Is This Your Paleo Diet?

As y'all probably know by now, part of my daily web reading is to check in on what's happening on followed blogs ... which landed me at Dr. BG's Animal Pharm in a post discussing a 2009 study by Linda Frassetto,  (Frassetto presented at AHS12):  Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.

This post is not addressing Dr. BG's post and the results of this study ... perhaps another time for that one ... but rather the diet used in the study.  From the abstract, bullet-pointed and formatted for clarity:
Methods:   We performed an outpatient, metabolically controlled study, in nine non-obese sedentary healthy volunteers, ensuring no weight loss by daily weight.
We compared the findings when the participants consumed their usual diet with those when they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets of increasing potassium and fiber for 7 days, then a paleolithic type diet comprising lean meat, fruits, vegetables and nuts, and excluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, for 10 days.

Outcomes included arterial blood pressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and insulin areas under the curve (AUC) during a 2 h oral glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery reactivity in response to ischemia.

Results: Compared with the baseline (usual) diet, we observed:
  • Significant reductions in BP associated with improved arterial distensibility       (- 3.1±2.9 , P=0.01 and  +0.19±0.23,  P=0.05)
  • Significant reduction in plasma insulin vs time AUC, during the OGTT (P=0.006)
  • Large significant reductions in total cholesterol, low-density lipoproteins (LDL) and triglycerides (-0.8±0.6 (P=0.007), -0.7±0.5 (P=0.003) and -0.3±0.3 (P=0.01) mmol/l respectively).
  • In all these measured variables, either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, near consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.
OK ... now when you hear paleo diet, what comes to mind?  Bacon and eggs for breakfast?   Fatty meats and organs cooked in coconut oil or ghee?  Heavy cream in your coffee and dark chocolate covered macadamias for a snack?   Low carb, high fat perhaps?  Higher on the saturated fat, easy on the PUFA?   Well ...
In 1985, anthropologists Eaton and Konner (1985) introduced the general medical community in ‘paleolithic nutrition. A consideration of its nature and current implications’.  ‘Paleolithic’ refers to the period of history of the genus Homo, beginning more than 2 million years ago and continuing until about 10 000 years ago (10 kya, when the neolithic period began) when humans began to cultivate plants (predominantly cereal grains) and domesticate animals (Brandt, 2007). During that interval (more than 2-million year), culminating in the emergence of today’s sole Homo species, Homo sapiens, about 200 kya (McDougall et al., 2005), our ancestors, including Homo sapiens, lived as hunter-gatherers, eating wild animal-source foods (lean meats, internal organs, bone marrow, but no dairy) and uncultivated plant-source foods (mostly fruits, nongrain, vegetables, nuts, but no legumes).   As the 10 000 or so years since the beginning of the agriculture and animal domestication began,that is less than 1% of Homo evolutionary time—leaves little time for evolutionary forces to redesign the core metabolic and physiological processes in a major way in response to the major dietary changes introduced by the agricultural revolution and food animal domestication, the genetic makeup of contemporary humans may more closely optimize core metabolism and physiology when they consume a diet more closely resembling our ancestral hunter-gatherer’s preagricultural diet (Eaton et al., 1988; Cohen, 1989; Jansson, 1990; Eaton and Cordain, 1997; Neel, 1999; Simopoulos, 1999; Eaton and Eaton, 2000; Sebastian et al., 2002, 2006; Lindeberg et al., 2003b, 2007; Mann, 2004; O’Keefe and Cordain, 2004; Cordain et al., 2005).
Now, I was taken to task a bit here in comments recently for suggesting pretty much what is written above in the introduction of this paper:  In short, that the paleo diet is predicated on the notion that the genome has not changed in the 10K or so years of neolithic agriculture and that a diet comprised only of foods that might have been available back then would be more appropriate for our human physiology.  

While it's perfectly acceptable to "tweak" off of a paleo diet, acknowledging, for example, adaptations to dairy and such, this creates a problem with the few clinical trials like this one that have been done on paleo diets.  (Trials on carbohydrate restriction suffer similar issues in terms of what constitutes a low carb diet).    So what diet produced these wonderful metabolic changes?

They ramped them up (there appears to be concern over increasing potassium too abruptly) to where the final paleo diet consumed for 10 days was:

Usual diet: 18% of calories from protein, 44% from carbohydrates and 38% from fats
Paleo diet:  30% of calories from protein, 38% from carbohydrates and 32% from fats

They were eating almost 15% more calories, but there was no significant change in carbs or total fat intake here, thus almost all of the increased caloric intake came from protein.  Also sat fat intake was cut in half while PUFA intake tripled and MUFA intake increased 40%.   It's too bad they didn't give portion sizes for the foods, but it would appear there was a significant increase in fructose consumption (they consumed quite a bit of OJ during the ramp up week as well).    

OK ... so increase protein (insulinogenic and IGF stimulating) , drop the fat and carbs equally by percent but not by absolute amounts, and see metabolic improvements in glucose metabolism in short order.  

Is this your paleo diet?   Is it "by default" low carb?  I would notice that the *usual* diet was not the 500g carb/day we're accustomed to hearing for the SAD, but rather half that at around 250g.   Dr. BG lists a number of 2009 blog entries about this study.  Since he's the biggest wig amongst them, I'll simply highlight Mark Sisson's contribution, which consisted mostly of "I'm not going to say I told you so" but hailing the results of this study as some sort of endorsement of his Primal Blueprint.   This highlights the one thing that gets rather usual in these studies -- When you look beyond the headlines, the tested diets bear little to no resemblance to the diets those heralding the studies are promoting.  These subjects ingested roughly 100g of insidiously weight gaining carbs in addition to the 150g regular insulin surge inducing carbs.  They lowered their "healthy primal" saturated fat intake while increasing their MUFA and PUFA (if ratio improved, absolute increase in O6's would be inevitable).  They ate pork tenderloin (lean), tuna (lean) and chicken and turkey breast (lean, lean).  

One last comment -- what with this current 2012 trend of being a "fat burning beast" or (gag) in "nutritional ketosis" eating fewer and fewer carbs and more and more fat.   I think this study serves as a great reminder of the folly of TWICHOO and its cousins including any variation of carbs causing insulin resistance and metabolic syndrome and all manner of metabolic derangement, mitochondrial mahem and wreaking havoc and irreparable damage upon one's metabolism.


Unknown said…
2500 calories/day

38% carb = 950 calories = 237.5 grams
30% protein = 750 calories = 187.5 grams
32% fat = 800 calories = appx 89 grams

Cordain also co-authored a paper

Optimal low-density lipoprotein is 50 to 70 mg/dl Lower is better and physiologically normal

"Thus, although an LDL level of 50 to 70 mg/dl seems excessively low by modern American standards, it is precisely the normal range for individuals living the lifestyle and eating the diet for which we are genetically adapted."

How do you reconcile the two? Is it possible to lower your LDL-C to this " physiologically normal level" without reducing the fat content to <10%?
bentleyj74 said…
Just FYI Dr BG is a woman and [I believe] a pharmacist. It's very interesting to see the difference between what is perceived as the paleo diet vs what the clinical diet actually was comprised of.
Lerner said…
From what I'd seen, there is a big difference between Cordain style original Paleo (which was sort of a sidelight) and Wolf style Paleo (which is at the heart of the modern Paleo movement). Wolf's has lots and lots of tasty, tasty fat. It's no wonder which one became the biggest trendy thin which is now modern Paleo Inc.

It was not unusual for Cordain to be reviled in some circles (like PH) because he was against SFA (or let's say not-in-favor of unlimited SFA), in particular saying that palmitic acid is atherogenic. Cordain's frozen Eskimo woman was dismissed in the usual way - it doesn't fit with what modern Paleos wanted to eat, so they didn't want to hear about it.

Aside from whether Cordain is right or wrong (Kurt disagreed with Cordain, but I don't know on what basis), Cordain is one of the very few Paleos that I hadn't seen slanting things as a matter of course.
Lerner said…
Like that perennial caveman favorite, carrot juice @ 4 times per day. Why include that? Likely because it's high in sugar (aka calories), and has lots of K.

The DASH diet (anti-hypertension) is said by many to work mainly because it's high in K. The study authors might have some rationale about study participants not wanting to spend hours per day grinding down vegetables with their molars, so they use a machine to do it. (That is processing, but still not in the same vein as canned carrot juice).

The want/need sugars to make up for the lost starch. When you cut starch, you'd waste away - so you need to make it up with fat (Wolf, Eades, Jimmy) or sugars (this study).

Paul Jaminet said…
Hi Charles,

The claim that such low LDLs are optimal is mistaken. Nor is it present in hunter-gatherers, unless they have parasitic infections which lower LDL.

I did a series on that issue. See for links to earlier posts in the series. It started here:

Best, Paul
Lerner said…
Which leads to the point that this study does not measure or mention the much vaunted (in LC circles) LDL size pattern.

Btw, there are RCTs using potent statins to get to those low levels mentioned by Charles. What they find is not only significant plaque regression, but it can happen fast. So to get there by natural means would seem to be ideal - but then again you might be missing the anti-inflammatory effects of the statins.

Speaking of inflammatory, I don't use or advocate statins - but those studies do provide very interesting clues as to what goes on wrt atheromas. It's not even known for sure what causes plaques - but regardless, it does seem that getting LDL very low is protective - even if it means what you're really doing is lowering LDL-P or something else altogether.
Lerner said…
Paul says: "... unless they have parasitic infections which lower LDL."

LDL lowering is not limited in cases of parasites. It's widely known that viruses do the same. I'll just grab a quick reference at random:
"Hepatitis C associated hypolipidemia has been demonstrated in studies from Europe and Africa... Hepatitis C is associated with decreased cholesterol and LDL levels."

quoted from:
Hepatology. 2009 Oct;50(4):1030-7.
Hepatitis C virus infection and its clearance alter circulating lipids: implications for long-term follow-up.

Unknown said…
You can take a food item that isn't Paleo and convert it to Paleo by dousing it in butter. Take an item like a slice of cheese pizza, which is loaded with polynanosachirides. If you slather butter on the slice of pizza the nanochondrialites in the butter modify the molecular structure of the polynanosachirides and converts them into mononanosachirides, making the pizza safe for consumption.

Butter acts on non-Paleo foods at the quantum level through the Higgs boson mechanism and fundamentally changes the strings of molecules from non-Paleo to Paleo.
Unknown said…

So, the size -- the lipid proteins aren't uniformed in size. You can have some that are very small and very dense and then you can have some that are intermediate density and volume and then you can have others that are larger and lower density. And for those of you who have heard of the VAP test, or the vertical auto profile, or other, you know, technologies for measuring particle size, there's pattern A and pattern B. And pattern A means you have a whole bunch of large fluffy LDL particles.
Rob Wolf: Theoretically low reaction?
Chris Kresser: Theoretically not as big of a risk factor for heart disease. And then pattern B would be that you have a bunch of small dense, LDL particles and the idea was that these are -- were more harmful, more likely to damage the endothelium and initiate the whole process of atherosclerosis.
But more recent research has shown that there are a couple of problems
with that theory. There's no doubt that smaller dense of LDL particles can be a sign of something gone wrong. But in studies that control for LDL particle number, they found that the association between small dense LDL and heart disease disappeared. So in other words, if they did a study and it only measured small dense LDL protocol number and heart disease, they found a correlation. But if they also measured just a number of all LDL particles, then the predicted value of small dense LDL particles disappeared. So what that suggest, of course, is that it's the total number of LDL particles regardless of whether they're large and fluffy or small and dense. That's the most important factor. And getting back to your earlier question, how do we measure that? The gold standard for measuring that is a test called the NMR, nuclear magnetic resonance test. And it's offered by a lab called Lipid Science. It's the only lab that's FDA approved for determining LDL particle number, which is often referred to as LDL particle concentration. So you take that test and the result comes back and it tells you the number of LDL particles that you have. And that turns out to be the main driving factor in atherosclerosis because it's a gradient-driven process, which means that the more particles that you have floating around in your bloodstream, the more likely it is that some of them are going to migrate into the endothelium, damage it and start this process of platforming.
Rob Wolf: So it's just kind of a statistical gig, like, even though small dense LDL maybe more reactive even large puffy LDL particles, at some point, if we have enough of them, just statistically, we're going to call some damage in the endothelium, get some inflammatory response and then...
Chris Kresser: Right. And that's one of the -- actually, one of the -- actually, was one of big holes in the theory of -- that large buoyant LDL was not a problem, is that people with the condition called familial hypercholesterolemia, which is a genetic problem that we'll probably talk about in a few minutes here where people produce -- they have a much higher number of LDL particles than someone without that condition. Well, people with this condition have a whole bunch of particles and then mostly large buoyant LDL particles. But they have a three times greater risk of heart disease than someone without that. So even though all of their LDL particles are large and fluffy, they're still having, you know, they have 300 percent higher risk of heart disease?"

