Tuesday, April 10, 2012

FIRKO-isation without all the hassle?

OK, I've treated myself to a few hours at the blog.

If we look at Veech's 2011 paper we can see that he is driving towards a drug which induces ketosis, side stepping all of that starvation or very low carbohydrate eating normally required, outstripping octanoate for carbohydrate defying ketosis. You can even FIRKO-ise your mice without all that standing around on a hill top in mid winter. It would, essentially, allow all of the benefits of ketosis on metabolic efficiency while still consuming a diet of utter crap. That's not something which interests me terribly much, though I can completely see where he is coming from. It will do some good but probably do very little to influence the underlying progress of the disease.

We had friends of friends round to supper the other day. They were interested (as Veech is) in ketosis as a tool to try and modify the progress of Parkinson's disease. So we had a baked mushroom each, filled with bacon and melted soft cheese with a smidge of fried onions and a micro smidge of spinach then topped with half a round of goat cheese for starters, belly pork goulash with soured cream, broccoli and asparagus for main course and Optimal ice cream (minimal dose of honey, no sugar) with a few raspberries for desert. Coffee and double cream. Modest red wine portions. The funniest part was trying to explain to them that serious researchers/nutritionists genuinely explained away the reduced appetite on LC diets as being due to either boredom or lack of palatability.

As Veech commented:

"Further, to achieve effective ketosis with KG diets, almost complete avoidance of carbohydrates is required to keep blood insulin levels low to maintain adipose tissue lipolysis. Such high-fat, no-carbohydrate diets are unpalatable, leading to poor patient compliance."

Eeeh, the stuff people come up with. Personally, I think Veech should sack his chef. Or stop eating F3666 and hire a chef.

The other gem from the paper was this line here, talking about his ketone ester fed mice:

"The ketone levels are similar to those found in humans during prolonged fasting (33, 34) and are 3- to 5-fold higher than the levels reported for mice fed KG diets (13, 15)."

It's the last section of that quote that really made me sit up. Both ref 13 and ref 15 are sitting on my hard drive. They use F3666, 8.6% protein, 3.2% carbs and lots of fat. They found ketone levels of 1.3mmol/l and 1.6mmol/l.

That is amazing. Amazingly pathetic ketosis. Nine percent protein, minimal carbs, the rest fat. If you or I ate this diet for more than a few days we would be peeing brilliant purple on our Ketostix.

What is really special about this Veech study and the other two mouse ketosis papers is not what they tell us about how to get in to ketosis (or not), it's much more what they tell us about C57BL/6 mice. That's right, C57BL/6 mice.

These mice are very special.

I've long thought that these poor rodents behave, when fed a high fat diet, rather like MSG lesioned, ventromedial hypothalamic lesioned or gold thioglucose lesioned animals. Their VMH breaks. They develop neuronally mediated acute insulin hypersensitivity in their adipocytes, they then abnormally store fat at low levels of insulin, increase eating to compensate for this calorie loss in to adipocytes and eventually develop adipocyte distention induced insulin resistance, which shows as metabolic syndrome.

It is impossible to over emphasise how important these ketosis studies are to C57BL/6 mice. Especially if you happen to be a C57BL/6 mouse.

BUT let's pretend none of us is a C57BL/6 mouse, just imagine you are a Wistar rat on 11% protein added to your traditional diet of neat Crisco (Mmmmm, Crisco, yumeeee). You will be in to ketosis with a beta hydroxybutyrate at 4.8mmol/l, and probably develop another mmol/l of AcA, within days and stay there. Are humans more like C57BL/6 mice or Wistar rats? I have no doubt that a human can damage their VMH by the same process by which they become obese. I doubt very much that this has anything to do with eating fat. Sucrose is much more likely. But even if you are obese and have damaged your VMH while becoming obese, you can still get your BHB over 7mmol/l. It may take some time, or even a little water fasting, but you can do it.

BTW Crisco induced ketosis is neuroprotective although I'd personally rather do the same with butter!

If you are a human looking to manage Parkinsons you can quite easily get to 6mmol/l of ketones in your bloodstream. You are not a C57BL/6 mouse. You don't even need Crisco, selected Food will do it.

The massive benefit of a ketogenic diet over the "SAD spiked with ketone esters" approach is that ketogenic diets avoid hyperglycaemic episodes. If you think hyperglycaemia is good for neurons you are probably well in to some nasty neurodegenerative disease!


