OK, what do I eat? It's been a long time since I posted anything about myself. Another hastily written post during Hazel's nap.
Breakfast is always the same. I melt about 100g of butter in a frying pan. I crack 11 eggs yolks in to this (I fry the whites later for the chickens!) and fry them until they hold their shape. I then pour 8 yolks for myself and Hazel, with all of the free butter, in to a bowl and mash them with a fork before stirring the mix in to an "egg soup". Hazel has a dollop, I have the rest. We like it quite solid. I finish any Hazel doesn't want, hopefully I get six yolks worth. Daniel likes his yolks just fried, he has the other three.
If I feel like it, I have a creamy cocoa, ie about 4g cocoa powder, 2ml honey, maybe somewhere between 30 and 60ml double cream. Usually a decaff coffee too. Sometimes with caffeine, though I tend to prefer my caffeine in the evenings.
Lunch on work days is portable stearic acid as 100g of Lindt 90% cocoa solids chocolate. Sometimes with 100g macadamias, sometimes not. Occasionally 300ml of soured cream along side some chocolate.
Supper is a meal. It varies a lot. If you scroll down the index to the set of posts starting with "Food" you get the idea of the sort of things I eat for a main meal. I have been known to eat green leaves with supper. I have been known to eat parsnip chips. I have been known to have gluten free home made cake for desert under a centimetre of butter or drowned in soured cream. If fat has been a little low with supper I might make ice cream with just a little added sugar. Or rhubarb baked in cream and flavoured with cinnamon. Or another creamy cocoa.
Alcohol, some. I like dry wine and gluten free beer. Never a huge amount.
I don't weigh any food nowadays (I went through the Fitday kick years ago), especially since the digital scales passed away. I weigh myself about once a year. My jeans are 28" waist, depending where I buy them.
There are oddities that need to be borne in mind, ie that I have never been overweight. I eat this way as a result of an accident at an anaesthesia meeting, chatting with a friend who had dropped from 18 stone to 12 stone on Atkins induction. I had just discovered Pubmed and devoured studies voraciously.
It didn't take long to realise that Kwasniewski's Optimal Diet was where I wanted to go. I don't eat enough offal and I don't make enough bone broths, but otherwise I keep fairly close. My biggest transgression is excess protein.
Quite why excess protein is bad is interesting. If you read the DNA chapter in Nick Lane's "Life Ascending" it brings home quite how closely integrated amino acid metabolism is to the TCA. It's way too complex to see how any given protein would interact, so aiming for high grade low quantity is how I work, when practical. If you eat more than you need it goes in to the TCA.
In my Fitday days I used to run at around 2000kcal/day for weight stability but I probably run a fair bit higher than than nowadays, most days. But no two days are the same and there is far too much to enjoy in life without agonising over +/- 5g of butter.
Is it worth it? Well, I sort of forget that eating this way is odd. You have to giggle at the nurses with their little tubs of salad and half an apple but they're just kiddies... But I went from being early middle aged to pretty much how I felt as a teenager, once I had adapted (full adaptation took me about 6 months). I don't feel I have changed much, beyond the needs of a second family, in the last 10 years healthwise. Beard is a little greyer.
I feel well. You sort of forget what it used to be like to need to eat NOW. And to fall asleep for three hours after a huge bowl of rice before being awake half the night. Anyone with a bad back will be very familiar with using one foot to pull your underwear up the other leg to where you can actually reach it without bending down. All gone, along with the little pot belly.
I have no expectation of living for ever. But I have no intention to going back to where I was at 40 years of age. Aging un-noticed would be nice. When you find something which works this well you don't throw it away.
Peter
Tuesday, May 21, 2013
Monday, May 20, 2013
A bit more on ketones and diabetic nephropathy
Just in haste, sorry for the missed typos! Liz sent me the full pdf of this paper:
Treatment of Diabetes and Diabetic Complications With a Ketogenic Diet
It's primarily a review, both of the work by Phinney and Westman and of the lab animal studies by the group producing the review.
Deranged glucose metabolism appears to be what causes the problems in diabetes, type 1 or 2. More on this when I get back to the chronic hyperglycaemia post. It's not forgotten.
