Sunday, March 06, 2011

Potatoes and weight loss (1)

I tried and failed to produce a comprehensive post about weight loss on an all potato diet. It runs to too many pages. This is a brief simplification.

Eating 2-3000kcal/day of potatoes spikes blood glucose. The more potatoes you eat the more you spike glucose. The pancreas responds to hyperglycaemia by secreting insulin but also by upregulating pancreatic glucokinase production, which increases insulin secretion per unit rise in glucose. After a couple of days on an all potato diet your pancreas will be producing impressive amounts of post prandial insulin.

Adipocytes respond to the insulin by shutting down lipolysis. Plasma free fatty acids drop and fat loss stops.

Insulin is degraded by insulin degrading enzyme. Very, very, very crudely (with a ton of qualifications, read the paper!) insulin action leads to insulin degradation. All insulin sensitive tissues degrade insulin. The liver is a massive sink for insulin, especially on a high carbohydrate diet. Anything which increases hepatic insulin sensitivity should increase hepatic insulin degradation. A sudden ceasation of free fatty acid supply from adipocytes will increase both hepatic insulin sensitivity and hepatic insulin degradation. A potato diet supplies relatively little in the way of fatty acids so there is also little dietary fat to supply the lipid intermediates to encourage hepatic insulin resistance.

Much of the hepatic uptake of glucose occurs without the direct intervention of insulin. The liver has large numbers of GLUT2s on its cells, which allow insulin-independent hepatic glucose uptake via a simple concentration gradient. The gradient is maintained by the intracellular phosphorylation of glucose, which allows its prompt removal to metabolism or storage as glycogen. Hepatic glucokinase does this phosphorylation and the production of the glucokinase enzyme in the liver is, of course, controlled by insulin. Increased insulin leads to increased glucokinase production and enhanced GLUT2 mediated glucose uptake.

Without fat, bulk calories are stored as glycogen, excepting that there is a little de novo fat synthesis from glucose in the liver. Hepatic glycogen does not cause hepatic insulin resistance. In the near absence of FFA supply the liver maintains insulin sensitivity and the ability to degrade insulin. Nothing like as much insulin reaches the periphery as is produced by the pancreas in response to 2-3000kcal of potatoes.

The second effect of shutting down free fatty acid supply from adipocytes and diet is the loss of fatty acid intermediates in muscle. Insulin sensitivity increases, the amount of insulin needed to facilitate glucose uptake by muscles decreases. Insulin secretion from the pancreas will then decrease but hepatic extraction of insulin continues while ever carbohydrate adaption continues.

The ultimate determinant of weight loss is fasting insulin. This determines how much lipolysis occurs during the period before the next meal. No one expects to lose weight during the 4 hours immediately after any meal. The following 8 hours, especially overnight, is when weight loss occurs.

Post absorptively, without dietary glucose input, there is no stimulus for anything other than basal insulin secretion. Fasting insulin will be low because muscles are insulin sensitive so relatively little insulin is needed for glucose uptake. As fasting insulin levels drop lipolysis will restart. Free fatty acids will feed back to the liver to cause some degree of hepatic insulin resistance, decrease first pass metabolism and stop too profound an hypoinsulinaemia occurring. But fat loss will happen.

So you have to ask whether an almost all potato diet genuinely leads low fasting insulin and subsequent weight loss. For my perspective the answer is yes. The precedent for this has to the Kitavans with fasting insulin levels of 4.0microIU/ml.

The next question is whether anyone could do this. That, I suspect, depends on how broken your liver is, ie is there irreversible hepatic insulin resistance. If you are overweight secondary to simple fatty liver, which is completely reversible, I suspect the answer is yes. If you have pathology in your liver such as NASH, especially with fibrosis, I think you might not respond in the same way. 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.

Is it healthy for someone with a functional liver to live on potatoes? It is clearly possible in the medium term. Cooked tubers have a respectable history of human usage. If you are not broken it might be a reasonable diet. There are no trans fats in spuds. There are minimal omega 6 fats. There is no gluten. There is just enough fructose to activate hepatic glucokinase without generating de novo lipogenesis. There is adequate high quality protein. On the down side there are a stack of vitamin and mineral deficiencies waiting in the wings.

I have no doubt that Chris Voight lost weight on an all potato diet. I also have no doubt that he was neither chronically hyperglycaemic nor hyperinsulinaemic.

There is no way of putting numbers to the framework with the data I have at the moment, but the physiology is comprehensible.

OK, up for shredding.

Peter

There are a whole stack of follow on posts to this one but let's see how this one holds up first...

82 comments:

garymar said...

The man lost weight on his all-potato diet. Wasn't he also experiencing caloric restriction?

Nigel Kinbrum said...

He was. You can't lose weight without caloric restriction, whether conscious or spontaneous.

Asclepius said...

If he lost weight, I'd be more interested in knowing how this diet changed his body composition.

gunther gatherer said...

I tried that. Used glucose powder and sweet potatoes almost exclusively for 3 weeks to see if the Kitavan diet worked. Kept fat intake low and protein quite low.

I definitely lost weight, but not the kind you want to lose. When my pants got tight around the middle but the shirts got loose at the upper body, I knew it was time to stop.

