Tuesday, February 02, 2016

Personalised nutrition: Eat fat

Personalized Nutrition by Prediction of Glycemic Responses

In the comments after the last post, dissertante asked about the above study. It's been around for a while and many folks have talked about it, Bill Lagakos being one of the more articulate. The study is enormous. The paper is quite long and, for various reasons, not exactly gripping reading for myself. So I may well have missed certain facts which are not immediately obvious. This is the summary of the study from the abstract:

My initial thought was to ask how the insulin response varied between people with a normoglycaemic response to junk food vs hyperglycaemic response. Typical junk foods considered in the study are the bananas vs the cookies in section G of Figure 2:

If normoglycaemia is bought at the cost of hyperinsulinaemia, it's not particularly attractive, to me anyway. Banana, cookie, who cares? The only way I can see that either of these is acceptable as food is if they are taken by the gut bacteria, converted to short chain fatty acids and so bypass the whole insulin/glucose signalling system. Many people seem to be happy to trust their health and glycaemic control to their gut bacteria. It takes all sorts I guess.

So, the implication is that we can use this massive level of investigation to make choices between carbs which spike glucose and carbs which don't. For us, on an individual basis, tailored nutrition. Without any idea of what these given sources of carbohydrate do to an individual's insulin levels. But, to be quite honest, it's junk vs junk anyway.

There is a snippet which shows a glimmer of interest in the use of fat to blunt the glycaemic response to carbohydrate by the group. This is what they say:

"The PDP [partial dependence plots, part of their model] of fat exhibits a beneficial effect for fat since our algorithm predicts, on average, lower PPGR [post prandial glucose response] as the meal’s ratio of fat to carbohydrates (Figure 4C) or total fat content (Figure S5A) increases, consistent with studies showing that adding fat to meals may reduce the PPGR (Cunningham and Read, 1989). However, here too, we found that the effect of fat varies across people".

Fat cannot reliably save us from carbohydrate induced hyperglycaemia. We still need personalised nutrition, even if we eat fat.

But what if we eat only fat? What would be the glycaemic response to 100ml of double cream, drunk on its own, for breakfast?

Dandona, on his way to drawing incorrect conclusions, gives us the glucose and insulin data for 100ml of double cream:

Drinking cream alone mildly reduces  insulin after a transient rise and point blank drops glucose throughout the study period. There may be minor individual variations in response but these are all contained within standard deviations which narrow with time after exposure... There is little scope for a pathological rise in glucose or insulin within those SDs.

So how much do we have to go begging, cap-in-hand, to our gut microbiota for a nice glucose AND insulin response to 100ml of cream? Not a lot. Ditto butter, lard, beef dripping...

The simple approach to personalised nutrition is to eat fat, cut out the middle man of our microbiota, limit glucose and reduce signalling through the insulin pathway while eating just enough protein to meet our needs. Anything else is going to need an awful lot of laboratory investigations to even get half the information we need to keep our blood glucose levels remotely normal while still using unknown amounts of insulin.

Personalised nutrition: Eat fat.


Oh, dissertante also mention that, for some people, chicken came through as a "bad" food in terms of post prandial glycaemia. That's another post I guess.


Unknown said...

I'd love to eat more healthy natural fat, preferably meat. I only have to figure out how to convince the butchers not to trim all the meat to death. It's a culinary wasteland.

Beef: too lean
Pork belly: must be coming from truly anorexic pigs
Cooked ham: no fat to be found

There is some hope though, a Turkish butcher shop selling lamb once a week!

Fatty lamb ribs, to die for.

Jürgen Wildhardt said...

I have the same problem: preparing the meat with lots of good butter helps a lot!
My butcher seems to be very proud on his "lean" products: there are many with the label "Our lean..."

Try Lardo, it's almost pure fat!

Peter said...

Essentially, I live on butter. Chicken fillets + butter = minimal omega 6 PUFA, ditto pork. Beef we can get 20% fat mince in the UK. But butter saves the day, as does cream...


Charles Grashow said...

So the ideal diet would be 80-90% fat with the rest in protein and zero carbohydrate?

normalcarb said...

I hate cliffhangers. Gives us a clue about the chicken! Is it just the protein and GNG?

Peter said...

normal carb, the post is roughed out.