So - it's the total particle count not the pattern size that matters.

Paul - I would love to hear your thoughts on ths
Sanjeev said…
coconut oil is preferred, ideally from grass fed coconuts

> acts on non-Paleo foods at the quantum level through the Higgs

I think you mean the grok boson, AKA grawksawn. And for women it's the grokette meson.
LeonRover said…
The food choices used in this study to mimic a Hunter Gatherer diet are very close to those recommended in Dukan's reducing diet.

Fish, turkey, chicken as protein choices, but no lean beef or eggs.

The average protein increased by 91 gm to 207 gm - an amount that would horrify JM - and that Donald Layman would find excessive. However, I'm sure George Bray would be happy that it could lead to an increase in muscle mass.

I quite like roast parsnip at 13 gm CHO/100 gm uncooked, but what about some sweet potato to the same CHO count, or EVEN Idahos ?

The drop in BPs is quite small even tho' the result is statistically sigificant.

I do not recognise the units for BG: 18 vs 17 - WTF are they?
The drop in Fasting Insulin from 69 pmol (borderline) to 21 (low) is a good result.

As I personally do not regard LDL of 3 mmol/l as an Health Crime I could care less that it dropped to 2.3 on these food choices.

All in all: I score it 6 out of 10 for Effort.

Lerner said…
Charles, is that quoting of yours from Wolf's show in Sept 2012?

Meanwhile, readers of Carbsanity would have known about that (the LDL-size pattern just being an artifact of LDL number) long before followers of Wolf would have known - I know so because I myself posted on exactly that here in Dec 2011:

There's a link there to read the commentary by the author of the MESA sub-analysis.

Btw, I'm pretty sure I've heard Wolf previously describing large puffy LDL specifically as "non-atherogenic", which was never a valid claim. The claim was that it was less atherogenic. You can search Wolf's archives and might find that. (Jimmy has made the same incorrect claim.)

Meanwhile, Kresser should have mentioned (I don't know if he did or not) the historical evidence which suggests that people who lived before ~1900 or so and had FH did *not* have shorter lives. That suggests that their diet had a protective effect. I'd suppose that one possibility is because the LDL probably has to be oxidized (oxLDL) before a macrophage's scavenger receptor will be interested in the LDL... and won't gobble them up and become a foam cell.

Regarding oxidation, one reason the small LDL might indeed be more atherogenic is that it can be more prone to oxidation - the idea is that the ApoB-100 protein, when wrapped around an unnaturally small particle, is mis-shapen and therefore less likely to bind well to the LDL receptor (in the liver, for clearance). It's exposed longer to oxygen in the serum an therefore more likely to become oxidized. That's been a theory for a while.

But, to show that not much is known for sure: the Pritikin group has research showing that their hi-carb subjects' LDL was small but also was *less* prone to oxidation - therefore presumably less atherogenic. On top of that, they also demonstrate a wide genetic variety in who gets small or large LDL when eating the same foods.
Lerner said…
wrt viruses and LDL, HVC of course involves the liver (site of cholesterol production) but that's not the only virus to cause hypolipidemia.

E.g., "Human immune deficiency virus (HIV) is associated with hypocholesterolemia during the asymptomatic phase..."
Hypolipidemia: A Word of Caution

Probably many more. If I run across the ref that I'd read just a couple of days ago, I'll post it. It's difficult finding them in a websearch because search engines these days now assume that they know more about what you meant to search for than you know yourself. They keep returning results for "hyper", even when not asked for that.
Unknown said…
So - what is correct - is it particle size or particle count

For example - on my last NMR test - 5/10/12 my LPL-P was 1500, my small LDL-P was 127, my HDL-C was 59, my Triglycerides were 36, my TC was 254 and my LDL-C was 188 (using the Iranian calculation it was 141)

SO - is my particle count too high or is it okay because my small LDL-P is relatively low

OR - is it not good because my LDL-C is too high

This is why people like me get very confused.
Unknown said…
The grass-fed coconut is an interesting case, in that highly scientific studies have shown that consuming it creates a worm-hole in time and across many universes so that the result is that you are alive in a version of the universe in which you have rock-hard abs and buns of steel.

Before I started chugging coconut oil I did not know what it was to be an Adonis, now when I walk down the street people stop me and ask "Excuse me, are you a Greek God?" and I answer "Yes, as a matter of fact I am."
Steven Hamley said…
The study where people with FH lived longer before 1915 is this
It's not very strong evidence and I'm not aware of any others

Researchers don't seem to know exactly how LDL oxidses, but some ideas are related to endothelial dysfunction, mitochondrial dysfunction and immune related mechanisms (myeloperoxidase, ceruloplasmin, NADPH oxidase, etc) including an excessive immune response (low Treg cells)
Lerner said…
Charles, there's a simple answer: nobody knows for sure. But the latest view is that LDL-P is the best guess. Even LC advocate Volek uses that as one of the outcome measures in his latest "eggs are good" study - along with LDL pattern and some others.

But then there's the whole matter of inflammation. The Masai drank milk all day and didn't have heart attacks, so some Westerners said that dairy was somehow protective despite its fat content. Then LFer Pritikin goes there many years ago and sees on autopsies that they do have 'extensive atheromas' in cardiac arteries. They had the plaque buildup, but just didn't rupture to create the actual heart attack.

A plaque has a fibrous cap - which if stable can effectively contain the lipids and cells inside the plaque. Only when the cap gets thinned by enzymes (Matrix MetalloProteinases --- MMPs --- from inflamed macrophages) can the plaque then rupture, and expose the plaque contents to the blood. The blood then quickly forms something like a sludgy scab, the thrombosis which blocks off blood flow. One process builds the plaque, another opens it up through rupture (or erosion).

So that's another possibility why the people with FH before 1915 didn't have heart attacks even though they might have had their own extensive atheromas. The same could be true of Cordain's Eskimo, and conceivably even the Kitavans... low inflammatory diets.

(Yes, I know that there are theories such as the Masai milk wasn't itself really harmful, that Europeans left a bag of flour there which created all the plaque buildup. Might be true, might not... but only theories for sure.)

Or, as Steven says, maybe the idea of FHers living long lives pre 1915 isn't true after all. Going from memory, the researchers identified modern people with FH by using modern medical means, then traced their ancestors and did calculations on who back then was likely to have FH. So it's sketchy, but gives people with FH a possible avenue to try.

Oh yeah, and MUFA raises HDL and lowers LDL. But then the good HDL can go bad. The confusion never ends, except for blustering/bluffing types.

So anyway my approach is to hedge all bets and don't follow any radical trendy 'new paradigm'.
Unknown said…

We believe that wheat upregulates metalloproteinases. It upregulates metalloproteinase 2 and metalloproteinase 9. If you look at the final dissolution of that fibrous plaque, what causes that fibrous plaque to rupture– it’s made out of collagen and smooth muscle and cholesterol. What causes it to rupture is metalloproteinases. They up-regulate and degrade the collagen, and when the fibrous cap breaks, that is the event that kills you. We believe elements in the Western diet, including Wheat and corn and grain and legumes and high glycemic load carbohydrates, these upregulate the enzymes that directly cause the rupture of the fibrous cap.

So that spaghetti meal could be what triggers the heart attack.

Right. But to unequivocally say that saturated fats do not cause atherosclerosis, is sheer folly. We know that they do. We awarded the Nobel Prize in medicine to Brown and Goldstein for saying that Palmitic acid down regulates the LDL receptor. Unless we’re going to take that Nobel Prize back, you cannot deny that information. So, I would like to hear a response of how in the world LDL receptors are not down regulated by palmitic acid.
Lerner said…
I've heard through the years that carbs are pro-inflammatory, that fat is, that insulin is. But I'd never heard about spaghetti triggering a heart attack.

There is however, the well known medical phenomenon of the "Single Fatty Meal" -which does trigger heart attacks. The data was inconclusive about which fat is worst and in whom - but it might be that SFA was least dangerous... I forget. If so, that'd be one point in favor of the Paleos. Olive oil is highest in MUFA, but the 2nd highest content is SFA. Who could be against olive oil? Yep, we know who.

(A high fat meal can stimulate the endothelium to release Tissue Factor which starts the cascade with Clotting Factor VII and downhill it all goes. But that's a different pathway, I think, than the plaque rupture pathway.)
Steven Hamley said…
As for the Eskimos - the amount of long chain omega 3s they were eating is not healthy and would make LDLs more vulnerable to oxidation. The amount of smoke they were exposed to is also an issue.

Charles: HDL-C and trigs correlate with LDL particle size, which correlates with LDL particle number. When these are adjusted for LDL particle number remains a significant risk factor. A suggested mechanism is a concentration gradient/more particles >> more likely to penetrate endothelium. Even with that there are other factors like endothelial permeability and the immune response.

I would rather look at the possible mechanisms than debate whether the Masai/Kitavins had atherosclerosis
Lerner said…
"I would rather look at the possible mechanisms than debate whether the Masai/Kitavins had atherosclerosis"

That's where I would disagree, Steven. The world has been full of possible mechanisms, very well thought out and convincing on the surface, which ended up going nowhere. Mechanistic arguments are often very deceiving. One case in point: McCully and "The Homocysteine Revolution", which was perfect on paper in theories yet failed over and over in actual outcomes studies.

All that matters are outcomes, mechanisms are just the way to decide what outcomes studies to perform - though sometimes mechanisms are all that are available to base a current guess on what to do.

Another case in point: Wolf and Lalonde spent a lot of time elaborating their VLC theory: that no one ever needs to eat any carbs. So they drove that off the cliff, degrees and research backgrounds in hand. When they actually tried it, it didn't work.

P.S. Kitavans "smoked like chimneys" and didn't die of heart attacks.
Unknown said…
LDL Receptor Activity Is Down-Regulated Similarly by a Cholesterol-Containing Diet High in Palmitic Acid or High in Laurie and Myristic Acids in Cynomolgus Monkeys

It seems that independent of species, the saturated fatty acids lauric, myristic and palmitic acids consistently elevate plasma LDL cholesterol concentrations in the presence of dietary cholesterol,whereas caproic acid (10:0) or lower (8:0 or 6:0) and stearic acid (18:0) have little impact (Hayes and Khosla 1992, Woollett et al. 1992b).

In conclusion, these data suggest that the concentrations of lauric, myristic and especially palmitic acids in the oil blend diet exerted suppressive effects on LDL receptor activity, resulting in elevated plasma LDL cholesterol concentrations compared with the unsaturated fat diet. The fact that consumption of the highly saturated coconut oil diet (saturated fat) abundant primarily in lauric and myristic acids resulted in a reduction in LDL receptor activity (Table 4) similar to that of the oil blend diet suggests that the quality of the fat in the oil blend diet exceeded the threshold for optimal receptor activity. These data further suggest that even if the total fat intake of the Western diet remains as high as 36-40% of energy, a reduction in total saturated fatty acids, especially palmitic acid, will contribute to a reduction in plasma LDL cholesterol concentrations. Therefore, future diet recommendations may need to consider the concentrations of these fatty acids if they are to be effective in reducing plasma LDL cholesterol concentrations.
The Paleopathology of the Cardiovascular System

Those blood glucose units of 17 and 18 in the Frasetto article are in mmol/l, not the mg/dl used in the U.S. To convert to mg/dl, you multiply by a 18. So those fasting blood sugars you note are around 300 mg/dl. These were supposedly healthy participants, so the reported figures must be misprints.

