), resulting in the recruitment of inflammatory cells (659). This particular step appears critical as mice lacking the receptor for monocyte chemotactic protein1 are resistant to atherosclerosis (72, 323). More heavily in vitro oxidized LDL, commonly termed “ox-LDL,” is chemotactic for monocytes (742) and T lymphocytes (611), perhaps as the result of lysophosphatidylcholine formed during oxidation (886). Oxidized LDL has also been shown to stimulate the proliferation of smooth muscle cells (890) and to be immunogenic by eliciting the production of autoantibodies (710, 795) and the formation of immune complexes that can also facilitate macrophage internalization of LDL (334, 492). The recruitment of inflammatory cells may result in the continued oxidation of LDL, setting the stage for catalytic expansion of the atherosclerotic lesion and the full-blown spectrum of atherosclerosis.

Lerner said...

--- Thus the "collision theories" seem misguided to me,

to me, too. Especially if transcytosis is indeed the biggest method (IIRC Larry's cite is from 2003 so it bears looking to see if that has stayed in vogue). With transcytosis, an endothelial cell might have to behave like a liver cell (internalizing a receptor for endocytosing, and not just docking, the LDL); but instead of destroying the LDL, it deliberately moves the LDL along the internal railways of the cytoskeleton to the opposite wall. That doesn't seem as if it could be random. The cell then has to deliberately export the LDL; the LDL can't move anywhere on its own, it is always being pushed or pulled.


Speaking of CETP (cholesteryl ester transfer protein): the idea is to inhibit transfer of cholesterol from HDLs to ApoB100s as Larry said. Such an inhibitor would result in greater retention of C in the HDL-C, plus it would lower LDL-C. The 1st such drug, torcetrapib, failed as it produced even more death. But there was lots of stated valid reasoning that problems were with that particular drug (hypertension, for one), not with the general concept... unless you take the Dayspring-style view that it's the numbers of transporters that matter (not the C content).

So yesterday came the results from another drug in the class: dalcetrapib. The trial, dal-OUTCOMES, was stopped for non-efficacy. The analysis is too varied to even post excerpts.

But I'll select this one tangential bit: "... the AIM-HIGH study, where a small 15% increase in HDL cholesterol with niacin did not translate into a reduction in the clinical end point"

---I'd expect HDL-C to not only be non-crucial in stopping or reversing plaque progression, but more pointedly to be not very involved in plaque rupture.

---why don't these studies measure HDL-P already?

-- in the short run, you prevent events with anti-inflammatory agents (JUPITER, using rosuva, was halted for efficacy - it worked too well to unfairly keep the controls on only placebo)

ProudDaddy said...

Re anti-oxidants: I recall a recent study to the effect that ingested anti-oxidants do not make it into the blood stream very well. Hence, "taking anti-oxidants has not been helpful"?

ProudDaddy said...

Would it make more sense if we stopped talking about cholesterol and just talked about apoB particles? It wouldn't seem to matter how much cholesterol is in the LDL particle that gets modified or oxidized or whatever.

Sanjeev said...

depends on the exact chemical, some go right through digestion into circulation tissues, many don't.

Polyphenols IIRC don't make it through digestion & liver. Even massive doses of resveratrol got minimally into tissues.

Some stuff that the life extension crowd was taking in the 80s and 90s - BHT, BHA gets absorbed and retained pretty well.

Another one that was heralded as the greatest ever antioxidant

Lerner said...

There was a big meta not too very long ago on using antioxidant supplements, it showed no benefit in CVD. Then shortly afterward came another with the same lack of benefit, this time in cancer. So naturally, people said that the antioxidants and whatnot had to come from food and not from supplements.

Not long after that came a meta-study on the same lack of benefit for CVD in people consuming many fruits and vegetables per week. Then the same for cancer.

Nothing was so elegantly elucidated as the many rationales and pathways and mechanisms that prompted all of those studies. People like Bruce Ames actually were very smart, unlike Taubes. But it didn't work out for actual outcomes, which is all that matters in the end.

