Wednesday, June 13, 2012

Insulin, the Un-dead and coffin nails

Things keep getting in the way of the next post, which is roughed out but needs tidying. I've also been meaning to post on the Somogyi overswing effect in diabetes treatment for some time, so here is a minor diversion down that route, mostly because it's very illuminating.

The Somogyi effect is quite common in those unstable diabetic dogs which tend to get shunted in my direction at work. Any clinician will recognise the effect. A dog is given 8iu of lente insulin at 7am with a meal of utter crap (ultra low fat Chappie usually). Blood glucose spikes to 22mmol/l by 9am from the carb load then falls progressively until about mid day, as the slow onset insulin struggles with the hyperglycaemia. It looks like there is a nadir at about 6mmol/l around mid day. The 1pm reading is unexpectedly high at 30mmol/l. No food, no behavioural signs. Just sudden hyperglycaemia. The Somogyi overswing. This fades slowly to around 15mmol/l by the next meal time at 7pm. The cycle repeats.

Management (if you can't change anything else) is to reduce the dose rate of insulin, which stops that sudden surge in blood glucose at 1pm. Somogyi attributed the effect to a reflex release of glucose from the liver to prevent catastrophic hypoglycaemia in response to insulin overdose. Most clinicians seem to still think in these terms.

Logical but incorrect. The advent of continuous glucose meters has pretty well disposed of the "hidden hypo" explanation and people are now looking at the effects of hyperinsulinaemia per se. The sudden rise in blood glucose appears to be associated with progressively rising or even peak levels of insulin in the blood.

Let's have a think about what is happening. Under insulin deficiency conditions glucose can still be used as a fuel, in a somewhat unregulated manner, using concentration driven supply through GLUT1, independent of insulin. Hyperglycaemia is essential for this. It's not good. The poorly regulated glucose supply generates free radicals in the electron transport chain. Superoxide is the main one and this appears to be the key to causing insulin resistance. Hyperglycaemia causes insulin resistance. This is not controversial, as far as I am aware.

As the insulin kicks in we have a period where glucose levels are falling so GLUT1 transport is decreasing and insulin regulated GLUT4 transport is increasing. Initially excess glucose above cellular needs diverts to glycogen and the respiratory chain is kept happy by insulin. As insulin levels continue to rise above physiological needs we end up with a situation where insulin is putting a ton of GLUT4s out, far more than are needed. This happens because we have inadvertently injected a supraphysiological dose of insulin.

All those excess GLUT4s allow glucose molecules to pour in to the cells. You might as well have hyperglycaemia and GLUT1 mediated oversupply, as far as the respiratory chain is concerned. Glucose in excess of the cell needs generates superoxide. Superoxide triggers, as an antioxidant defence mechanism, insulin resistance. With thanks to Dr Guyenet. Again. It is difficult to emphasise how good this paper is.

Somogyi overswing is likely to be caused by acute onset insulin resistance occurring as a direct result of excess glucose uptake in to cells due to supraphysiological insulin concentrations.

The temporal association with hypoglycaemia, which misled Somogyi, comes from the time course of switching sources of glucose oversupply. The hypoglycaemia is not causative, it is just common for it to occur at around the same time that insulin/GLUT4s oversupply substrate to the mitochondria and they say no to it, using insulin resistance.

Let's summarise. This is very, very important:

Excess insulin causes insulin resistance

End summary.

This is just day to day internal medicine. You have to pay the mortgage somehow.

If anyone is interested there is a rather nice discussion paper here, it's pay per view and doesn't say much more than is in the abstract but it has a nice set of references. I have access to a great Athens account. All the comments on insulinomas ring so true to clinical life too.

It's also interesting to go back to the controversies around the Somogyi effect, you can read Somogyi's ideas here and the continuous glucose monitoring evidence here. All very fascinating stuff (well it is to me!) but what does it have to do with shooting fish in a barrel?

Question: Who are the Un-dead?

