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 ...  

WHAT FOLLOWS IS SOME THINKING OUT LOUD, I AM NOT CLAIMING THIS DOES OCCUR WITH ANY CERTAINTY, ALTHOUGH I DO BELIEVE THE EVIDENCE MORE STRONGLY SUPPORTS SOME OF THESE SUPPOSITIONS THAN SUPPORTS VARIOUS CLAIMS MADE WITH CERTAINTY BY THE LIKES OF WHEAT BELLY, EADES, NAUGHTON, MOORE, SHANAHAN, ETC.ETC.

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".