Boiled mashed potatoes for miracle satiety?

The effects of potatoes and other carbohydrate side dishes consumed with meat on food intake, glycemia and satiety response in children.

With thanks to Mike Eades for the full text.

This is an interesting study. Given a meal of meatballs plus a choice of five different carbohydrate sources, a group of children ate a great deal less (in calories) of boiled mashed potatoes than of pasta, rice or either of two types of chips.

"The five treatment sessions consisted of ad libitum servings of (i) rice, (ii) pasta, (iii) boiled and mashed potato (BMP), (iv) baked French fries (BFF) and (v) fried French fries (FFF) with a fixed amount (100 g) of meatballs".

What did they find?

"... children consumed 30–40% less calories at meals with BMP (p less than 0.0001) compared with all other treatments, which were similar".

That's a LOT less calories! Potatoes seem to have some sort of magical satiety property. If you believe in magic. Table 1 gives an inkling of the problems with the study:

As you read through the cooking description you realise (red box) that the carbohydrates had very different amounts of added fat per unit carbohydrate and that some had butter (+/- added milk) while others had canola oil in varying doses. So when we look at Table 3 we have to realise that "CHO amount (g)" means an assorted mix of various fats and carbs:

We have to work back using Table 1 to find out what amounts of carbohydrate and fat were actually eaten and read the cooking details to find out what the fats were in each dish. Some arithmetic gives us this for what was actually eaten:

To my mind the trial here splits in to two. We have BMP, boiled mashed potatoes with 3g of carbohydrate per gram of butter, which is fairly well matched with FFF, chips deep fried in canola oil, with 2g of carbohydrate per gram of canola oil. Both are potatoes. Both provide a roughly similar ratio of calories/grams from glucose and fat. Both are relatively low carbohydrate per unit fat (compared to the other three meals, ie just in this study).

From the Protons point of view the relatively low carb BMP and FFF are supplying glucose from potatoes to drive complex I. However butter also supplies FADH2 at ETFdh, so generates a resistance within adipocytes (and elsewhere) to an excessive insulin facilitated calorie ingress during the period of maximal blood nutrient levels. When calories stop falling in to adipocytes, satiety kicks in. Using FADH2 this happens after eating 508 kcal. With FFF based on canola oil, ie potatoes steeped in 18 carbon omega 3 and 6 PUFA, the beta oxidation generates a much lower input at ETFdh (one less FADH2 per double bond) and so insulin sensitivity at peak nutrient uptake is maintained for longer, fat pours in to adipocytes for longer and almost twice as many calories are consumed (912 kcal) before satiety kicks in. I expect satiety to rise as blood nutrients rise. Not sequestering them in to adipocytes seems the best way to do this. More physiological insulin resistance. I'm guessing the brain does the actual sensing of both glucose and FFAs.

I like that. You can say what you like about the hypothalamus. I prefer to think about the adipocytes and their mitochondria as determining what gets done with food and hunger. There is some input from leptin of course, but that's another post.


The other three carbohydrate dishes are essentially lowish fat foods with between 7g and 10g of carbohydrate per gram of butter or canola oil.

In these lower fat preparations it takes three or four teaspoons of butter to generate satiety vs just under 6 teaspoons of canola oil, roughly twice as much fat is needed when carried with a similar amount of starch. A reasonable fit with a Protons point of view, though not as pleasing as the BMP vs FFF comparison.

How the study was developed is fascinating to think about.

What decisions were made at the planning stage? Obviously, someone had worked out, well before any grant application was submitted, that higher saturated fat with lower carb meals are by far the most satiating. Or maybe they are dumb and they were just lucky to get a result? Personally, I can't see how you engineer a study like this unless you are pretty clever and well informed, not at the mitochondrial level of course, but certainly at the butter level. Mashed potatoes, which already have something of a reputation as a miracle weight loss food, getting a helping hand... From a dollop of butter. It makes sense.

