Friday, March 19, 2010

Butter, insulin and Dr Davis

Sigh. Okay, here we go. It's the weekend and I'll correct the typos when I get chance!

Better read Dr Davis' post here here to get the lie of the ground before reading this post. Now, before we get to the Spanish study, let's look at the insulogenic effect of cream (the closest I can find to butter in a study which, unlike the Spanish study, controlled its variables). Please bear in mind that cream contains small amounts of both casein and lactose. So does butter. BTW look what casein does to insulin. But it doesn't budge glucose levels (they should drop!) so there has to be a counter regulatory system here, glucagon was not measured. It's not relevant to the role of palmitic acid in the Spanish study, but it's interesting never the less.

Taken from Dandona's paper here. This is the effect of 300kcal of cream (equivalent to about 30g of butter) or the equivalent in casein calories:

Okay, on 300kcal of cream alone insulin "spikes" from 39.6pmol/l to 49.2pmol/l at 1h (remember the casein and lactose?) and then insulin drops below baseline at 2h and 3h.

During this period there will be palmitic acid in to the blood stream and muscles. Palmitic acid is the primary metabolic signal to switch from glucose burning to fat burning. Because essentially zero carbohydrate is supplied with cream there is neither a rise in blood glucose or in insulin.

The Spanish study uses about 40g of carbohydrate (22% of about 800kcal) with their fat load. It gets eaten along side just under 60 grams of fat or oil.

The rise in glucose is trivial for all groups. It is neither statistically nor biologically significant. We can ignore it.

Now, let's look at insulin. The full figure and caption is here

Butter is the black squares.

Obviously, the best meal for minimising insulin response is the control meal. That's the one with round dots. That's the one we should eat to maximise weight loss, if it is a simple matter of minimising insulin! Ah, but the control meal is 40g of carbohydrate and no fat at all! Eating just 40g of carbs before an eight hour fast drops your insulin levels all right, this is starvation! But does it allow weight loss? Calories in, calories out, 40g of carbohydrate is only roughly 170kcal.

To answer this we have to look at the free fatty Acids (FFAs):

The study started with FFAs around 500micromol/l in all groups. The carb-only 40g snack DROPPED FFAs from fasting levels of 500micomol/l down to 150micomol/l at 2hours and it took until 5 hours for FFAs to get back up even close to the fasting levels seen at the start of the experiment. After a 40g fat-free carbohydrate "snack" the only source of FFAs is lipolysis and we can say that the small 40g carb snack blunts lipolysis, and so weight loss (rather I should say fat loss), for 5 hours! And you're hungry too.

Now the butter group produced the least fall in FFAs while the insulin was elevated from the carbohydrate and also allowed the most sustained rise in levels of FFAs once the carbs were dealt with. The FFAs were still significantly elevated at the end of the study. The area under the curve for chylomicrons (no VLDLS involved in this study) is also bigger and peak chylomicron-triglyceride level is higher in the butter group than after any other fat meal.

Butter provides palmitic acid which is the physiological signal to switch from using glucose to using fat. It also provides medium chain triglycerides which will produce ketone bodies for a few hours, which also produce physiological insulin resistance and a rise in insulin in their own right.

So in the presence of 40 grams of carbohydrate extra insulin is need to maintain normoglycaemia. The insulin should inhibit lipolysis. It certainly does in the 40g carbohydrate snack group! What about the butter group? The butter provides plenty of FFAs to run metabolism on and storing some calories is no big deal. But does this insulin effectively store calories? What if the adipocytes become physiologically insulin resistant with palmitc acid in exactly the same way as muscle cells do?

You know, my mantra: The function of insulin is the inhibition of lipolysis.

This study makes it look as if it is not quite that simple.

In fact, you have to ask some interesting questions about exactly where all of these FFAs come from and where the chylomicrons go to. ALL of the fat meals provided the SAME number of fat calories, but the FFA levels in the butter group where ALWAYS higher than other fat meal groups, even before chylomicrons levels became different between groups. Now, FFAs do not pop in to existence merely to prove that butter is going to kills us through obesity. They come from SOMEWHERE. And chylomicrons. These are lower in the oil meal groups than in the butter meal group. Where are the chylomicrons going to? Because all fat based meals provide the same number of fat calories then either:

a) the butter group has to be allowing more lipolysis from adipocytes or from chylomicrons to get those extra FFAs. Lipolysis means fat loss.


b) the non-butter groups are allowing more fatty acid storage and less FFA release. Insulin sensitive fat cells store fat! Low FFAs means less fat release. You CANNOT burn fat without lipolysis!