Charles, it's not that straight forward. There may be some benefits from carb intake, even if it's just hormesis from the nasty toxins in the veggies. What level is an open question, but my bet is low.


Charles Grashow said...

How low is the question. What are your thoughts?

bill said...

Yes. I asked a couple of butchers
what they do with the fat they cut
off the beef and they said they
"throw it away."

We've got a long way to go...

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

Personalized nutrition has become a nauseating buzzword unfortunately; this is the first time I've read it and kept my appetite, because.....it was followed by good advice: EAT FAT!

Bill's analysis was interesting but it's contaminated by the underlying erroneous assumption that [in his words] "Low carb diets can help weight loss in some people but low fat is better for others". No, LC works for everyone and a lucky few do well on either intervention (probably still better on LC). He cites Ebbling, Pittas & someone else I can't recall now for this, but....they don't support his claim given that the diet comparison groups are not LC vs LF but high-carb vs moderate-to-high-carb. Oh, and recently another nail in the LF coffin surfaced in the form of Christopher Gardner's study putting people with differing levels of insulin resistance on LF or LC diets...surprise surprise, the "Conclusion: Substantial weight loss was achieved overall, but a significant diet 3 IR status interaction was not observed". This is a sweet 'I told you so moment' hahaha...

I rest my case. Dietary fat for the win.

karl said...

RE - chicken - seems to have a high level of linoleic 18:2 n-6 compared to other meats.

see fats list

The question remains as to what bit gets broken - someone in their late 40's starts gaining weight after years of rather normal weight. I've been thinking about autonomic nerves that go to fat tissue. There is the case of progressive lipodystrophy - picture

Thin on top - seriously fat on the bottom. Same hormones in the blood stream - but could it be a break in a nerve? Autonomic nervous system? Can we make an experiment to stimulate nerves that feed adipose tissue? Could it be a form of neuropathy - similar to PN(Peripheral Neuropathy) which is often co-morbid in T2D?

Found these


There are a number of people that get PN before disregulation of BG. The medical community has only palliative treatments at this time for PN. There is an association with homocysteine. So what if PN of adipose tissue is driving this? And what if the damage is driven by Linoleic acid? Treat with some form of nerve stimulation?

In this paper they did cut some nerves - seems it matters.

DLS said...

I live on food. IF saves the day. used to eat 6 yolks a day... now do just 3 eggs dont even bother to use butter ( add 1k of pure fat to my minced meat @ lol omega 6) still strong @ lean. no protein? no silly food? = not living.

Galina L. said...

A while ago I complained in a natural food store about their ground beef being too lean. They offered me for free any amounts of fat trimmings. I enjoyed free staff for couple of years, until they started to sell it to the public for a small price. The problem is - it is often sold out nowadays. You can influence your butcher, especially in a small local store. Ethnic stores are also good sourses of fatty meat. Most ethnic traditions value fatty cuts, and ethnic stores are the goldmine of traditional foods.

Joanne said...

I've understood that carb feeding is the best way to pate, so this article focused on fats as causes of NASH/NALFD caught me flat-footed.

Saw this article at Science Today/PubMed last week. It finds a link between dietary SFA but not PUFA in development of NASH. I believe this is rats on a HFD (high fat diet). I didn't see a full description of the HFD, but I suspect it's really a HFHS diet (high fat/high sugar) if indeed it does promote the development of NASH/NAFLD. Pathway activation through sphingolipids (S1P).


Peter said...

Joanne, it's a review so there is no single diet specified but you can be sure each individual study will be using a sucrose centred diet along with the fat. Or uses rodent strains which develop NASH on USA pork derived high omega 6 pufa lard.


R Cobb said...

Ok so details, details, details. I like to buy grassfed ground chuck 85/15 ratio bc of the so called better omega 3 to 6 ratio, but if I buy stew meat it is so lean its almost not worth it- but I found really fatty pastured raised stew meat that leaves a good inch beef fat covering after slow cooking- but am I inadvertently eating higher omega 6 to 3's on pasture raised? Is there still a good ratio after 90 days of grain feed?

Also tell me- I've heard that some people have a large insulin spike from heavy cream- not sure if the percentage in the UK is higher but I think USA heavy cream is about 35% fat... your thoughts?

It is one of my favorite ways to eat fat so I am hoping the rise is negligible- I also heard that there are sex differences in response to heavy cream and dairy in general but not sure there is any truth to that- trace amount of endogenous hormone?