Which can be rephrased as: Can we control the Somogyi effect?

If we take the average bodybuilder from a few years ago and watch him self-inject with insulin for its anabolic effects and then forget to eat the carb load needed to balance it, we can see the acute effects of insulin overdose. Insulin rises very rapidly from the regular insulin used and every GLUT4 receptor in his body pops on to every cell surface which uses them. There is a free fall of glucose from plasma in to the cells, blood glucose plummets and the chap ends up in A&E or, quite possibly, in a mortuary. There is no time for the massive cellular caloric overload from over-translocation of GLUT4s to generate enough insulin resistance to stop the hypoglycaemia. Glucose pours out of the bloodstream until it drops to levels low enough to kill the brain. Sad but true. Somogyi effect is too late, too little. Insulin overdosed bodybuilders are not the Un-dead.

So who really are the Un-dead?

What if you give insulin as a constant rate infusion, initially at a low rate and gradually crank it up?

Think it through. Progressively increasing insulin levels allow progressively greater amounts of glucose in to cells. If the cellular glucose supply is greater than cellular needs there is increased generation of superoxide by the respiratory chain which signals the cell to become resistant to insulin. A balance is achieved. Increase the insulin CRI, overcome the insulin resistance, generate more superoxide, generate greater insulin resistance, achieve a balance. Do it again. And again. More. Again. How high can you get plasma insulin by playing this sort of game? Here's the table we need:

Okay, they stopped at a total of 6iu/24h/per rat. They could possibly have gone higher but hell, we have here a set of rats with a mean insulin level of 588.9microIU/ml. No, that is not a typo. The SEM was 89.7. Anyone like to guess how high the highest insulin level measured was? Quite high perhaps?

These are the Un-dead. They walk around, without any genetic modification, with an insulin level which, if achieved acutely, would have put them rapidly in to a clinical waste bag. They are very, very, very, (repeat ad nauseam) insulin resistant, otherwise they would look like the bodybuilder in the mortuary.

WARNING: There is a black box paradox warning about the paper providing Table 1. I'll stick an addendum on the end of the post.

Soooooooo. They are, undoubtedly, hyperinsulinaemic. Are they fat? Of course not. Why should they be fat? They are the Un-dead. If they were remotely sensitive to insulin they would be not be the Un-dead, quite the contrary. But insulin induced insulin resistance does not spare adipocytes. These have mitochondria and generate superoxide. They too will ignore insulin, to a level determined by their mitochondrial superoxide production.

Here's a bit of an aside: The process is physiological. It involves a careful titration of cellular insulin resistance to the cellular energy needs. This is no blanket insulin blocking drug. The responsiveness to insulin is carefully adjusted to just allow enough glucose in to cells to meet their needs. This applies to adipocytes as well as well as to muscle cells. With the number of GLUT4s being translocated by the residual insulin sensitivity, in an environment of 588microIU/ml of insulin, you don't need much of a blood glucose level to supply glucose needs. Table 1 suggests the body settles to a plasma glucose of about 71mg/dl, as opposed to 148mg/dl in the control rats. Metabolism is still largely glucose based, with some responsiveness to insulin preserved despite the need for resistance to survive at 588microIU/ml. Transplanting tissues to a petri-dish allows you to pick up this responsiveness. Free fatty acid release from adipocytes is not significantly inhibited because the adipocytes are insulin resistant to a level where they maintain normal function. Weight gain is similar to that of control rats.

And another BTW. The process is cellular. Bugger the hypothalamus.

A nail in someone's coffin?

Apparently these rats are a nail in the coffin of the insulin hypothesis of obesity.

The actual coffin nail [nb if the link comes up with a failed log-in just refresh the page] is a pay per view article in a journal not covered by Pubmed and I'm unwilling to shell out $40 for it. Perhaps I could ask The Good Doctor for a copy. Fortunately the information on CRI rodent models is freely available in the paper which provided Table 1 above. What is crashingly obvious is the utter lack of understanding of insulin induced insulin resistance by people who are fixated on insulin as a satiety hormone.