As I see it butter produces sustained chylomicronaemia. The chylomicrons are used to provide FFAs to run metabolism on rather than going in to storage. There is no hyperglycaemia to glycate apoB48s, so who cares if they hang around. Either they (or possibly adipocytes) are supplying energy.

Oil based meals can only produce lower levels of chylomicrons if they are storing the chylomicron fat ON YOUR BUTT and lowered FFAs means the INHIBITION of lipolysis from chylomicrons or from YOUR BUTT.

There is no other explanation that I can see, whatever the insulin levels are. Take you pick.

More fat gain and/or less fat loss: The gift of olive oil!

To summarise:

Insulin controls bodyweight. Physiological insulin resistance modifies this.

Of course if you think apoB48 was evolved to kill you, run from the butter and knock back the vegetable oil/fish oil combination. Maybe cut a few calories too!

Me, I'll stick to FFAs and butter as my energy source.


BTW 40g is close to the total daily carb intake for a reasonable LC diet. After that it's fat on its own and, as we all well know, fat on it's own causes ZERO insulin spike and allows FFA run metabolism where fat can be both stored and accessed freely. Okay, add a little protein somewhere along the line.


LynneC said...

This study of amino acids was posted by a member of TYP in a discussion about dairy products and Dr Davis' response that all dairy are insulinotrophic. Full text available for free, and there's a nice graph that shows insulin response and glucagon response by each amino acid.

LynneC said...

The predominant amino acids in dairy are leucine, isoleucine and lysine, according to the TYP member that posted the study...

Juho said...

It seems that I've been reading this blog for a while, because I can mostly follow your line of thought now :) Jargon is lodging itself into my brain. And if I understood correctly here, your essential point is that the chylomicronaemia (and elevated insulin) caused by butter consumption is all fine and dandy if the blood glucose levels are low. If it is so, does it mean then that SAFA + carbohydrates = dietary catastrophe or have I misunderstood some here?

zach said...

And does anthropology count for nothing, Dr. Davis? There were not a few traditional cultures that used dairy and butter as a staple. On the average, their pancreases kept them going for more than 80 years while eating milk products every day!

Sue said...

I don't understand Dr Davis lately.

kilton9 said...

Another study showing an even smaller insulin response:

donny said...

Do you think that the "endothelial dysfunction" caused by consuming glucose and saturated fat vs glucose and corn oil could just be cells in particular need of fat secreting lipase?

Oh, and I found this;

"Mania in a Case of Hyperparathyroidism"

My thoughts really did race a lot less when I went back on vitamin d. I seem to be better now, but I may not be the best judge. :(

Sorry 'bout all that.

Ned Kock said...

Very interesting post and study Peter!

When we look at chylomicrons (link below with pictures), they do seem to come in various sizes, with several small ones included.

This has led some researchers to hypothesize that postprandial states are the ones that contribute the most to CVD. These researchers refer of course to postprandial states after fatty meals.

This doesn't make sense to me, based on empirical data on CVD, but it is a intriguing hypothesis. It seems to me that chylomicrons are cleared from the blood a lot faster than LDL particles, and for this reason do not contribute much to CVD.

John said...

Thanks for that Peter. The Heart Scan post was disappointing...

Helen said...

Thanks, Peter. You are as smart and funny as you are iconoclastic. Maybe there is a connection here.

And, like Juho, I'm beginning to be able to understand you better at first read.

Ned Kock, I've read a lot of studies about postprandial CVD damage and find the thought extra depressing. Did nature not want us to eat? I'd wager that, while looking at things through a postprandial microscope could reveal some useful information, we need to assume that nature wants us to eat (though what is still a question), and that a big picture, like a lifetime, like a large group on the same diet, is really necessary to figure out what's happening. That is, I don't want to get too caught up in postprandial cautions. Especially since, reading Dr. Davis, there is nothing good that happens post-prandially with any food. There is only bad and more bad.

Kurt G. Harris MD said...


Sorry to ruin your morning by mentioning that one!

Several other papers that model actual meals more closely suggest less significant differences in AUC for insulin when different fat sources are used, but almost all the evidence shows adding butter to a carb meal lowers the AUC for GLUCOSE - the thing we should be more concerned about than insulin anyway.

@Ned and Helen

Belief that postprandial lipemia of any kind is some kind of lipotoxicity is just the latest version of the lipid hypothesis. It's all BS.

cholesterol, fats, lipoprotein fractions, lipoproteins etc. none of them are "causing" anything, especially atherosclerosis. These molecules are either fuel or tools we use to manage fuel.

Aaron Blaisdell said...