Ketones, the metabolism of which remains normal, appear to be key in replacing abnormal glucose metabolism, more so than simply achieving normoglycaemia without ketosis.
Protein limits ketosis and the use of low carbohydrate diets with unrestricted protein intake may explain some of the failures to maintain the benefits of carbohydrate restriction. I have to say, Jimmy Moore comes to mind here. I like his success with ketosis.
It looks to be as easy to substantially reverse diabetic nephropathy in mice as it is to limit nephropathy progression in humans, but ketones are essential.
Mouse, human, diabetic nephropathy, reversal with ketosis. Shrug.
The take home message is very simple. If you have severe metabolic problems the answer is not simply carbohydrate restriction. It also involves protein limitation, to adequate but not gluconeogenic levels. Low carb, adequate protein, high fat. With the emphasis on the fat.
Taterism is fine for any Tato Head without metabolic problems. As everyone will eventually develop metabolic problems, so Taterism will eventually injure everyone. Some folks probably have dialysis blood on their hands already.
The high fat brigade are correct.
Peter
Treatment of Diabetes and Diabetic Complications With a Ketogenic Diet
It's primarily a review, both of the work by Phinney and Westman and of the lab animal studies by the group producing the review.
Deranged glucose metabolism appears to be what causes the problems in diabetes, type 1 or 2. More on this when I get back to the chronic hyperglycaemia post. It's not forgotten.
Ketones, the metabolism of which remains normal, appear to be key in replacing abnormal glucose metabolism, more so than simply achieving normoglycaemia without ketosis.
Protein limits ketosis and the use of low carbohydrate diets with unrestricted protein intake may explain some of the failures to maintain the benefits of carbohydrate restriction. I have to say, Jimmy Moore comes to mind here. I like his success with ketosis.
It looks to be as easy to substantially reverse diabetic nephropathy in mice as it is to limit nephropathy progression in humans, but ketones are essential.
Mouse, human, diabetic nephropathy, reversal with ketosis. Shrug.
The take home message is very simple. If you have severe metabolic problems the answer is not simply carbohydrate restriction. It also involves protein limitation, to adequate but not gluconeogenic levels. Low carb, adequate protein, high fat. With the emphasis on the fat.
Taterism is fine for any Tato Head without metabolic problems. As everyone will eventually develop metabolic problems, so Taterism will eventually injure everyone. Some folks probably have dialysis blood on their hands already.
The high fat brigade are correct.
Peter
Wednesday, May 15, 2013
A Peek at Paleo
I don't eat a paleo diet, I'm just a saturophile. If it's saturated fat and it happens to come from a neolithic block of butter, that's fine by me. But I hadn't realised going paleo could be actively worse for your health than eating some version of the SAD. You can download Eric Trexler's thesis from here. Catchy title is:
"Paleolithic Diet is Associated With Unfavorable Changes to Blood Lipids in Healthy Subjects"
Some people may have noticed that I have minimal interest in blood lipid levels. I know people angst about them, but I've yet to be convinced that they have anything to do with heart disease other than as a surrogate for how much sugar you eat.
The thesis reports pre and post diet lipids but only gives end-of-paleo-diet food breakdown, and only the fat/saturated fat at that. Go figure. Guess they forgot to ask what folks were eating to have better lipids than their study diet was going to produce! Perhaps they had a defective crystal ball.
I've always viewed HDL as a surrogate for saturated fat intake. The sub population with the best HDL on pre diet lifestyle (around 82mmol/l) dropped it to around 69mmol/l on paleo diet plus exercise and weight loss. My assumption is that these folks actually dropped their saturated fat intake or increased their PUFA intake by so much that even the exercise induced rise in HDL and weight loss induced rise in HDL couldn't offset the fall in HDL induced by the study diet. Impressive.
Triglyceridess rose non significantly. I view trigs as a surrogate for sugar intake. You have to guess how much SAD high fructose corn syrup was replaced by paleo fruit. Or whether fruit juice [Peter vomits quietly in the corner] was allowed. Well, the trigs went up (slightly), not down... Gathering was good that day, every day, for 10 weeks!