I don't know why Kitavans, though healthy, don't go pear-shaped with their diet. At least the men. It may just simply be due to high activity. Let's remember they have also been quite isolated up until recently, so they may just be genetically more tolerant of that diet. Studies with mice and other rodents show increasing glucose tolerance and insulin sensitivity with each generation on a high-carb diet. Those of us on the mainland didn't have that kind of luck!

gunther gatherer said...

I also found myself cold all the time, with low body temp and poor circulation, and my TMJ returned. I was also in a brain fog most of the time.

It took about 4 days of high fat to get back to normal.

blogblog said...

Gunther said:

"I don't know why Kitavans, though healthy, don't go pear-shaped with their diet."

10,000 years of adaptation to a crap diet! They probably have hundreds of genetic and physiological adaptations.

Paul Jaminet said...

Hi Peter,

Sounds right, but I think the hormonal situation is more complicated and that you can have weight loss on any macronutrient mix, including mixed fat and carb diets. So I don't think it's necessary to be all-carb or all-fat.

In a healthy metabolism, you'll still place all dietary calories into safe places by 4 hours after the meal, and be able to lose weight in the subsequent fast.

Hi gunther - Sounds like some kind of chronic infection, at least in the gut, that the carbs were feeding. Brain fog indicates systemic immune activity, possibly due to endotoxins entering through a leaky gut. Thyroid and TMJ can both be infective symptoms.

blogblog said...

Most of the Irish population used to eat 4kg of boiled potatoes every day without any problems. They just added some greens, butter, fermented milk and fish to their diet. This gave them all the nutrients they needed.

In fact the Irish were far healthier than the wheat-fed people of England.

gunther gatherer said...

Blogblog, I think the Kitavans have been on their islands even longer than that, like 30,000 years. Though when they got hold of sweet potatoes and made them the main staple I don't know. I agree that there is a great spectrum of tolerance levels to Cr@pinabag Diets that we have yet to properly understand.

Dr. Jaminet, you're right that I could have been suffering from some kind of pathogenic bacteria caused by lots of starch and glucose fermenting in my gut. I don't know why the bacteria would have crossed into my bloodstream though. Perhaps the Kitavans also have more gut tolerance of carbs and fiber as well, or more beneficial bacteria which counteract pathogens before they infect you systemically.

Anyway, I'm glad I did the experiment to confirm that I was on the right track with VLC. There are tons of indigenous diets and we should be considering the local population's regional tolerance levels whenever we adopt them. This is why diet books just don't work. You simply gotta find out what "population" your body is from by trial and error I guess...

Joe said...
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Joe said...
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Joe said...

So what happens to me weight if I add a gluttonous load of FFA's through saturating my potato with butter?

I'm genuinely interested as this is one of my favourite foods at the moment and I'm trying to get down from my 20% body fat.

The studies mentioned in this post suggest that a high fat high GL diet would be a bad combination for weight loss. You either go high fat or high carb to lose weight due to how the diets are affected by insulin sensitivity.

Jenny said...

Peter,

I'm curious on what you base your claim that simple fatty liver is completely reversible. The data do not support it. What is reversible are the enzyme changes associated with fatty liver. But when the people at Duke did liver biopsies six months after patients embarked on a very low carb diet, they found only very small decreases in the amount of intracellular liver fat.

This is depressing, and not something the people who earn big money writing diet books want you to know, but it seems to be the truth.

The same was true of Metformin. It lowered the liver enzymes, but on biopsy the liver still had the same amount of intracellular fat.

--Jenny

John said...

On your link for "hepatic glycogen does not cause hepatic insulin resistance", I'd like to add that the study linked only shows that acute hyperglycemia, followed by glycogen production does not immediately result in hepatic insulin resistance.

It is almost a surety that when the liver is at near-maximal capacity for glycogen (such as that seen in many obese individuals), that feedback mechanisms do tune down insulin sensitivity in the liver.

Stephan said...

Hi Gunther,

Kitavans' ancestors have not been eating their current horticultural diet for more than 9,000 years max. Although New Guinea was colonized 43,000 years ago by hunter-gatherers who were probably the ancestors of modern Melanesians, the first evidence of horticulture dates to ~9,000 years ago. So roughly the same as Southern Europeans.

I don't know when humans actually showed up on Kitava, but I doubt it was before the Austronesians showed up with advanced seafaring technology around 4,500 years ago. It would be mighty tough to make it to the Trobriand islands on a log raft. Kitavans are considered Melanesian, but I think they're actually a mixture of Australoid (Melanesian) and Austronesian (Polynesian) stock.

That being said, 9,000 years is enough time for a certain amount of genetic adaptation, and in fact it's known for a fact that all long-term agricultural and horticultural societies have undergone measurable genetic adaptation to diet.

But, I think it would be hard to argue that they are genetically "carb resistant". There are too many healthy high-carb cultures around the world, including a few hunter-gatherer cultures.

gunther gatherer said...

Thanks for filling in the dots, Stephan.

So maybe it's a little bit of adaptation on both sides: the Kitavans have adapted somewhat to eating a mostly starch diet, and Europeans have perhaps lost some of that resistance to high carb while finishing off all the indigenous European game over the last 9,000 years.

I hope you've seen some of the studies on Pubmed on how mice become more and more carb "resistant" with each successive generation of a high carb diet. I'm not advocating a high carb diet, just noting how one species' metabolisms can adapt to their environment.

But for those of us having chosen the wrong parents, well VLC it is.