BTW this is Canada. I can't see how such a study would ever have gotten past any ethics review committee in the US of A. Imagine trying to feed BUTTER to American children. Immoral. Plus they might not eat up their carbs!

Peter

High fat fed mice on stearic acid

The concept of finding anything positive about palmitic acid is still tantamount to research suicide. However, stearic acid is a rather different matter. It's lipid "neutral" for those poor folks who still bow their heads and kneel before the altar of the lipid hypothesis. So you can publish good stuff about stearic acid with relative impunity.

Raymond sent me the PhD thesis of Valerie Reeves, Kentucky University.

Reeves, Valerie Lynn, "A DIET ENRICHED IN STEARIC ACID PROTECTS AGAINST THE PROGRESSION OF TYPE 2 DIABETES IN LEPTIN RECEPTOR DEFICIENT MICE (DB/DB)" (2012).Theses and Dissertations--Physiology. Paper 3.

Before we think about leptin receptor defective mice (another day), we can ask questions about the control groups. Such as:

What happens if you feed a fairly typical C57Bl/6 mouse 40% of its calories from fat, based on fully saturated stearic acid?

They stay significantly slimmer than they do on CIAB (chow) and probably slimmer than when fed on 40% oleic acid (olive oil w/o the PUFA).

(EDIT As Tucker pointed out in comments: You might be able to explain the relative weight gains in terms of omega 6 PUFA. Chow was about 13% of energy as PUFA, stearic acid diet about 5% PUFA and the oleic acid diet about 14% PUFA. The correlation of PUFA with fat gain isn’t perfect but it’s quite close… END EDIT)

Now this is clearly impossible, as anyone who has read anything about Bl/6 mice and fat will be very aware. So the poor girl did it again:

This time we have p values sprouting all over the graph like mould in a Winter bathroom. For mice, chow makes you fat. Olive oil makes you fat. Stearic acid doesn't. Impossible I know, but that's twice it has happened. For fat mass the p values never make pay dirt but the writing is on the wall for oleic acid and fat gain too:

The wild type control mice were so nice in this PhD thesis that I thought I'd just put up these few figures before we consider what might happen if (gasp) you put an obese, diabetic db-/- mouse on a highly saturated stearic acid based diet.

I think palmitic acid would do exactly the same as stearic acid did for these mice. But who would risk their career with a finding like that? The corollary is that when you see a C57Bl/6 mouse get fat on a high fat diet, you know there are lots of double bonds in that fat........

Peter

Not really much about swimming underwater (2)

Just a one liner after all the discussions about breath holding on a fat based diet:

Effects of Twenty Days of the Ketogenic Diet on Metabolic and Respiratory Parameters in Healthy Subjects.

The first person I came across doing this practically was a LC blogger back in my early days (probably 2002-ish) and I didn't realise why she was LC eating to manage her chronic lung disease, from the metabolic perspective. She was very focused on saturated fat, obviously (with hind sight!). I've not been through the above link's full text but you all know the depths of stupidity of most saturophobes. If this was corn oil and MCT based... Perhaps we could get a significant O2 consumption drop given some butter, dunno. Nice to see some medics taking this seriously!

Peter

With apologies to whoever put this up on Facebook, one of those saved links but no idea who it came from.

Life (11) Ferredoxin

Anyone who has read through the Life series will know that I have a great deal of time for reduced FeS moieties as the core energy source used during the transition between pre-biotic chemistry and something resembling life.

Bottom line: An electron from a reduced FeS moiety is able to reduce dissolved CO2 to a Ni bound CO- group using molecular hydrogen. If you supply a couple of geochemical CH3-SH molecules you can then generate acetyl-SH, precursor to acetyl-CoA, from this Ni-CO. After that it's down hill all the way to metabolism. This is where the watchmaker comes from who is going to make the watch which you might find in the jungle.

One of the earliest biological problems was to detach this reduced FeS from the inorganic cell wall and make it mobile. The solution is ferredoxin.