OK, so what sort of a paleo diet was this? Quote:
"Subjects were advised to increase their consumption of lean meat [Peter vomits quietly in the corner again], fish, eggs, nuts, fruit, and vegetables and were instructed to strictly avoid all grains, dairy products, and legumes."
Obviously spuds appear to have been on the menu in paleoland and animal fat is the devil incarnate!
What was their source material for these well thought out recommendations? They were based on Eaton and Konnor's 1985 paper:
"Paleolithic nutrition. A consideration of its nature and current implications"
You can't get at the full text or even an abstract on line. Luckily Anna, over at Lifextension, fills in the details for us. She pasted a copy of her information over on ItsTheWoo's blog here, explaining both where Eaton got the data and pointing out the 2000 correction he published, amending his paleo fat intake estimates (upwards of course). I get a faint impression that Anna may not be best impressed by Eaton's ideas. Or by Taterism in general. BTW, did anyone run through the list of references? Given a year or two I might try one day, but perhaps just sticking with simple saturophilia might be easier.
I rather like Anna's commentary. I like her suggestion that Eaton's ideas seem uncomfortably influenced by politically correct beliefs aligned with the AHA's diet advice. Reading Trexler's thesis I was also struck that it could easily have been written by an AHA cardiologist. The naked fear of LDL cholesterol shines through the whole text.
My take home message is that if you are going to align your paleolithic diet advice with the AHA, people are going to get hurt.
Peter
"Paleolithic Diet is Associated With Unfavorable Changes to Blood Lipids in Healthy Subjects"
Some people may have noticed that I have minimal interest in blood lipid levels. I know people angst about them, but I've yet to be convinced that they have anything to do with heart disease other than as a surrogate for how much sugar you eat.
The thesis reports pre and post diet lipids but only gives end-of-paleo-diet food breakdown, and only the fat/saturated fat at that. Go figure. Guess they forgot to ask what folks were eating to have better lipids than their study diet was going to produce! Perhaps they had a defective crystal ball.
I've always viewed HDL as a surrogate for saturated fat intake. The sub population with the best HDL on pre diet lifestyle (around 82mmol/l) dropped it to around 69mmol/l on paleo diet plus exercise and weight loss. My assumption is that these folks actually dropped their saturated fat intake or increased their PUFA intake by so much that even the exercise induced rise in HDL and weight loss induced rise in HDL couldn't offset the fall in HDL induced by the study diet. Impressive.
Triglyceridess rose non significantly. I view trigs as a surrogate for sugar intake. You have to guess how much SAD high fructose corn syrup was replaced by paleo fruit. Or whether fruit juice [Peter vomits quietly in the corner] was allowed. Well, the trigs went up (slightly), not down... Gathering was good that day, every day, for 10 weeks!
OK, so what sort of a paleo diet was this? Quote:
"Subjects were advised to increase their consumption of lean meat [Peter vomits quietly in the corner again], fish, eggs, nuts, fruit, and vegetables and were instructed to strictly avoid all grains, dairy products, and legumes."
Obviously spuds appear to have been on the menu in paleoland and animal fat is the devil incarnate!
What was their source material for these well thought out recommendations? They were based on Eaton and Konnor's 1985 paper:
"Paleolithic nutrition. A consideration of its nature and current implications"
You can't get at the full text or even an abstract on line. Luckily Anna, over at Lifextension, fills in the details for us. She pasted a copy of her information over on ItsTheWoo's blog here, explaining both where Eaton got the data and pointing out the 2000 correction he published, amending his paleo fat intake estimates (upwards of course). I get a faint impression that Anna may not be best impressed by Eaton's ideas. Or by Taterism in general. BTW, did anyone run through the list of references? Given a year or two I might try one day, but perhaps just sticking with simple saturophilia might be easier.
I rather like Anna's commentary. I like her suggestion that Eaton's ideas seem uncomfortably influenced by politically correct beliefs aligned with the AHA's diet advice. Reading Trexler's thesis I was also struck that it could easily have been written by an AHA cardiologist. The naked fear of LDL cholesterol shines through the whole text.
My take home message is that if you are going to align your paleolithic diet advice with the AHA, people are going to get hurt.
