I was looking around pubmed for the effects of fasting on homocysteine concentration. I'd seen a reference which claimed that HCy rose progressively with extended fasting beyond 12h, making a 12h fast the ideal time to measure. For some reason (probably to do with having 10 windows open in two web browsers) I lost it. While pubmeding to relocate it (and failing) I tripped over this rather nice paper on starvation.
It looks very like the second author is the chap in the box and this news report gives an idea of how the first and second authors interacted. It also explains why there were no "pre box" blood values for Blaine!
The paper has a number of gem lines in it. First was that, whatever homocysteine levels do in acute starvation, by 44 days of water fasting they are normal. Normal does not appear to be zero.
Next was the acute hypophosphataemia induced by re feeding. This kicked in by the end of day one. By this time Blaine had been given three cartons of a commercial liquid "food" including a total of just under 40 grams of sucrose. I wouldn't like to mention fructose as a trigger for hypophosphataemia, but it does get an honourable mention here and we've all listened to Lustig discuss fructose the net. Glucose also requires its place in the syndrome too. Dr Powel-Tuck seems to feel that this hypophosphataemia is to do with the energy intake. I suppose this is true if you are stuck in the time warp that energy=glucose, before anyone realised that free fatty acids could be used for energy. As far as I am aware no one has ever precipitated acute hypophosphataemia with an Intralipid infusion, disgusting though the thought of soya bean oil intravenously might be.
You just have to wonder what a supply of calories as fat and protein might have done by perhaps using, gasp, cheese. High in phosphate anyway.... Then add that essential nutrient, sucrose, later. In fact on day five Blaine took himself to the hospital canteen and had fish and chips against doctors orders. Marked fluid retention was the end result but nothing worse.
The fluid retention is very interesting. This is what they noted:
"A raised haematocrit on admission (reflecting haemoconcentration) changed to progressively lower values, despite cautious refeeding, and total avoidance of saline or additional salt during the hospital stay (Table 3). Albumin concentration on admission to hospital was slightly raised and declined gradually over 5 days probably due to plasma expansion. By day 10, 5 days after he left hospital on a free diet, he demonstrated mild pitting oedema."
and here is my favourite
"As refeeding raises plasma insulin, [then] potassium, phosphate and magnesium are driven intracellularly, and sodium extracellularly, expanding circulating volume and causing haemodilution, as indicated in D B by changes in his haematocrit and albumin levels."
It doesn't mention that insulin also causes renal sodium retention, but it does. I rather like this paper, I've not worked through the free full text but I note from the abstract that an insulin infusion with normoglycaemia causes sodium retention even in control rats, never mind spontaneously hypertensive rats. You learn so much from the control groups, even if thay are only rats. And we all thought that folks with hypertension while hyperinsulinaemic on a high carbohydrate diet were born with an in-built frusemide deficiency! Sounds more like Fanta poisoning to me. So, for Blaine, you have to ask whether the immediate return to a "balanced" diet, rich in nourishing sucrose and insulin spiking starch, is what precipitated the fluid retention and whether a more lipid based diet with gradual transition at real food for a few days before diving in to the "sugar as the main course with spuds for dessert" regime might have been less problematic.
I can't imagine anyone testing this idea, so perhaps it's a good job we have phosphate infusions available in UK teaching hospitals to pull post-starvation patients back from the brink of iatrogenic sugar poisoning during refeeding!
Peter
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You know, when I first heard of refeeding syndrome, I also had the thought that it could be avoided or reduced by refeeding starving patients on fats with minimal protein and carb. Seeing as fatty acids are the least insulinogenic food (assuming the diet is very low in carb and low in protein), and seeing as refeeding syndrome is essentially caused by a form of insulin shock on electrolytes... then, you really want to make sure a starving person begins refeeding with food most similar to the food their metabolism already has been using : fat.
I wonder if anyone has even attempted to use a high fat diet low carb / protein for refeeding. I suspect it would be much safer.
First increase the amounts of fat calories to SLOWLY bring up insulin, then you can add in more calories from protein and carb which cause much more significant increases in insulin.
It is the increase in insulin that causes refeeding syndrome. It only stands to reason the diet should be constructed in a way as to avoid insulin release as much as possible.
Maybe even using octreotide might help, as it is my understanding octreotide prevents release of insulin after eating.
This is what happens when nutritionists outline therapies. ... things get real illogical and unscientific. You just KNOW it's nutritionists handling the refeeding process with physicians only being instrumental in the physical stability parts.
I would disagree to refeed on cheese... a lot of evidence suggests cheese and all dairy can be pretty insulinogenic due to the casein proteins. You want to avoid protein as well as carb since protein is very insulinogenic, particularly casein.