People have looked at the ferredoxin used by those bacteria which have done well for several billion years by developing the form of metabolism most closely allied to this very basic pre biotic chemistry. One of these ferredoxins was sequenced very early in the 1960's, while I was just a kid playing in the streets of Nottingham and Mike Russell (thanks Jack) had just gained his geology BSc from  London University.

Working with the ferredoxin sequence from Clostridium pasteurianum Eck and Dayhoff noticed some interesting things. There looks to have been a very early gene duplication, this allows the two sections of the protein to be compared to each other and this facilitated all sorts of speculation about its possible origin. A sort of molecular Rosetta Stone. Here is the sequence they started from in the nicely descriptive three letter code (it becomes more legible if you click on it):

To make comparisons easier to fit on a given line they then changed the three letter notation to the less descriptive single letter notation for amino acids during the rest of the discussion, which goes like this:

The legend to Fig 1 is quite self explanatory but, if anyone wants the full text to work though it line by line in more detail, I have the pdf. The end conclusion is that primordial ferredoxin could be derived from a simple repeating pattern of just 4 amino acids. These four:

From these four amino acids they suggest you can reverse engineer the process giving this as the process of generating ferredoxin:

Apart from a nice discussion about why a very early protein, given billions of years to evolve, remains so remarkably similar to its primordial sequence, they also have a think about what the ADSG polymer might have been doing before it was co-opted to pick up an FeS cluster. Possibly some sort of simple structural polymer. They also throw in the concept that the FeS might initially have been only chelated to cysteine, I would suggest as a solubilising agent. Again, cysteine is one of the most primordial of amino acids:

I found the paper and its proposals fascinating. They are talking about concepts which fit extremely well in to Mike Russell's ideas about hydrothermal vents at a time before there was any evidence that the vents existed. As far as I can tell it has no bearing on anything we might do today but I still like it. It says a great deal about where we might have come from.

Peter

Insulin glucagon and protein

Again from dissertante's query: How can chicken be found to raise blood glucose, acutely?

Many years ago, as a beginner at treating diabetic animals, I tried to balance insulin dose rate/timing against carbohydrate intake. Owners always asked if there was anything they could feed as treats etc. I used to suggest meat and fat as they shouldn't need insulin for processing.

This was a mistake. Dogs are, by the time we diagnose them, functionally type 1 diabetics. While fat is perfectly OK, protein certainly isn't.

Eating protein, for a type 1 diabetic, produces an immediate rise in blood glucose. This is nothing to do with gluconeogenic amino acids, the effect of which would expect to be delayed for several hours, if it occurs at all. While protein for an normal human being/animal is neutral on systemic blood glucose it never the less produces an immediate spike (by around 60 minutes) in blood insulin.

Dandona measured insulin and glucose, although not glucagon, after casein ingestion as we saw in the last post:

Eating 75g of casein protein more or less triples your blood insulin level but doesn't budge blood glucose down any more than cream does, which leaves insulin pretty well alone. Under normal conditions the casein induced spike in insulin is counterbalanced by a rise in glucagon. If the insulin rise does not occur (through beta cell failure) the glucagon will still rise and is unopposed, so hyperglycaemia is the net result, coming from a rise in hepatic glucose output.

This took me years to realise. Slow, I know but ah well.... It's now common knowledge and Dr Unger's glucagonocentric view of diabetic hyperglycaemia makes a great deal of sense.

So protein will provoke hyperglycaemia in the absence of an insulin response, via glucagon, in a type 1 diabetic. I would guess that the same would apply to an advanced type 2. It very recently occurred to me that an elevated blood glucose after protein intake might be a useful supplementary test for certain oddities in OGTTs.

I had an email a few weeks ago about OGTT results in long term, non diabetic low carb eaters. I don't know the exact details of duration of LC eating or the period of carb loading before the OGTT, but the end result after glucose ingestion was a sustained hyperglycaemia with profoundly depressed C-peptide levels.