This might have been acceptable in 1980 when the physiology of insulin resistance was completely unknown. But to see this explanation promoted by the same obesity researcher who provides us with the concept of insulin resistance as a cellular antioxidant defence mechanism, mediated through superoxide, is utterly depressing. We are, after all, talking about a complete failure to understand the basic physiology of insulin resistance, with the key paper sitting as a free download from Pubmed.

Does the Good Doctor not understand his own citations or is he stuck with terminal cognitive dissonance?

Or perhaps he's just utterly confused.

I feel the coffin nail is misplaced.


OK the paradox: In the paper providing Table 1 the rats have a blood insulin level of 588microIU/ml with physiological blood glucose levels. BUT isolated muscle and fat cells taken from these rats are highly insulin sensitive, more so than those from the control rats. How is this possible? I can imagine the Good Doctor or some other idiot shouting that the rats aren't insulin resistant at all, because the paper clearly shows their tissues are extra insulin sensitive, ergo the insulin hypothesis of obesity is wrong. Peter is misquoting a paper, you know what I'm like!!!! Gotta read all those papers cited, the Good Doctor knows how few people follow the links.

But the rats are definitely Un-dead.

If you culture adipocytes at consistently supra maximal insulin levels they behave exactly as the whole rats do. So if you pull out a muscle or fat cell from an Un-dead rat, having made it an un-Un-dead rat by decapitation, how long will the insulin resistance last? This is probably determined by the elimination half life of superoxide. Which is, err, not very long... Actually, it's probably determined by the cellular redox state providing the superoxide, which should last at least a few seconds after decapitation.


Puddleg said...

Here's the mechanism for the hyperglycaemia; superoxide decreases phosphorylation of the Fox01 transcription factor. This is the same transcription factor that fructose stimulates (, but in the ROS case Fox01 production is normal, but diminished phosphorylation means that Fox01 is retained in the nucleus for longer than otherwise.
(so the net effect is much the same)
Here's a model where HCV core protein has this effect via ROS (by inhibiting mitochondrial enzyme complex 1)

Interestingly, Fox01 is inhibited by PPAR-alpha in the fructose model: what elevates PPAR-alpha? Ketogenic diets, also, calorie restriction.

Scott Russell said...

Perhaps the insulin hypothesis, now undead, has been feeding on the brains of obesity researchers?

Dr. B G said...
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Dr. B G said...
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zazendo said...

Peter you really need to get a Facebook or at least a button so I can repost all this stuff. Your blog is pure gold.

psychic24 said...


Morning blood glucose is high, not low, due to the somogyi effect. That would suggest t2d is actually overdiagnosed, no?

blogblog said...

An interesting paper:

Cell Metabolism, Volume 15, Issue 6, 848-860, 17 May 2012

Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet


While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a nonpharmacological strategy against obesity and associated diseases.

This is almost certainly why the Kitivans are healthy on 80% carbs. Kitivans normally eat all their food in one large meal each evening. [On Kitiva it is taboo to eat during the day unless you are doing strenuous work.]

blogblog said...

Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet

Cell Metabolism, Volume 15, Issue 6, 848-860, 17 May 2012

Probably why the Kitivans are so healthy on a high carb diet - they only eat one large meal each day.

Melchior Meijer said...

Peter, thanks for sharing these insights! It really explains a lot. I'm afraid I'm slowly coming full circle round. Again.

Dr. B G said...

scratch!! (thanks pyschic 24)

I meant the rebound hypoglycemia in the AM...and yo-yo BG of those with reactive hypoglycemia!

*chuckle chuckle*

You made my day... OK. MONTH!

The Somoygi effect (and dawn phenom in untreated folks) reminds me of insulin overtreatment which leads to low AM blood glucoses (BG) (or how rebound, counter-regulatory, high insulin leads to 'low' BGs in untreated folks).