BTW Apologies for the total lack of contribution to conversation in the comments. I have the choice between the occasional post or trying to get comments answered and a lot of the time neither gets done. Here's the occasional post. Obviously the next step, given time, is back to Veech 1995 where he talks electron transport chain, mitochondrial inner membrane voltages, proton leakage and a whole load more about very basic concepts, some of which are quite fascinating. Including the benefits of insulin. He then is talking in Nick Lane territory. And I hope everyone noticed that Stan has been to Nick Lane's website and has linked to this publication. I just loved this quote about the acetyl CoA pathway:

It's "a free lunch that you're paid to eat," in the words of Everett Shock.

My own light reading at the moment is this one, as a kid I thought tunnel diodes were cool.


Nigel Kinbrum said...

You don't need to eat a ketogenic diet to avoid postprandial hyperglycaemia.

And what about the chronic hyperglycaemia from all of that poorly-controlled hepatic glucose production?

The lengths that people will go to, to live an extra second. What next, cold baths? ;-p

Puddleg said...

For me, life expansion comes before life extension any day.
Ketosis is a reliable tool for the former; what causes the second is still anyone's guess.
I don't usually buy lotto tickets, and I don't usualy gamble on the odds of any diet prolonging a life which, on family form, is likely to be quite long enough already.

Anyway, I thought you might be interested in this paper.
It looks like the usual "saturated fat good for liver" paper, but there is interesting stuff happening with the controls, and quite a spread of SFA/PUFA ratios.

I believe I read at one point that the rats eating more SFA gained less weight.

It's called:
Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition

right now I can only pull up this table, and the abstract, but full text is available as I have it on my harddrive.


Puddleg said...


did the authors of that paper mean to imply that rats eat subject to "food reward" and palatability considerations?
Maybe the rats should be the chefs.

Puddleg said...

Yes, it does show a dose-response trend whereby more SFA = less weight gain.
Assuming the feeding was unrestricted, does this mean that SFA is more satiating, or that it is less palatable?
What, indeed, is the tool used to distinguish between high satiety, and low palatability?
I will give a Food Reward to anyone who can find it.

Puddleg said...

full text:

Bill said...

Good stuff Peter. the "occasional post" is OK by me.

Nigel Kinbrum said...

Thank you George!

I read Dietary Saturated Fat Reduces Alcoholic Hepatotoxicity in Rats by Altering Fatty Acid Metabolism and Membrane Composition, and the following thought occurred to me:-

How about not drinking so much that you get alcoholic hepatotoxicity in the first place?

Nigel Kinbrum said...

Also, "We fed male Sprague-Dawley rats intragastrically by total enteral nutrition..."

Sounds like zero food reward, to me.

Nigel Kinbrum said...

George Henderson said...
"Yes, it does show a dose-response trend whereby more SFA = less weight gain.
Assuming the feeding was unrestricted, does this mean that SFA is more satiating, or that it is less palatable?"

Neither. It means that Calories out are higher. Sadly, humans aren't rats!

Scott Russell said...

Of course this always raises the question: was it the raising of SFA that was protective, or the removal of harmful PUFA?

Also of interest, the SFA they used was primarily coconut oil (MCT), which is metabolically in its own category in my opinion.

So make your pina coladas with coconut oil and you can go to town!

Zorica Vuletic said...

Well I suppose on a superficial level it would be 'convenient' to have some pill that puts you in ketosis and you can eat w/e CRAP there is...for pesky ppl that never leave you alone with what you eat...HOWEVER, I care about hormonal milieu of my cells, and general health of my cells and telomeres.


So I'll keep doing keto-ish and the cold thermogenisis protocol as described by Dr. Jack Kruse.

Zorica Vuletic said...

@ Nigel...just saw your comment...LOL!

Yes, cold baths are really good. I've been doing them since end of Feb. and honestly it's a miracle for me! Hormones all sorted out, muscular build as if I've been lifting weights but haven't been...ya it's good stuff. I recommend it. And sure, I would def. like a few 'seconds' extra on the back end of my life. :-) I will be the 80 yr old woman with the six pack!


Nigel Kinbrum said...

@Gladina: You women are well 'ard! Yes! LOL!

Anonymous said...