So that's why I don't care much for the whole-food-real-food-natural-food blah blah blah. As far as reducing calorie density and therefore caloric intake, sure that makes sense. But for health, it didn't pan out. So I'd wondered how it would get resurrected, since the lure of back-to-nature is so powerful and sounds so good on its surface. It turns out that those failures in studies to show benefit are just being ignored. End of story.

ProudDaddy said...

Thanks, Lerner.'Tis as I suspected. So, is the key to somehow not generate the oxidants in the first place? Or somehow find a way to increase production of glutathione? Or?

I am really, really interested in this because all my male relatives have died from heart disease.

ProudDaddy said...

On a new tack wrt oxLDL, serum oxLDL doesn't seem to track with CVD much better than other biomarkers. Could this be because it is the oxLDL in the intima-media that needs to be measured?

George Henderson said...

Actually I think a good doctor should maybe not be such a great scientist. Much of the science we discuss here is about finding the mean value, and knowing its probability. Most patients lie far enough outside that to benefit occasionally from a more particular approach, which may sometimes involve the doctor ignoring what they would expect from most other people.
Anyone who endures in the health system long enough will hear some fully scientifically informed doctor say "it can't be what it seems, it has to be what it says"... and be very, very wrong.

George Henderson said...

Define little meat. And what about fat, marrow, organs? Do they count?

What about insects, molluscs and grubs? Seafood, river and pond life. Frogs, snakes and lizards.

Before fire, we could not get starch from roots as easily as we do now.
Many starchy roots - taro, cassava - are toxic raw.
So what was our starch source? Smaller roots like yams, nuts, seeds, wild grains, squash - none of it adds up to much quantity.

Meat consumption was high in all traditional societies where lots of meat was actually available - no-one ignored an easy kill to go dig up roots. But all the HGs left for study are those who live on marginal land (e.g. highland PNG, or the arctic), or who live where explorers and settlers have already killed the big game, or where settlers and other authorities have suppressed hunting, or missionaries have proscribed cannibalism.
We changed the traditional world before we studied it.
If you go back to the first contact reports, you often discover a more carnivorous world.

George Henderson said...

Here we go - this is what I'm taking about.
The Andamanese are perhaps the last unspoiled, isolated people living in the midst of plenty.

"The amount of fatty meat consumed daily during the rainy season when pork was at its fattest was large and could on occasions rise to the truly gargantuan. People with an average adult body weight of around 40 kg (88 lb.) could, on occasion, eat up to 1.8 kg (4 lb.) of food. This could rise to a staggering 4.5 kg (10 lb.) during a 24-hour period on special occasions. At major feasts , during colossal honey-and-pork orgies, participants stuffed themselves to bursting point, leaving everyone barely able to walk and with severe indigestion for days. Such "food pig-outs" are known from many primitive societies that are precariously dependent on an insecure food supply. Comparable "pig-outs" involving intoxicating beverages are also known in rather more advanced societies. In a hunter-gatherer group, a single day's unsuccessful hunt could lead to a night on short rations, while a failure lasting for more than three days could be the beginning of a life-threatening famine. An attitude of let-us-enjoy-when-and-what-we-can is understandable in such circumstances.

A diet rich in animal fats together with the occasional over-indulgence cried out for a counter-balance in the form of starchy roots, vegetables and fruit. These were available throughout the year but most abundant during the dry season. Gathering the unglamorous but necessary supplements was left to the women. If an all-male hunting party, especially an unsuccessful one, happened to come across such items, they might stoop to gather and bring them home. We may suspect a form of hunters' re-insurance against hurtful wifely comments on inadequate hunting prowess and related matters."

Evelyn aka CarbSane said...

I agree and disagree. Docs should certainly treat the patient rather than say "well X worked better than Y in this study so I'd like you to stop Y and start X" ... stuff like that. Then again (pipe dream) it would be nice if Docs took a scientific "method" approach to treating difficult patients. Rather than lumping 3 of a list of 7 symptoms together and calling it a Syndrome, suggesting modest dietary changes that will almost always fail (because they are not rigorous enough) and then trying medications at random until it "fixes" things, a more individual/methodical approach is in order.