To all...
Clinical studies of the paleo diet are still in infancy. The leading clinical researchers ideally should get together and decide how the paleo diet should be defined. Don't laugh - it could be done, probably in an academic setting. Otherwise we'll have the Frasetto paleo diet, the Lindeberg paleo diet, the Cordain paleo diet, etc. One of the reasons we got a flurry of very low-carb diet clinical studies in the early 2000s is because they could hand the participants Atkins New Diet Revolution.

I actually heard from a paleoist that the reason that the French by in large are in good health is because they use heart healthy butter to negate the negatives of wheat. The trend in some paleo/LC circles to slather everything in butter to absorb the nutrients and blunt the insulin response is another personal favorite.

Lol at "grass fed coconuts".
"is this your paleo diet?"

Besides the fact that I eat dairy yet way less meat/protein, it is fairly similar to how I eat. Well, similar when compared to the poundsoffattymeat/cookedincoconutoil/limitedfruit/addmorefat style paleo diets that I see.
CarbSane said…
Grass-fed coconuts and pastured carrot juice. Num!
CarbSane said…
Don't you mean the Dorkan diet? LOL. I do find the insulin drop impressive. Not because I fear the hormone, but low insulin on a normal OGTT indicates good insulin sensitivity.
CarbSane said…
I knew Dr. BG was a woman, she also goes by Grace when she comments of blogs and PH. The "he's the biggest of the wigs" referred to Mark.

@Lerner, I don't get the impression that Robb is particularly high fat. He's a Cordain protege Cordain has somewhat changed his stance of sat fats, but I always wonder if that was bowing to pressure or for more appeal to the masses rather than based on newer information.

The Eaton Konner papers are almost universally cited -- even in The New Atkins. There is apparently some circular referencing going on in that wing Eaton/Cordain/etc.etc. Jimmy said that Cordain said in a recent podcast that you would be hard pressed to get over 25% carb on paleo. I'm looking forward to S. Boyd Eaton's AHS12 talk ... the tweets from AHS were all aghast at his eating shredded wheat and wondering where the bacon was in his diet.

The acquiescence to dairy in primal (a la Sisson) is, to me, a marketing coup. Giving up grains and legumes is not near as scary as also giving up cheese and cream and butter.

I think Robb wrote a blog post about whether this and the safe starches concepts were good for paleo in terms of the balance between increasing the mass appeal vs. diluting the basis.

The bizarre dark chocolate thing is what's really interesting to me. Chocolate is a highly refined/processed product. It's OK to say it's an acceptable non-paleo treat -- part of your 10 or 20 or whatever percent non-purity -- but it's absurd to promote it as paleo, real food, whole food or anything of the sort.
Unknown said…
More confusion
"Our goals are more stringent compared to the lax national cholesterol guidelines. For plaque regression, we aim for LDL cholesterol <60 mg/dl, HDL > 60 mg/dl, and triglycerides <60 mg/dl."
All wheat-based products (all breads, all breakfast cereals, noodles, pasta, bagels, muffins, pancakes, waffles, donuts, pretzels, crackers), oat products (oatmeal, oat bran), cornstarch-based products (sauces or gravies thickened with cornstarch, prepared or processed foods containing cornstarch, cornmeal products like chips, tacos, tortillas), sugary soft drinks, candies

Enjoy unlimited:
Vegetables-except potatoes; fresh or frozen, never canned
Raw nuts and seeds-raw almonds, walnuts, pecans, hazelnuts, pistachios, Brazil nuts, cashews; dry-roasted peanuts (not roasted in oil); pumpkin and sunflower seeds
Healthy oils (unheated)-olive, flaxseed, coconut, avocado, walnut
Meats-red meats, pork, fish, chicken, turkey, eggs. (Consider free-range, grass-fed and/or organic sources.)
Non-wheat grains-ground flaxseed, chia seeds
Teas, coffee, water, unsweetened almond milk, coconut milk or coconut water
Cheeses—real cultured cheeses only (not Velveeta or single-slice processed cheese)
Avocado or guacamole; hummus; unsweetened condiments, e.g., mayonnaise, mustard, oil-based salad dressings; ketchup without high-fructose corn syrup; pesto, tapenades; olives

Fruit-No more than 2 servings a day (one serving is a level handful), preferably in this order (best first): berries of all varieties, citrus, apples, nectarines, peaches, melons. Minimize bananas, pineapples, mangoes, and grapes
Fruit juices-only real juices and in minimal quantities (no more than 2-4 oz)
Dairy products-No more than 1 serving per day of milk, cottage cheese or yogurt, unsweetened (Fat content does not matter.)
Legumes/beans; peas; sweet potatoes and yams; rice (white and brown); soy
Dark chocolates-70-85% cocoa or greater; no more than 40 grams (approximately 2 inches square) per day
Sugar-free foods-preferably stevia-containing, rather than aspartame

Fried foods
Fast foods
Hydrogenated “trans” fats
Cured meats-hot dogs, sausages, bacon, bologna, pepperoni
High-fructose corn syrup containing foods; honey; agave syrup; sucrose
Processed rice, rice flour or potato products-rice crackers, rice cereals, pretzels, white breads, breakfast cereals, potato chips
Fat-free or low-fat salad dressings
”Gluten-free” foods

Quick tips:
For healthy breakfast choices, consider ground flaxseed as a hot cereal (e.g., with soy milk, milk, or unsweetened almond milk; blueberries, strawberries, etc.). Also consider eggs; raw nuts; cheese; consider having “dinner for breakfast,” meaning transferring salads, cheese, chicken, and other “dinner” foods to breakfast.
Add 1 tsp or more of taste-compatible healthy oil to every meal. For example, mix in 1 tbsp flaxseed oil to ground flaxseed hot cereal. Or add 2 tbsp olive oil to eggs after scrambling. Adding oils will blunt appetite.
If you suspect you have a wheat “addiction,” use the first week to add healthy oils to every meal and reduce the amount of wheat by half. In the second week, aim for elimination of wheat while maintaining the oils.
Reach for raw nuts first as a convenient snack."

Question - has anyone ever had LDL-C levels <60 mg/dL on a "paleo/ancestral diet"?

Basically the vast vast majority of the paleo bloggers say to IGNORE LDL-C

Question - is it possible to have LDL-C <60 mg/dL on this type of diet?

Question - or is Davis full of you know what?
CarbSane said…
There have been some notable reports on PaleoHacks of not only no reduction in LDL-C, but skyrocketing levels when going VLCHF paleo.

Curious. Has Davis published any studies based on his data?
Lerner said…
Quoting Evelyn: "I don't get the impression that Robb is particularly high fat. He's a Cordain protege"

Evelyn, I was there as it happened, for the first 100+ podcast episodes. Wolf was about VLC, very high meat and fat. People keep talking here about coconut oil - no, then it was mostly coconut milk, drinking several cans per day every day. Bacon, butter... you need the fat for *fuel* if you're not taking in carbs. It's the opposite of weight loss.

Imagine hearing, "Andy keeps pushing me to finish this book". How's that for historical reference? Or, "We now have 6 listeners because we lost one" :) It was fun, and Wolf is very personable. It was a kick for me to listen (just as with Gabe Mirkin's show before then), I was never a practicer per se. I became surprised when I saw people taking it very seriously.

I was more than surprised to hear that "you don't need to ever have any carbs, not even PWO, because gluconeogenesis will take care of everything". It had already been well established, scientifically, that getting carbs within a limited time-window PWO resulted in greater mass of glycogen storage in myocytes.

When latecomer Paleos now show up here and there saying that Paleo was never wedded to VLC, they don't know what they're talking about. Wolf was on the forefront of making Paleo cool and therefore popular... Crossfit, margaritas, counterculture, etc. Cordain was only on the shelf in the science section. And yes, the arrival of Taubes for an interview was talked about as if the arrival of a king. I eventually complained a few times about being all about one-sided advocacy, then left.

Speaking of Cordain, it was always hard to determine what his stance on SFA was back then, at least online. I'd asked about that on his site way back. After a week or two one of the grad students that was manning the boards answered something inconclusive.

Unknown said…
I can't find any studies that Davis has published

Jimmy Moore interviewed Dr Thomas Dayspring

It's actually a very good podcast

Dr Dayspring says that LDL-P is most important - Dr Dayspring says if your LDL-P is too high you should go on a drug regimen

SO - the question is WTF? I'll have new blood work results in 2 weeks and I'll take another NMR test in 2 weeks and have results in appx 1 month BUT my last LDL-P count A/O 5/10/12 was 1500 - the reference range is for low is <1000 so 1500 is borderline high - also the LDL-C was 188 (iranian formula = 141) which is also considered to be high

SO - do I abandon the HFLC diet for something else in order to drive down the LDL-P and LDL-C without resorting to drugs?
LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management

Paul Jaminet tried to address this

Jimmy says when he gets his weight stable for 3 months he will take another NMR test to see if his LDL-P has gone down

My question is this - it doesn't seem logical that one can consume a high fat diet AND at the same time have low LDL-C and low LDL-P

Am I wrong? How many people on a paleo diet have LDL-C <60, LDL-P <1,000, HDL-C>60 and Triglycerides <60?

Unknown said…
Now - people can criticize this all they want BUT

Postgraduate Training
After graduating from Emory, and despite his previous experiences in anatomy and surgery, Roberts served as an intern in medicine at Boston City Hospital before pursuing a 3-year residency in anatomic pathology at the National Institutes of Health in Bethesda, Maryland. It was here, working with attending physicians such as Glenn Morrow and Eugene Braunwald that his career began to focus on cardiovascular pathology, and he focused his training exclusively on autopsies and surgical pathology. He also began reading the works of Jesse Edwards, which he credits with helping to develop both his style of writing and strong interests in medical authorship and publications. He next served as a resident on the Osler Medical Service at The Johns Hopkins Hospital in Baltimore before spending an additional year as a fellow in cardiovascular disease at the National Institutes of Health. This extensive training conferred upon Roberts unique credentials both as an anatomic pathologist and a clinically trained cardiologist.

he pathology section of the NHLBI was substantial but in Roberts' first year only 25 cardiac specimens were available for study. Determined to catalog the largest possible collection of anatomic cardiac pathology, Roberts personally canvassed more than a dozen institutions each month to collect heart specimens which he would examine and return with completed autopsy results to their parent institutions. Among those hospitals contributing to his collections were Georgetown, George Washington University, Children's National Medical Center and Johns Hopkins Hospital as well as the Washington, D.C. Veteran's Affairs hospital and National Naval Medical Center. Collectively, Roberts was soon studying more than 50 hearts per month, a twenty-fivefold increase over those available from the NIH alone.
Despite major achievements by the institution in the understanding of cardiovascular diseases, Roberts was frustrated by growing difficulties attracting pathologists interested in cardiovascular disease. These difficulties were compounded by the closure of the NIH cardiac surgery program in 1987, greatly limiting the quantity and diversity of pathology available for study.
[edit]Baylor University Medical Center
In March 1993, 32 years after starting at the NIH, Roberts left the National Institutes of Health to join the faculty of Baylor University Medical Center, the flagship of a large hospital network located in the Dallas/Fort Worth metroplex. Working in a laboratory built for him by the hospital, he continues to study cardiac pathology and has published more than 300 articles since.[2] He is also an active participant in the ongoing training of cardiovascular disease and pathology fellows.