Peter said...

R Cobb, yes, details. Largely it comes down to looking for the data, much of which are not easily available, certainly on a LC background. Personally I happen to eat fish about once a week because I like it. After that it's UK supermarket meat, chosen to avoid accidentally purchasing the halal meat which contaminates much of the UK food chain. I always think of the largest brained hominids to have lived, the neanderthals. There's no evidence they ate anything other than large herbivores so the total dose of omega 3 needed to support a large brain seems remarkably small and needs no sea or river food consumption.

UK double cream is 50g fat per 100ml, protein is 1.5g/100ml. I think Dandona's cream was 70g fat/100ml. The std deviations didn't change much at an hour so in his small group there probably weren't any outliers whose insulin quadrupled on cream ingestion...


normalcarb said...

Great to see how you apply your research to your own diet, Peter. Has it evolved with your understanding of mechanisms, or has it been pretty constant over the years? Any health metrics you pay attention to in order to measure efficacy?

Consider a blog post outlining your diet and your justifications for it. I think a lot of people who find in interesting.

Fructose = poison. Minimize omega-6. Enough omega-3, but no need to go crazy. Enough veggies to stimulate hormesis. Cholesterol = neutral. MUFA = neutral? SFA = preferred fuel? Any limits on protein?

R Cobb said...

good marker- Would you also say neanderthals ate grass fed by default and therefore naturally higher in omega 3's? I am properly scared of omega 6's now... but yes take DHA/EPA fish oil for good measure.. eat fish 1-2 a week-

"What would neanderthal eat?" might be a good guide for fat foraging...heck- zero carb looks mighty appealing from my colon's perspective!

Nostril Damus said...

I guess Rosedale is right after all !

Matt Aleph said...

R Cobb, I think dairy's insulinogenic reputation comes from whole milk, with the protein and lactose. I've thought before about insulin's growth promoting effects and how I've heard Ray Peat talk about how egg protein is insulinogenic. Both dairy protein and egg protein are made to feed animals at the early stages of their life, so growth promoting [insulin promoting] proteins would make sense in this context.

I think the omega 3:omega 6 ratio is only really relevant in the context of our modern, unnaturally high omega 6 consumption. If you don't eat much vegetable oil, you probably don't need to worry about omega 3's.

Peter, I recently saw some article talking about how they found some evidence of Neanderthals eating legumes, barley, dates, and water lilies. Do you think carbs become less harmful in the context of an active lifestyle, with increasing levels of activity supporting increasing levels of carb consumption? In an environment where calories are hard to come by, I can't see an opportunistic hominid avoiding carbs for any reason.

Peter said...

normalcarb, I started from the huge eye opener that LC eating sorted out all sorts of problems, somewhere around 2002. It’s all been confirmation bias since then. Luckily I seem to be barking up the correct tree!

I don’t measure much nowadays except the occasional random glucose and post prandial glucose after my main meal, 1 or 2 hours after eating. HbA1c would be my next stop. After that… The question really is, what else is available (other than LCHF) with any sort of solid basis?

Nostril, I still have a great deal of time for Rosedale and he was a very early influence.

Matt, I don’t doubt that any neanderthal dying of starvation would eat anything. I would sort of assume everyone has read Miki Ben-Dor’s “Man the fat hunter” paper. He does lots of arithmetic about what might have been available and what was needed by early hominids. Elephants come out as number one preferred food. Then large herbivores, once the elephants disappeared. Some plant material. But eating raw legumes and grains may not have been too kind to GI function.


Miki Ben-Dor:

normalcarb said...

Hmm, health markers with a solid basis? I guess that rules out lipid panels. hsCRP maybe?

I saw an old post of yours in which you expressed concerns with chronic ketosis due to cortisol. Do you manage to avoid long-term ketosis?

Sodium losses on LC are a puzzle for me. I try to minimize ketosis so I don't have to replenish lost sodium to maintain blood volume. But in general, it seems weird to dump sodium at below ~100g carbs and retain sodium above ~100g carbs. Very fragile and finicky state. Not something I would expect neanderthal to have to deal with unless he was a constant blood drinker to get sodium.