George, taste is acquired, hormones are innate. Taste is not universal, but hormones are. Something may taste good to one, but crap to another, yet cause the same hormonal response in both, therefore the same satiety in both. Hunger is regulated by hormones, and hunger makes crap taste better, therefore both will eat more crap when they're hungry. But if one eats actual food, he'll be more satiated, and ultimately eat less. Since he's more satiated, he's less hungry, therefore any crap tastes not as good.

So you ask if fat is more satiating or less palatable? It's both. It's more satiating therefore causes a reduction in hunger therefore fat tastes not as good the next time. Round and round we go.

TedHutchinson said...

@ Martin Levac "It's more satiating therefore causes a reduction in hunger therefore fat tastes not as good the next time" If we want to regulate appetite by activating the ileal brake we must ensure secretion of the satiety parameters (that regulate hunger and fullness) and cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY). Length and site of the small intestine exposed to fat influences hunger and food intake shows us simultaneous treatments to duodena,jejunal,ileal significantly reduced hunger. Sounds like fat for starters, main course, desert and maybe also with coffee is required.

Puddleg said...

Martin wins the Food Reward; a free CD download

"De gustibus non est disputandum"
("in matters of taste there can be no scientific debate")

About the control rats and differential weight gain:
either this is a "metabolic advantage" of some sort from MCT ketones plus CLA in the SFA,
it is evidence of differential caloric values of different fats (or both)
Barry Groves, in Trick and Treat, says that whereas long-chain PUFAs yield about 9 kC per gram, MCTs are closer to 7 kC/g. (from memory, the exact figures are more specific). The longer the fatty acid chain, the less glycerol in the triglyceride, is, I think, the reason.
If these diets were designed using a flat rate of 9 kC/g, that could account for some of the differential.
As could a uniquely fattening effect of PUFA...

The hepatoprotective effect is not soley due to PFA restriction; diets with less PUFA but no extra SFA promote more inflammation in this model of alcoholic liver disease; a 5% corn oil diet will do it, whereas the high-SFA groups in the beef-fat/MCT experiment still consumed significant corn oil.

M said...

Hi Peter. I searched your blog for "Cold Thermogenesis", but couldn't find anything. I was curious to know if you have any opinion on its alleged benefits, namely in improving metabolism.


If sounds like a fabulous way to amplifying and accelerating all the benefits of LC dieting, but I have to say that personally I'm afraid of being cold, as it literally gives me a cold. Should one force oneself to go through it anyway, I wonder.

Fox said...

hi Peter, long time fan of your site (and your sense of humor). thanks for revealing the mysteries of lab-mouse types and science diets to those of us who don't get to spend time with mus muscadus. prior to reading at hyperlipid, I had no idea how important this could be to results!
(and I'm with you on laughing at those who think high-fat diets are low-palatability diets. butter is awesome.)

Puddleg said...

Combine high palatability with high satiety, energy density, and optimal micronutrition, and you're on the way to the perfect meal, one would have thought....

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

Peter, just got a google alert with this paper:

Lethal Mitochondrial Cardiomyopathy in a Hypomorphic Med30 Mouse Mutant is Ameliorated by Ketogenic Diet


Thought you might be interested, and would love to see a translation if you have time.

Stan Bleszynski said...


Tunnel diodes and quantum tunneling effect are cool indeed!

I am fascinated by Nick Lane's papers! I came across Lane's papers very recently and got struck by a similarity of his thoughts and those of prof W. Sedlak (a friend and mentor of Dr.J.K.). I used to think that Sedlak's ideas (electromagnetic nature of Life) were a bit off. Actually I thought they were way off if not completely cookey. I am realizing now to my amazement that he was basically right, though perhaps not in every detail.

[purely speculative rant]

The second issue is that there seems to be some subtle distinction, on the quantum-mechanical level in the electromagnetic processes involving proton (and ionic) transport as in the living cells, and those involving electrons only (i.e. conventional solid state electronics).


Anonymous said...

Hi Peter,

You state: "But even if you are obese and have damaged your VMH while becoming obese, you can still get your BHB over 7 mmol/l."

I find this highly unlikely. If you look at the paper you referenced as "water fast", you will see that at the 35-38 day mark, BHB levels were only ~5-6mmol/L. This seems to be as deep as you can get by nutritional ketosis.