I am shocked by the # of low carbers who do not know insulin causes hypertension and the retention of minerals. It's a lot. They are always watching sodium when they need to monitor foods which prompt insulin release if they want to stop bloating.
Peter, or any of your knowledgeable readers:
what is the mechanism by which glycogen is replenished in the liver/muscles on LC?
if we store about 200g in the liver and about 200g in muscles, what happens when those get used and you only bring in 100g carbs / day? you're always in a chronic deficit? or does the liver manufacture reserves from the fat?
@ David:
Liver depleted of glycogen when there's less than 100g of it? lol
According to the books I read, liver can store only around 75 g of glycogen. And, since liver can produce daily up to 250g of glucose (from dietary sugars, dietary proteins, excesses and remnants from body's amino pool, dietary or in-body glyserols left over from fat transport...) there is plenty of material to keep the liver glycogen storages non-empty, i.e. non-depleted.
To fill liver glycogen storage up to the brim means problems in the next meal. So, in order not to panic, liver starts changing excess glycogen into fat well before that. Which one would you prefer: fatty liver fat or the triglyserides which show up as elevated trigs in your fasting lipid profile? I prefer LCHF, since then this problem will not even occur.
Regards,
LeenaS
It's worth noting David Blaine performed this stunt in the UK which was and still is a heavily "low-fat" orientated nation.
I found an interesting study recently also that shows although the insulinogenic spike of protein is much lower than that of carbs, protein kept insulin elevated for much longer interval, possibly leading to a higher AUC although I cant be sure since you have to pay for the full article.
Protein also kept ghrelin supressed for the longest, fasting ghrelin and obesity are inversely correlated.
http://www.ncbi.nlm.nih.gov/pubmed/16508254
This study was good evidence for me that carbs can be handled reasonably well by the body provided they are ingested only once per day.I.E. Intermittent Fasting.
Although I feel a ketogenic diet is the healthiest way to go, (eggs cream and butter your favourite peter :) ), I think the problem with carbs start with multiple ingestion windows thoughout the day....
Toast, Orange Juice, Cereal at 8:30am, Sandwhich's, Crisps at 1:30pm, Then Potato's, Chips, Pasta at 6:30pm. You know, the 3 meals a day bullshit.
Kindke wrote: "Although I feel a ketogenic diet is the healthiest way to go, (eggs cream and butter your favourite peter :) ), I think the problem with carbs start with multiple ingestion windows thoughout the day...."
I totally agree with you! See also this:
Snacking and glucose/ketogenic cycling
A few years ago my pet cat ran away shortly after I moved house. He returned 8 weeks later having lost about half his body weight. Because cats don't read textbooks he simply acted on instinct and ate every 2-3 hours. Within four weeks he had regained the 3kg of weight loss and had made an almost total recovery.
Wow, not only does David Blaine do all those stunts, including prolonged fasting, but he also publishes too!
:)
Here are a few posts on glycogen depletion and replenishment:
http://healthcorrelator.blogspot.com/2010/06/fructose-in-fruits-is-good-for-you.html
http://healthcorrelator.blogspot.com/2010/05/growth-hormone-may-rise-300-percent.html
The first link above makes a point that Peter may not agree with - fructose in fruits may be good for you, especially if you are low in glycogen.
As far as glycogen storage, the numbers are more like 100 g in the liver, and 500 g in muscle.
Muscle glycogen use is very localized, so the 500 g is not a pool that is available to regulate blood sugar.
Hi Kindke. The insulin AUC for cheese is much lower than for white bread, even on a gram-adjusted basis:
http://healthcorrelator.blogspot.com/2010/04/insulin-responses-to-foods-rich-in.html
Opposing effects of dietary sugar and saturated fat on cardiovascular risk factors and glucose metabolism in mitochondrially impaired mice
I wonder how natural ending a periods of fasting with carbs is; European Ice Age hunters would be going hungry at times of the year when carbs (ie plant foods) were not available.
(Review article) How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis)
Kindke,
I agree. HGs typically only eat over a 3-6 hour period in the late afternoon/early evening. In effect they fast around 18 hours/day. This avoids insulin spikes. I do likewise.
"You just have to wonder what a supply of calories as fat and protein might have done..."
That would surely ease the hormonal shifts and the transition from (endogenous) fat/protein metabolism by refeeding. Perhaps egg and egg yolk may also work besides cheese?
I wonder if the patient's previous hormonal setpoints (due to his prior dietary habits) should be considered as well. If your pancreatic beta-cells are accustomed to copious and rapid production of insulin you may be more susceptible.
It's good to see you posting again (welcome back, Peter) and DB sacrificing his body (partially) for science this time.
John
this is amazing....for a 'study' i refed myself on a high fat diet... a lot of this makes sense to me now i dont knwo how i missed it before
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