Peter
Sunday, April 28, 2013
Hyperglycaemia is bad
Hyperglycaemia does whatever you want it to. Want to show it increases glycolysis and/or oxidative phosphorylation? No problem. Want to show it decreases both? Equally no problem. Choose your tissue, choose your duration, choose your insulin level, choose your glucose level, choose your tissue culture medium before test, choose... With the correct combination you can show anything.
But certain patterns emerge from lots of papers. In the short term hyperglycaemia increases both glycolysis and oxidative phosphorylation. Acute hyperglycaemia in neurons induces an equally acute hyperpolarisation of the inner mitochondrial membrane (a pre requisite for reverse electron flow through complex I), followed by a burst of free radicals (from reverse electron transport in the face of a low NAD+/NADH ratio?), followed by a collapse of the inner mitochondrial membrane potential (from free radical induced loss of cytochrome c?), soon to be followed by apoptosis, as you might expect
These guys set out the events nicely but suggest the mechanism is unclear. I would be willing to bet on G-3-P dehydrogenase as driving reverse electron flow using the high membrane potential from glycolysis. It seems that, under "mitochondrial preparation" conditions, ignoring reverse electron flow, G-3-P dehydrogenase also spills a reasonable dose of free radicals not only inwards towards the matrix but also outwards to the inter membrane space, in roughly equal amounts. As does complex III of course, but complex III is not specifically driven by a short side branch of hyperglycaemia-induced hyperactive glycolysis. Goodness only knows if this happens in-vivo, but let's accept that it does. Cytochrome c is on the outer surface of the inner mitochondrial membrane and spilling free radicals outwards seems a good way to oxidise the cardiolipin anchors and release one of the most important pro apoptotic proteins we have, cytochrome c.
So acute hyperglycaemic injury, in a cell type where glucose entry is essentially concentration driven, is potentially apoptotic if the injury is severe enough. Lesser but sill significant injury may come from spills of superoxide from complex I on to the mitochondrial DNA, another potentially interesting effect. Research on G-3-P dehydrogenase is still in its infancy and there are no clear cut answer as to how important this scenario might be, but I rather like it. Is it true? Who knows. It's hard to tell.
Exactly how difficult it is to transfer information from "preparations" to any semblance of "in vivo" is reviewed by Martin Brand. I like this chap, he really looks at the limitations of how much we currently know (not much, it appears) plus he came up through Naked Mole Rat research, another positive. Here's his summary of where free radicals might be produced:
Outwards spillage, directly on to cytochrome c, from G-3-P dehydrogenase and complex III...
It's quite clear that hyperglycaemia is not invariably acutely fatal to all neurons on first exposure. It takes years of following the advice of the ADA and AHA to develop diabetic neuropathy or to kill off enough central neurons (around 70%) to get the clinical label of Alzheimers and, while recurrent hyperglycaemia might get us there directly, the indirect effects are much more interesting to a mitochondriac like myself.
Chronic hyperglycaemia is where we have a depressed inner mitochondrial membrane potential, reduced glycolysis and electron transport with subsequent failure to generate superoxide.
Badness too.
Peter
But certain patterns emerge from lots of papers. In the short term hyperglycaemia increases both glycolysis and oxidative phosphorylation. Acute hyperglycaemia in neurons induces an equally acute hyperpolarisation of the inner mitochondrial membrane (a pre requisite for reverse electron flow through complex I), followed by a burst of free radicals (from reverse electron transport in the face of a low NAD+/NADH ratio?), followed by a collapse of the inner mitochondrial membrane potential (from free radical induced loss of cytochrome c?), soon to be followed by apoptosis, as you might expect
These guys set out the events nicely but suggest the mechanism is unclear. I would be willing to bet on G-3-P dehydrogenase as driving reverse electron flow using the high membrane potential from glycolysis. It seems that, under "mitochondrial preparation" conditions, ignoring reverse electron flow, G-3-P dehydrogenase also spills a reasonable dose of free radicals not only inwards towards the matrix but also outwards to the inter membrane space, in roughly equal amounts. As does complex III of course, but complex III is not specifically driven by a short side branch of hyperglycaemia-induced hyperactive glycolysis. Goodness only knows if this happens in-vivo, but let's accept that it does. Cytochrome c is on the outer surface of the inner mitochondrial membrane and spilling free radicals outwards seems a good way to oxidise the cardiolipin anchors and release one of the most important pro apoptotic proteins we have, cytochrome c.