People tend to use urinary ketones as a surrogate for plasma BHB levels. But has anyone measured his/her plasma BHB directly? I have. Mine got only as high as 1.4mmol/L, if Im not mistaken. In either case, it was less than 2mmol/L. This was despite eating a "complete" ketogenic diet with all the nutritional and lifestyle tools: almost zero carbohydrates, low protein, high fat, fasting and exercise. I was not calorie restricted, however. It may get a little higher using MCT oil (not to mention dehydration), but not as much as 7mmol/L. Ketosis is not just about carbs and protein, its more dependent on calories. In a normal human, ketone bodies inhibit ketogenesis. Unless you have an hormonal imbalance, you cant expect BHB levels to rise to very high levels.

Metabolic inferences from rat studies are tricky: energy expenditure is way higher than humans, as well as the activity of regulatory lipolytic/lipogenic enzymes.

My guess is that the benefit response to ketosis is not linear. Trying to get around 2-5mmol/L seems to be a good target, although hard. It seems to me that trying to achieve higher levels would not cause increased benefits.

About Veech. I think he is just trying to make things as practical as possible. Implementing a ketogenic diet as a therapeutic tool, in complicated and dedicated patients is feasible. But in most people its too hard. If eating a ketogenic diet and implementing lifestyle measures can get you to the 2mmol/L mark, then some ketone-ester can up your levels some more. This is interesting and important in people who needs it.

Dr.Veech is, in my opinion, THE erudite in metabolism (student of the one and only Hans Krebs). Having studied ketosis for years and seeing no practical application beyond a few researchers/doctors, trying to expand the benefits of ketosis by an artificial compound is a valuable job.

Kindke said...

Lucas can you expand on some points, you say that ketosis is dependent on calories? How exactly?

I was under the impression only liver glycogen and insulin inhibit ketogenesis. After that, its simply a matter of FFA availability coming from adipocytes. ( which serum ketones control via the niacin receptor )

How did you measure your serum ketone levels, id like to do what sometime. Some simple kit you can buy from a chemist?

Lacie said...

@Kindke, Lucas: Ketones are pretty easy to measure with a diabetic's handheld glucose/ketone meter. Peter Attia (Taubes's friend who is doing an n=1 experiment on nutritional ketosis and athletic performance on his blog) uses one and says it runs a bit high over a blood test.

This study found it reasonably accurate:

Attia says he averages between 1.0 and 2.0 mmo/L but was able to push as high as 4.4 mmo/L after a 6 hour, 104 mile bike ride with 5,600 feet of vertical. The ride apparently made him spill FFAs that lingered even 24 hours later. So I'd have to agree with Lucas that 7 mmo/L from diet would be unusual. The question is whether 1.5 to 2 mmo/L is sufficient for neuroprotection, since this level seems pretty easy to achieve with diet.

Peter said...

Hi Lucas, I was looking at Figure 2 from the water fast paper. Although this used frank starvation it fits in to the correct ball park for the same effect as the Wistar rats on Crisco.

When you checked your blood ketones did you check your urine ketones at the same time? I cannot logically see how anyone could have higher urinary ketones than plasma ketones unless they are generated in the kidneys, otherwise I'd expect near equilibrium under steady state conditions. We are then left with the accuracy, or lack of it, in ketostix.

I agree Veech is trying to do what he can with people who are self selected for behaviours which have probably resulted in repetitive hyperglycaemia over decades. The ketones may in fact ameliorate the effects of hyperglycaemia by lowering the inner mitochondrial membrane potential, a classic ploy to minimise reverse electron transfer through complex I and the resultant marked free radical generation..

Re Veech's understanding, yes, he is very good. I'm working through some of his early work on alcohol, acetate and membrane potassium and Mg ion fluxes and subsequent effect on membrane voltage and on ATP energy of hydrolysis. Ditto deltaG of ATP hydrolysis under ketosis and/or insulin+glucose in the 1995 paper. Luckily I've found an elderly cellular biology text which explains it down to my level. Possibly.


I agree Nick Lane's recent papers make great reading.

I remember making an oscillator out of a tunnel diode, a couple of resistors to set the bias, a 1.5 volt battery and a RF quartz crystal. Not much else. Peanut power morse transmitter. But I then had a device I could control quantum tunneling in. Very cool. Now I just look at the electron transport chain and see the effect so neatly applied to redox couples... Quantum tunneling use here is so focused and elegant compared what is probably quite crude in the TD. Do you feel that ions though the ATPases are a bit large for quantum effects compared to electrons being manipulated down the ETC? Would that give a different impression?