Hi Peter,
Very nice analysis! I share other commenters' concerns about Dr. Davis' Heart Scan Blog as of late. I love butter from grass-fed cows, cream, and full-fat yogurt and kefir. But I've been getting an earful, lately, of Dr. Cordain's concerns about the dangers posed by proteins found in dairy. Especially their contribution to autoimmune responses. What are your thoughts on this?


Emily said...

this post is so helpful to me, a lay person, and butter lover. i was perplexed by davis's statements about him personally being a former vegetarian and still not "liking" meat, and saying milk products are all bad for you. butter, lard, human fat, they are all about the same makeup of fats, why is butter so evil...just because it comes from a cow? and vegans arent for eating animal foods? lame. anyways, thanks you. i would not have stopped eating butter regardless of davis, but your interpretation is solid.

Helen said...
This comment has been removed by the author.
Helen said...
This comment has been removed by the author.
Helen said...


I have nothing but my own experience with autoimmunity and dairy to offer you (and I know you asked Peter :), but since I've been eating more dairy, especially yogurt, and more butter fat, my allergies have dwindled to a shadow of their former, horrible selves, and my eczema is gone. It could be partly what I'm not eating also, but butter and yogurt are very anti-inflammatory, and I think that could be part of the reason.

I haven't gotten my anti-thyroid antibodies tested lately, so I don't know what's doing with my other autoimmune disease.

Edward said...

Dr. Davis's focus at TYP is to halt, reduce, or regress arterial plaque and calcification.

Peter's focus appears to be on nutrition and the science behind health and disease.

Much of what Dr. Davis shares in his blog may not be accurate; indeed, his TYP diet as evolved over the years. He does, however, have a solid track record of halting and reducing his patients' arterial plaque.

My focus is to avoid the same fate as my father, grandfather, and great-grandfather - all died of heart disease.

Do those of you eating lots of dairy, especially butter, have recent heart scans? I'm not afraid of dairy or butter, but have been hesitant to over-indulge. I'm not savvy enough to understand the science of this debate.

Peter, have you had your second scan yet?

Ned Kock said...

Hi Helen and Kurt.

I don't buy into the postprandial CVD hypothesis either. This comment by Helen sums it up nicely: "Did nature not want us to eat?" If eating is so important for survival, there are certainly mechanisms to clean up the mess afterwards (as with physical exercise).

My interest is in the reason why the hypothesis may be incorrect. I think it has a lot to do with how the body deals with chylomicrons.

And, as Peter pointed out before, it is not really about the cholesterol. There are other things that seem to be of more importance: oxidation of cholesterol, and glycation of fats and proteins.

Kurt G. Harris MD said...


Butter has been about 30% of total kcal for me for over 2 years. My CAC at age 48 is 0. It also has not made me fat. I weigh 153 at 5'11'.

Kurt G. Harris MD said...


I think even referring to chylomicrons or pp TGs in any form as a "mess" is sort of buying into the Lipid Hypothesis version 5.0.

donny said...

Beta cells need to be very insulin-resistant, don't they? Do they do physiological insulin resistance?

Edward said...

@Dr. Harris,

Thanks much for sharing. I have been wanting to eat more butter, but have been hesitant. Personal stories such as yours help me form my decisions more than detailed scientific research/analysis as I simply don't have the background to understand it all in proper context.

Aaron Blaisdell said...


Thanks for responding to my question. That's been my experience with dairy, too. I finally mowed my lawn (which was 2' high in spots!) for the first time in a year. I was expecting the usual onslaught of runny nose, cough, sore throat in the morning and evening, and possibly even mild fever. But nary a symptom at all this time! Going lacto-paleo, with the lacto part restricted primarily to pastured butter, high-vitamin butter oil, FAGE yogurt, and kefir has really improved my health and allergies dramatically!

zach said...


I have a jersey milk cow. Milk, yogurt, butter, and cheese probably make up 50% of my Calories. I consume it raw. I haven't had as much as a sniffle or a stomach ache in the years since I've been doing this. Giving up sugars and grains did not do this for me, though it did help in other areas. My skin looks healthier too.

The only negative thing that I'll mention is that drinking a lot of fresh milk with meat is constipating. By itself or with fruits and vegetables it doesn't seem to be.

O said...


I eat 180g of fat each day (53% of kcal). 77g of it is saturated, the rest mostly monounsaturated. I eat coconut oil, butter, olive oil, and lots of cheese (4.5 oz each day). My CT heart scan score is 0.

I am 43, 5'7", 163lbs, muscular, with visible abs, and have an HDL of 88. The HDL has nearly doubled since I started eating a paleo diet.

Valtsu said...