Lerner said...

ProudDaddy, I don't know the answer as far as lessening oxidation.

But there inevitably will be surprises in research. Here are some:
which shows that it is the *oxidized* fish oil that provides benefit in CVD and elsewhere.

Since you already know the difficulties in increasing glutathione (you can't just take some daily... but maybe NAC helps, etc), I'd mention that in an Fx of CVD without overeating or diabetes (IOW, moreso of mystery causation), I'd look at any genetic SNPs to be tested for.

My personal view is that combating inflammation is a better avenue for self-help than oxidation. Purely a guess.

Measuring oxLDL within arteries might be only done in research as of yet.

As Sanjeev says, you do have to match the antioxidant to the oxidant. It also needs to be soluble where you want it used.

Lerner said...

As I wrote the last sentence in my previous comment, I thought of melatonin (both water and fat soluble, not found in whole food). So a quick look shows some research taking place wrt oxLDL.

An added benefit of melatonin occurs in people who have heart attacks, or strokes: a lot of the tissue damage (maybe even the majority) occurs from "reperfusion injury" when the oxidants formed during ischemia (especially the iron based ones) wreak more havoc than the ischemia itself did.

I recall this study: Take a rat, tie off a brain artery, wait a few minutes, then release the artery and wham! That's when the real damage occurs - which is very greatly lessened with melatonin.

Sanjeev said...

looks like this has not been linked to before

Hernandez, Sutherland

"Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet1,2,3"

or click here

George Henderson said...

Lerner, food that the poor were allowed to eat because the rich were monopolizing the more nourishing stuff is not optimal. Nothing wrong with snobbery here.

Glucosinolates might give oil a "hot" taste, like mustard oil, rather than bitter.

traderdoc said...

To me these results are very simply explained. And people blaming this on their thyroid gland are way off the mark, especially when they have near normal TSH.

Excess non-esterified fatty acids (NEFA) can be packaged up by the liver into VLDL particles...which as we all know then turn into LDL particles.

Like it or not, Jimmy is still very overweight. All adipose tissue at baseline, regardless of diet, will release *some* NEFA into the circulation (or in Jimmy's case A LOT). Insulin greatly decreases this baseline NEFA release, but even so there is still some minimal level that always occurs.

NEFA can be used either for energy production, turned into VLDL by the liver, or re-esterified by adipocytes.

I think of the circulation as a big conveyor belt that fat mass is always "dumping" into. The more fat mass you have, the more that conveyor belt is loaded up with NEFA from the fat cells. Add in lots of dietary fatty acids from the gut, particularly saturated fatty acids, and that conveyor belt will only get more full.

Furthermore, the non-insulinogenic nature of Jimmy's diet does not shut down NEFA production from the fat cells. They just keep pushing it out, even in the fed state! Adding some insulin action would slow this down, which explains why some people see major lowering of LDL with some starches added back into their diets.

In order to continue on his current diet without continued extraordinary levels of LDL, Jimmy MUST exercise more (use up NEFA = less LDL). Or he MUST lose the majority of his excess weight (lower baseline fat mass = less LDL).

That is his only way to reduce the conveyor belt of fatty acids --> VLDL --> LDL that's continually moving from his gut into his blood, and probably into his arteries as well.

Evelyn aka CarbSane said...

This all makes perfect sense to me! The NEFA are the "missing lipids" -- even at 230 lbs Jimmy had excessive abdominal fat. At around that weight, he "carries it well" in clothes, but he posted shirtless pics that say the reality is quite otherwise. For his build -- narrow shoulders and lean limbs -- a healthy metabolic weight for his current activity level is under 200 lbs. I've heard him laugh about such more recently, but it was a realistic goal for him all along and he knows in his heart of hearts that is so.

pathdoc said...

Exactly. I've been trying to wrap my head around why my own LDL increased on a paleo/lowish carb diet. This thread and its comments have really, really helped me work this through. As soon as I get to my goal weight, I'll retest my own lipids and see what my N=1 study has to say.