The worry here is that long term LC might have led to endocrine pancreatic insufficiency. My initial thought was to wonder what the response to exogenous insulin might be, but this was probably the wrong line of thought.

What would be far more interesting would be to run an oral protein response test, looking at blood glucose, insulin, glucagon and C-peptide. Although, at a pinch, all you need is the blood glucose result. If a person has developed a significant loss of beta cells then the unopposed alpha cell glucagon response to this protein would produce hyperglycaemia. A normal insulin reaction in response to protein would produce normoglycaemia after said protein load.

We all know that after a month or two of LC eating that three days at 150g/d of carbs will restore a normal response to glucose. But the question is what time scale of carb loading is needed after several years of LC eating. The regulation of insulin secretion in response to glucose requires active glycolysis, regulated by glucokinase in the pancreas. Glucokinase gene expression is controlled by dietary glucose supply. If long term glucokinase down regulation takes longer than a few days of carbohydrate loading to reverse, this would produce intolerance to glucose but would have no effect on insulin secretion when driven by amino acids. It would be quite simple to differentiate between down regulation of the pancreatic glucose sensor from newly acquired type 1 diabetes during LC eating.

Summary: Elevated blood glucose after an oral protein load suggests genuine diabetes. Poor responsiveness to glucose after sustained LC eating simply reflects a mothballed glucose sensor, provided response to protein is normal.

Peter

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.

Peter

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.

On drinking varnish

Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet.

Raphi sent me this link early in the New Year. It’s nice. It demonstrates, at some level of complexity, that omega 6 PUFA at 8% of calories are obesogenic in mice, even if they are fed otherwise fat free CIAB. It’s all about endocannabinoid ligands and receptor activation. Potentially useful when folks get round to starting class actions against the cardiological community and any other health advisors warning against saturated fat. If you limit fat to 30% of calories and saturated fat to 10% you still have 20% PUFA/MUFA in your diet. That’s easily obesogenic. Your cardiologist made you fat. Sue now.

But all of this endocannabinoid stuff is what I call high level signalling. At the core mitochondrial level we know that omega 6 PUFA fail to limit insulin activity under situations where a saturated fat would shut down insulin mediated calorie ingress. In an adipocyte this means that, during oxidation of omega 6 PUFA, insulin continues to signal and fatty acids (and glucose) fall in to the adipocytes, stay there, and you get really hungry. Modified chemicals derived from this system of omega six fatty acids are overlaid on top of the core mitochondrial signalling. A modified derivative of arachidonic acid becomes an endocannabinoid ligand and makes you hungry and fat. The system takes something basic and develops an overlay of enormous complexity, this is what I call higher level signalling.

I hate higher level signalling. Give me the core process anyday.

On this front people may realise I have issues with omega 3 PUFA fats. From the ETC perspective they are worse than omega 6 PUFA and should be more obesogenic. But, in general they’re not. In fact there is a massive industry showing us how good they are for us. But there are suggestions that the core process which makes omega 6 PUFA obesogenic really do apply to the omega 3s. Bear in mind that we are only talking about linoleic and alpha linolenic acids here. Longer fatty acids go to peroxisomes for oxidation and have little influence on core mitochondrial processes, though they do perform a great deal of high level signalling. Here we go:

Sucrose counteracts the anti-inflammatory effect of fish oil in adipose tissue and increases obesity development in mice.

Notice the obesogenic effect of fish oil only shows when sucrose is present in the diet. Replacing sucrose with protein eliminates the effect. Fructose is an unstoppable source of cellular energy intake which needs insulin resistance to limit insulin signalling facilitated ingress of glucose. As insulin continues to act, fat cells sequester calories. Fish oil combined with sucrose is the worst, corn oil is intermediate and, without sucrose, none of the fats are obesogenic.

This makes me happy. I can see the core process at work, never mind what EPA and DHA say to g-protein coupled receptors.