"This is the effect of 300kcal of cream (equivalent to about 30g of butter)"

As butter usually contains about 80-82% fat, 30g of butter contains usually just about 220-230kcal, not 300kcal. You'd need 40g of butter for 300kcal.

Peter said...

Thanks for posting this Peter. I didn't know what to think when I saw Davis' post. What I did forget was, probably the same as everyone else who previously felt that they can trust Davis, to read the study myself.

I must say I am very disappointed with Davis. Claiming things like "butter makes you fat", when experience shows something completely different and his claim is imo based on questionable science, is very, very disappointing.

Pasta, bread, sugar and fat in combination makes you fat? Not really a novel idea.

J. A. Deep said...

First time poster here! As a couple of others have already mentioned, I've just come to understand your Hyperlipid mantra: "The function of insulin is the inhibition of lipolysis".

I've commented on my new found appreciation of your work over at Whole Health Source. Thanks, Peter!

Eric said...

This is entirely tangential to the post, but what Aaron said has triggered it ... I used to get colds regularly every quarter, four times a year. I could rely on it (and I didn't mind ... time off work). But since cutting down the carbs, I appear to have become immune to 'the flu'. Really, I've had one cold in three or four years. This when my wife and child are regularly struck low by the same thing. It's enough to make me doubt the entire germ theory of disease hahah (everyone around me is regularly ill and I don't get anything).
Oh and by the way, going low carb seems to clear up caffeine withdrawal headaches. As in, you won't get one.
Just my own worthless personal observations.

Togo Sled Dog said...

I remember in a previous thread the mentioning of having what feels like a hypoglycemic crash after the consumption of coconut oil alone or with a meal. I have added butter to the mix recently and still occasionally experience this post meal effect. Looking at the charts and reading the article makes me wonder if during this process as described I'm experiencing a gap in the period where FFA are slow to come up, thus creating the energy slump. Make sense to anyone?

陽明山花季 said...

很喜歡你的blog哦...加油唷 ........................................

praguestepchild said...

Alas, mainstream media has caught up with Kwasniecki! Presently, the third most popular BBC article is about 'good fats' lowering the risk of CVD. They did make a small typo and labeled PUFAs as the good fat responsible, but I'm sure some copy editor will catch the mistake soon . . .

lightcan said...

Are you joking praguestepchild?
That article is just another one telling you to cut sat fat.

L said...

Eric, your anecdotal evidence about not getting colds is good, but I have anecdotal evidence too, lol. I have never known my husband to get a cold! In our 15 year marriage, he NEVER gets a cold! He is a fanatical hand washer, and I'm sure that makes a difference, but he still gets exposed to them (through his family), and doesn't get sick. Weird. He eats carbs, grains, whatever he wants.

He does, however, get seasonal allergies. Allergies totally kick his butt.

I get colds every year (but I started low carb in Nov., so maybe that will change? I hope I hope), but I really don't get seasonal allergies at all.

Go figure.

Not arguing with you or anything. Just saying that for every rule, there is always an exception to the rule.

Mindscaper said...

Peter, I'm wondering if you've seen this article on TYP. I'm trying to figure out what it means. It seems to me that most of the fat challenge meals it reports did not segregate the types of fat ingested. Some did. It is very important to me to understand this.

I think I'm doing great on a PaNu diet but I am concerned about whether or not all factors considered my intake of saturated fats could be silently contributing to greater atherosclerosis. I had a heart attack a year ago. After about 7 months, I switched from the cardiologist's recommended Mediterranean diet (which seemed to be doing very little re: weight loss)to PaNu. I have not yet cut out dairy but switched to raw whole milk, whole cream, some goat cheese and kefir. I also do intermittent fasting--usually eat two meals per day, on alternate days eat once. I adhere to all the other paleo steps now.

It seems to me that the more saturated fat I ingest the faster I lose weight so I have greatly increased my saturated fat intake while cutting carbs to a bare minimum. But does loss of weight per se outweigh other factors? I just had a heart scan but will have nothing to compare it to until 6 months or more from now.

If fasting triglycerides are in a good range does one need to worry about post prandial TG's from high s.fat meals?

Thanks for all of your fascinating inquiries and critical analyses. Cee

praguestepchild said...

Lightcan, yeah I was joking, of course. This meta-analysis published on PLoS is complete crap. But I briefly held high hopes when I first saw "good fat". Alas, my naiveté got the best of me . . .

ET said...

Since switching to a high-fat, low carb way of eating, my post-prandial triglycerides and glucose have never risen above 100.

Jack C said...