M and Gladina,


The water temperature was about 4 degC. I only do it for the buzz, never occurred to me it might generate UCPs. Maybe I should ditch the dry suit! Plus getting some time on the water would be nice. Still, the children are only young once, best make the most of them.

Ellen, interesting. There are a number of studies showing benefits of fats on damaged mitochondria but most use rather extreme models. It seems like you can suggest almost anything with these models. But, overall, no one is suggesting that elevated glucose is good, plus ketones do seem to come out rather well...


Lacie said...

Went back over my notes and found several days where I hit 4 mmo/L BHB on Ketostix by restricting carbs and eating some coconut milk. So I guess I don't have to ride a bike 100 miles to hit 4. That's reassuring.

M said...

I have to say the more I think about Cold Thermogenesis the more sceptical I feel.

If the idea is that it forces your body to fight cold by burning off fat, much like your body sweats when it's warm to cool off, then it's not very effective. If it's hot outside, sweating does not significantly make you cooler, and if it's cold you just get colder. You can't be burning off a lot of fat.

If it does work it must be on the same principle of aerobic type of exercize, like jogging, biking, etc. Everybody knows that type of exercize does indeed burn off a lot of energy in the short term - one can feel it too, as one gets very warm indeed! Which just begs the question, why not go for a run instead?

As for it improving one's metabolism, I thought I read somewhere that aerobics doesn't accomplish that, that rather the best type of exercize to improve metabolism is strength training, like lifting weights.

The only way I could see the same principle applying to Cold Thermogenesis, is this: 1) strenght training works on the principle that in order to make a muscle strong you must force it to exercize maximum strength. The more you tense it up, the stronger it gets. and 2) An isolated muscle or group of muscles can never exercize as much strength on their own as when all the muscles in your body are exerting themselves together, i.e., if you try to squeeze a ball just using the muscles in your arm you can only apply so much strength; but if you tense up all the muscles in your body at the same time you find you can squeeze that ball much more. Therefore, the ideal type of exercize is weight lifting, because it forces your body to do just that, to tense up all of its muscles at the same time, working together.

What happens when you are suddenly dipped into a bathtub of ice cold water? All of your body tenses up, from top to toe, at the same time. That might indeed make your muscles stronger, and therefore improve your metabolism.

Which begs the question: why not just lift weights instead?

Maybe Cold Thermogenesis might be useful to the bed ridden? If they can stand it?

Renaud said...

@M : I'm still wondering about "cold thermogenesis" for weight loss. Getting there may be effective, but tough!
On the other hand i'm pretty inclined to think it's good for cardiovascular health (but certainly ice cold bath not mandatory).

Makro said...

OT: Interesting that Lustig now has a very heavy mitochondrial focus in his new "popular" obesity vids...


Anonymous said...


If only glucose and insulin would regulate ketogenesis, fasting hyperketonemia would be easy to achieve. Ketones inhibit ketogenesis by distinct, but sinergistic mechanisms: stimulating insulin, inhibiting lipolysis, etc.

See: http://www.ncbi.nlm.nih.gov/pubmed/1152676

Calories determine the energy status of the cell, which in turn has direct influence on regulatory proteins involving mitochondrial respiration, fatty acid metabolism and autophagic pathways.

For instance, one study praised by some people about ketogenesis & glioblastoma shows the following:

"Due to the hyperuricemia the patient was gradually shifted to a calorie restricted non-ketogenic diet, which also delivered a total of about 600 kcal/day. This diet maintained low blood glucose levels and slightly elevated (++) urine ketone levels due to the low calorie content of the diet."


If your calories are low, then you are eating also a low carb diet (unless you eat a very high carb, low fat, low protein diet). It would help, however, to restrict carbs intentionally, even during CR if one wants to get into deep nutritional ketosis.

I tested myself in a standard lab, it was a special test. In my country you can get almost any analysis without prescription.

@Peter: I didnt measure urinary ketones. Urinary ketone concentration is determined by the balance between tissue extraction/utilization vs. excretion. If you are producing high levels of ketones and utilizing them, ketonuria would not correlate with the level of ketones (this is comparing VARYING levels of ketosis, not the presence or absence of it, which is what ketostix are for; this is inherent to the method, its semiquantitative). Increased renal absorption can also reduce urinary AcAc excretion (ketostix measure only AcAc, not 3HB). With increasing levels of ketone bodies the correlation between ketonemia and ketonuria is reduced.