This is also why modern medicine misdiagnoses and underestimates the current epidemic of pre-diabetes/T2DM in children and obese Americans. The perceived 'low' BG morning swing caused by dinners full of healthywholediseasecarbs is utterly miscontrued when fasting BG 'screenings' are ordered and measured. Sure. It matches and goes well with the 'low' LDL cholesterol too...

Wide spread small and dense cognitive dissonance...

Asclepius said...

"Let's summarise. This is very, very important:

Excess insulin causes insulin resistance

End summary."


Dr. B G said...


I think T2DM is vastly underdiagnosed... OGTT, oral glucose tolerance test, is the gold standard but requires too much time and labor. It is reserved for gestational diagnoses since the ramifications effect both baby and mom for mortality and complications. T2DM (which is Metabolic Syndrome) should be more vigorously screened because it is associated with a 2-10x increase in cardiac mortality, erectile dysfunction, hormone havoc, and basic life suckiness.

Thanks for the catch!!

Dr. B G said...

(add'l T2DM and severe insulin resistance affects skinny people too, particularly recovering or current vegan/vegetarians -- it's not just an obesity disease)

FrankG said...

It has been my understanding, through all these recent years that: IR results, at least in large part, from chronically raised insulin. It makes sense that a constant high level would lead to a down-regulation of receptors -- much like how folks living alongside a busy road no longer notice all the traffic noise -- but of course this parsimonious explanation would fall on deaf ears for someone who is building and safeguarding a professional career by down-playing the role of insulin and sugar.

Anonymous said...

I love this back and forth, very interesting.

Nigel Kinbrum said...

Hold it right there...again!

Insulin increases the rate at which glucose (& AAs) enters cells.

Therefore, more insulin = cells fill (with glycogen) faster.

Cells that are full (of glycogen) = insulin resistant cells.

As cells are emptied (of glycogen) by doing resistance training with weights, they become increasingly insulin sensitive.

Being sedentary does not empty cells (of glycogen).

Therefore, it's not insulin that causes insulin resistance.

It's a failure to empty cells (of glycogen) faster than they're being filled that causes insulin resistance.

Anonymous said...

I'm hoping you (or another smart commenter) can explain one part for me.

The rats had very high insulin and yet weren't overweight. Evidently some took this as disproof of the insulin hypothesis of obesity.

You then point to "Chronic insulin infusion suppresses food ingestion and body weight gain in Rats" as the real disproof of the insulin hypothesis of obesity. Or at least I think that's what you meant, though when I read the abstract they note that insulin promotes weight gain in diabetics (which matches my experiences).

I can understand from the first part of your post how insulin caused insulin resistance. What I'm confused about is are you saying/agreeing that insulin resistance doesn't cause weight gain? I guess I'm missing your point about IR and weight gain and would really like to understand.

I was happily following you at first then got terribly lost. :)

ItsTheWooo said...

Right on! Not exercising enough and enjoying lying on your butt causes obesity! It's not insulin, it's the not moving and lying like a pig in shit. Insulin is a good thing which decreases appetite and promotes amino acid uptake storage, it only causes obesity if you are driven to eat too much and move too little, which is a random personality driven phenomenon. People eat too much and move too little when they give into impulses and eat very "moreish" food. They move too little when they are lazy by personality.

It's also true that the heart muscle failing to circulate blood is the cause of heart attacks. These people who persist in taking plavix/blood thinners and omega 3 fatty acids to prevent heart attacks are total moron idiots. Just make your lazy heart muscle circulate blood all the time and you won't have heart attacks. Duh, that simple. If you have a heart attack its probably because your heart muscle is content in sloth and decided to stop properly working, perhaps it enjoys inactivity as so many fat mildly diabetic persons clearly do.
People who don't have heart attacks never require a blood thinning medication and their heart works all the time without succumbing to clots and tissue death, so this is all the evidence I need that blood thinning medication is totally useless and it is just an excuse to explain why your cardiovascular system SO LAYZEE.

praguestepchild said...