Charles R. said...

I found this passage to be key:

"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)"

I think that's a great concept to begin to get across. Much of the effect of the kinds of diets we're suggesting have the effect of appetite normalization, and that's critical to their success. And that feeling, when you realize you're just not hungry anymore, is really quite a revelation. The constant huger one feels on a crap, HC diet is maddening when people around you are just suggesting you eat less.

Appetite normalization. I'm going to start using that phrase a lot. It will appeal to people...

Ralleh said...
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Travis Culp said...

http://www.ajcn.org/content/48/2/240.full.pdf

This seems to indicate that once glycogen stores are saturated, excess glucose is stored as fat, even in the absence of appreciable amounts of dietary fat. I would imagine that the 3% fat diet is similar to what would occur on a potato diet.

The potato diet fellow lost a lot of weight initially as a result of loss of appetite. Indeed, potatoes are often cited as being one of the best sources of satiety, the effect of which might be amplified due to just how disgusting such a diet would be. Upon realizing how much he was losing, he forced himself to consume more calories so that the weight loss would not be so rapid. What weight he lost would have been the result of a significant caloric restriction initially, intentional or not.

If my BMR is, say, 2800 calories and I consume that amount in potato, I will quickly saturate my glycogen stores and store the excess as fat. I suppose I could mitigate the fat storage process by continually depleting my muscle glycogen stores via resistance workouts or sprinting etc. My brain, organs etc. will continue to tap into the hepatic glycogen stores for energy and my muscle mitochondria will continue to (via the beta-oxidation pathway I assume) use fatty acids from my adipocytes as fuel between meals. My brain, muscle and organs will consume the same amount of energy roughly as always, so I don't have a net gain in adiposity because even though significant amounts of it are stored as fat in an immediately post-prandial state, the energy balance is the same.

I would not expect the same result to occur if instead of potato, high-fructose fruits were used, even if the number of grams of carbohydrate are the same, since the fructose would lead to various forms of metabolic derangement and would itself only be available for storage as hepatic glycogen.

Wolfstriked said...

Peter,hello from a long time lurker of your blog.I like that you are giving a lowfat diet a chance by doing this and the upcoming blogs on it.

A question I have is....would a lowfat diet of potatoes plus lean meats give the same insulin sensitivity benefits that a potato only diet does?Would make sense on how lowfat dieters can get very lean.

If so then which do you think is healthier over the long haul....or are they both healthy since insulin is kept low??

Tony Mach said...

The healthy liver is an important point, because any glyco-alkaloids (AFAiK the major antinutrient in potatoes) that leaky int the body need to be disposed off by the liver.

In my n=1 I got problems when I reintroduced 'taters in my low-carb (pre-paleo) diet and those problems got relative massive (I felt like sedated) with a big portion of fried potatoes... Maybe this was some other problem I had, maybe I'm somehow broken, but it certainly wasn't the carbs and it wasn't the blood-sugar because if I eat a big portion of fried platains I don't have these problems... Just like Kurt Harris said, carbs are not a problem (unless you are somehow broken), but the anti-nutrients are the problem. Can you name a carb-source that is anti-nutrient free? Besides liver? Ok, I settle for low in anti-nutrients...

BTW: Besides causing all kinds of havoc in the body (like glueing together with cholestrol to cause cell-leakage) Glyco-alkaloids have a steroid group that could interfere with the steroid-hormone-system - ups.

And the sweet-potatoes the Kitavan use certainly have a different anti-nutrient profile than "our" white potatoes. Does anybody know how the Kitavan perpare their food?

Peter said...

Hi Gunther,

My suspicion is that those of us who cannot adapt to a high carb diet free of trans fats and excess fructose may not have the nice undamaged liver needed... I doubt may people on Kitava have ever had chronically elevated ALT before going to 70% carbs...

Paul, yes, almost any calorie mix should be fine, with a switch from fats to carbs and back as needed, I'll come back to this again. But in the current civilised world low carb, with certain caveats, seems to win hands down... But I don't think this generalises to all societies and diets. I doubt high carb would work for me now I've had nearly 50 years of carbs/PUFA/grains/occasional trans fats to cook my liver (however mildly). Luckily I'd read Pure, White and Deadly in my 20s and had backed off on sucrose in a fairly big way.

blogblog, yes, it doesn't take too much to render potatoes safe.

Joe, that depends on your insulin sensitivity, especially that of your liver, which might be good bad or mediocre. The more obesity prone/insulin resistant you are the less you can mix your foods seems a reasonable take. In fact you could rephrase that to say the more obesity prone you are the less carbs you can tolerate with your butter. We none of us are Kitavans.

Jenny, reversal of simple steatosis is just accepted in pathologyspeak. I have no problem with metformin being ineffective (this one? http://www.ncbi.nlm.nih.gov/pubmed/19811343) as the folks with steatosis did nothing other than take a drug, however good, and keep chowing down the Big Gulps. Not that I've seen the full text. Westman's pilot study was encouraging (http://www.ncbi.nlm.nih.gov/pubmed/17219068), was there a bigger study which failed? I can't find it if so. I'm no lover of bariatric surgery but there are a fairy number of studies like this one (http://www.ncbi.nlm.nih.gov/pubmed/17376042). There is also this elderly case report (http://www.ncbi.nlm.nih.gov/pubmed/3829884).