There is another paper which shows a similar effect and I like it rather a lot because the cognitive dissonance, which shines through every word of the text, is rather entertaining. How can you get a life-sustaining source of funding if your data show that omega 3 PUFA are grossly obesogenic? They improve insulin signalling exactly as the ETC effects would predict. The cost of improved insulin responsiveness in adipocytes is obesity. Here we go again:

Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids.

The values to look at begin with the weight gain. All we have to do is to subtract weight at the start of the study period from weight at the end (perhaps the authors don't do arithmetic?). Low fat group gained a gram, added saturated fat group gained 0.6 g, added omega 6 group lost* 2.4g and omega 3 group gained 10.4g.

Ten point four grams.

These are db/db mice which lack a functional leptin receptor. They are diabetic and I feel their chronic hyperglycaemia represents a similar drive to obesity as the fructose loading in the last study, ie an unregulated source of calories which drop in to adipocytes and which require insulin resistance to shut down whatever further caloric ingress it can practically do. Free fatty acids, a reasonable surrogate for the action of unmeasured insulin, are low so this suggests adipocyte sensitivity to insulin is high, hence the weight gain.

Weight gain in the alpha linolenic acid group was over 17 times that of the saturated fat group and 10 times that of the low fat group. Notice saturated fat protected (admittedly ns) against the weight gain seen on the low fat diet. The logic is obvious. What do the authors say? Well, I can find no mention in the discussion of this massive weight gain in the omega 3 group. Zilch. This is the quote from the only mention it gets, in the results section:

"Body weight at the end of the study was somewhat higher in db/db mice fed HF/3 compared with HF/S (Table 1)".

My emphasis.

There is no other mention of the hard fact that omega 3 fats are obesogenic. Also note that in relatively normal, non hyperglycaemic db/+ mice, the omega 3s are not obesogenic. Much the same as for non-fructose fed mice in the previous study.

Now look at the * I put in above. The omega 6 diabetic group LOST 2.4g. Ouch, at the core mitochondrial function level! How can this be? This needs no mention at all in the paper because p is greater than 0.05 (in the twisted stats used by the authors). But brownie points if you have noted the oddity about this particular group of mice.

Well done! Yes, in a group of 5 animals the standard deviation at the end of omega 6 feeding is 8.6. No other group had a standard deviation greater than 3 at any time. How do you get a standard deviation of 8.6? These are diabetic mice. Four gained weight, one became ill and this one lost a lot of weight. That's my guess, just trying to reverse engineer information out of the data supplied by a group of dissonant thinkers...

So, I went to an on-line standard deviation calculator and fed in various options where 4 mice gained some weight and one mouse lost a tonne of weight. Using a 2g gain for 4 possibly healthy mice and a 20g loss for the fifth poorly mouse we get four mice at 44g and one at 22g. This gives a mean weight at the end of the study of 39.5g to with an SD of just over 9. I think something like this is what happened. Would this group notice one skinny mouse in with four fat ones? Hahahahaha!

Summary: When PUFA are being oxidised in the mitochondria of adipocytes, those adipocytes are unable to resist the signal from insulin to distend with fat. The more double bonds in the PUFA has, the greater the effect. Linseed oil should be used for making varnish.

Peter

Paignton Zoo

So funny that both articles come from Paignton Zoo in Devon. Has anyone contacted the victims of Lynne Garton's Going Ape "Evo Diet"? To tell them to knock off the fruit and live on raw kale leaves? Good enough for monkeys....Luckily Garton's stupidity seems to have done no permanent damage to it's victims, beyond 12 days of flatulence in the "study"!

Going ape.

Monkeys banned from eating bananas at Devon zoo.

Thanks to Amber O'Hearn via Faceache for the second link.

Peter

Not really much about swimming underwater

Just before I hit post: I think the arithmetic and the logic here are sound on a ball-park basis but if anyone can point out any major flaws I stand to be corrected and will take the post down in embarrassment. But is is so simple in concept that I don't see why it's not standard fare... Here we go.