So acute hyperglycaemic injury, in a cell type where glucose entry is essentially concentration driven, is potentially apoptotic if the injury is severe enough. Lesser but sill significant injury may come from spills of superoxide from complex I on to the mitochondrial DNA, another potentially interesting effect. Research on G-3-P dehydrogenase is still in its infancy and there are no clear cut answer as to how important this scenario might be, but I rather like it. Is it true? Who knows. It's hard to tell.
Exactly how difficult it is to transfer information from "preparations" to any semblance of "in vivo" is reviewed by Martin Brand. I like this chap, he really looks at the limitations of how much we currently know (not much, it appears) plus he came up through Naked Mole Rat research, another positive. Here's his summary of where free radicals might be produced:
Outwards spillage, directly on to cytochrome c, from G-3-P dehydrogenase and complex III...
It's quite clear that hyperglycaemia is not invariably acutely fatal to all neurons on first exposure. It takes years of following the advice of the ADA and AHA to develop diabetic neuropathy or to kill off enough central neurons (around 70%) to get the clinical label of Alzheimers and, while recurrent hyperglycaemia might get us there directly, the indirect effects are much more interesting to a mitochondriac like myself.
Chronic hyperglycaemia is where we have a depressed inner mitochondrial membrane potential, reduced glycolysis and electron transport with subsequent failure to generate superoxide.
Badness too.
Peter
Wednesday, April 24, 2013
Axen and Axen (4) Ketogenic insulin resistance. It's all over now...
I have so many posts I want to get finished, all of which are inter-related and all of which need waaaaaay too much work, that I thought I would just throw this one out in the interim. I began with this paper which came as a pdf from Liz. While I was getting the pubmed link to it I noticed the same group had another rather similar paper out which was equally interesting and then the third link down the page was an accidental find which is this one, subject of this post.
I don't know if it's worth going through the figures individually, they are very similar to those from Axen and Axen which produced a series of posts a few years ago, except that the feature of COMPLETE reversal of insulin resistance is, here, presented right up front in Figure 6 and in the abstract too:
That figure for insulin looks a little dubious at 120 minutes but I'll let that go, I guess p was still > than 0.05... Pretty close to full reversal.
It's quite hard to know exactly how much this group understand about their results. They give roughly equal weight to the adverse (sic) effects of a ketogenic diet as they do to the fact it is reversible within a week (or less, they only checked at a week) of re-introducing carbohydrate.
What they seem to lack is the concept that rats fed a very restricted carbohydrate diet MUST be insulin resistant to survive, as happens in starvation. But maybe they are creeping towards some sort of understanding. It's about time. Good.
When people cite Axen and Axen to prove ketogenic diets are going to make you diabetic (there are folks who believe this, or at least wish you to believe it!) you have an answer in Kinzig et al 2010.
BTW, the links which led me here relate to using ketogenic diets to control both pain and inflammation. This is a potentially very useful tool but the beneficial effect does appear to be as rapidly reversible as the physiological insulin resistance... Ketogenic diets are a fix, not a cure (in the short term anyway). But inflammation appears to be a feature of ageing, long term, and if KDs work in "ageing inflammation" all we have to decide is the age at which we should all start on a KD. Unless someone has a method of stopping the ageing process of course....
Peter
I don't know if it's worth going through the figures individually, they are very similar to those from Axen and Axen which produced a series of posts a few years ago, except that the feature of COMPLETE reversal of insulin resistance is, here, presented right up front in Figure 6 and in the abstract too:
That figure for insulin looks a little dubious at 120 minutes but I'll let that go, I guess p was still > than 0.05... Pretty close to full reversal.
It's quite hard to know exactly how much this group understand about their results. They give roughly equal weight to the adverse (sic) effects of a ketogenic diet as they do to the fact it is reversible within a week (or less, they only checked at a week) of re-introducing carbohydrate.