To be quite honest I'm amazed that LC eating decreases hepatic steatosis. If you are in ketosis there shouldn't be a lot of glycogen anywhere and that only leaves fat to run your liver on. Having a few TAG molecules around might be useful...

John, possibly. The paper does discuss conflicting studies. I was also interested in good old GSD1a where you can have a liver so full of glycogen it extends well below your umbilicus and still suffer chronic hypoglycaemia/insulinaemia. Of course if hepatic energy sensing needs glycogenolysis this argument is futile. I would agree that there must be an energy sensor for glucose as well as lipid in the liver. I guess I would argue that 4kg of spuds with minimal fat is physiological...

Stephan, thanks for the dots too.

Travis, thanks, I'll read through the pdf when I get the chance. I was going to integrate DNL, along with visceral vs peripheral fat and a few other aspects. It got too long. I would also ask what you mean by satiating... To me that implies access to adipose calories (if we have plenty), which suggests low insulin. Then we're back to mechanisms. And then, how would weight loss stop if we just kept on potatoes for more than two months...... Ah, leptin.

Fructose in modest amounts repletes glycogen but is great for DNL in the sort of amounts found in the current SAD...

Peter

Peter said...

Hi Charles, I think Gary Taubes/Bob Kaplan beat me to it on the appetite normalisation under LC at the end of the Dr Oz blogpost...

http://www.garytaubes.com/2011/03/dose-of-intervention-land-of-dr-oz/

Hi Wolfstriked, low fat per se is idiocity, eating "real Food" which happens to be low in fat is potentially acceptable. The fiasco of pushing low fat vegan "near Food" on diabetics is religion gone very bad, even if they gave the victims B12 rather than pooh supplements. Have to post about that one. Once you are diabetic you are broken and have got to go LC... But understanding the physiology of how low fat real food can be done, if you are not broken, is very interesting. Most of the medics treating people with metabolic syndrome using LC are dealing with people who are undoubtedly carb-broken... That's not the normal human condition, but it does include an awful lot of us which is why LC works for so many problems.

I'm betting on LC for best health. But you have to consider the options...

Hi Tony, humans seem to go to enormous lengths to detoxify their carbs, but still they go for them. I've not looked at cooking on Kitava in detail. All societies will differ I guess.

Peter

Wolfstriked said...

Peter,this post started an idea that maybe my diet needs to be very lowfat to enable better insulin sensitivity.I have tried so many mixed diets with large amounts of carbs and fats and I suffer the consequences.What if I need to go very low fat to help my bad glucose metabolism.

Severe hypo symptoms on carb ranges from 180deg recommendations to the recently tried carb amount in the "perfect health diet".Unhealthy bloated looking and severe hypoglycemia is not what I want no matter what my weight loss is....or lack of.I go to Optimal diet ratios and feel good but find my weight room workouts then suffer.

Yet also at times I recall feeling very good on carbs.Your post opened my eyes to the possibility that a diet for a severe hypoglycemic is a balance of carbs w/lean proteins.How long do you think this higher insulin sensitivity will take to occur?

Ed said...

Jenny,

Unfortunately I can't add much useful to the fatty liver topic. But I would figure that dietary choline status could be a major confounder when trying to reverse fatty liver. Not enough liver or eggs and you may not have enough choline to package up triglycerides in LDL particles for export.

LeonRover said...

Hey Peter

Great post. Recently I switched my ratios to that of the Kitavans - about 70% CHO from potatoes and "an apple a day". The rest was my "real food" of eggs, bacon, breast of lamb etc. (My favourite cookbook is Poor Cook" by Caroline Conran.)

During the experiment I maintained my weight at72 kg and BMI of 25.

I too read "Pure White and Deadly" when first published,and had stopped taking sugar in tea and coffe at age 8. My basal insulin is 3.6 and ALT's etc are in middle of range.

My lucky Irish citizenship?

Alan said...

my feeling is that carbsanity.blogspot.com has demolished the insulin-prevents-lipolysis theory.

blogblog said...

Gunther,

the Kitivans and their neighbours in New Guinea have been living almost entirely on starchy foods such as cassava for tens of thousands of years. They had no choice because there are no large native land mammals in Melanesia.

blogblog said...

It depends how you eat your potatoes.

In the Andes and Ireland potatoes were traditionally eaten half-cooked.

Potaoes contain retrograde starches which revert to back to a non-gelatinised form when cooled.

In this situation the starches are not gelatinised. This ensures the affect on blood glucose is minimal and that a lot of colonic fermentation occurs.

Peter said...

Hi Wolfstriked, the enzyme changes appear to track over a few days. Whether there is a longer adaptation period, as in transition to LC, I don't know but I doubt it. I think going the route to low fat really pushes your reliance on having normal liver and pancreatic histology/function. Reactive hypoglycaemia suggests LC is the way to go but adapt your carb intake to your weights. JK talks about 100g/d for heavy work. Overall I keep coming back to LC mimicking starvation. The system should be very highly conserved. High carb with very low fat is an agricultural approach with far too big a dose of random chance in it for my liking...

Ed, well yes, eggs are good and not exactly promoted by main stream medicine, though egg bashing is not as bad as it was even 10 years ago. Unless you are a cardiological dinosaur of course.