@ Aaron Blaisdell, regarding the comment on "Dr. Cordain's concerns about the dangers posed by proteins found in dairy. Especially their contribution to autoimmune response."

The book "Devil in the Milk: Illness, Health and the politics of A1 and A2 milk" by Keith Woodford is a very thorough analysis of health problems associated with a tiny protein fragment of A1 beta-casein, called BCM7, that is found in milk from A1 cows.

Milk that contains A1 beta-casein is known as A1 milk: milk that does not is called A2. All milk was once A2 until a genetic mutation affected some European cattle thousands of years ago.

Most commercial milk in the U.S. comes from A1 cows (Holsteins). Jerseys and Guernsey cows that are favored by raw milk producers are A2 cows and do not have the problem BCM7.

The problem fragment, BCM7, will not pass through a healthy mature gut but can pass through the gut wall of babies and those with leaky gut from IBS or other gut problems. Once in the bloodstream it can cause many auto-immune problems, including type one diabetes and autism.

The incidence of gut dysbiosis has increased in recent decades due to increased use of antibiotics, birth control pills and other potent drugs, and there has been a related increase in the incidence of type 1 diabetes and autism.

It is my opinion that part of the benefit of raw milk consumption is due to the fact that most raw milk comes from A2 cows.

In cheese making, BCM7 is broken down in fermentation, so BCM7 is not a problem in aged cheese. It is not a problem in butter either because there is very little protein in butter.

The initial studies on the problems associated with A1 milk was done in New Zealand which dominates the worldwide dairy industry. All initial studies supported the A1 hypothesis, but at some point the New Zealand dairy board conducted a very large study, which involved six different countries, that cast doubt on the hypothesis. Subsequently it was revealed that the study was flawed by contaminated milk, but the authors refused to withdraw their conclusions. This is an interesting story itself.

The A1 problem is just one of many problems with "regular" (A1) milk. (Grain fed cows, hormones, antibiotics etc.) so it won't make much difference to readers of this blog.

"Devil in the Milk" should be of interest to those interested in nutrition.

aNorCalifGuy said...

check this out Peter...

Atorvastatin Reduces Plaque Vulnerability in an Atherosclerotic Rabbit Model by Altering the 5-Lipoxygenase Pathway

Jack C said...

Several important points were omitted in my post on "Devil in the Milk" concerning beta-casomorphin (BMC7) which is in most commercial milk in the U.S.

Beta-casomorphin is a powerful opiate. A similar opiate, gliadomorphin, is found in gluten. A gluten free, casein free diet is often recommended for those susceptible to immune problems, and is usually prescribed to children suspected of having autism.

The solution to the problems associated with A1 milk can be solved simply by converting dairy herds to A2 cattle. New Zealand dairymen are well on the way to accomplishing this, partly by design and partly by happenstance as most of their best bulls happen to be A2 cattle.

The book "Gut and Psychology Syndrome" by Natasha Campbell-McBride addresses the association between autism and beta-casomorphin. Apparently most autistic children have poor gut flora which results in a leaky gut that permits passage of opiates from casein and gluten which result in autism.

Jack C said...


To further your enjoyment of eating butter cheese and cream and reduce your concerns about arterial plaque, I suggest you take a look at the Rotterdam study:

The study examined whether dietary vitamin K1 and K2 were related to aortic calcification (which other studies show is related to arterial calcification) by following 4800 men for eight years. The risk of CHD mortality and aortic calcification were studied in tertiles energy adjusted vitamin K intake.

None of the outcomes were related to vitamin K1 intake which comes from vegetable sources.

Vitamin K2 (menaquinone) is a fat soluble vitamin primarily from animal sources that inhibits arterial calcification). Intake of vitamin K2 was inversely related to CHD mortality (odds ratio .43 for highest tertile vs lowest)and aortic calcification (odds ratio .48 highest tertile vs lowest.). About 75% of the dietary vitamin K2 came from butterfat with the rest from meat and eggs.

You can better enjoy your butter knowing that it reduces arterial calcification.

Thomas said...

Peter-found this article link on Art Devany's site-would enjoy your comments on it.

Ned Kock said...

Thomas, thanks for the link.

I read the article in The Economist with interest. It is a very good example of how the media can distort the message. They make it sound as though the researchers, including Dr. Unger, are saying that being fat is healthy.

Roger Unger is a widely cited and respected researcher in the area of fat metabolism, which has been saying the opposite, but with some added details that probably confused the author of the article in The Economist.

Here is one of Dr. Unger's most widely cited papers, linking obesity to diabetes:

blogblog said...