Evelyn aka CarbSane said...

A comparison of the Toukelau and Pukapuka would support the notion of CO as a culprit:

The habitual diets of the atoll dwellers from both Pukapuka and Tokelau are high in saturated fat but low in dietary cholesterol and sucrose. Coconut is the chief source of energy for both groups. Tokelauans obtain a much higher percentage of energy from coconut than the Pukapukans, 63% compared with 34%, so their intake of saturated fat is higher. The serum cholesterol levels are 35 to 40 mg higher in Tokelauans than in Pukapukans. These major differences in serum cholesterol levels are considered to be due to the higher saturated fat intake of the Tokelauans.

Apocryphon said...

It wouldn't and it doesn't; that's a study from the 1960's, about total cholesterol (not LDL), regarding coconut cooked in meals (not VCO), and concluded "Vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations."

Forward to 2011 "Coconut oil is associated with a beneficial lipid profile" -

Evelyn aka CarbSane said...

Last I checked, coconut fat is coconut fat, whether or not it is refined. Tis true that both of these populations were healthy as well so this is but one piece of evidence that cholesterol is not the whole story -- I sure hope my postings here have not led you or anyone to think I believe otherwise.

As to your link, it begins with "Coconut oil is a common edible oil in many countries, and there is mixed evidence for its effects on lipid profiles and cardiovascular disease risk. "

Evelyn aka CarbSane said...

Oops ... hit publish too soon. Fast forward to 2011? You are seeing some sort of information in this paper that compares in any meaningful way to the CO consumption of many LC and paleo folks, particularly Jimmy who consumes multiple tablespoons at a time?

"Stratifying the women according to their menopausal status revealed that post-menopausal women tended to be older, had experienced more pregnancies, had lower BMI, were less educated, and were from households with fewer assets." They also consumed less CO it would appear by T2.

" Post- menopausal women had higher CVD disease risk as indicated by their lipid profiles, including higher total and LDL cholesterol, triglycerides and TC/HDL ratio, and lower HDL-c levels compared to pre-menopausal women. On average, women in the sample consumed 9.54 grams of coconut oil each day, with pre-menopausal women reporting higher intake than post-menopausal women."

Gee, any surprises there? Post meno women are always at higher CVD risk "on average" so to attribute the pre-meno lipid profiles as somehow due to differences in coconut oil consumption???

9.5 grams average for CO = approximately 2 teaspoons. (+/- ~ 2tsp I would add)

In terms of cholesterol impact, the 1960's population comparison with significantly different consumption of coconut (and thus coconut fat) are more relevant. True, we don't know the lipid breakdown, but looking at your study we see that CO raises both LDL & HDL, in conjunction with eating more, higher BMI, getting younger, better socioeconomic status, and becoming far more educated. And???

Apocryphon said...

And you gave Jimmy sound advice, except for "Ditch the coconut oil." which you haven't backed with evidence. In fact I provided evidence to the contrary. If you really believe oils extracted from olives and nuts are more healthy than coconut, why not do some extensive research and make a new blog entry?

Evelyn aka CarbSane said...

I back that with the "weblinical evidence" that innumerable people have reported when they start consuming coconut oil. I don't think the nature of the fat makes much difference for people eating normal amounts, but both CO and butter seem to cause problems for some people. I don't think Jimmy had yet jumped on the CO bandwagon in 2005. I have also edited in a "partially" to my advice, because I don't know if 1:1 replacement would help for him. The suggested replacements were options other than butter and higher MUFA.

Your cite, by the way, concurs with mine in terms of intake, TC increases with CO consumption -- and yes, part of that is HDL, but not all of it. The changes appear to be nominal, and according to Table 3, are quite different in pre vs. post menopausal women. There's no control for meno status, BMI, caloric intake, etc. for nominal differences in CO consumption. Mostly it reads like something a "Miracles of CO" website would tout.

I'm not inclined to spend much time on fat consumption research as I do not believe it makes much of a difference for people consuming normal amounts of whole and added fats, getting most fat from whole sources.

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