Hi Leon, I agree it is certainly do able for some of us and those 30% non carb calories fit in with blogblog's ideas. Yudkin may not have seen things quite the way many of us do nowadays but he was pretty close. I was going to say ahead of his time but LC has been around for so long that I thought I'd better stop!

Hi Alan, she or yourself can come and treat my ketoacidotic patients then. Save me having to faff around with all that insulin, potassium and glucose at 3.00 in the morning.

Peter

Peter said...

Asclepius, the interview with Stephan suggested fat loss. It is believable.

Peter

blogblog said...

Unfortunately when "native" lifestyles are researched the studies are usually done by physicians or anthropologists who know virtually nothing about diet or exercise.

A Kitivan sweet potato is probably completely different to a western sweet potato - much more fibre, more resistant starches and considerably higher vitamin and mineral levels. If it is eaten half-cooked it will have a low impact on blood glucose and a strong prebiotic effect on colonic fermentation.

The other problems is that researchers grossly underestimate physical activity in pre-industrial societies.

The amount of time spent on physical activities is essentially irrelevant. It is the intensity that counts. Spending an hour a day walking barefoot up a steep muddy path is actually an extremely intense workout.

Drs. Cynthia and David said...

Re Jenny's comment, JD Browning just published a follow up paper showing only two weeks carb restriction reduced liver triglycerides by 42% in NAFLD patients. see http://www.ncbi.nlm.nih.gov/pubmed/21367948

Cynthia

antispirit said...

Re: NAFLD still persisting on a low carb diet-

I would like to suggest the possibility that not all fatty livers are created equal. A low carb fatty liver may as physiologically threatening as a normal one. The low carb liver might just be trying to be ironically unhealthy. You can identify them by their mutton chop facial hair and aviator glasses. Along with the requisite adiposity, of course.

"Oh I'm sooooo insulin resistant"

antispirit said...

May *not be* as threatening, rather.

gunther gatherer said...

If one is low-carbing using lots of PUFAs, I reckon you can still get weight loss while keeping your fatty liver, or even making it worse.

Peter said...

Gunther, absolutely. http://www.ncbi.nlm.nih.gov/pubmed/17318260 uses 59% of calories as safflower oil (near pure omega 6) and produces fatty liver in 3 days! Omega 6 mayo could do this if you ate enough of it. Any LC but cholesterophobic cardiologist would wet their knickers for the cholesterol lowering effect and encourage you in your folly. Your liver will still cook, you will still lose weight if you dropped carbs enough and you can join the queue for a liver transplant...

Peter

Andy said...

Jenny: The data **you** have been reading doesn't support it, but there is plenty of other data that does.

I cut & pasted your phrase "fatty liver is completely reversible" into Google & got this: http://www.lmgtfy.com/?q=fatty+liver+is+completely+reversible

Even the very first sentence in Wikipedia says "Fatty liver, also known as fatty liver disease (FLD), is a reversible condition where..." http://en.wikipedia.org/wiki/Fatty_liver#Treatment

I'd like the reference to the Duke study you cite. I suspect the subjects were fed or continued eating a diet low in natural saturated fats & cholesterols, high in toxic, adulterated, OXIDIZED processed TRANS configured PUFA corn & vegetable oils, high glucose carbs & probably even alcohol.

Chris Masterjohn has good info: "A 2007 study published in the journal Nutrition and Metabolism found that although corn oil-based high-fat diets can induce non-alocholic fatty liver disease in rodents, long-term feeding of high-fat diets based on coconut oil or butter cannot." http://blog.cholesterol-and-health.com/2009/10/maternal-intake-of-saturated-fat-causes.html

Also: "A brand new study published several days go in the journal BMC Gastroenterology showed that a diet rich in coconut oil dramatically protected mice against fatty liver disease induced by a methionine and choline-deficient diet when compared to corn oil." http://blog.cholesterol-and-health.com/2010/06/coconut-not-only-protects-your-liver.html

The key to fatty liver, CAD & other lipid related conditions lies totally in the difference between the molecule chains of TRANS fats versus CIS fats. Oxidized TRANS molecules pack tightly & space efficiently like a bundle of straws, CIS molecules are bent & can't pack as tightly & are more easily emulsified, which is why natural saturated fats & others are so good for you.

Don't be depressed, which is also caused by a deficiency of good saturated fats & O6 & O3 EFA's, just start reading better studies & sources that say otherwise.

Wolfstriked said...

Thanks Peter,I read where JK says up to 100gms for heavy labor but its just not for me.Sitting here after my workout with 40gms whey/15gms sugar PWO drink on top of my normal diet and my blood sugar is super stable.In past I would do 50gms whey and 100gms sugar and would crash hard. LOL

That stable blood sugar is very important to me since once I go hypo its all downhill getting worse and worse until I reset for a few days on JK ratios.

Things are good so why go all bland chicken breast with plain rice. ;(

Stabby said...

I was just doing some research on fatty liver yesterday. It was interesting that a high saturated fat diet ameliorated hepatic inflammation through downregulation of TNF-a and COX-2 through adiponectin synthesis, and also reduced endotoxins and peroxides through reducing in omega 6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1398076/?tool=pubmed

This is a major advantage to the butter and beef diet. If we would just balance/reduce our PUFAs the lower carb diet would confer more benefit than the potato diet, supposing that they were nutritionally equivalent. Higher protein intake also helps dejunk the liver http://www.ajcn.org/content/90/4/1002

Now I know why Robb Wolf has such dramatic results with his diet. It does everything to make love to the liver.