In the comments after a previous post it became pretty obvious that several LC eating folks noted a significant improvement in their ability to breath-hold while running their metabolism on fat rather than on glucose. Although this is rather counter intuitive based on the RQ (more oxygen is required per unit CO2 generated when you oxidise fat compared to glucose) what matters is the generation of ATP per unit oxygen or ATP per unit CO2 produced. I started with oxygen. Arithmetic goes like this:

Glucose oxidation is simple. Six carbons give 2ATP from glycolysis and a mix of NADH and FADH2 from the TCA:

6(CH2O) + 6O2 = 6CO2 + 6H2O      
RQ: CO2/O2 = 6/6 = 1.0
2 ATP + 10NADH + 2FADH2


A theoretical six carbon section of a chain of a fully saturated fatty acid gives this:

6(CH2) + 9O2 = 6CO2 + 3H2O        
RQ: CO2/O2 = 6/9 = 0.67
15NADH + 6FADH2


Three of the FADH2s are from acetyl CoA turning the TCA, the other three are from beta oxidation. For PUFA a theoretical alternating sequence of single and double bonds yields this:

6(CH1.5) + 8.25 O2 = 6CO2 + 4.5 H2O
RQ: CO2/O2 = 6/8.25 = 0.73
15NADH + 3FADH2


The first step of beta oxidation for PUFA yields no FADH2, so we just have the three from the TCA. Assuming the ETC works efficiently we pump these protons from our hydrogen supply:

NADH = 12H+
FADH2 = 8H+

And, very crudely, let’s assume at complex IV, ATP synthase, we have 4H+ = 1 ATP (not true IRL!)

So we can calculate protons pumped, what this is worth in ATP and combine this with the O2 needed (from the chemical equations above) giving:


Glucose protons
10NADH = 120    2FADH2 = 16, total = 136 H+
ATP 34 + 2 = 36

ATP-gluc/O2 = 6.00

Saturated fat protons
15NADH = 180     6FADH2 = 48, total = 228 H+
ATP = 57

ATP-sat/O2 = 6.33

PUFA protons
15NADH = 180 3FADH2 = 24, total = 204 H+
ATP = 51

ATP-pufa/O2 = 6.12


Clearly fatty acids are better at generating ATP per unit O2 consumed. If a 70kg person, at rest, is consuming 200ml of oxygen per minute to produce a given amount of ATP while burning glucose they should be able to maintain that same amount of ATP on less oxygen.


But the difference seems pretty small. How small?

Through sins of education I tend to think of O2 consumption for an anaesthetised, mechanically ventilated patient. That person needs about 200ml/min of oxygen.

200ml O2 gives 6.00 x10^bw ATP if running on glucose (where 10^bw is a crude scalar to whole body ATP needs). On saturated fat:

200ml O2 gives 6.33 x 10^bw ATP

Or, more realistically:

190ml of O2 gives 6.00 x 10^bw ATP on fat, equivalent to 200ml O2 used on glucose. An oxygen sparing effect of 10ml/min is underwhelming on first consideration. It’s a 5% improvement. But this should be maintained at VO2 max. When oxygen delivery is the limiting factor in performance, running on fat gives you a 5% advantage.

This is simple arithmetic applied to the most basic of biochemistry processes.

Is butter a performance enhancing drug?

Yes, provided it displaces carbohydrate.

Should folks with ischaemic problems eat butter?

Yes, provided it displaces carbohydrate.

Does it taste good?

Yes, unqualified.

Of course, once you add in ketones, magic starts to happen to the energy yield of ATP hydrolysis. Ketones are not as arithmetically simple as fatty acids but we all know, from Veech and D'Agostino's work, that magical indeed they are.

Peter

Oh, I calculated CO2 per unit ATP produced too. On carbs ATP/CO2 = 6.00 as you would expect but on saturated fat the amount ATP produced per unit CO2 evolved is 9.5. CO2 build up makes you breathe, you make less per minute on fats. Breath holding is, arithmetically thinking, expected to be easier running on saturated fat. This is what we find.