He doesn't strike me as some dumb schmuck - he recommends a pure plant based/fruit diet to drive LDL down to physiological levels
Twenty questions on atherosclerosis
Optimal low-density lipoprotein is 50 to 70 mg/dl
Lower is better and physiologically normal

BTW - this was coauthored by Cordain

So - confusion reigns
Lerner said…
Charles, here's a lecture from UCSF Mini Med School, 90 minutes:

If you've only been exposed to ideas of preventive cardiology from online Paleos and LCers, then you've only gotten a very biased outlook. Generally there's a kernel of truth somewhere, but all opposing evidence is ignored.

One example: after listening to Eades and Wolf for a while, I later read a study on non alcoholic fatty liver disease and was actually surprised to discover that the usual way to induce fatty liver in studies with rats was to feed them lots of *fat*. So obvious in retrospect. But in the LC world, it was always only about fructose, always one-sided advocacy.

Unknown said…!

LDL Cholesterol vs. LDL Particle Number, LDL-P and ApoB Measurements
Lerner said…
No confusion about what affects LDL and HDL:

SFA = LDL up and HDL up
PUFA = LDL down and HDL down
MUFA = LDL down and HDL up
TFA = LDL up and HDL down

I don't have a read-it cite but that's in the UCSF lecture.

HOWEVER, getting any of those numbers to goal doesn't necessarily prevent CVD. I'd suggest withdrawal from Paleo advice for a while and hang out at, then decide.
Lerner said…
I remember his face, he is part of or owns a company doing the (expensive) testing. Doesn't mean he is wrong, but it does mean he is not neutral.
Lerner said…
Evelyn says: "There have been some notable reports on PaleoHacks of not only no reduction in LDL-C"

You would naturally expect an increase with all of the SFA consumption. You might, however, get reductions if you are calorie restricted. Calories matter, a lot. As always, genetics might change any one person's response.

Twinkie diet guy reduced his LDL-C. So did Potato Diet guy.

Whenever I know of anybody who's had a CVD event or CVA, I personally say to get into weightloss mode ASAP. The time when any person is most likely to have an event is when they'd already just had one. Secondary prevention is different from primary prevention on a lot of things.

Craig said…
That 20 questions piece was interesting. So carnivores don't develop atherosclerosis, but herbivores do. I wonder if herbivores ever develop type 2 diabetes if overfed? Do carnivores develop diabetes if fed a high starch diet?

Perhaps being an omnivore is inherently a compromise: you get the vulnerabilities of a herbivore to fat, and the vulnerabilities (if there are any)of a carnivore to carbs, but you also get the benefit of a much larger range of food, and food that can easily be stored. And as long as you live long enough to reproduce and raise your childern, evolution cares not what happens when you pass the age of 35.

As to the confusion over cholesterol - It is like a lot of things in life: learn as much as you can, and then place your bet.
Larry Eshelman said…
I discovered Thomas Dayspring's lipid writings about two years ago and found them very enlightening. His views on lipids (i.e., high LDL-P is bad, whereas LDL-C is just a not very reliable marker) seems very representative of the MAINSTREAM lipid researchers and experts, as opposed to the medical bureaucracy, which is still stuck on LDL-C. Given his mainstream views, I was surprised that Peter Attia in his cholesterol series (which BTW is quite good) relied very heavily of Dayspring. I was even more surprised to learn, when I listened to Jimmy Moore's two interviews of Dayspring, that Dayspring is a recent Taubsean convert. Dayspring now believes that carbs are the main cause of high LDL-P (via insulin resistance). He admits that a FEW people on a low carb diet may see their LDL-C and LDL-P shoot up, including Jimmy Moore, but this doesn't seem to make him reconsider his Taubsean position.

A much more balanced view is Chris Kresser's. In his recently published High Cholesterol Action Plan he agrees with Dayspring and others that high LDL-P is the main culprit, but he recognizes that a low carb diet may not always be the solution, and may even be the problem (via causing hypothyroidism). He also integrates Chris Masterjohn's views on oxidized LDL into the overall picture.

Jimmy Moore, in the recent Dayspring podcast, said that he is on a 3% carb diet to see if, among other things, it brings his LDL-P down (from extremely high levels). It will be interesting to see what he does if his LDL-P doesn't come down. Will he abondone his low carb diet (unlikely), or take a statin (which seems to by Dayspring's backup solution), or will he disavow Dayspring and go back to believing that his large pattern A LDL particles are going to protect him?
Unknown said…

Myocardial Infarction in a Large Colony of Nonhuman Primates With Coronary Artery Atherosclerosis
Unknown said…
As part of my latest blood test I took the Oxidized LDL Triple Marker Test from Shiel Medical which measures oxidized LDL

the test was developed by Paul Holvoet

I will - in the next 2 weeks also get a new NMR Test to compare with my previous test in May

So - we shall see

If my LDL-P is still around 1500 I will have to rethink my diet, etc.
CarbSane said…
Thanks for the first hand account Lerner! Counter to some opinions of me, I don't have unlimited time to go back and read/listen to lots of back things. I know of Sisson's positions b/c he was cited often enough on Jimmy's forum in 09/10 especially, Kurt was cited quite often but not too much. I'd heard of Robb, but didn't really know much about his stances. I also didn't really start listening to a lot JM's podcasts until Summer 2010 ... and there were enough relatively current ones that I didn't listen to lots of archives. It seems as if he's undergone some evolution in his thinking himself then -- or changed with the flow of the times. You are right, relatively newbies to paleo are incorrect about the VLC roots ... I just think that the AHS11 Taubes/Guyenet altercation was that last straw that pushed most to move past that and many see VLC now as hijacking the movement.

I did listen to Robb on Jimmy's latest ATLCX podcast. If you listened I'd be curious your take compared to his older works. Thanks!

Puddleg said…
"nine non-obese sedentary healthy volunteers"

I think that such people are pretty resistant to negative effects of any dietary changes, what the study picked up were the "marker" benefits of avoiding grains and other neolithic toxins, improving electrolyte balance, and many other interventions.
Adverse effects of high omega6/3 ratios are a matter of years. 10 days? Just jokes.
Unknown said…

November 23rd, 2009

The results of Jimmy Moore's NMR Test
LipoScience's NMR LipoProfile Test: A Revolutionary, More Accurate Lipid Profile Particle Size Screening

my vein rolled so they had to jab me twice. But I wanted to have my blood tested so bad I sucked up the pain. This was just too important NOT to have done.

So, what were the results? Here were my numbers:

Total Cholesterol 351
LDL-C 278
HDL-C 57
Triglycerides 79
LDL Particle Number 2130
Small LDL-P 535
LDL Part. Size 22.0
Large HDL-P 10.9
Large VLDL-P 0.4

He thought these numbers were great

"Although my particle number of 2130 is considered “very high” for this test, the particle size of the small LDL-P was just 535 of that — considered “low” according to the test. Additionally, the LDL Particle Size of 22.0 nm is indicative of the “large” fluffy kind and the Large HDL-P and Large VLDL-P numbers I had put me in the “low risk” category. In other words, 1595 of my LDL particles were this protective kind and the graph was off the charts. Meanwhile, the small LDL-P number was less than half of the “goal” that is considered desirable. The numbers were well within the safe range. WOO HOO!"
Unknown said…
Unknown said…

Concept #8 – Why is it necessary to measure LDL-P, instead of just LDL-C?
Gabriella Kadar said…
Lerner, the problem with comparing the effect of various dietary 'ingredients' on rats, mice, rabbits, cats, dogs etc. is not necessarily valid for humans.

Cats are obligate carnivores, so feeding them carbs results in fatty liver, diabetes, and renal failure. Why? Because cats will gorge on kibble even though it's not healthy for them. Cats fed their appropriate diet do not over eat and do not become obese. Dogs are a bit more tolerant of carbs but are not really as omnivorous as some people think. Rabbits are eaters of green things, which are low in fat and must be consumed in large quantities to provide energy. Rabbits have very little fat on their bodies. Feeding them other than their natural diet causes metabolic stress. Mice are largely seed eaters. Yes, probably high in fat, but it's a particular type of fat found in grass seeds (and the bread in your kitchen!), rats prefer a vegetarian diet but when starved will eat your face. As, btw, will squirrels. Dead bodies found after a winter usually have had their faces chewed off by squirrels. I guess they are really hungry and the fat in the tissues provides them with a calorie boost.

I would assume that any *excess* calories consumed by a human, whether the source is fat, carb, alcohol or even protein would first result in fat accumulation in the liver and then fat accumulation in whatever area that person's genetic make up preferentially stores fat. Since the portal vein system from the GI tract goes to the liver, it only makes sense that the liver grabs whatever it can. When it's full up, then it proceses the excess, in whatever form it enters the hepatocytes, into blood borne molecules destined for storage elsewhere in the body. (triglycerides)

This is why it is easiest to lose fat in certain parts of the body and more difficult in others. I.e. abdominal fat (not subcutaneous) goes first along with the fat in the liver. Then when a person continues to consume a deficit in calories, the subcutaneous fat starts to go as well. The 'pear shaped' people have the greatest trouble losing their weight because that fat is most resistant to being utilized.

Therefore, fortunately, it is the people with the worst fat (intra-abdominal on the greater and lesser omentum) are the people who can most easily mobilize that fat out of there.

This stuff looks impressive on autopsy. It looks like great teardrop shaped globs of fat hanging off a relatively clear 'curtain' that covers the internal organs.

The pear shaped people usually have little abdominal fat of any kind unless they are severely overweight. Usually they end up with fat arms, really chubby thighs, fat on the hips and in women, small breasts. But these people have the hardest time losing weight in a proportionate way.

I was in the autopsy suite and it was very interesting.
So I've made observations over the years and do not entirely rely on bloggers who've never experienced what I have.
Gabriella Kadar said…
..........and now for bears...........?
Sherry said…
Well, Charles Grashow, you asked about the blood lipid numbers, and whether it is possible for anyone doing "paleo" to have ideal results on any or all markers, especially for LDL-C.

I'm one of those people who, after doing low-carb, high-fat for a while, ended up with skyrocketing LDL-C (around 180). However, my triglycerides were ideal at 55, and my HDL-C was 80. This meant that the trig/HDL ratio was 0.68, which is great. I have not done any labs to measure particle counts yet. My immediate solution has been to add more carbs, which I have tried to be consistent with over the last two months. This means that I don't skip many meals (which is a temptation, because I'm not very hungry). If I'm going to eat more starches, naturally, I want to consume them with a real meal. Besides, I'm very slender now, and feel that I need my calories. We'll see what happens on future tests.

But, yes, there are some people who start going HFLC, and all numbers improve dramatically, though they will change again, and nobody really knows where their fractions will settle. The people who have their LDL-C go up sharply are probably larger in number than Thomas Dayspring, M.D. wants to admit. I did listen to Dr. Dayspring on Jimmy Moore's site, and found him to be an engaging guest. If you'll remember, he remarked on the death of Tim Russert, and said "Tim's doctors were able to get his LDL-C down to around 65, and a lot of good it did him!" Dayspring even said that he was once a ticking time bomb with "great lipids." So there are plenty of anomalies one could locate.

In regard to Tim Russert, he might be a good example of stress causing a cardiovascular event. Maybe there is not enough emphasis on the type of personality who ends up with heart disease. I heard a radio host speculate that Russert was likely a Type A person who should have rested after returning from his trip to Italy. Jet lag is very hard on a person in their late 50's, and one does not recover as easily as a 22-year-old. Add to that, you've been away for a number of days in a foreign country, eating too much unusual food, and probably not sleeping well in a strange bedroom. Russert insisted on returning to work right away, and that may have been what caused the MI.

You mentioned Dr. Brown and Dr. Goldstein at UT-Southwestern. I was working at UTSWMC when it was announced that they had won their Nobel Prize. I can't say I got too excited about it, but then, I always thought that the lipid hypothesis was highly suspect anyway. I remember the first time I heard a distant relative of mine speak about her high cholesterol, and that the doctor wanted her to limit her consumption of eggs, and I thought that was pretty weird. Years later, my father developed some coronary artery disease, yet always seemed to have the right numbers on lipid panels. The best thing I can say is that he kept his weight down after undergoing bypass grafting, and he exercised every day, and things went well subsequently.