It is true that many traditional societies consumed dairy foods. However consuming fresh milk is a relatively modern phenomenom due to refrigeration. In traditional socities milk was either fermented or made into cheese and butter.

In western countries fresh milk consumption was uncommon until the late 1800s. Drinking fresh was actively discouraged due to the risk of tuberculosis. Milk was nearly always made into cheese and butter. The skim milk from butter making was used as pig food.

Before the late 1800s butter was always made by slowly boiling and then cooling the milk. This denatured the protein causing the cream to float to the surface. After the 1870s centrifugal separation of milk became common. This meant that milk and butter began to contain biologically active casein.

Anna said...


I'll offer my CAC score experiences as an illustration that coronary plaque buildup isn't just about diet; there must be lots of other factors.

I "cleaned up" my family's diet considerably in the past decade, esp since 2006. Between more home cooking with traditional foods I source direct from the local and semi-local producers (raw dairy, eggs, meat, produce), to eating out less often and being choosier about Real Food when we do eat away from home - our diet is hardly ever SAD anymore, unless there is simply NO choice.

My CAC scan score in Dec '08 was 0 and increasingly I've been eating "lots" of grass-fed butter (pasteurized and raw), aged cheeses, egg yolks, and some raw milk (in addition to other natural fats like coconut oil, home rendered lard and bacon drippings, and olive oil now only for non-cooked salads & homemade mayo). I don't generally calculate or analyze macronutrients or calories, though I eyeball carbs and avoid industrial seed oils and concentrated fructose. I'm 48 yo, have a 22 or 23 BMI, and and am still pre-menopausal (so that may account for at least part of the score), however, I spent many years undiagnosed with hypothyroidism and hyperglycemia (now treated with natural thyroid hormone & carb restriction). Those conditions perhaps offset any protection from still being pre & peri-menopausal. I didn't expect a high score, but I also didn't expect a 0.

On the other hand, my husband aged 55 had a CAC score that was worrisome (I'm using my husband's laptop now so I can't remember if it was 181 or 281, but either way, it wasn't a good score for his age).

Our difference in scores can't really be explained by diet. For the 15 years we've been together, we've eaten quite similarly (good food is a mutual interest, but I'm the cook and shopper). But he eats out/travels more and is somewhat less knowledgeable and definitely less careful than I am about avoiding excessive PUFA oils & carbs (esp wheat) away from home. He doesn't get enough exercise except for weekend gardening. AND, he's been a 1/2 to 1 pack a day smoker for 30+ years and has moderately high BP, which probably trumps everything.

As a result of his worrisome scan score (for him it was a needed wake-up call that he needs to pay more attention to his health and not rely only on my efforts) he's adopted a lot of the Dr. Davis/TYP-oriented approaches, like niacin, Vit D, and some other supplements, plus a "somewhat regular" Slow Burn strength routine at home. As a result, most of his subsequent lab test results have moved in a positive direction, like a reduction in small LDL particles, higher HDL, better BP, & nice Vit D levels, etc. I've always thought the TYP diet advice has some significant weak areas, but there have been some improvements. I still tend go with my own interpretations though ;-). Honestly, it drives me nuts to read the "tell me what I can and can't eat" comments. Sheesh.

My husband hasn't had another CAC scan yet, but probably will do so this later this year after another round of blood tests, if they're still moving in a better direction. The real benefit of the scan is likely to be the ability to see how it compares to the baseline scan (sure wish I'd known to do these a few years earlier). He's not been able to quit smoking, though he has cut back somewhat and switched to a cigarette without tobacco additives (so-called "natural" tobacco). If he could have quit easily, it would have happened already, so I don't hold my breath or nag on that issue (he doesn't smoke in the house or around the rest of us). So
I'd be happy with slowed progression of his coronary plaque; it's probably unrealistic to expect significant plaque regression if he continues to smoke, etc.

praguestepchild said...

Traditional societies that are lactose intolerant don't consume fresh milk except as a purgative (such as recommended by Galen). Roman authors recorded that the people of northern Europe drank unprocessed milk, and the gene for lactose tolerance is 99% prevalent in the northern European gene pool, even though it is a relatively recent mutation. Obviously this mutation bestowed a huge advantage.

Still, it is a neolithic mutation, all dairy products are no more 'natural' than other neolithic foods such as grain.

pjnoir said...

There are no lactose intolerant issues with fresh milk aka Raw milk. Pasteurization causes that problem in milk.

Jack C said...

Milk has been consumed throughout recorded history in many societies including ancient Greece and Rome. An excellent book on subject is "The Untold Story of Milk" by Ron Schmid.