Nigel writes:

"As cells are emptied (of glycogen) by doing resistance training with weights, they become increasingly insulin sensitive.

Being sedentary does not empty cells (of glycogen)."

It's times like these that I think you are trying to be intellectually dishonest.

High intensity exercise only drains *muscle* cells of glycogen, and only the muscle cells that are being used. In order to drain most of the glycogen out of the muscles one needs to lift to failure, in which case one would need to several days to recuperate.

You honestly think insulin resistance is the result of everyone not lifting like a bodybuilder?

Of course exercise does have positive metabolic effects but this is ridiculous.

Jorge said...

"I stumbled on to nutrition completely by accident. Once you have been taught to think, it's hard to stop." -Peter

And it shows. Thank you for your work.

Nigel Kinbrum said...

@Sean: Fat cells don't contain glycogen, so naturally I was referring to muscle cells. Muscle cells don't need to be almost completely emptied to restore their insulin sensitivity. They just need to be *not* *full*. This doesn't take much intense activity.

Also, fat stored inside a fat cell isn't used up unless there's physical activity by *muscles*. IR in fat cells is also caused by a failure to empty them faster than they are filled, long-term.

Therefore, IR in both muscle & fat cells is the result of consistently eating too much and moving too little *for* *whatever* *reason*.

Trust Woo to chime in with her usual emotional "Gluttony & Sloth" nonsense + some new nonsense about heart attacks.

FrankG said...

So the only "cells" in our body that use and store energy are Muscles and Fat? Is that right?

And "As cells are emptied (of glycogen) by doing resistance training with weights, they become increasingly insulin sensitive." has now become...Muscle cells don't need to be almost completely emptied to restore their insulin sensitivity. They just need to be *not* *full*. This doesn't take much intense activity.

I agree with Sean that your are purposefully "trying to be intellectually dishonest" ...either that or you consider everyone else here an idiot who cannot think for themselves.

FrankG said...

What about IR in the Liver or the Brain? I like to think that I "exercise" at least one of those, quite often each day.

FrankG said...

@Daytona: the above was just a 2 week study on rats infused with insulin that (IIRC) Stephan Guyenet suggested was a model for chronic hyperinsulinemia in humans with IR... but as Petro has pointed out serves to show that ramping up insulin leads to IR.

In my understanding: those of us with Metabolic Syndrome (including obesity) did NOT rapidly ramp up insulin over a week to 2 week period but rather over many months, years or decades. IR may occur at different rates in different tissues (and we do have more than just muscle or fat tissues) which may help to explain why IR can also lead to (and be worsened by) excess fat mass.

FrankG said...
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FrankG said...

Correction: this was the study cited by Stephan Guyenet at his blog, where he writes... "In the first study, published in 1980 by Dr. Dennis A. Vanderweele and colleagues, rats were implanted with mini-pumps delivering insulin at a steady rate throughout the day and night for 7 days (4). They tested four different doses: 0, 1, 2 and 6 units per day, and measured food intake and body weight. This is a model of chronically elevated insulin reminiscent of what is seen in insulin-resistant people."


A 7 day trial of infused insulin on otherwise healthy rats may be "a" model for "chronically elevated insulin reminiscent of what is seen in insulin-resistant people"... but I submit that it is no a very good one

Nigel Kinbrum said...

FrankG said...
"So the only "cells" in our body that use and store energy are Muscles and Fat? Is that right?"
No Frank. That's not right. Take off your "Cognitive Bias" goggles. When I write about muscle & fat cells, that does *not* mean that those are the only cells that use/store energy in the human body. Do you seriously expect me to write about *all* of them each time, just to keep *you* happy? Jeez!