Frankly, I get disgusted and a little angry that we put so much weight on these lab tests that are supposed indicators of coronary artery disease. Do we truly know what causes heart disease? All these years, and I just can't see what has been accomplished, as heart disease is still directly responsible for most deaths. What is sometimes deemed as medical progress would have been better left unexplored, IMHO.

I also wonder if most humans (not all, but most) are simply very adaptable to many different ways of eating, as long as they are eating whole foods.

I hope you are able to get your LDL-P and LDL-C improved, Charles. Though I'm not particularly worried about my own, I might consider eating some oat bran for breakfast every day and see where that takes me!
Susanne said…
Could someone direct me to the source of the paleo/LC idea that "saturated fat is a good thing to have in your diet and you should add lots of it" (not just "not all saturated fat might not be as bad as we thought," which I've actually read studies on.

Also Charles, I eat basically the Frasetto diet above BUT also 4-5 servings of whole grain a day, and 2-3 of dairy in place of the red meat. (I only eat red meat about 2 servings a week, about the same as I eat legumes and fish). A Greek Mediterranean-ish diet. My LDL on the last test this summer was (if I recall correctly) about 117, my HDL 77, triglycerides 55. (It was a TC of 203 so I'm a bit off on something, maybe the LDL). I also get about 30min of aerobic exercise almost every day, which I suspect is part of the key for me. ('m a 44-yo woman and the aerobic exercise is the main difference between me and the other similar-aged women in my family, who have similar diet but slightly worse blood markers, and more central adiposity.)
It's funny watching different dieters pick and choose what they think is more important parts lipid tests.
Here's Jimmy moore lecturing a vegetarian about their "concerning" cholesterol numbers because he doesn't have a sky high HDL.

Now I'm certainly no expert on blood lipids and cardiovascular disease, but I'm pretty sure Jimmy isn't in the position to be lecturing vegetarians with low cholesterol about their lipids given his shaky looking cholesterol numbers.
Unknown said…
I am going to give the Bullet Proof Coffee a try, the people at Paleo Hacks love it. That's where you put a whole stick of butter in your coffee to healthify it.

Supposedly it makes you invulnerable to mortal wounds, though it does make you sensitive to sunlight, garlic and silver.
CarbSane said…
Could someone direct me to the source of the paleo/LC idea that "saturated fat is a good thing to have in your diet and you should add lots of it" (not just "not all saturated fat might not be as bad as we thought," which I've actually read studies on.

I can't find this anywhere myself. There are the "big game" paleos who insist we humans sat around eating fat from large fatty mammals and little else. There are the Nourishing Traditions Fallon and Enig who extol the virtues of natural fats. The major impetus for the sat fat promoters seems to be HDL. Mostly though there's the Jimmy sorts who read sat fat's not bad and turn it into healthy fats. Much like the fluffy LDL magically became "protective". This is one reason I "pick on" him so much, because his reach through podcasts is quite wide, and he influences the content with everything from his guest selection (many experts have no real expertise), to questions he asks or doesn't ask, to guests genuflecting to LC, to inserting his commentary.
Derek H said…
A little late to the game, but Lerner is accurate regarding Wolf's stance. He now states more of an ambivalent stance tagged with, see how you "look, feel, and perform" regarding how many carbs (and only/mainly from sweet potatoes or yams).

I dare say I've listened to 98% of Wolf's podcast, now typically for entertainment value.

Another famous line from Wolf (not him alone, however) is a gram of protein per lb of bodyweight. It may be because I weigh 225, but that seems a little nuts and difficult to maintain.
CarbSane said…
Hey Steve,

Not laughing here, just not sure how it could be done. The paleo that academics outline is not the pop-paleo being promoted. And when we're talking pop-paleo there's really two big names with their own brand/businesses. Almost everyone cites the Eaton papers, but almost no plans seem to follow them. It is impossible to get to around 40% calories from carb without either a lot of fruit or starchy root veggies. I'd even go so far as to say there needs to be starchy veg, because when one looks at the sheer volume of food the raw vegans consume, there's gotta be some malabsorption going on. Don Matesz' wife Tracy ( is doing a raw "banana girl" challenge and for a tiny thing she's eating enormous amounts of food -- 8 bananas for breakfast? And bananas are even high cal. I noticed Frasetto chose to juice the carrots and used pineapple. Cantaloupe is pretty high sugar, but high water too so it's rather low calorie.

Speaking of those LC studies, one of the biggest complaints is that some of them actually followed DANDR -- e.g. added back in some carbs.
CarbSane said…
Thanks Derek, Are you sure that's not 1g/lb lean body weight? Doesn't make quite as much difference for a guy depending, but for most women it would. I listened to his ATLCX podcast with Jimmy and if I didn't connect "paleo" with him and that had been bleeped out, it came off more like an elimination diet. Cut out everything, add back as tolerated. Sisson is adamant about one thing: grains, and this seems to be based on his own issues with grains and IBS. Wolf called gluten Satan's excrement in that podcast.

I just found this:
It's always hard to know exactly who is writing these things. I believe this is Amy Kubal writing. Suggested reading Taubes WWGF?? Consume 1-5T coconut oil daily??


Larry Eshelman said…
Jimmy Moore is so deluded, he is embarrassing to listen to. For me to force myself to listen to one of his podcasts the person he is interviewing has to be someone I expect will have something REALLY interesting to say, such as Thomas Dayspring.

Unfortunately, most lowcarb/paleo defenders give Jimmy a free pass. In the comments to Part VI of Pete Attia's "The straight dope on cholesterol" series one commenter, who had achieved a high LDL-P on a low carb diet, pointed out that Jimmy Moore and others in the low-carb/paleo crowd have achieved > 2000 LDL-P. Attia replied: "I’m not sure where the assertion comes that Jimmy Moore et al. all have LDL-P > 2,000 just because you might? My guess is very [few] folks out there even know their LDL-P." I know my LDL-P. After going very low carb it topped 2000 LDL-P. That's when I really got interested in lipid proteins and their relationship to CVD.

As Thomas Dayspring points out, the vast majority of people with CVD are insulin resistance and typically have a high number of small LDL particles. A subset of these people are the ones with normal or low LDL-C but high LDL-P (e.g. Tim Russert). Those of us who have high TC and LDL-C on a low carb diet, unlike the insulin resistant cases, may have large, "fluffy" LDL particles, but we may also have a lot of them. We are more like those with Familial Hypercholesterolemia (FH). The large LDL particles of people with FH don't protect them.
Lerner said…
To revisit square one: it's well known that SFA raises LDL (and HDL). It's even hard to find a quotable paper on pubmed saying so, because they were so long ago and show up as only title with no abstract. But here's a more recent one:
"It has been known for 40 years that dietary saturated fat (SAT FAT) increases plasma cholesterol, including LDL-C and HDL-C." 1997

Then efforts were made to determine which particular SFAs were doing it, in combination with what other nutrients, why did it happen, etc.

Then enter the LC smokescreen. When I used to read Eades' blog, there would always be discussion of how LCHF was superior for improving lipid panels. Then one day, I saw the most insightful comment that'd ever been posted there when somebody said that "everybody's LDL goes down during weight loss dieting, no matter what they eat". (Of course, that went unremarked on.) But that's why I wasn't surprised when the Twinkie Diet (lots of fat and sugar and carbs) provided a reduction in LDL - he was restricting calories.

Taubes, of course, is and should be infamous for insisting that calories don't matter, only carbs make you fat. Bloggers went wild on how brilliant that supposedly was in all it's analysis of mechanisms - yet meanwhile the carb eating Japanese weren't fat because calories do matter.

So now the same pattern is arising wrt heart disease... ignoring the effect of calories. If somebody's LDL actually goes down after starting LCHF, then they are restricting calories or they are genetically unusual. Anecdotes don't reverse decades of published research in the science world, though they might do so in the LC world of Alice in Wonderland.
Lerner said…
Besides which, I'd never seen in past years that any LCer (not Eades or Wolf) would actually claim that LCHF reduces LDL. The claim was always that it didn't matter, because large&fluffy was not harmful. However, from comments being made here, it *seems* like some LC bloggers and others out there are beginning to claim that SFA won't raise LDL. If so, the smokescreen is expanding.

That said, it should always be remembered that about half of people who have heart attacks do have 'normal' lipid numbers.
Lerner said…
Larry says, "Jimmy Moore is so deluded..."

and IIRC, he has one or more MDs egging him on in the "don't worry about it" delusion that large&fluffy is protective. It reminds me of how very overweight people will be plodding along with calorie-laden foods in the cart - plus a container of the blueberries that will save them.
garymar said…
Well I drink it every day, but I use coconut oil, not MCT oil, so my coffee is only bullet-resistant.

Actual prefer it now to cream, but only 2 teaspoons each of butter and coconut oil, around 150 kcalories.
Lerner said…
1g/lb is used as in muscle gaining, but is still the upper end of suggested ranges. Yes, it is hard to get that much, especially without powders. If one ounce of ground beef has ~6 grams, that'd be over two pounds per day for me at 205. Personally I'd think most of that much protein is wasted as fuel - except maybe in steroid junkies. Or how about over 2 dozen eggs?

Evelyn, I hadn't listened to that recent podcast you mention. But I'll tell you what, I'm fairly sure that very roughly around podcast episode 40, Wolf says "We're all taking a big chance here" [concerning all the fat consumption].

Maybe Derek remembers that.

Evelyn, Wolf has had severe coeliac problems, so his view is very much altered by food sensitivities of all kinds.

I didn't know that about Sisson; but wow, that fits the mold. Once again I'll remark here at the asylum: be wary of people who have conquered bad health problems of their own and then say that *everybody* should be in the same nutritional boat. That includes Masterjohn, who had big health problems as a vegan and now *apparently* AFAIK claims that unlimited cholesterol is not only harmless but beneficial.
Derek H said…
I've heard both. Robb always stated this recommendation came from his personal training days when individuals would always complain about being hungry, and eating these large amounts of protein is quite a task. And as Lerner pointed out, he also recommended copius amounts of coconut milk.

Lalonde had his article "Crossfitting on a Low Carb Diet" (paraphrasing), in which he admits to finding himself staggering to a Coldstone Creamery and eating a couple pints of ice cream to revive himself.

Even John Welbourne experimented with his crossfit football training and low carb, and he stated that Robb had him over for dinner and he was feeling terrible. He ate 6 sweet potatoes during dinner and explained to have felt like someone "wrapped him in a warm blanket" and he slept better that night than he had in a while.
Derek H said…
Sorry, I don't have Evelyn's memory. :). I don't remember him specifically saying that. It seems like they have all simply played the game of trying to balance the macro's. You can't suggest low carb without providing replacements. More meat, more health MCFA's - coconut milks and oils. There isn't any other option. So I can see where he may have said such a thing.
CarbSane said…
Gabriella, I believe you have the fate excesses incorrect there. It goes to the adipose tissue first. Indeed most dietary fat (less in fasted state, most in recently fed/large meal) goes straight to the fat tissue and the liver only gets a real shot at chylomicron remnants.

I'm not sure what your point is with cats and bears oh my! Cats aren't used in metabolic studies, they are mostly used to study sleep and the brain. Well, actually I do see your point, I think, that we can't translate results in animals to humans, but that is complicated. This is where some of the in vitro stuff is most helpful in identifying receptors, enzymes, hormones, etc.etc. that are common between humans and the animal models we study.

Yeah Lerner, feed them fat. Or even better, feed them a human junk food diet with lots of fat -- they'll overeat and get really fat and really trash the liver. The CAF rat study was priceless in this regard.

Lerner said…
Here is what I'd think of as being the official end to Wolf-style VLC, the interview with Lalonde about the failure of VLC and Crossfit style workouts:

To his credit, Lalonde readily and without excuse admits that it was a big failure. (The site also has transcripts of podcasts.)