In the warm climate of southern Europe the majority of milk was made into butter and cheese as a method of preservation. In contrast, in the cold Scandinavian countries, cheese and butter consumption is half that of southern Europe while milk consumption is double that of southern Europe.

Regarding "lactose intolerance":

Lactose is readily digested by lactose digesting bacteria, such as E. coli, in those with healthy gut flora regardless of whether or not a person produces the lactase enzyme. Physiological strains of E. coli appear in the digestive tract in huge numbers soon after birth and have many beneficial functions in addition to digesting lactose.

Many who have been diagnosed as lactose intolerant are actually allergic to the casein fragment BCM7 in A1 milk and can drink A2 milk, pasteurized or unpasteurized, with no problem, including milk from goats, camels and A2 cows.

Many of those who actually are lactose intolerant have gut dysbiosis, or poor gut flora, and it is found that once the gut dysbiosis is corrected, many, but not all, of "lactose intolerant" individuals can digest lactose.

There are a number of reasons that many "lactose intolerant" people can drink raw milk but not pasteurized milk. One major reason is that raw milk producers favor A2 cows (Jersey and Guernsey) because of the high cream content of the milk, and these cows do not have the problem casein fragment, BCM7. The "channel island " cows originated in France where all cows are A2 cows. Further, raw milk contains lactase that helps digest lactose and many bacteria that aid digestion, and these factors are destroyed by pasteurization.

I can't buy decent milk where I live so I do without it. I do eat a lot of butter and raw cheese from grass fed cows.

Edward said...

@Anna and "O",

Thank you both for sharing your personal experiences. As my faith in the "scientific community" has been undermined, I appreciate Peter's interpretations and commentary; I find it informative (the portions I can comprehend) and entertaining.

I find your personal stories compelling. I'd rather be wrong about the science while moving my health in the right direction than the reverse.

I added saturated fat to my diet 6 months ago. HDL remained constant at 67. Particle size increased (though was already solid Pattern A). But, LDL and total C increased by 50% to 170 and 250 respectively.

Thanks again,

Dr. B G said...


Please see O Primitivo's site. He conveniently lists the studies that associate the higher the LDL, the higher the longevity and vice versa (which Peter has discussed at length as well, J-Litt, etc).(it's Portuguese)
Category: 'Hipótese Lipídica'

We know this to be true in the paleo world despite what some cardiologists are indoctrinated to think.

Survival definitely entails critical thinking and honest evaluation of the evidence, as I believe you are doing so.


blogblog said...

Jack C:
Milk is just as much a neolithic food as wheat. Milk proteins from both fesh A1 and A2 milk are almost certainly as unhealthy as wheat.

Lactose intolerance is due to an absence of lactase. This affects 90-95% of the world's people older than seven. Pasteurisation has no effect on lactose tolerance.

Avi Saha said...

Can you do a follow up post or SOMETHING more explanation/analysis because I am so confused.

Did you say insulin resistance = more lipolysis?

Post workout/exercise muscle and fat cells are insulin sensitive right, what do you think butter would do then regarding this study.

ANd what if the other fats simply burned faster, saturated fats do tend to burn slower (although butter contains 20% MCTs) can we really assume that they just went to storage if not detectable?

Peter said...

Hi Avi,

Yes. Just think of type two diabetes. If we ignore all of the hepatic and pancreatic issues involved, essentially your fat cells listen to insulin and, while they remain dutiful listeners, they store fat and you get fatter because they refuse to release fatty acids. Hence even the insulin from 40g of complex carbs inhibits FFA release for many hours.

Once your adipocytes have accepted so much fat under the command of insulin that they cannot accept any more, they then refuse to listen to insulin and become insulin resistant (I suspect this happens at the mitochondrial level, it's not a physical size issue). Once insulin resistant they then spill free fatty acids without metabolic control (they're resistant to insulin by now, yes?) and people with type 2 diabetes end up with elevated FFAs.

To a simple cardiologist the FFAs from eating fat have the same significance as the spilled FFAs from failure of adipocytes to listen to insulin.

The hypothetical aspect of the post is the possibility that FFAs from food, particularly palmitic acid from butter, might make adipocytes release their stored lipids as FFAs by making them ignore the message of insulin to hoard fat. Palmitic acid is the molecule to produce physiological insulin resistance in muscle, why not in adipocytes?

You would then predict that butter should aid weight loss. I cannot imagine how much palmitic acid I eat per day. Loads. I'm skinny. I wouldn't go so far as to claim palmitic acid keeps me thin, but it certainly has not made me fat!

Does that make a little more sense?


Avi Saha said...