Good article.

Stabby Raccoon.

Lucas Tafur said...

@ Alan:

No, she has "demolished" the carbs drive insulin drives fat gain myth. That insulin prevents lipolysis is a well known biochemical effect. You only need minimal amounts of insulin to inhibit HSL. That means you cant lose fat while on a high carb diet? No. And nobody is arguing that.

justdoinglife said...

I tried all potato breakfasts for a couple of mornings. It is a volume issue; eat 400 gms of potato, 300 calories, fried with a little fat, total say 400 calories. I did not get hunger for 7 hours, ~ 60C/hr, less than my BMR, which makes potato a suitable diet breakfast, but I cut it to 150 C and added 2 eggs. Much better, and it still lasts 6 hrs.

blogblog said...

Peter,
like you I'm a chilli and chocolate fan. Have you tried adding cocoa to your chilli to combine your vices? It is apparently very popular in Mexico.

Dr. N said...

Peter,

This isn't really about potatoes per say but several posts comment about about low blood sugar.

I hear a lot of talk about episodes of hypoglycemia but found very little documenting that in the contest of low carb. Certainly it occurs when patients take medications such as insulin, etc.

But my experience is that my patient's who consume high levels of carbs are often experiencing excess stomach acid (dyspepsia) when they think they're having 'hypoglycemic spells'.

These dyspepsia symptoms often improve just as easily when someone takes a quick-acting antacid such as Tums as they do when they eat.

Dyspepsia and its big brother, GERD, are felt to be the result of autonomic impairment. These dramatically improve with a reduction in carb intake. I generally target my patients to be less than 100 grams per day.

There is growing evidence that impairment of autonomic function may actually preceed and might even trigger the development of insulin resistance.

Any thoughts?

Anyone else seeing this?

blogblog said...

re: Dr N,
with respect I would totally disagree with your entire post.

a) A patient is very unlikely to confuse the symptoms of hypoglycemia and dyspepsia. They are nothing alike.

c) Tums and similar antacids all contain sugars. So they will obviously help treat hypoglycaemia.

b) There is almost nothing published in the mainstream scientific literature about low-carbing. So it is necessary to rely on blogs etc to gain an insight. It is obvious from reading blogs that reactive hypoglycemia is a very common occurrence in low-carbers.

d) A far better explanation for GERD is that gases produced via fermentation of carbohydrate in the small intestine force acids into the esophagus.

e) Only refined carbs, particularly sugars, seem to cause GERD. Even a high intake of unrefined carbs (eg brown rice) does not seem to cause GERD.

blogblog said...

An addendum to my previous post.

High dose polyols cause dyspepsia and reflux yet have no effect on insulin.

Cliff said...

Blogblog says" "potatoes are traditionally halfcooked"

According to who?

If your doing exercise it only makes sense that a high carb diet is better for weight loss(and performance which leads to more weight loss).

Peter said...

Hi Dr N,

I've not come across syndrome of hypoglycaemia vs reflux mimicry, but it is very clear that reflux is not only influenced by carbs, which it obviously is, but also by gastric pH per se. My wife's GERD, with regurgitation of coffee 8 hours post consumption was so violent the coffee would come down her nose, went completely on omeprazole, it's not just a change in the pH of the reflux, the reflux stops. I think it went with Gaviscon too. Obviously LC was the long term solution.

Whether the pH affects the GERD or it is the massive hypergastrinaemia or another knock on of crippling acid production I don't know. Clued up human anaesthetists are now offering a light meal on the morning of a GA because the reduction of fasting gastric hyperacidity by food administration decreases the amount of reflux as well as the pH of the fluid. Not sure if I would go for an omeprazole tablet or a hospital meal... Better avoid surgery as much as possible!

Peter

CarbSane said...

Re: The ultimate determinant of weight loss is fasting insulin.

There is no evidence for this! For example see my discussion of Grey & Kipnis

I can't find them all at the moment (had a bunch of links gone missing), but at least in diabetics from this study we see that fasting insulin tends to correlate with BMI: http://www.sajpc.org/vol7/vol7_3/bodymass.htm
I have others that correlates with fat mass.

blogblog said...

Blogblog says" "potatoes are traditionally halfcooked"

"According to who?"

According to The Propitious Esculent: The Potato in World History

"If your doing exercise it only makes sense that a high carb diet is better for weight loss(and performance which leads to more weight loss)."

Not true:

a) Your muscles only use a significant amount of glucose during high intensity exercise. The other 95% of the time they use fat as the primary fuel.

b) Exercise does not cause weight unless combined with calorie restriction. In most cases intense exercise simply causes excess appetite resulting in weight gain. Manual labourers have - on average - a greater BMI and higher body fat than sedentary people.

blogblog said...

Peter,
low stomach pH (high acidity) is important to suppress the growth of pathogenic bacteria such as clostridia.

Severe, or even fatal, cases of clostridium difficile infection have beeen associated with omeprazole and similar proton pump inhibitors.

Peter said...

Absolutely re omeprazole. I guess it would be bacon and eggs before a general anaesthetic then, but I'm not sure these are all that available on the NHS! Getting my wife off of omeprazole was our main drive to LC eating. Her current most reliable trigger for minor acid reflux relapse (rare) is accidental gluten exposure, rather than sucrose.