All of the degrees and 'research backgrounds' and especially the purported mechanisms ad nauseum fall by the wayside with the simple concept of testing to see if it actually works, aka outcomes. Graciously admitting that it was a failure should not obscure the fact that it was a big failure readily embarked upon because of all the misguided mechanistic arguments.

Derek, that's interesting about the ice cream. I've been going around saying that sugar-isn't-always evil. Do you happen to have a URL for that Lalonde article? (If it's not too much trouble.)
Lerner said…
And of course, carbs must be the approved sweet potato; and non-exercisers can still be VLC 'til the end.
CarbSane said…
I have wondered for a long time how much those MDs are egging him on, and how many say just enough of what he wants to hear.

In 2008 he went to Westman who told him to increase his fat/protein ratio but decrease portions. Guess which advice he really took?

Mary Vernon told him his whacked lipids after the eggfast were normal for having just lost 30 lbs so rapidly. He heard "normal".

What happened to the mystery doc who diagnosed and treated the low testosterone?

Most of the docs who go on his podcasts and such probably have no clue what his lipid panels look like, and have looked like for a very long time. Yet he repeats "spectacular" and "healthy" and OMG he is going to be writing a book on the topic for the layperson?

Right now Jimmy's situation is improving because he's losing weight and in caloric deficit. He says he often eats only once or twice a day now. When the weight loss stops, what next? I shudder to think about that.

I would be very curious to know the IMTG (triglyceride levels in the muscle cells) of some of these VLCHF people.

I need to listen to the Dayspring podcast.
CarbSane said…
I'm skimming Robb's book chapter on fat now. Gary Taubes. Sigh.

I'm trying to follow along with this discussion here. Hopefully tomorrow I can catch up fully
Derek H said…

When the font turns bold, you can begin reading at the 5th paragraph if you want to skip a little of his introduction.

He does provide a week's worth of what he ate.

The article was written highlighting the many benefits of this plan, in fact Mat said this towards the end (sorry so long):

"So where to go from here? I’m going to keep this up because I know I’ll be healthier in the long run by consuming fewer carbohydrates. Does this mean that post workout carbohydrates are bad? Absolutely not! In a situation like the CrossFit games, with multiple workouts throughout the day, PWO carbs are essential. Replenishing glycogen stores takes approximately a day on a low carb diet whereas wolfing down some mashed sweet potatoes will get the job done in a few hours. In addition, the fact that fat slows down gastric emptying probably means you don’t want to be eating a whole lot of it during competition. Easily digestible protein and carbohydrates are still the way to go in a games setting. However, I think my experiment highlights the fact that PWO carbs are a powerful tool that should be used sparingly under the right conditions. Avoiding a carb load after a workout will allow you to hold on to the insulin sensitivity you gained from exercising. This is a huge boon, especially for clients who are trying to improve their body composition. Whether you are a CrossFit, weightlifting, endurance, or any other type of athlete, I don’t see why a high carb diet should be considered “necessary” to fuel your endeavors."

I'm not sure how much longer he did it for, but the ice cream event he admitted to much later in a podcast (I'll work on finding which one).
Unknown said…
My last blood work - 5/10/12 - Triglycerides were 36 and HDL-C was 59 - ratio was .61

BUT - LDL-C was 188 (141 using the Iranian formula) and LDL-P was 1,500 - BUT small LDL-P was 127

So - which is a better predictor - the Triglyceride/HDL-C ratio OR the LDL-P?

Derek H said…
Transcript of Podcast 68, which was 2 years after the above article:

"So let me discuss an example of that where, you know, Robb has changed his mind. So Robb used to be highly pro low-carb and mostly for using carb sparingly post workout. But, you know, Robb and I talked extensively while he was proofreading – while I was proofreading the book and I mentioned to him that I wasn't convince glucose from starch as problematic."

Only took 3 to 4 months for the low carb/crossfit experiment to go awry; begins on page 23 of the transcript.
Lerner said…
Gabriella, I'm glad that I read your comment about the fat and autopsy only *after* I'd already eaten :)

Yes, bears storing fat is unusual for animals living normally. I think woodchucks get fat, also. How a rabbit makes it through the winter, I don't know.
Lerner said…
Derek, thank you kindly for looking that up. Hey, you might be just the one to ask: is it true that the two of them have backed off about phytates being a big problem in mineral absorption?
Larry Eshelman said…
There are actually two Dayspring podcasts. The first is on June 20, 2012 and the second is October 4, 2012. The second is quite long and includes questions from listeners. Jimmy included a long summary list of points covered, so it is fairly easy to navigate the podcast.

Peter Attia's cholesterol series is basically a summary of Dayspring's writings, and I would recommend it. The long version is on his website, but there is a shorter version of Mark Sisson's website (Aug 29, 2012).

One of the interesting points made by Dayspring (and repeated by Attia) is that HDL-C is not all that important. Basically, low HDL-C reflects high trigs, and high trigs lead to a large number of small LDL particles (so it is the trigs that are important). The reason I find this interesting is that a lot of lowcarbers take comfort that their HDL-C is very high. This, in turn, often leads to a very low TC/HDL-c ratio. This ratio is a fairly strong indicator, but I am beginning to question whether it has much meaning when the reason one has a low ratio is because of an abnormally large denominator (high HDL-C) in spite of a fairly high numerator (high TC). There is evidence that a low HDL-C is not a good sign, but there is not much evidence that high HDL-C is protective (at least for CVD).
Derek H said…
I think Lalonde has - particularly when cooked. His more recent podcast with Robb may talk about that. I think the gliadin component of gluten may be the last one he suggests avoiding. And of course, fructose is "dose dependent" - which would obviously factor in activity levels and such.

He also did a "Low Carb Experts" podcast with Jimmy highlighting the importance of calories while explaining the many nuances about them that people don't realize. A good listen. I was always wondering what Jimmy must have been thinking during the discussion.

I like Lalondes ability to change with experience and improved information, but often leaves me thinking (which you mentioned above) - with all the doctorates, research experience, explained mechanisms, and a larger brain than mine, it's amazing how many times they need to change their stance.

It's no wonder everyone get's tired of the changing tides.
Lerner said…
and as LDL has been analyzed by sub-fractions so that a simple LDL-C doesn't tell enough, so too with HDL sub-fractions by size - but perhaps more importantly by oxidation status. Lecture here:
"HDL: When Good Cholesterol Goes Bad"
Dr. Jay Heinecke, professor in the University of Washington's Department of Medicine

HDL also seems to be the lipoprotein with the widest variety in surface proteins, by far; and it might be involved in many functions besides lipid transport (which is what Larry might have been alluding to)
Lerner said…
Yes indeed, the trendy movements and "new paradigms" are usually based only on purported mechanisms. People get all excited about being part of the new wave, then eventually find out it isn't true after all. Everybody goes through it, but some never stop. As for the gurus, they often end up showing feet of clay - only lurching from topic to topic to try and prove that their pre-determined stance (and guruness) is correct. I imagine that vegans have the same.

To bring things generally back to Charles' original questions: all that counts as real evidence are outcomes. That means that studies tracking deaths or events are number one. Studies using scans that show plaque progression or regression are next. Everything else is far behind, with maybe inflammation markers being next. PhDs, Mds or 'science writers' using lots of jargon about pathways make for movements and internet sensations that come and go.

Nevertheless, without strong evidence you still do have to take a guess regarding what to do. It'd seem less than prudent, at least to me, to gamble one's life on some trendy, new radical movement. That is why medical guidelines take a long tine to change, while patients might be griping about their doc not being up on the latest thing.

Okay, I'm off the soapbox and packing it in for the afternoon :)

"However beautiful the strategy, you should occasionally look at the results."
Winston Churchill
Lerner said…
One last study for Charles:
"Weight loss, regardless of diet intervention, can reverse carotid disease"

(and no study ever settles things for good)
Unknown said…
Weight is not a problem for me - age 58 - height 6'1" - weight 163 +/- a pound or two
Larry Eshelman said…
HDL "might be involved in many functions besides lipid transport". Yes, that was what I was alluding to (e.g., immune function). Dayspring thinks HDL particle count (over various sizes) is important even from a lipid transport point of view, but that it is very complex and not well understood. His main point is that HDL-C doesn't tell us much beyond the fact that high HDL-C usually is associated with low trigs.
Craig said…
For the benefit of Charles, here is my history:

When young (<30), lean (< 160lbs), and very active, my total cholesterol was around 160-170. That is about as far as they tested it back then.

In my 40's and early 50's, I got heavy (190-200lb) and less active. Ended up with high cholesterol (>250), high LDL (>130), low HDL (<40), and high triglycerides (>150). Later on, also saw my blood sugar numbers drifting into danger territory. Classic metabolic syndrome (except that my blood pressure was always OK, even ran to the low side).

Eventually, was put on lipitor. Brought my LDL down (<100), and thus my total cholesterol (<200). But HDL was still low and triglycerides were still high.

Then began carb restriction, lost 35+Lbs, and started taking fish oil. With that, plus continuing the lipitor, I now get 'good' numbers: total cholesterol 140-150, LDL 75-90, Triglyceride ~50-70, HDL ~55-60.

I do eat some red meat, maybe 3 or 4 times a month. Tend to avoid bacon and sausage, except for the low fat turkey/chicken varieties. For protein, I eat mostly chicken, fish, eggs, reduced fat cheese. The rest of my diet is mostly nuts, veggies, a bit of fruit, some 'safe' starches, a little wine, coffee with half and half. Use olive oil and butter for cooking. Try to avoid 'industrial seed oils'.

In terms of variations in these numbers:

- When I up the carbs and decrease fat intake, HDL will drop a bit, and LDL will drop a little.

- My LDL seemed to remain pretty stable during my rapid weight loss phase, and did not rise when I stabilized at my present weight.

- The rise in HDL may have been partially induced by an increase in the amount of fish oil I was taking. I also have, in the past 12-18 months, done more exercise of the high intensity interval type. This is also known to boost HDL.

I am not as active as I was in my 30's, but I think I am exercising smarter. Instead of running 30 miles a week and lifting weights twice a week, I now lift weights once per week, and then do one or two high intensity interval sessions of about 20 minutes in duration.

Would like to get off the lipitor, but suspect it would put my LDL at a level that conventional thinking deems unsafe. Since I don't seem to have side effects, I'm gambling that it is doing some good for me. I may try 5 mg dose for a bit, just to see what happens.

What does this mean for my risk of heart disease? I have no idea. I occasionally let myself feel good about the numbers. Then I remind myself that people with 150 cholesterol have dropped from heart attacks, and that people with HDL > 100 have had needed surgical intervention for significant blockages.
Unknown said…

Do You & Your Doctor Know All 10 Heart Disease Risk Factors?

Because Total Cholesterol (TC) and LDL cholesterol are not the most reliable predictors of heart disease, they are not posted in the following chart.
Sanjeev said…
I have not studied the cholesterol -> CHD enough to comment really.

My reaction to what's come and gone over the last 10 years is it's been an unending stream of

"my old cholesterol idea was invalid, but my new, NEW idea fixes it (like that fixed the one before, and THAT fixed an older one). This time I mean it. Really, I mean it this time ... "
Gabriella Kadar said…
Evelyne, find an overweight person whose liver isn't fatty on CT scanning. It's a 'reportable finding' but it's to be expected. Most patients don't realize how important this is and their doctors don't say much about it either except to mention it. Explaining the significance doesn't fit into the 10 minute appointment time. Doctors aren't in the diet business. Not here, anyway. The government won't pay them to weigh patients every two weeks, that's for sure. There is only concern when patients are losing weight rapidly or anorexia nervosa/bulimia. If someone wants to lose weight and be monitored, they've got to 'pay to play'.

You got my point about different animals and diet and metabolism. Rats especially, sure if you do to them as you stated above, the predictable happens. But really, rats are being fed a diet that is not natural to them by doing that experiment. So, a mechanism is demonstrated which is not any different than producing fois gras. We could use geese and ducks too, I suppose. Just they are bigger, messy and geese can be quite nasty. But at least we can eat the birds after bits of their livers and internal organs are harvested. Rats, not so much. Rat corpses are just incinerated. (I'm being a bit bizarre here, but just my own, thankfully, limited work and exposure to ethanol research dismayed me as to the numbers of rats that were sacrificed.)