Interesting theory I heard from a nephrologist: forget neanderthal and look at more recent European history. We preserved foods with salt to get through the winter. If you couldn't tolerate high levels of sodium, your genes didn't get passed on. So we may need more sodium than neanderthal.

Peter said...

I had an excellent GP when we lived in Compton who I asked to test me for HLA B27 (negative). He threw in an ESR and CRP (not the hs type). Both were bottom of ref range. I still subscribe to the best level of cholesterol being one which has not been measure, though my TC level 10 years ago was 8.6mmol/l.

I stopped avoiding ketosis as I found occasional post prandials with my sweet potato chips could hit 7.0mmol/l and Amber O'Hearn put up a couple of nice post about cortisol and ketogenic eating some time back which I found useful. Because nowadays I'm pretty well retired, my exercise level is such that I can't really avoid ketosis. Not gym exercise, just I now choose to work less, live more etc and I've always been an outdoor sort of person. If I get a decent walk I now run fasting BG in the low 3's mmol/l and post prandial is often still under 4mmol/l and always well under 5.0mmol/l. It may not quite be JK's Optimal Diet but it seems to be doing OK at the moment...


Peter said...



R Cobb said...

Normalcarb I've found proper amounts of magnesium potassium aspartate and time in ketosis helped with sodium regulation, don't know exactly how that works

normalcarb said...

@R Cobb, I supplement with the citrate form -- supposedly helps reduce kidney stone risk.

Mechanism of sodium loss seems to be a combination of hormonal regulation and simple ion coverage. As we leak ketones in the urine as cations, they need anion coverage and sodium is the first to volunteer.

With time and changes in protein burning, ammonium ions seem to take up some of the slack, and that's why the "flu" only lasts a week or two for most people.

My carb intake is high enough that I go into and out of ketosis often (exercise will do that to me), so that seems to make me dump sodium pretty much constantly.

I guess cutting carbs more would allow me to adapt better, but I have to believe that we evolved to eat carbs opportunistically, and you'd think we'd be able to switch in and out of ketosis seamlessly....

normalcarb said...

Opps, ketones=anion, sodium=cation.

Matt Aleph said...

Thanks for the links Peter. That's definitely a compelling idea, that if you've got giant fat depots lumbering around you probably don't need to be quick or intelligent to stay fed, just strong enough to do the slaughtering.

The "physiological ceiling on plant food intake" part of the paper reminds of the tour I took at mesa verde, where they talked about the natives spending hours and hours every day grinding corn that they cultivated. They ground the corn on stones, and small particles of stone supposedly made their way into the corn meal and wore their teeth down over time, making dental infections common, which the tour guide said partly accounted for their shortened life expectancy. Apparently they were also very short.

I think the article I saw about neanderthal carb consumption implied that there was some processing going on [stone grinding for sure, not certain about cooking.] Also just remembered a WAPF paper that talked about the diets of Africans and brought up some interesting stuff about carb consumption:

"The healthiest tribe that Price studied was the Dinkas, a Sudanese tribe on the western bank of the Nile. They were not as tall as the cattle-herding Neurs groups but they were physically better proportioned and had greater strength. Their diet consisted mainly of fish and cereal grains. This is perhaps the greatest lesson of Price’s African research-that a diet of whole foods, one that avoids the extremes of the carnivorous Masai and the largely vegetarian Bantu, but incorporates both nutrient dense grains and seafood, ensures optimum physical development."

They talk later in the article about how the Dinkas would ferment their carbohydrate into a paste, and consume it while working in the fields. This was the point that got me interested in the link between carbohydrate consumption and physical activity, and how in the context of a highly active [agrarian] lifestyle, perhaps some of the negative effects of carbs would be mitigated, what with consistent glycogen depletion. Hunting and gathering, by contrast, is much less energy and labor intensive, and perhaps bears more similarity to our current lifestyle, wherein fat becomes a more appropriate source of calories as glycogen is not being consistently depleted.

Matt Aleph said...

The fermented carb paste they ate was highly processed, aka hulled, fermented, squeezed through sieves, etc. This seems pretty common, where a culture will find an energy source and then ferment it to eliminate the less friendly components [cassava, sour cream, sour dough, yogurt, cheese] or process it [white rice, white flour, etc], or even cultivate it [giant corn kernels, white, low fiber potatoes].

Matt Aleph said...