Peter

Peter said...

Hi CarbSane,

Nice study, I'll deconstruct it for you sometime after I've done as much reading as I need to. BTW Thanks for the lead in to Axen and Axen's work.

I got the email about this comment but couldn't see it on the blog. Turns out the blogging software put it in the spam folder. Hysterical.

Peter

Cliff said...

"Your muscles only use a significant amount of glucose during high intensity exercise. The other 95% of the time they use fat as the primary fuel."

You only use fat as your primary fuel at rest or during low intensity and even then your only using like 60% fat and still using 40% carbs. Once the intensity goes past 50% of your maximum, carbohydrates become the main fuel source. If what you said was true marathon runners would never bonk and could run forever.

http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2001.00295.x/full

"Manual labourers have - on average - a greater BMI and higher body fat than sedentary people"

This is an average based on a correlation and as we all know from your guru gary taubes correlation doesn't equal causation. Manual laborers generally have very stressful jobs which lead to cortisol production which leads to fat gains not to mention manual labourers eat some of the most unhealthy food.

Exercise is the only thing that is proven to cause weight loss according to the science. Calorie restriction only causes short term weight loss for the most part.

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

Cliff said,

You only use fat as your primary fuel at rest or during low intensity and even then your only using like 60% fat and still using 40% carbs. Once the intensity goes past 50% of your maximum, carbohydrates become the main fuel source. If what you said was true marathon runners would never bonk and could run forever.

We only use 5-10g of glucose an hour during rest. Most of that is used by the brain.

In fact marathon runners have far more efficient fat metabolism than untrained people. This is due to increased muscle vascularisation and metabolic adaptations.

Humans didn't evolve to run 20km/h for two hours. We evolved to run long distances at intermittent pace or low speed.

A well trained amateur runner can only run at the Olympic marathon race pace for a few minutes.

A trained runner can run over 100km at an 8-10km speed without bonking - the main problem is sore feet.

Exercise is the only thing that is proven to cause weight loss according to the science. Calorie restriction only causes short term weight loss for the most part.

No long term weight loss study based only on exercise has ever been conducted.

Most exercise physiologists consider that exercise is totally useless for weight loss unless combined with a calorie restricted diets.

Manual laborers generally have very stressful jobs which lead to cortisol production which leads to fat gains not to mention manual labourers eat some of the most unhealthy food.

Heavy exercise increases appetite far in excess of the actual calories used. Most professional athletes are kept on strict diets to prevent weight gain. Body builders go on extremely strict diets before competitions to lose excess body fat - even 15-20 hours a week training won't keep them lean.

allison said...

Peter,

How does this process play out in the case of obesity and fatty liver? Lutz has opined that some obese patients do not respond to a HFLC diet, typically middle age women. He suggests a tipping point. It appears that a prerequisite to weight loss is a normal functioning liver.

blogblog said...

re: allison,

Lutz has opined that some obese patients do not respond to a HFLC diet, typically middle age women.

Moderate obesity is probably the natural state for most middle-aged women. Stefansson noted that traditional Inuit women were generally moderately obese (despite a life-long diet containing less than 2% carbohydrate).

Poisonguy said...

Hey, Peter, are you saying/implying that a dysfunctional liver is the be all and end all of metabolic syndrome? Something to chew on for sure.

Peter said...

Just a few loose ends:

Hi Stabby, yes, I have a paper to blog on about failure to induce hepatic lipidosis (prob rats) using saturated fat. I'll dig it out some day.

Lucas, too true.

justdoinglife, I think it was Gunter who mentioned spek (sp?) and potatoes as the preferred breakfast for sustained hard farm labour. Spek is a high lard bacon I think...

blogblog, cayenne pepper, paprika and chili powder all find their way in to my cocoa on occasions. Nutmeg and cinnamon have their places too.

allison, I think a healthy liver is very important for spontaneous weight control. Obviously anyone can starve themselves for a month and lose weight. JK also has failures for weight control. I find the failures fascinating, you have to try and fit them in to a logical framework. The problem is that finding how normal people seem to work is hard enough, let alone looking at the outliers... The other set of problems I send quite a lot of time thinking about are the skinny type 2 diabetics.

Poisonguy, It seems rather important. I doubt it is everything. You have to look at mutations in IDE, pancreatic glucokinase, exactly what is happening in haemochromatosis...

Peter

gunther gatherer said...

Peter, the chili powder, cayenne and even the cocoa itself are all hormetic agents, according to Pubmed. So are the lipopolysaccharides given off by the bacteria in your fermented cream. Funny how our natural tastes can lead us to things like these. You are inadvertently "exercising" your cells with your cream!

PS: Speck is the best. The Bauernfrühstück (farmer's breakfast) when I lived in Germany was traditionally eggs, potatoes and Speck (pork belly) fried in butter. After that, you don't even think about food until about dinnertime.

blogblog said...

Peter:

regarding speck. I had a friend who lived in Austria in the mid 1950s. He was a refugee and worked on a farm. Breakfast was always speck (a very fatty spiced ham) and a boiled potato. He told me he never got hungry and had heaps of energy.

http://en.wikipedia.org/wiki/Speck

blogblog said...

Bauernfrühstück (farmer's breakfast)

Ingredients
6 slices bacon
1 tablespoon butter
1 onion, chopped
4 potatoes, cooked and finely diced
6 eggs
½ teaspoon salt
freshly ground black pepper
¼ cup milk

Directions:
In a frying pan, fry the bacon until crisp.
Remove and drain on paper towel.
Remove the bacon fat from the frying pan, add the butter and saute' the onion until soft.
Add the potatoes and brown lightly.
Beat the eggs lightly and add the salt, pepper and milk, and finally the chopped bacon.
Pour the egg mixture over the onions and potatoes and stir occasionally until cooked.

blogblog said...

Bear Stanley killed:

http://www.nydailynews.com/news/national/2011/03/14/2011-03-14_lsd_icon_owsley_bear_stanley_dead_at_76_killed_in_car_accident_in_australia.html

One of his other claims to fame was living for over 50 years solely on meat, butter and eggs

Peter said...

Thanks for the heads up blogblog. I think it was Bear who made the comment somewhere on the net that he attributed his health to never letting anything green pass his lips. At the time I had no idea as to quite how close to this point of view I would come!

Luckily I can use hormesis as the justification for my occasional vegicide.

Peter

gunther gatherer said...

The NYT obituary said he suffered a heart attack some time before getting throat cancer. Anyone know more details?

Chris said...

According to the LA Times, he attributed his heart attack to childhood broccoli poisoning.

Peter said...

Hmmmm, there is no limit to the ability of we humans to wriggle under our weight of our cognitive dissonance...

Peter

blogblog said...

Bear Stanley was an old man (76) He had a minor heart attack in 2004 when he was 69. His throat cancer was due to HPV and was in remission.

David Isaak said...

"Beat the eggs lightly and add the salt, pepper and milk, and finally the chopped bacon."

Oh, no! All that and "Killer Salt," too? ;-)

Peter said...

Oh yes, salt restriction activates the renin/angiotensin/aldosterone axis. A Bad Thing. By the time you have dumped processed food you often need to add some salt back in... Mmmmmm, bacon and eggs or their yolks scrambled in the bacon fat. Sound's like today's brunch. Oh, it was!

Peter

David Isaak said...

"You can't lose weight without caloric restriction, whether conscious or spontaneous."

And how do you knw someone restricted calories? Why, they lost weight!

Bit circular, innit?

Chris said...

David,

It's not circular reasoning, it's definition from simple thermodynamics. Your body can only do so much with what you eat. You can either burn it, store it, or excrete it.

Why you burned or excreted what you ate instead of storing it are the interesting physiological questions that thermodynamics doesn't answer.

justdoinglife said...

http://www.drsharma.ca/obesity-reducing-liver-fat-does-diet-composition-matter.html - implies liver fat is first fat to go.

Lionel said...

I noticed that Chris Voight ate mainly precooked taters that had cooled down for a fair while before being eaten later. This would suggest a fair portion of resistant starch - good for his intestinal bacteria and no influence on his BG.

Despite the solo diet, it seems that it turned out to be a sort of VLC/HF thing with the bulk of calories coming from fat reserves.

wanderinghybrid said...

Would the same effects be achieved by eating corn and oats? And why wouldn't this apply to sugar, too?

wanderinghybrid said...

Peter, aside from the satiety index, wouldn't this theory apply to a diet of corn and oats, too? And why wouldn't this apply to sugar/glucose? Or is this potato-specific because of the role of resistant starch? Thanks!

Fred Hahn said...

"There is almost nothing published in the mainstream scientific literature about low-carbing. So it is necessary to rely on blogs etc to gain an insight."

Say what?

http://www.nmsociety.org/low-carb-research.html

Fred Hahn said...

Peter - Why would a fat free, all potato diet cause more fat loss than a VLCD of the same calories?

Peter said...

Fred, my current suspicion is that, with near zero (20g/d) fat except from lipolysis, that the only way to limit caloric ingress to an individual cell is by using glucose so induce insulin resistance. This looks to be the point of the mitochondrial glycerol 3 dehydrogenase shuttle. This puts glycerol 3 phosphate, a close derivative glycolysis, in to the electron transport chain at the waste of 300mV of redox potential and the lack of pumping of 4 protons across the inner mitochondrial membrane. It will also reduce the CoQ couple which is the normal physiological way to generate reverse electron flow through complex I which generates superoxide to resist the action of insulin and limit calorie ingress to match metabolic needs.

The main place with unusually high levels of mtG3Pdh is located (outside of beta cells) is brown adipose tissue of carb fed rodents.

I think a similar situation will apply to rodents on a high sucrose diet. They stay slim and don't become insulin resistant, just so long as calories from fat are under a few percent. Adding fat alters the control of insulin sensitivity at both mitochondrial and adipocyte levels.

Peter

Fred Hahn said...

Thanks Peter. Your explanation is a tad (or a couple of tads) over my head.

Are you just speculating here or are you offering up good science?

I think perhaps the reason is that you switch from one thing to the other and that switch is metabolically expensive - in the short term.

Peter said...

Fred, I'm speculating. I've not got any hard data on blood sugar levels, let alone blood insulin levels. As far as I'm aware there aren't any (but I don't follow this sort of information with any avidity). I think I did revisit this subject at some point and I do have a plan to go back again as more real data come to light (probably mtG3P related), especially at the mitochondrial level. I have no doubt the effect occurs and I remain interested in quite why, even if I have no interest in going there...

Peter