What they seem to lack is the concept that rats fed a very restricted carbohydrate diet MUST be insulin resistant to survive, as happens in starvation. But maybe they are creeping towards some sort of understanding. It's about time. Good.
When people cite Axen and Axen to prove ketogenic diets are going to make you diabetic (there are folks who believe this, or at least wish you to believe it!) you have an answer in Kinzig et al 2010.
BTW, the links which led me here relate to using ketogenic diets to control both pain and inflammation. This is a potentially very useful tool but the beneficial effect does appear to be as rapidly reversible as the physiological insulin resistance... Ketogenic diets are a fix, not a cure (in the short term anyway). But inflammation appears to be a feature of ageing, long term, and if KDs work in "ageing inflammation" all we have to decide is the age at which we should all start on a KD. Unless someone has a method of stopping the ageing process of course....
Peter
Sunday, March 31, 2013
TCA rap
From Bert. Not advocating carb consumption but I can see that electron transferring flavoprotein dehydrogenase would need some serious effort to rap... So enjoy glycolysis and the TCA:
http://www.youtube.com/watch?v=aMBIs_Iw0kE&feature=player_embedded
Click-able, sorted!
Ta Bert. I enjoyed.
Peter
Now if I can get Ryan started on beta oxidation. Hmmmm....
http://www.youtube.com/watch?v=aMBIs_Iw0kE&feature=player_embedded
Click-able, sorted!
Ta Bert. I enjoyed.
Peter
Now if I can get Ryan started on beta oxidation. Hmmmm....
Wednesday, March 20, 2013
Sta'ins, CoQ, diabetes and Dr Andreas Eenfeldt's link
I'm not very conscientious about reading many blogs as I don't really have time to look after my own blog properly, but I will occasionally flick through the links from Stan's site and I felt that Dr Andreas Eenfeldt's link to the official Swedish data sheet for simvastatin was rather excellent. Via Google translation:
"Diabetes is a possible side effect. This is more likely if you have high blood sugar and high blood fat levels, are overweight and have high blood pressure. Your doctor will monitor you while you are taking this medicine."
Statins deplete CoQ. This means that for every electron carried from any input, NADH or FADH2, down the ETC there will be less CoQ available in the redox couple and the CoQH2 levels will be relatively high. An highly reduced CoQ couple (ie low CoQ per unit CoQH2) will drive reverse electron flow through complex I and generate superoxide. Insulin resistance. Diabetes.
I suspect that EVERYONE on a statin will step their insulin resistance up by an amount proportional to the CoQ depletion. Everyone. Just a few will cross the arbitrary boundaries between "normality", "impaired glucose tolerance" and "diabetes".
Hyperglycaemia doesn't care about labels or boundaries. You get it, you suffer.
Obviously this rather nasty side effect can be COMPLETELY avoided by putting the statin script in the bin.
If you are going to take simvastatin anyway then some coenzyme Q10 might ameliorate some of the damage you have chosen to do to yourself.
Peter
"Diabetes is a possible side effect. This is more likely if you have high blood sugar and high blood fat levels, are overweight and have high blood pressure. Your doctor will monitor you while you are taking this medicine."
Statins deplete CoQ. This means that for every electron carried from any input, NADH or FADH2, down the ETC there will be less CoQ available in the redox couple and the CoQH2 levels will be relatively high. An highly reduced CoQ couple (ie low CoQ per unit CoQH2) will drive reverse electron flow through complex I and generate superoxide. Insulin resistance. Diabetes.
I suspect that EVERYONE on a statin will step their insulin resistance up by an amount proportional to the CoQ depletion. Everyone. Just a few will cross the arbitrary boundaries between "normality", "impaired glucose tolerance" and "diabetes".
Hyperglycaemia doesn't care about labels or boundaries. You get it, you suffer.
Obviously this rather nasty side effect can be COMPLETELY avoided by putting the statin script in the bin.
If you are going to take simvastatin anyway then some coenzyme Q10 might ameliorate some of the damage you have chosen to do to yourself.
Peter
Let them eat fat: Ron Rosenbaum
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