They favored the carb paste because of the "quick energy boost" it gave them, kind of akin to a long distance cyclist eating some energy gel. Its not like they were deprived of calories and forced to eat the carb paste. They actively chose to, because of a favored effect.

kellyt said...

"If normoglycaemia is bought at the cost of hyperinsulinaemia, it's not particularly attractive, to me anyway. Banana, cookie, who cares? "

exactly.. And for a person to "hope" that they have the right makeup of gut-bugs to eat bananas and cookies without the need for hyperinsulinaemia behind the scenes to maintain normal BG smells of grasping at straws to rationalize/justify a continuation of a less than optimal-health diet...

I did a quick text search for "INSULIN" on Bill's writeup that you link. Not a single hit in the article... saved me the time of reading it. No discussion of insulin = missing 1/2 the picture.

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

Sorry, one more comment..
Peter you're probably familiar with Dr. Kraft..

Dr. Kraft wrote a book - "Diabetes Epidemic & You". He was the father of OGTT with Insulin Assay and performed over 15,000 of them over the course of his career. He proved with his life's work that before anomalies in BG show up the pathology of diabetes has been playing out behind the scenes for years and years doing all kinds of damage to our cardiovascular system, etc.

So, according to the life's work of Dr. Kraft, these "special snowflakes" who can supposedly tolerate all this junk food really aren't so special after all.. They are simply individuals who are in various stages of "broken" and the last place it shows up is in BG abnormalities...

js290 said...

50% coffee + 50% heavy cream = 100% delicious.

Petra Hildebrandt said...

cream: a lot of cream (heavy cream) has carrageenan. Since my body reacts to this, I am pretty OCD in checking the labels. it might mess with the insulin (= cause spikes) among other reactions.

Galina L. said...

My own migraines almost 100% disappeared. I guess because the most difficult trigger to control - hormonal fluctuations has gone. I am 55 now. Now, with less need in ketosis, I am trying to eat more proteins than before because my blood test indicated insufficient level of vitamin В12. From my experience I can tell that relying too much on a cream consumption may leave too little room for other sourses of nutrition.

Peter said...

Galina, Yes and there's a lot to be said for occasional liver. Fried with some oinions and bacon... mmmmmmm


Galina L. said...

Thank you, Peter.I am afraid my pate contains too much butter, and I guess your bacon/liver/onion version has higher liver content. I will definitely
upgrade my cooking. My own vitamins B12 insufficiency is a mystery for me. I thought I ate enough meat, and an occasional organ meat was in my menu. May be practicing fasting, eating less than I wanted in order to avoid a natural weight gain normal during menopause prevented me from getting enough nutrition. Fortunately, with increased dose of thyroid hormone now I can eat more than before. Next blood test will give me an answer.

George Henderson said...

You're gonna love this.

The microbiome is NOT saturophobic. Lactobacillus metabolises dietary palmitate and stearate.
It can't saturate MUFA and PUFA easily so these inhibit its growth, especially LA and ALA.
In the context of alcohol feeding (29%) and low CHO (13%) hydrogenated soy oil (almost pure stearate with some palmitate) restores healthy microbiota, protecting gut cells and liver.


1945 research shows same difference with L. Helviticus -


Notice MCSFA are not much good, I suspect peroxisomal oxidation is important in lactobacillus.
So all that nonsense about high-fat diets being bad for the microbiota referred to PUFA and MUFA; oil and lard; had they looked at butter, tallow, or dark chocolate, different story.

Peter said...



jo said...

Hi George- lactobacillus actually linked to obesity in a few studies. May prevent akcohol/liver problems. But dont seem that good fr met syn. They may even have too much lactobacillus. It seems alcohol/liver problems more to do with excess of gram negative bacteria, which are good fr metabolism, if not excess. May be that sat fat-- lactobacillus balances out excess gram negative bacteriacaused by excess /chronic alcohol.

Unknown said...

I'd be happy with less bacteria per SIBO and LPR-silent GERD-wretched!... but wondering if I'm not too late to ask, what's worse PUFAs or fructose?

Peter said...

That depends who you ask. To me, both sidestep physiological control of glucose access to glycolysis pathways in the cell. PUFA have some physiological role, fructose probably we have no dietary need for. I also suspect (w/o hard evidence) that a diet based on palmitic acid might be relatively unforgiving to significant fructose intake...