"I agree with Sean that your are purposefully "trying to be intellectually dishonest" ...either that or you consider everyone else here an idiot who cannot think for themselves."
What was I saying about "Cognitive Bias" goggles? I don't care what you think or who you agree with. I've argued with you before (on Pål Jåbekk's blog) and I *still* have the taste of straw in my mouth from the logical fallacies you used then.

Nigel Kinbrum said...

FrankG said...
"What about IR in the Liver or the Brain? I like to think that I "exercise" at least one of those, quite often each day."
Ha-ha. Very droll. The liver empties relatively slowly due to hepatic glucose production. Filling the liver faster than it empties produces IR in the liver.

What about IR in the brain? The brain doesn't have any GLU-T4 transporters AFAIK.

Beth said...


much like how folks living alongside a busy road no longer notice all the traffic noise -- but of course this parsimonious explanation would fall on deaf ears

Being subjected to a lot of noise can make people deaf, yep. :-)

George Adventures In Health said...

I too feel a little confused, and would like some degree of clarification about whether those fats that became IR in this process also became obese?


ItsTheWooo said...

Very interesting, excellent post per usual!

I was wondering if perhaps the very high insulin and total resistance to it may relate to antibodies against insulin, or receptor defects which are unique to exogenous insulin.

In the leptin therapy studies it was often observed predictable dosing/blood levels until circa month 3 of therapy... then blood measurements of leptin could become very wildly increased. The drug dose was the same, the issue is the body made antibodies to the leptin preventing accurate measurement. For example, early on in therapy my level was 20, 25. This is high physiological, the sort of level you might expect in a not particularly thin reproductive aged woman. By the end of measurement my levels were 80, 90, or higher. I took no more of the drug than before and took less if anything but my body was clearly making antibodies which messed up attempts to get an accurate blood level.

So I wonder if this steady insulin infusion resulted in a similar thing occurring for the rodents... the blood insulin seems high here but perhaps it is just a measurement error secondary to immune system reaction to foreign insulin.

ItsTheWooo said...

If my nonsense is too convoluted for you, here is a short reply:

Inactivity is a symptom of abnormal metabolism and endocrine dynamic, before a cause. There is a cyclical and reinforcing nature between inactivity and metabolic/endocrine disease, but the point of origin defect is the metabolism. ALWAYS.

Your self assessment is that you are happy to be lazy and this is just your personality, and that promotes problems with blood sugar and weight. I would argue you have things backward, problems with blood sugar and weight lead you to enjoy lying around. I've been on ALL EXTREMES of weight and energy. I've been super energetic and unable to eat and very thin. I've been ridiculously fat unable to much lift my arms or stand. Energy is always produced from within. Some people are more active than others, but no one is supposed to have a couch glued to their ass...that is a sign ones metabolism and endocrine system is not healthy at all.

Look, I didn't say gluttony or sloth either, wowz!

Puddleg said...

@ Nigel,
look at what happens when Fox01 is retained in hepatocyte nucleus;
increased lipogenesis AND increased gluconeogenesis.
This looks to me like a cell that has taken in too much energy trying to export that energy again.

Nigel Kinbrum said...

@Woo: Thank you for not using the g & s words. The fact is that even on a low-carb diet, I wasn't ever hyperactive or fidgety. When I'm on-line, I lie on a sofa. It's very comfy! On a high-carb diet, I sleep more, so I am more active on a low-carb diet. As I've said many times, you and I have completely different personalities.

@Frank: RE The verb "to empty". Consider a glass that is full of water. If I empty the glass a bit, the glass is no longer full, but it isn't empty either. Pouring water out of the glass is emptying the glass.

If I completely empty the glass by pouring all of the water out of it, the glass is then empty. Got it?

@George: If hepatocytes (also adipocytes) didn't either reduce their import of stuff or increase their export of stuff, they'd eventually explode.