Some people might be in mild ketosis but do not show positive results in ketostix.

Veech's papers are an excellent mental exercise. They literally squeeze your brain.

Anonymous said...

Peter, I think blogger ate my response (probably due to links).

Peter said...

Lucas, correct re spam. You make a good point re blood levels of anything vs utilisation levels. Flux and blood level are not the same thing, ditto glucose, FFAs etc.

We're still left with a ++++ on ketostix representing > ++++ (can't remember the mmol equivalent on the sticks) in plasma, within the accuracy of ketostix.

Interestingly we use ketostix on plasma in A & E work as I don't have access to a ketone meter. Plasma always reads lower than urine but I assumed that this is because the sticks are designed for urine rather than plasma, so don't work on plasma correctly. I still feel this is the case, certainly under near steady state conditions.


Scott Russell said...

Another thought re: ketostix

Ketostix typically just test acetoacetic acid, and don't show levels of BHB. I think it was Phinny/Volek who discussed how longer periods of ketosis (keto adapted as they put it) tend to manifest a shift in the types of ketones we produce, so that we make less acetoacetic and produce more BHB. At least I think that was the conclusion. In either case, the point was that ketostix can eventually become a poor test of ketone production.

David Isaak said...


"Sadly, humans aren't rats!"

I have been confused about this for some time, so I did extensive research on the topic. Here's what I have determined:

On the internet, humans are in fact rats (or sometimes mice) when assuming so confirms someone's pre-existing biases. They are not rats (or mice) when assuming so disconfirms someone's pre-existing biases.

Meanwhile, as Peter requested, I'm pretending not to be a C57BL/6 mouse...

TwitchyFirefly said...

As someone with a nasty neurodegenerative disease, and attempting to ameliorate it with a ketogenic diet (15 months now), I have two questions.

1. (Posed by Lacie) "The question is whether 1.5 to 2 mmo/L is sufficient for neuroprotection, since this level seems pretty easy to achieve with diet."

2. Is it legitimate to extrapolate studies on the effects of ketones on brain cells to motor axons in the hands and feet? There are tons of studies for things like Parkinson's and Alzheimer's, and zero on multifocal motor neuropathy.

TwitchyFirefly said...

As someone with a nasty neurodegenerative disease, and attempting to ameliorate it with a ketogenic diet (15 months now), I have two questions.

1. (Posed by Lacie) "The question is whether 1.5 to 2 mmo/L is sufficient for neuroprotection, since this level seems pretty easy to achieve with diet."

2. Is it legitimate to extrapolate studies on the effects of ketones on brain cells to motor axons in the hands and feet? There are tons of studies for things like Parkinson's and Alzheimer's, and zero on multifocal motor neuropathy.

Peter said...


My feeling is that +++ on ketostix from Atkins induction will probably have a useful effect and that the full blown ketogenic diet, with its associated renal stones and pancreatitis, may well be overkill. But I don't see any studies out there looking at various shades of purple vs therapeutic effect. We're just at the stage of looking for any beneficial effect from normoglycaemic ketosis.

Fascinating from the epilepsy abstracts to see the massive drop out rate. People prefer epilepsy to steak????? Mmmmm bread and jam, that's a big monkey!


Icedcoffee, yes, I see ketostix only measure AcA, and certainly with starvation AcA stays relatively constant after a few days while BHB climbs progressively over a couple of weeks. Who knows what happens on good compliance ketogenic dieting? I guess Volek et al might well know this.

TwitchyFirefly said...

Neuroprotective and disease-modifying effects of the ketogenic diet at


is one of my favorites, though in the last line of the abstract, as in almost all articles about keto diets, they make the same old tired complaint about the "unhealthy" high fat diet.

As for the dropout rate...I couldn't find it just now, but I remember reading a magazine article where a group of Parkinson's patients spent a month on a keto diet with some dramatic improvement (VanItallie et al. 2005). One participant, interviewed at the end, said she was not going to stick with the diet because she "just couldn't give up her carrots."

The Neuroprotective Properties Of Calorie Restriction, The Ketogenic Diet, And Ketone Bodies at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649682/ is full-text and has some good details.

And our guy Veech, in The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism at http://www.ncbi.nlm.nih.gov/pubmed/14769489
says: "The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states." Notice he said mild.

Puddleg said...

Look at this abstract on high-fat mice: