Monday, May 02, 2011

Hepatic insulin resistance in KD fed mice

Let's look this abstract. Thanks to Liz for the full text.

The key quote is, of course:

"In conclusion, despite preventing weight gain in mice, KD induces hepatic insulin resistance secondary to increased hepatic diacylglycerol content. Given the key role of nonalcoholic fatty liver disease in the development of type 2 diabetes and the widespread use of KD for the treatment of obesity, these results may have potentially important clinical implications."

I'm not sure what the word for a collection of idjuts is. A moronity?

Despite this the data are very interesting.

Look at those hepatic diglycerides, up 350%!!!!!!

Failure to suppress hepatic glucose output. Not just reduced, but reduced to zero percent suppression. Zero percent!

Wow, are these mice gonna die of diabetes, fatty liver, metabolic syndrome, Spawn of Satan induced inflamasomation.... Okay, I'll calm down now.

These mice are running their metabolism on a combination of free fatty acids and ketone bodies. What would you expect their liver to be full of? Sugar?


Maybe fatty acids?

Well, in ketosis FFAs come from transport by albumin or release by lipoprotein lipase as exactly that, free fatty acids. They are not stored in this form, they are re-esterified to triglycerides for hepatic storage. The 350% increase in diglycerides is not from being swamped with diglycerides exogenously. They are generated in situ specifically to stop the liver responding to insulin.

These mice have no source of dietary glucose. They are generating and outputting small amounts of glucose from their liver, despite extreme protein restriction, to keep their blood glucose levels compatible with life. Possibly from glycerol.

Then some joker comes along with an insulin infusion. What would happen if their ability to trickle out glucose actually did suppress in response to this malevolent tease? Death would ensue in a few minutes without a rescue glucose infusion as is needed for the mice on CIAB. Hepatic diglycerides are generated to stop the liver responding to insulin when survival makes this an absolute necessity. It's an absolute necessity under extreme ketosis conditions, even without the joker with a bottle of insulin.

To get a breath of KetoSanity we can go back to the paper by Maratos-Flier's group (thanks to John for the heads up on this "non conformist").

These folks didn't look at diglycerides but they did measured the liver triglycerides and found they were nearly twice those of the mice fed crapinabag. Gasp! Fatty liver is where it's at. But these folks did a little histopathology too, using PAS to stain for glycogen. As they say:

"PAS staining showed decreased glycogen deposition in KD animals vs. both HF- and C-fed groups (data not shown)"

If your liver is glycogen depleted what, exactly, should it have as an energy store? Thin air? A small nuclear reactor?

Maratos-Flier et al understand exactly what is going on and see no need to trot out hysteria about ketosis generating a fatty liver which is physiological. It has nothing to do with fatty liver under a carbohydrate based diet.

Now, what would happen if we increased the carbohydrate content of the diet to 15% of calories in the same way as Axen and Axen did in their 2006 blooper?

Ketosis would stop and hepatic insulin sensitivity would return. Probably within three days and certainly within the three weeks A & A allowed. The diglycerides would be gone. Probably so would the bulk of the triglycerides. Under these conditions carbohydrate would clear the fatty liver.

Would the mice be diabetic? You've got to be joking.

So why does carbohydrate restriction improve fatty liver in humans? I would suggest the lack of de novo lipogenesis due to fructose reduction coupled with chronically lowered insulin allowing VLDL output to clear the excess of hepatic triglycerides. The situation is completely different.

I doubt many LC dieters would push themselves to the ultra extreme of the diet enjoyed by these KD consuming mice. If they did, their hepatic lipids, especially diglycerides, would have to increase to produce an utterly essential survival gift of hepatic insulin resistance. Their hepatic triglycerides would rise too.

I think it's an open question about whether placing yourself at the very extremes of physiology is a good or a bad thing. It should certainly assist weight loss, but would it improve health? Interesting question.



Anonymous said...

Oh boy. Do you remember one study where they looked at PPARalpha in mice? It's this one:

""New" hepatic fat activates PPARalpha to maintain glucose, lipid, and cholesterol homeostasis."

How is that the same as "Hepatic insulin resistance in KD fed mice"?

Anonymous said...

Sorry Peter, I just noticed my post could have been misinterpreted as if I was knocking your post. I meant to knock the study you were quoting. Carry on.

John said...

So it is the degree of extremity. As you mention, most low carbers never get that low in protein+carbs. I think I remember Gunther saying he was going to try protein cycling. Most probably don't even get up to 84% fat, like the mice from the popular paper... ...and here the fatty liver is still not necessary.

What would happen if you gave mice on 95% fat diets lots of choline?

John Speno said...

You're welcome. :-)

I asked Dr. Maratos-Flier about the fatty liver in the KD mice and she was nice enough to write back with this:

"Also there's fatty liver and fatty liver. The KD diet mice had "microdroplets" and a different histology. We've had some mice on the diet for as long as six months -- at some point we should go back and look at inflammatory markers and see how they compare to high fat/high sucrose diet NAFLD."

Aravind said...

[Begin sarcasm] I'm sure some idjut will point out the de novo lipogenesis is not significant in humans so your fixation on insulin and other conclusions are wrong. Will you ever learn?[End sarcasm]

I am torn between laughing aloud at your wonderful humor (If your liver is glycogen depleted...Thin air? A small nuclear reactor?) and being deeply disturbed at the continuing bad science that has gotten the world into this mess.


gunther gatherer said...

Hi John, yep been there done that with protein cycling. It was all because I wanted to lower IGF-1 as much as possible, trying to get to where calorie restriction practitioners can only dream of, but without the hunger.

The problem was that it left me without much to eat, and as Peter says "hunger is not an option" for long-term success. As I was already eating about 80% fat anyway, I had to settle for staying lean and disease-free without feeling deprived and socially alienated. What's an extended life without friends, or an entrecote from time to time?!

mathman said...


My LDL-215, HDL-80, and Tri-52. My doc is insisting on Statins and my wife is worried that this crazy "low carb diet" is killing me. Is there an easy to understand explanation that I can give them that shows these numbers are not dangerous during CHO restriction? Also my FBG is up to 98 which I believe you have mentioned is also a by-product of HF/LC, is this correct?

Христо Раднев said...

I have been on an extreme KD for two and a half years. A recent liver scan showed a clean liver, unlike 5 years ago when I was on a protein/carb/low fat diet and had fatty liver. I'm constantly at 4% bodyfat. I consume about 300 gr of animal fat per day, 90 gr of protein and about 25 gr of carbohydrate. I follow this diet because i have crohn's disease in my cecum and rectum and a badly septated gallbladder which would cease to function in hours without the fat. I have brought crohns upon myself by eating whole wheat bread.
Without my gallbladder I wouldn't be able to survive for too long.My digestive system tolerates carbohydrates poorly, not to speak of fiber. I'm 21

Peter said...

@John Speno: Peter dances a little happy jig around the room singing "There are people who know, they understand. They're doing to do HISTOPATH on the mouse livers. Wooo hooo". More little happy dance... Some of us are so easily pleased.

Hi Martin, nice how the knockout mice developed fatty liver... saved that one.

John and Христо, yes. Very few of us get to 4.5% of calories from protein and under 1% from carbs... Serious LC eating at adequate protein and 25g/d of carbs wouldn't need full liver switch to fat-only running.

Aravind, we now have the extremes of diet and hepatic insulin extraction in place, we can go back to diabetes next.

Gunther, entrecote, mmmmmmmmm....

Hi mathman, this is really impossible. Your Dr has no choice and your wife has simply accepted what most of the world has accepted. This is completely normal behaviour for the vast majority of humans, it's just how we work. I guess you could print out the full text of observational study from Japan and ask your Dr what, exactly, would he like you to die of if he lowers your TC out of the 200-219mg/dl range? Ultimately you are stuck, as we all are, with making our own decisions. You need table 5 p1091, lines 1-4.


Peter said...

Hi Jorge, can't see any reason why the comment won't post. But yes, I think these are directly comparable to the peripheral effects. It would be interesting to track people who have used full water starvation for treating carbohyhdrate associated fatty liver. Would they go from standard NAFLD to ketogenic form fatty liver? It sounds like the histopath might be different. Or does HP from severe fatty liver under high carbohydrate intake never really completely go back to normal? There will be some fibrosis I guess and that will be there to stay... I doubt ketogenic lipid would lead to fibrosis which is why I would love to see HP on mouse livers which have liked in severe ketosis for 6m. Maybe one day they will be published...


Wonderful Blog Peter. We have learned so much from you. For some reason Blogger is not letting me post my comment, so it is below. Feel free to respond on your blog (and post my comments if you want.)

Directed at 2011/05 post:

This great post reminds me of your October 23, 2007 post on how eating a very low carb diet can cause physiological insulin resistance in muscle cells in order to focus the energy consumption of muscle cells solely on fatty acids so that BG can be preserved for nerve and brain tissue. Do you think this kind of insulin resistance is fully reversible when carbohydrate intake is high or do you think there is some kind of permanent physiological change? What is the mechanism that returns the insulin sensitivity when BG rises due increased carbohydrate consumption? Could we think of this as a kind of benign and temporary insulin resistance? I question whether this is really insulin resistance at all. If there isn’t permanent physiological change (damage), there might be a better name for it. Maybe it is really glucose intolerance in muscle cells not insulin resistance (i.e. the cell receptors still bind to insulin, but the GLUTs do not operate to absorb glucose into the cell)?

Similarly, regarding today’s post, although you say hepatic insulin sensitivity would return in 3 days or more, do you think this insulin resistance in the liver is fully reversible when carbohydrates are eaten or do you think some permanent change occurs? In other words, what I said above about muscles seems to apply to liver. What do you think?

We appreciate your blog so much!


Христо Раднев said...

Wow, 4.5% protein That may as well be protein starvation regardless of the rest of the diet

Its true that you can somewhat lower protein requirements by the glucose derived from glycerol, but to what an extent....

Aravind said...

Hello Peter,

This post and few others of yours that I've recently read are starting to connect the dots for me.

In your potato post, you wrote the following -
"The more of a problem you have with obesity the less likely you are to lose weight or experience appetite normalisation (translates as access to adipose tissue calories). Ultimately the ability to live on varied macronutrient ratios comes down to how broken you are, especially your liver. Why a broken liver requires low carbohydrate eating is another post."

You now have written-
"So why does carbohydrate restriction improve fatty liver in humans? I would suggest the lack of de novo lipogenesis due to fructose reduction coupled with chronically lowered insulin allowing VLDL output to clear the excess of hepatic triglycerides."

Thanks for the dots!

Just to be explicit, for those of us that are slightly metabolically deranged (i.e. overweight but not diabetic, etc), is your definition of a "broken" liver synonymous with a "fatty" liver induced by fructose/alcohol consumption? Or is that a subset of a greater whole?

Maybe an ignorant question, but it's the best I can do at this time :-)

Thanks and warm regards,

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

Great Post - Seems like science has turned into a grant exploitation industry.

mathman -

You could ask them to run more appropriate tests like Shiel Medical Laboratory's tripple marker. This test looks at oxLDL which is much more predictive than LDL. I'm not sure LDL it self is a risk factor other than oxLDL tends to go up with LDL. There are dietary interventions that can lower oxLDL if it is elevated.

You might also have your ApoE3/E4 tested (Search for Apolipoprotein_E on Wikipeidia).

You may have to pay for these tests out of pocket as the practice of medicine is quite a way behind the science.

It is getting popular to look at LDL size (is it more useful than reading tea leaves?). I'm not convinced that if postprandial BG is under control (less than 110) that it means anything. Could be that these expensive tests are an expensive way to measure average BG.

Peter said...

"Could be that these expensive tests are an expensive way to measure average BG"



Pieter said...


In January 2008 when eating a "normal" diet (lots of bread, soda, vegetable oils, pizza ... well everything basically :-p), my total cholesterol was around 150 (LDL around 90 I think, HDL 40+, Tri 65, FBG around 89).
Everybody happy.

In January 2010 while still eating bread (with some butter), some eggs, less sugar, less vegetable oils, my total cholesterol was around 190 (don't know what my LDL was, HDL 60+, Tri 45, FBG again around 89).
Everybody happy.

I changed my diet in August 2010: No more bread, pasta, pizza, soda, vegetable oils. Yes, I ate more eggs, more butter, but nothing really extreme. I still eat fruit, potatoes, white rice, so I’m not really low carb, I have just cut out the trans fats, wheat, fructose, linoleic acid, ...

In March 2011 I had my blood values checked for the first time since I changed my diet:
Total 252, LDL 150, HDL 94, Tri 36, FBG 89. The risk factor that is mentioned on the lab test stayed the same (2.7).

This is the first time my doctor mentioned my cholesterol being on the high side. He was a little worried: "... especially since it is mainly the bad LDL that went up".

I have not tried to explain why I think these values are ok. In the end, he's the doctor, I have just read some books/blogs. I just told him I ate less sugar and more fat.

I'm curious though what will happen next year if my cholesterol is still this high. A suggestion for statins? We'll see.

In 2009 I asked about particle size and count, but my cholesterol was fine so "it was not necessary". I forgot to ask this at my last checkup. I will try this again if I receive a prescription for some statin.

Or maybe I have to go back to eating all that crap again ...

mathman said...

According to the J-Lit study, people with TC > 240 are at an increased risk of death. So why are you not concerned Peter?

Peter said...

There is no information in J-LIT as to why the patients had the levels of TC which they had. There are many pathologies which might elevate TC and CVD risk. I doubt many J-LIT enrolees were on a low carbohydrate, high animal fat diet... Perhaps more telling is MRFIT and smoking

I don't have the full text for this but apparently the correlation between TC (and presumably LDL) and cvd is of marginal statistical significance and non-linear in the non smoking arm. ie, the MRFIT data did not correct for smoking any more than J-LIT did. The one proviso is that I've not got access the the prev med paper.


Unknown said...

Peter, you said:

"...apparently the correlation between TC (and presumably LDL) and cvd is of marginal statistical significance and non-linear in the non smoking arm."

You might have seen this paper:

"It is also seen that when a low TG–high HDL-C concentration was present with conventional risk factors of IHD, risk was approximately 5% or less."

Particularly figure 4:

Smokers with high HDL and low TG had almost the same risk for IHD than non smokers. Even those with high TC and LDL-C.

"The major new finding from this study was that men with major classic risk factors of IHD such as a high LDL-C level, hypertension, low physical activity, and smoking still had a low risk of IHD if they had low TG–high HDL-C concentrations. In addition, our results showed that a high TG–low HDL-C concentration was a stronger risk factor than several major conventional risk factors of IHD."

So what seems to be more important is HDL-C and TG-levels, independent of other "risk factors". And we know what kind of eating results in high HDL-C and low TG.

Dr. B G said...


So provocative with that link... smoking is as safe as eating cr*p and having a high 'bad' LDL (granted one has a high fat, low carb ratio of High HDL/Low TGs... like me 105/36)?? *haa*


Makro said...


Don Matesz has been blogging up a storm about the metabolic perils of animal fats over at Primal Wisdom.

Would be interesting to hear your take, if you are in need of topics.

Peter said...

Hi Makro,

I read Don's posts and I note that he was not getting the results he wanted with ultra low carb in either himself or his clients. Chris M has commented on the body composition of the ultra LC mice in this post's paper too. I would concur that ultra LC (and <5% protein!) will not make you look like Anthony Colpo.

My only problem with Don's posts is the concept that art imitates reality. Last time I was forced in to watching a few minutes of Friends or Sex in the City I had an epiphany.

Americans are all slim attractive people! No one is obese. I've seen the art!


blogblog said...


I had a cholesterol test done two years ago as a bit of a prank.

TC: 7.7 (298 in US terms).
HDL: 5.5.
LDL: 2.2.
Triglycerides: 0.2 (18 in US terms)

The poor doctor was very concerned and stated that I had one of the highest cholesterol levels he had ever seen.

To achieve this magical result I only eat meat, cheese, cream, butter, dark chocolate and a few berries.

Unknown said...

@Dr. BG,

They are only statistics so we cant draw any conclusions based on it. As most people here I think blood tests, generally, are useless. The key point should be why do these people had high HDL/low TG? We will never know. But, the thing that is interesting to me was that the "protective" blood lipid panel was exactly the same produced by a KD, OD, or similar.

Now, for the most part blood lipids are just a reflection of your diet. I dont think that you are healthy if you have high HDL/low TG but eat a SAD. Indeed, most of my patients have "healthy" blood tests, except for not so high HDL. But they feel awful and have a wide range of metabolic damage.

Re: smoking. I havent found convincing evidence for smoking being the only cause for diseases associated, specially with CVD. IMO, smoking aggraviates a damaged metabolism, but is not the cause. You see, people who smoke tend to eat a bad diet, high in sugar, PUFAs and overall carbohydrates. The metabolic effects of smoking resemble that of fasting and or a HFLC: increase in plasma FFA and energy expenditure, adrenergic and somatotropic stimulation, muscle insulin resistance, increase in O2 uptake, inhibition of glycolysis, etc. High PUFA means more risk of oxidation by oxidants in cigarette. High BG induces glucotoxcity and AGE formation, and metabolic dysregulation by the Randle Cycle, considering that thanks to smoking you have more plasma FFA. Seems that the metabolic effects induced by smoking are not compatible with a diet high in carbs, PUFA, fructose....

Is the damage the same when someone eats an almost no glucose/fructose, starch, low PUFA, high saturated fat diet? What if he fasts regularly? Exercises? This is a very interesting question.

blogblog said...

I read Don's article and have to totally disagree. The main job of an HG male is kill your enemies with a spear or club and steal their women and food supply. A few extra kilos of fat will help soften the blows and protect the organs.

The modern male gym physique is almost totally non-functional. A lot of emphasis is put on muscle groups that are relatively unimportant such as the lats and biceps. These are barely used in ground dwelling apes like us. The thighs and upper arms are far too big. The buttocks and chest are relatively underdeveloped, the deep core stabilising abdominal and lower back muscles are usually weak and trying to create a sixpack is an effective way to permanently damage your lower back.

A functional male body has a well developed chest, buttocks and shoulders, a reasonably thick muscular abdomen (without a sixpack) and relatively slender arms and legs.

Body fat is pretty much irrelevant as long as it is not much higher than 15% for males.

John said...

The only problem I have with Don's article is the tone (and the less than 30% fat, "mostly unsaturated"). What happens in 3 months if he ends up losing muscle and gaining fat? He then loses a lot of credibility. Instead of being so sure of himself (was he not sure 1 year ago?), he can openly treat it as an experiment.


I'm skeptical that the chest is important* for any athletic endeavor (besides powerlifting). I cannot think of one thing where its strength/power is the limiting factor. Lats play a significant role in many movements though. I like to emphasize glutes [spinal erectors (maybe hamstrings too) come for the ride] as I think they get the most work (and hence contribute the most) during the the best exercises (squats, deads, sprints, etc).

*In the sense that it probably doesn't need direct training. I have a well-developed chest (not compared to my back and legs though) doing mostly deadlifts, squats, olympic lifts, chins, sprints, and various hamstring exercises. My arms are quite small though in comparison.

Galina L. said...

After reading Don's article, I realized how important the mind-set of the person ,who is trying to find the healthy way of eating ,is. I think,his female clients who reported weight gain , breast abnormalities and other interesting things on the LCHF, became his clients on the first place in order to find a life-style nanny for themselves, so it made it not theirs, but his responsibility to make proper decisions about details of their diets. Listening to your own body is a very important part of finding what is working for you. Looks like those ladies concentrated on finding as much as possible pleasures in food while on the diet( because they payed another person to make diet decisions ) and manage to find a way to make even the LC diet fattening. How it was achieved - I don't know. My guess is - munching ,a lot of nuts, sugar substitutes.

donny said...

I don't see that the question of de novo lipogenesis matters, at least so far as whether fructose causes fatty liver or not. Fill the liver up with glycogen, and the brain will have a steady supply of glucose, as will the liver itself, so not much need to oxidize fats there, so maybe they accumulate. Some of the "inflammatory" hormones, like tumour necrosis factor increase free fatty acid/triglyceride cycling, so pairing inflammation with increased liver glycogen might not be the best situation.

If you look at big fluffy ldl, it's a more efficient way to deliver free fatty acids to the cells that need them. I think triglycerides become high usually because the body is trying to make up for a functional shortage of triglycerides. Type II diabetic's endothelial cells overexpress lipoprotein lipase--this seems an obvious sign of a local need for free fatty acids that isn't being properly met.

Does palmitic acid normally induce physiological insulin resistance in endothelial cells?

donny said...
This comment has been removed by the author.
blogblog said...


in our university exercise prescription classes we were taught to emphasise functional multi-joint exercises such as squats (even using body weight alone) as much as possible. Training isolated muscles using single joint movements such as biceps curls was discouraged (except for rehabilitation) and any movements involving repeated bending of the spine such as crunches, side bends and dorsal raises were not allowed. Perfect technique was considered far more important than the weights used (eg 5kg bench presses for the elderly).

If you look at photos and drawings of HGs and pre-industrial males you will see relatively thin arms and legs, thick muscular waists and large buttocks. This is about as far from modern aesthetic weight training as possible.

Heterosexual women typically show a strong preference for the classical male physique and a strong dislike of the bulky modern body building physique.

John said...


Yes, I personally think muscular hips and "waist" looks better as well, probably because I associate it with athleticism. Early 20th century strongmen had that physique. Heavy single-limb lifts or using lots of deadlift variations definitely achieves that. Nowadays, bodybuilders are considered lucky if their waists stay small during mass gains. Louie Simmons (of Westside Barbell) says almost all the best athletes he knows have thick muscular waists. I'm muscular but not hugely (175 @ 5'9), and you can't see my spine even at full flexion. My friends who seem to work hard only at bench and "arms" have very underdeveloped erector spinae (among much else). Funny how having good hip and back musclulature causes others to underestimate your weight.


Are you rewriting your comment? It was interesting.

Peter said...


I would agree this is an interesting line of thought without simple answers. I notice that Jenny Ruhl cited this rather interesting study

and I've been thinking about this paper for some time

but I've not had the time to see if the changes apply body wide or just to cardiac muscle.

Acipimox is the darling of FFAphobes. Not so popular with us lipophiles.


Chris said...

I can't say I'm impressed with the Venus posts. Particularly the second one.

Two groups are overfed the same number of calories of either fat or CHO, the researchers notice for apparently the first time that it costs energy to convert CHO into fat since it's not fat to begin with, declare that overeating fat will therefore make you fat faster than overeating CHO, and somehow the blogger thinks this means Greeks are fatter than Japanese because the Greeks get more of their calories from fat. "Maybe."

Because everyone knows we naturally overeat by an amount determined by geeks in lab coats with bomb calorimeters.

blogblog said...


I'm 85kg/182cm and often considered thin because most of my weight is in my core not my arms and chest. I would probaly need to be 100kg+ to look "big".

The great irony is that most females don't like huge muscles and most men aren't attracted to skinny or muscular women. Yet heterosexuals inadvertently spend huge amounts of effort to make themselves less physically attractive.

gunther gatherer said...

Honey, with its high fructose content, and nuts, high in carbs and PUFAs, can cause metabolic derangement to the point where you look like a Venus figurine. Both of these are and have been present in Europe for thousands of years and were certainly present when the figurines are supposedly dated. In addition, many cultures have been known to revere a sacred woman whom they overfeed and who doesn't have to engage in labour activities and so can lay around all day eating.

In short, if this woman even existed at all, she was not an average hunter gatherer. Making sweeping statements about the dangers of LCHF based on extrapolations from what the figurine looks like is pretty ridiculous. I don't know where his evidence comes from that she was eating pure protein and fat.

He also goes on to trash VLC because he tried it and his allergies came back. There are thousands of Neolithic things in the air now, including new agricultural creations, that never existed in the paleolithic and if they did certainly not in their present numbers. But he chooses to blame it on not eating carbs. Do people on the SAD not have allergies then?

blogblog said...


Allergies, such as hay fever, often become much worse in the early stages of VLC as the immune system becomes much more aggressive. This was noted many years ago by Dr Wolfgang Lutz. It is certainly my own experience.

Will some future anthropologist find a Barbie Doll and conclude that all 20th century women were two metres tall with incredibly long legs, weighed only 50kg, had gigantic breasts and tiny waists?

blogblog said...

The Japanese are only thin because the BMI says they are. The BMI doesn't measure body composition and always gives a lower result for shorter people. East Asians, such as the Japanese, actually have considerably higher average body fat percentages than causcasians. In fact quite slender Japanese women may have well over 30% body fat.

cavenewt said...

"Allergies, such as hay fever, often become much worse in the early stages of VLC as the immune system becomes much more aggressive. This was noted many years ago by Dr Wolfgang Lutz. It is certainly my own experience."

I also saw that in "Life without Bread" but it seemed almost a throwaway comment without any elaboration. You say in the "early stages". Does immune aggressivity continue, or does it slacken off? What if one has an autoimmune disease? I do, and ketones might help in peripheral nerve regeneration, but am concerned about increasing the damage from the immune system. I can't find much info about KD and autoimmune.

blogblog said...

the allergies taper off quickly and often disappear completely after a couple of months.

Dr Lutz advised a preemptive course of low dose corticosteroids for anyone with an autoimmune disease or severe allergies who went on a VLC diet.

cavenewt said...


Good to hear that the allergies (and hopefully, by extension, strengthened autoimmune response) tapers off. Corticosteroids are contraindicated in multifocal motor neuropathy, my personal lottery prize. Instead, I'm on immunoglobulin. Next thing to try is rituximab. The idea is to keep the immune system at bay while waiting for axon regeneration, for which, my Mayo neuro says, medical science has nothing to offer (hence the idea that ketone bodies might help, for which there are some rat studies that offer hope.)

blogblog said...


have you tried vitamin D?

Dr. B G said...

Hey Lucas,

It was very interesting also to me that 'protective' lipid patterns are the same produced by OD, ketosis, IF, low carb and most 'paleo' folks. These are also found in Ashkenazi Jewish long-living centenarians and their children (though the TGs are higher probably from the grains).

Smoking -- I was being facetious but glad you have made some thoughts about it. My consults with authors/bloggers who understand the stats better than I do have agreed like you smoking is not detrimental based on the context of metabolic derangements. Take the French, no associated CAD or cancers with smoking and their diet is more ideal than the US -- high fat, low transfat, low n-6, low carb/gluten/starch/fructose and perhaps I believe stress is reduced (by smoking *haa*).

Lab testing may or may not be useless -- it can illuminate in darkness and sometimes confuse without context. CONTEXT!! as Peter describes... For instance take potassium -- depends on context -- contrast normoglycemic K versus ketoacidotic K? Then add an insulin drip and check the K!! It doesn't work in isolation as does anything...

Thanks for your insights,

cavenewt said...


Vit D is one of the supplements I take. Is there more info about Vit D and neuroregeneration you want to point me to, in addition to what I can google?

blogblog said...


I don't have any unique information of vit D.

SSRI antidepressants help nerve regeneration.