Lerner, I see rabbit tracks in the snow during the winter so they must be eating something. Probably reachable bush bits with buds are nutritious. Same diet as deer but rabbits can't reach as high.

Unknown said…
Re: approved sweet potatoes - didn't Lalonde's AHS12 talk identify white potatoes as being more "nutrient dense" than sweet potatoes? Wonder if this will permeate The Paleo Solution... Greg occasionally will say something along the lines of "even eat white potatoes if you have to". Since it also seems antinutrients are not likely a problem (especially peeled - Masterjohn did an article on this?) and neither is the glycemic index (Jaminet amongst others), I still don't get the reluctance towards white potatoes still. No-one hates on tomatoes so I don't see it as a nightshade issue either. I guess it's just one of Cordain's pet hates and that's that!
Unknown said…
Re: approved sweet potatoes - didn't Lalonde's AHS12 talk identify white potatoes as being more "nutrient dense" than sweet potatoes? Wonder if this will permeate The Paleo Solution... Greg occasionally will say something along the lines of "even eat white potatoes if you have to". Since it also seems antinutrients are not likely a problem (especially peeled - Masterjohn did an article on this?) and neither is the glycemic index (Jaminet amongst others), I still don't get the reluctance towards white potatoes still. No-one hates on tomatoes so I don't see it as a nightshade issue either. I guess it's just one of Cordain's pet hates and that's that!
Simon Carter said…
For what it's worth, Art DeVany has never agreed with the adding fat and bacon to everything Paleo meme. He recently commented that he thought that Robb Wolf was in the weeds.
Lerner said…
Charles, that changes a lot. So, it seems to maybe be time to put away the trialist hats and put on the clinician hats. Without overeating involved, I'd suggest there are two paths to proceed on:
1) should you actually be worried at all, are there any other risk factors
2) why is your LDL-P high, when not overeating and not having many carbs

As regards #1, the biggest question is if your BP is okay.
Lerner said…
Craig says, "... done more exercise of the high intensity interval type. This is also known to boost HDL."

Craig, can you say a little more about that? The last time that I'd looked, it was duration that provided the HDL-raising effect, not intensity.
Lerner said…
wrt to liver: I happened to watch "Supersize me" for the first time last night (Hulu). If we look past the hatchet-job aspects, there are some interesting things there. The main adverse health effect he had was in the liver, and it came quickly. Now, the docs in the movie all say that was from the high fat food. The LCers can have a point being irritated that Spurlock was eating fat and sugar, and *mostly* the fat gets blamed. Then again, both Spurlock and the docs and the LCers (and probably LFers) all keep the focus off calories. [Though one woman (a nutritionist?) does say he eats twice maintenance calories and so he should stop guzzling the soda.]

Spurlock, while doing the segment on food addiction, kind of shoots himself in the foot by bringing in Don Gorske, the Big Mac addict, who eats two per day for years but isn't fat and has low cholesterol, no known liver dysfunction... because he apparently keeps calories in check. Sure, that has probably been discussed to death since 2004 -- but not enough because we still have gullible, deluded billionaires giving money to Taubes for looney tune ideas.

Dr. Barnard, btw, brings up some casein opiate, just as the LCers bring up carb induced neurotransmitters. That's parallel to how Clarence Bass is a counter to Art Devaney - which brings up again that LCers trot out DeVany as an example of how LC goes great with 70+ yr old people, but conveniently forget to mention LFer Bass.

I was just about to give Wolf some credit on that, because a websearch does show that Bass is mentioned there. But oops then again, I did look at the first two page results and see that Wolf only mentions Bass' minimalist training - nothing about his LF approach.

It's interesting what Simon posted about DeVany's impression of Wolf.
CarbSane said…
Apparently DeVany is going to be launching a public website (his is now subscription only) to try and reclaim paleo from the neolithic capitalistic pigs (grin). I saw him on Fox and Friends once where he said avoid all white things, which would explain his tan, but that's about the crux of what I know about him.
Lerner said…
Chris says, "white potatoes... glycemic..."
If we want to compare opinions, then we can add Kurt who IIRC says that PP BG isn't a problem in normoglycemics at all. That seems sensible. Still, I want high GI and Insulin Index PWO, but generally avoid massive carb overfeeding otherwise... a la frequent small meals for health (not comp). If I have half a loaf of French bread then I insure having fat and some cholesterol with it, to try and keep particle size up (but I don't agree that limitless cholesterol is harmless). Macros are mostly irrelevant to me. Is there any blogger out there who is even remotely like that?
Larry Eshelman said…

Looking at percentiles from the Framington study, an LDL-P of 1500 lies in between the 50th and 55th percentile, whereas an LDL-C of 188 lies in between the 90th and 95th percentiles (and and LDL-C of 141 is at about the 60th percentile).

The trig/HDL-C ratio is a good indicator of small LDL particles, met symdrome, and for discordance of low LDL-C and high LDL-P. But you are somewhat discordant in the opposite direction - high LDL-C and normal (median) LDL-P.

So I would guess that LDL-P is a better predictor.
Lerner said…
wrt new DeVany site: About a month ago I was thinking that the 'end of Paleo' as a fad would come two ways: it would mainly be absorbed into the 'whole food, real food...' thing when people got fed up with the Puritan-like food restrictions of Paleo, and then secondly when people were getting fed up with what I've been calling "Paleo, Inc". Because there are sincere Paleos out there who aren't in it for the cool trendy counterculture aspects, although they're probably in the minority.

So I'd went looking and found this page from August:
"Paleo Marketing 101: How people make money using shameless megadoses of self-promotion"

They don't quite go so far as to name names, though.

Lerner said…
Larry, here's talk of how LDL-P can be estimated from TAG and HDL-C: 2007
"Although it's good to be aware of LDL-P, it's expensive to test. We show that HDL-C and triglycerides provide similar predictive information."
That is the claim which Dayspring says isn't true. From Charles' figures, would you say that his HDL-C and TAG agree with his LDL-P?

Larry Eshelman said…

Since most people with high LDL-P are insulin resistant, TAG and HDL-C are good indicators. Dayspring in his interview with Jimmy Moore says that TAG/HDL-C ratio is a good indicator for these cases. Charles' TAG and HDL-C numbers indicate that he is not LDL-C < LDL-P discordant. In fact, he is somewhat discordant in the opposite direction, but unfortunately, not enough to put his LDL-P is at a low risk level.


Your case is of strong interest to me, since like you I saw my LDL-C jump while eating a low carb paleo style diet, and, like you, I was not over weight (5'11' tall, weight 150, 31 inch waist). When I was eating VLC, my measured LDL-C jumped to 254 (with a LDL-P of 2674, pattern A) and peaked at 295. Based on Paul Jaminet's advice, I started eating more carbs, and taking his recommended supplements (including iodine). My LDL-C started to fall, and my most recent measured LDL-C was 144. (I am getting another NMR in a couple of weeks.)

In an earlier comment you reference a blog post by Paul Jaminet on LDL and the thyroid. Has eating low carb affected your thyroid? For me, at least, it seems that the major contributor to my high LDL-C and LDL-P was that the low carb diet tanked my thyroid. My free t3 was below range. Now it is within range, but still at the low end. During my VLC stint, my body temperature averaged 96.5, now it averages 98.0.
Unknown said…
I'll have blood test results next Friday when I see my doc - I'll post them here

I had a complete thyroid panel done

TSH, Free T4, Total T4, Reverse T3, Free T3, T3 Uptake

as well as other tests

Homocysteine, HA1C, CoQ-10, Electrolyte Panel, Hepatic Panel, BUN, CBC, Vitamin D, 1,25 -Dihydroxy, PSA (Free and Total), IGF-1, IGFBP3, Ultrasensitive Estradiol, Testosterone (Free and Total), Ferritin

I also has the Shiel Triple Marker test which measures hsCRP, HDH and Oxidized LDL

I don't think anything was left out

I will also take another NMR test on the 18th to compare to my last one
Unknown said…
BTW - my last HA1C (in March) was 5.2 and on the last NMR Test my Insulin Resistance Score (LP-IR) was 6 should be <= 45 so that was very good

I may make some dietary adjustments - I'll wait until I get the test results in

I also took the BerkeleyHeartLab LP Plus3 at Quest Labs - should have the results on the 19th as well
ProudDaddy said…
I'm wondering if apoB might be the best and cheapest proxy for LDL-C.
Unknown said…

"Measuring newer lipid biomarkers with the aim of honing risk prediction for heart disease doesn't actually appear to help very much in this regard, according to a the largest study yet to look at this issue [1].

The study, published in the June 20, 2012 issue of the Journal of the American Medical Association, found that measuring a combination of apolipoprotein B (apoB) and apoA1, lipoprotein (a) (Lp[a]), or lipoprotein-associated phospholipase A2 (Lp-PLA2) gave worse predictions of risk than current lipid measures—total and HDL cholesterol. In addition, the study showed that measuring these alternative biomarkers added little information when added to conventional risk factors."

Emerging Risk Factors for Atherosclerotic Vascular Disease
A Critical Review of the Evidence

Unknown said…


Epidemiologic studies suggest that LDL particle concentration (LDL-P) may remain elevated at guideline recommended LDL cholesterol goals, representing a source of residual risk. We examined the following seven separate lipid parameters in achieving the LDL-P goal of <1000 nmol/L goal for very high risk secondary prevention: total cholesterol to HDL cholesterol ratio, TC/HDL, <3; a composite of ATP-III very high risk targets, LDL-C<70 mg/dL, non-HDL-C<100 mg/dL and TG<150 mg/dL; a composite of standard secondary risk targets, LDL-C<100, non-HDL-C<130, TG<150; LDL phenotype; HDL-C≥40; TG<150; and TG/HDL-C<3.


We measured ApoB, ApoAI, ultracentrifugation lipoprotein cholesterol and NMR lipoprotein particle concentration in 148 unselected primary and secondary prevention patients.


TC/HDL-C<3 effectively discriminated subjects by LDL-P goal (F=84.1, p<10−6). The ATP-III very high risk composite target (LDL-C<70, nonHDL-C<100, TG<150) was also effective (F=42.8, p<10−5). However, the standard secondary prevention composite (LDL-C<100, non-HDL-C<130, TG<150) was also effective but yielded higher LDL-P than the very high risk composite (F=42.0, p<10−5) with upper 95% confidence interval of LDL-P less than 1000 nmol/L. TG<150 and TG/HDL-C<3 cutpoints both significantly discriminated subjects but the LDL-P upper 95% confidence intervals fell above goal of 1000 nmol/L (F=15.8, p=0.0001 and F=9.7, p=0.002 respectively). LDL density phenotype neared significance (F=2.85, p=0.094) and the HDL-C cutpoint of 40 mg/dL did not discriminate (F=0.53, p=0.47) alone or add discriminatory power to ATP-III targets.


A simple composite of ATP-III very high risk lipoprotein cholesterol based treatment targets or TC/HDL-C ratio <3 most effectively identified subjects meeting the secondary prevention target level of LDL-P<1000 nmol/L, providing a potential alternative to advanced lipid testing in many clinical circumstances.

SO - my TC/HDL ratio is 4.3 NOT <3.0 - might this explain the LDL-P >1000??
Larry Eshelman said…
"I'm wondering if apoB might be the best and cheapest proxy for LDL-C." I'm assuming ProudDaddy means "LDL-P". Thomas Dayspring, and most other advocates of measuring LDL-P, agree that apoB is very concordant with LDL-P as measured by NMR, and so a good proxy.
ProudDaddy said…
Yes, Larry, I meant LDL-P (senior moment). Thanks!

Thanks, Charles, for the references. The ones I had been looking at indicated that apoB/apoA1 was better correlated to atherosclerosis than conventional measures.