Hmm yes that makes a lot of sense, thanks. But it is still perplexing since so many experts say that insulin sensitivity and longevity are related. That reminded me that there are a few pathways of insulin resistance right? The glut4 pathway is the bad one I think. Insulin resistance from saturated fat, BCAAs, etc, if allowing us to burn more fat, hopefully is not a terrible thing at all. Would you happen to know anything about those pathways and why this type of insulin resistance is better than say insulin resistance caused by high sugar?

CarrollJ16 said...

Peter, I'd be interested in your comments on the recent insulin series on the Weightology blog

Rick said...

Could someone tell me a few butter basics? What do people mean when they say "pastured" butter? And what is "fermented butter"?

Anna said...


I'm going to jump in because Peter has indicated he's only posting sporadically at the present time (and I love good butter). Hope you don't mind the pinch hitting.

Pastured butter is from the milk of cows that feed on pasture (grassfed), the natural diet of herbivores. The butterfat from pasture-fed cows is higher in various nutrients, including beta carotenes and Vit A, so it is a deeper yellow color, esp in spring and early summer when the grasses are growing rapidly. Pastured butter can vary in color throughout the year, depending on what is growing in the pasture seasonally. Compared to pastured butter, butter from CAFO herds is more white and anemic-looking all year long.

Increasingly, dairy herds are larger and confined into smaller areas instead of rotation grazing on pastures that recover between grazings. CAFO herds are fed rations of grain (soy and corn), chicken litter, and many other manners of waste products. No kidding, some dairy farmers feed their herds stale baked goods and expired Cheetos and candy bars.

A college friend's husband who tried to make a go of dairy farming in Upstate NY in the late 80s, early 90s (in a rural part of NY as good a place for pasture-fed herds as you'll find) told me about this practice a few years ago; I was gobsmacked! Trucks from the bakeries and convenient store snack suppliers drop off the stale products they remove from the shelves. If I remember correctly, the candy bars weren't even unwrapped (I guess the packing was considered roughage). He said the added milk quantity was quite a bit more when cows ate this garbage.

Dairy farmers who sell their milk to the co-op (the vast majority) get paid primarily for their quantity of milk, not milk quality. Still, he couldn't support his family on a small dairy herd, so he gave it up and went into teaching and coaching at the local high school (and we know how well-paid that career is!).

Fermented is not the word I'd use for butter (it's better for cheese), but European-style butter is often made from cream that is cultured before churning. Cultured butter has a slightly tangy flavor compared to butter made from "sweet" cream (it's not sweet in the sense of sugar, but sweet because it isn't salted or cultured). Butter can be salted or unsalted. Salted butter tends to stay free of rancidity longer, but many cooks prefer unsalted so they can season foods with salt as they wish. Butter made from fresh raw cream will culture over time, as the natural lacto-bacillus bacteria (probiotics) multiply and consume the lactose, creating lactic acid.

Anna said...


I'm going to jump in because Peter has indicated he's only posting sporadically at the present time (and I love good butter). Hope you don't mind the pinch hitting.

Pastured butter is from the milk of cows that feed on pasture (grassfed), the natural diet of herbivores.

Fermented is not the word I'd use for butter (it's a better word for cheese, IMO), but European-style butter is often made from cream that is cultured before churning. Cultured butter has a slightly tangy flavor compared to butter made from "sweet" cream (it's not "sweet" in the sense of sugar, but sweet because it isn't salted or cultured). Salted butter tends to keep longer, but many cooks prefer unsalted so they can salt foods as they wish. Butter made from fresh raw cream will culture with time, as the natural lacto-bacillus bacteria (probiotics) multiply and consume the lactose, creating lactic acid.

Peter said...

Thanks Anna,

Five day week plus weekend rota with an hour's drive to and from work does not leave a lot of free time!


Eric B. said...

Peter- Love your blog, I usually try to keep up with it when I can. I have a question about butter though. I've been pretty much stalled on Atkins for 7 months after having a good 3 months worth of weight loss and I've noticed a couple anecdotes so far; eating a lot of butter, either in the morning or before bedtime, usually results in a curious drop in weight by the next day (not a lot, maybe 1/2lb). I have plenty of examples where eating beef, bacon, pork, chicken, whatever results in my weight staying pretty much stable from day to day (I weigh myself daily, in the morning under the same circumstances and have a log running all the way back to the start of my Atkins run--only weight though, I don't log my food intake).

With this study suggesting new information about butter's role with insulin and FFA release do you suspect butter by itself has a potential as a fat-losing supplement of sorts?
In either case I'm going to experiment on myself here by making it a point to eat a chunk of butter with every meal ;) Breaking this "stall" would be wonderful...