The takeaway: if you are interested in your LDL-P, you might instead just check your aopB. However, it may not add much to your knowledges of CVD risk.

Methinks I'm going to stop worrying about a marginal lipid profile and get a CIMT ultrasound.
an3drew said…
When does a particle qualify as "PUFFY?" Is there some sort of quantifiable measure that makes something puffy? I used to read and vomit every time a keyboard PhD at Paleohacks advised someone that "LARGE and PUFFY" particles means you're "safe" with regard to the threat of CVD.

Literally, I'd vomit in my lap.
Larry Eshelman said…
I thought the adjective used was "fluffy". In any case, for the NMR, an average LDL particle size of > 20.5 mn is considered type A and are of the "fluffy" type. This has to do with the density of the particles. Large LDL particles have relatively more cholesterol (higher cholesterol to TAG ratio) and so are less dense. At one point evidence suggested that the small, denser LDL particles were more atherogenic, but more recent analyses suggest that this simply reflected the fact that people with a lot of small LDL particles for a given amount of LCL-C had more particles. In other words, it is the number of particles that one has that determines the risk. Fluffy particles, per se, are not protective. In fact people with FH typically have a lot of fluffy particles; yet, they are at very high risk.
CarbSane said…
Isn't it the other way around? It's the triglyceride content that makes for size and density -- chylo > VLDL > LDL with triglyceride content declining with size. It seems to reason that the small LDL are particles that are hanging around longer due to perhaps receptor overload? Dunno. Just thinking out loud in that last statement.
CarbSane said…
OH ... and having a lot of fluffy LDL could just mean the "backup" goes even further past the receptors to LPL removing triglycerides from the LDL. Still just thinking out loud here.
Lerner said…
wrt to density: it's the proteins (in the shell) that makes it dense

chylo->VLDL->->IDL->LDL by size, as they get smaller they generally have a higher proportion of cholesterol as the TAG has been offloaded for fuel or to be stored

A chylo has the ApoB-48 surface protein. Then all the rest have ApoB-100. ApoB-100 is one of the largest protein monomers that humans make. It's like a weightlifting belt wrapped around a basketball. Other surface proteins can be tiny, e.g. for CD20 there are tens of thousands... like tiny threads woven back and forth a couple of times through the surface of the basketball.

As VLDL gets smaller, it also swaps out some of the other surface proteins. Usually HDL is the agent doing that.

The phospholipid bilayer mainly composes the shell, though in LDL the shell is about half free/regular cholesterol (as opposed to the cholesterol ester inside as the cargo).

Here is a graphic showing relative sizes, not the greatest image but I just happened to be looking at that page:
(bottom right)

wrt LDL receptor binding:
"... in small LDL, apoB has alterations in configuration, which is associated
with a lower affinity to the LDL receptor."

Thinking out loud is good :) it promotes more conversation. Corrections are welcome.


"HDL is the smallest of the lipoprotein particles. They are the densest because they contain the highest proportion of protein to cholesterol."
Lerner said…
oops, should say--> phospholipid monolayer (made of diglycerides)

whereas a cell membrane is a phospholipid bilayer (watery environment inside and out, as opposed to a lipoprotein being watery outside and fatty inside)
Simon Carter said…
Hi Evelyn, some De Vany quotes:

Question: Do you buy commercially raised meat or organic/pasture raised?
The energy density would be pretty different, wouldn't it? Do you worry about potential toxins ending up in your system if you buy regular store meats?
De Vany: I don't worry at all. But, trimming the edge fat helps to remove the oxidized fats. I buy most meats at Costco, though I do try to find bison and other game meats there or order them as often as I can find them in restaurants.

Some other De Vany quotes:

“No manufactured fats are good for you.”
“Stay away from manufactured oils”
“Butter and lard are, again, are not needed as sources of fat because modern meat is so high in fat. I do avoid them completely. Butter has its own problems related to milk, an important allergenic source for many. Now that I see where these items come from I have to wonder how anyone believes that lard and butter are Paleo. See my human diet post for a bit more on this subject. Problem is our modern cattle are so fat that we are all on a high-fat diet if we eat significant amounts of meat and fatty fish, as I do.”
“More importantly, eating leaner meats, with my abundant intake of ribs and fatty fish, gives me all the fats I need without engorging me with excess energy. So, in the end, this is a strategy for keeping energy intake from going out of hand. Easy to do in this modern world. “
“I am a bit appalled at where this former Paleo or Natural movement is going. Things are getting weird and harmful. CrossFit has gone over the edge and Paleo is promoted by a lot of know nothings all over the internet, as well as by some people with some background in science (and no practical experience or bodies to show for it, albeit some dramatic weight losses, usually following a simple EF protocol)”
Lerner said…
Since more confusion is needed: it's generally accepted HC will indeed produce more of small LDL. But, there's always a but:
" the Pritikin Center we found that the LDL status of 6 of 22 subjects actually changed from pattern B to pattern A (a predominance of large LDL particles) while consuming a VLF diet, which is the exact opposite of the trend observed by Dreon".

And somewhere is another ref (I think from the Pritikin group) showing that getting Pattern A or B from HC is genetically determined - some behave the opposite of normal.

And wow, the Pritikin bunch run a "Spa an Resort". Talk about marketing.
Single Occupancy (Share a room and save $1000+) $ 4,200 $ 7,200
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Lerner said…
those were 1 week and 2 week rates
Larry Eshelman said…
Lerner is right - the protein is the source of the density. LDL particles start out (usually) as VLDL's. It is the initial ratio of cholesterol to TAGs in the VLDLs that largely determines the ultimate size and density of the LDL particles. If they have a lot of TAGs relative to esterfied cholesterol (EC), after they give up most of the TAG, they will shrink to small particles with very little cholesterol and so will be dense. So it is the ratio of protein to core contents (EC and TAG) that determines the density, but the amount of final core content is largely determined by the initial ratio of TAG to EC. (This is a simplification, leaving out the role of CETP.)
Lerner said…
Larry says, "It is the initial ratio of cholesterol to TAGs in the VLDLs that largely determines..."

AMEN to that!! That's why I try to take in some cholesterol when I have a lot of carbs. The mechanism might be this: with carb overfeeding (beyond the amount which gets taken up as glucose by cells), the overage needs to get DNLed so as to reduce blood glucose. But, if there is no ingested cholesterol to put into the VLDL core, the body has to grab it from elsewhere or make it... but the body is in a rush to take BG out of circulation and get it out of the way as TAG in VLDL, so the VLDL core is not as cholesterol rich as it would be from eating animals. Plus, the original VLDL (after eating carbs) might be a little smaller anyway.

Btw, does anybody know if a stick of cholesterol would float just as a stick of butter would?
Larry Eshelman said…

Is this reasoning original to you (eating cholesterol with carbs)? I've never seen it before. Very interesting!
Sanjeev said…

should sink: density 1.052 is greater than water at its densest 4 deg C, 1 g/cc

Sanjeev said…
but since in manufacturing it self-forms into a fine powder and I've never heard of it being formed into large crystals, it will probably have a lot of air inclusions, so any product you can buy would float.
CarbSane said…
Sanjeev beat me too it. We just used commercial cholesterol in a lab and it seemed to float (though obviously not dissolve) in water despite the slightly higher density. It's more soluble in hexane, so I suppose hexane IV's will help ;-)
Larry Eshelman said…

But isn't that referring to the density of free cholesterol? What is the density of esterfied cholesterol?
Lerner said…
Larry says, "Is this reasoning original to you?"

Thanks for asking, Larry. Yes, sir, it is my idea. I've been trying to take an independent and pragmatic approach to all of these topics.

Something else I'd been thinking, I don't know if it's written about: what is the final purpose of LDL anyway? Lipoproteins carry TAG to destinations, if no cell needs it then TAG goes into adipocyte storage. But cholesterol has no such storage areas, so LDL just might be intended to be mobile storage. What necessity would require immediate access to cholesterol? All I've thought of so far is for some use in trauma...

It'd be akin to how coagulation proteins are always floating around in the blood. If you get a cut, you don't want to wait to be manufacturing clotting factors - you want them right that instant.

That's a matter of curiosity, not really practical. Though, if there are a lot of inflammatory signaling molecules in circulation, then maybe that signals the body to also keep LDL in circulation just in case - and so not clear it. Any thoughts on that?
Larry Eshelman said…
Dayspring says something similar about HDL: "The primary lipid mission of HDLs is to deliver cholesterol to steroidogenic tissue .... The reason HDLs have a 5 day half-life is to be available as a reservoir of cholesterol in case the adrenal has to start manufacture large amounts of adrenalcortical hormones (infections, inflammation, bodily crises)."

Also I remember Dayspring saying that the main mission of the apoB particles is to deliver TAGs and speculating that the cholesterols main purpose in these particles is to provide structure (or shape so that they won't collapse when devoid of TAGs).
Anonymous said…
DeVany is demonstrating that he can be silly too with some of these comments.
an3drew said…
Yep, meant FLUFFY. I guess using CAPS LOCK overwhelmed my attention to detail. Anyway, good posts here.

I literally have no clue what to think and it makes me want to be one of those guys who simply check out and pay no attention whatsoever to any blood test for this sort of stuff.
Gabriella Kadar said…
Craig in CT: yes, cats fed large amounts of carbs (grain or potatoes) develop type 2 diabetes. The pancreas becomes inflamed. There is a protocol to reverse this and if the animal is then maintained on a carb-free diet (5% carb calories max) the blood sugars remain normal. This can be maintained for years although other factors can destabilize the situation, like inflammation in the mouth. Cats with diabetes, like humans, also get renal failure, ophthalmic problems etc.
Gabriella Kadar said…
This comment has been removed by the author.
CarbSane said…
Rat saccer here! Gabriella, I have seen more rat and mouse livers than anyone ever should from my years working for the devil. Many would have quite the little fat pad going with normal livers. I also handled, in clear tupperware like containers, maybe 75-100 human livers from autopsies on people of all shapes and sizes ... I just don't recall them being noticeably fatty ... of course this was the 80's ;-) Now of course they could have "fatty" livers without being visible, but if the liver took the excesses first, that much fat would be visible. Perhaps I'm misinterpreting your statement, but you said excesses go first to the liver and then to wherever else.
"There are the "big game" paleos who insist we humans sat around eating fat from large fatty mammals and little else."

(Warning: I had fun writing this response...)

I once accidentally found an arrowhead while looking for fossils. It was a profound experience. I looked around that wide open field and realized that at some point in the past there had been an ancient hunter near this spot. What was he hunting? Perhaps some wild Canola? Possibly the elusive safflower? Maybe even a devious stalk of corn?

My guess, call me crazy, is that he was hunting a source of saturated fat and protein.

It might have happened that he took a break during the hunt and milked a buffalo or made a peanut butter sandwich in the tradition of his ancestors. It is also possible that he gathered sacred herbs and made a potion of Lipitor to help his body recover from the saturated fat and protein he was about to eat. It is sad that those nomadic hunters didn't know they were killing themselves with such a diet.

I've heard stories of how indians used to gather around the carcass of the buffalo they killed and ask the Great Spirit to bring them a banana or a piece of reduced fat chocolate cake. The children would pray for ketchup...and a toy surprise. Mothers would stop suckling their babies in the hope the Great Spirit would rain grape juice and teething cookies for their infants.

Saturated fat is a killer and the human body is self-destructive. That is why the body produces saturated fat through de novo try and kill itself.

It's odd that if those native hunters had all sat around and gotten really obese from eating so much buffalo fat, they would have realized, without a doubt, something was wrong. But if modern man gets obese from eating so much saturated fat, well...there's nothing wrong...they just ate too much saturated fat.

I know how to turn my computer on and off, but that doesn't mean I understand how it works. Similarly, knowing how to reduce obesity or heart disease does not in any way suggest that we understand the cause of obesity and heart disease. Blaming saturated fat is clearly a swing and a miss. Again, call me crazy but I think there are many pieces of this puzzle we are yet to find.
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