Muscle cells can't export glucose, so all that they can do is reduce their import of glucose to zero when they're full.

blogblog said...


glycogen is the "fuel of last resort". It is normally only depleted during sustained high intensity physical activities such as long distance running or cycling. Body builders are very unlikely to significantly deplete their glycogen reserves because they typically train individual muscles for very short periods - ranging from a few seconds to a few minutes.

Jean said...

This is a great post! Things for the bits of facts! It's so juicy. :)
Want the finest and best exercise bands? Click here!

Makro said...

More Peter fodder for a rainy day:

FrankG said...


Definition of EMPTY
transitive verb

a : to make empty : remove the contents of -- empty a purse b : deprive, divest -- a phrase emptied of all meaning c : to discharge (itself) of contents d : to fire (a repeating firearm) until empty
: to remove from what holds or encloses

intransitive verb
: to become empty -- the theatre emptied quickly
: to discharge contents -- the river empties into the ocean

You wrote "Being sedentary does not empty cells (of glycogen)."

If you meant to write "Being sedentary does not use any of the glycogen stored in muscle cells." perhaps you should have written that instead. I can help you with your English if you like... my Father was a teacher.

Meantime the fact still remains that I did not become IR due to my lack of constant weight training.

As for your position NOT being one of blaming Gluttony and Sloth you could have fooled me (and, evidently others) with all your talk of balancing energy stored within "cells" against physical activity... you say tomato, I say weasel words.

You must be so happy that your patronising and goading has elicited a response but please don't be fooled into thinking that when I don't reply to you it is a sign that you have "won the point"... I just have more productive ways to spend my time.

Nigel Kinbrum said...

@FrankG: Maybe you should have paid more attention in class. I can write in a verbose style (like Gary Taubes) but it's boring to read, so I write in a concise style. I checked the definition of "empty" on Wiktionary.

In my head, I meant exactly what it said i.e. Verb (transitive) (ergative) To make empty; to void; to remove the contents of.
Note that "empty" is qualitative, not quantitative.

Due to your cognitive bias, you interpreted "empty" to mean "to completely remove the contents of". You are arguing a straw man, yet again!

RE Gluttony & Sloth: If you don't know the difference between conscious actions (gluttony & sloth) and unconscious actions (eating due to ravenous hunger & lethargy/sleepiness), any further discussion with you is a waste of my valuable time.

IR is multi-factorial, something that you would have known if you had read my blog post on Insulin Resistance. You choose to remain ignorant, another reason why further discussion with you is pointless.

Nigel Kinbrum said...

blogblog said...
"@Nigel, glycogen is the "fuel of last resort". It is normally only depleted during sustained high intensity physical activities such as long distance running or cycling. Body builders are very unlikely to significantly deplete their glycogen reserves because they typically train individual muscles for very short periods - ranging from a few seconds to a few minutes."
See It's all in a day's work (as measured in Joules) Part 2.

The body uses significant amounts of glycogen for activities >~25% of maximum exercise intensity e.g. brisk walking (something that I do for fairly long periods of time as I walk to/from shops in my town).

The body uses lots of glycogen for activities >~80% of maximum intensity i.e. sprinting/lifting heavy objects, putting them down again & repeating. I don't sprint as I have a long torso & short legs so it hurts, but I do low-impact bodyweight exercises.

Galina L. said...

Who would guess I will get a language tips on a nutritional blog. You guys are more useful for practicing English than my previous coworkers who were retired navy officers. Most of their adjectives started with "F", which was not very educational, but allowed me to build a very useful immunity to that sort of language. Helps sometimes even in reading some nutritional blogs.

FrankG said...

@Nigel: with respect (at least as much or little as you deserve) you are talking complete bollocks and you know it!

If I were to EMPTY a pint of beer over your head: the glass may start off full of beer, it may go through various stages of being partially full to empty BUT the inevitable final stage in the "act of emptying" (implicit in the very word "empty") is that THE GLASS WILL BE EMPTY! Devoid of its contents.

In other words: the phrase "completely empty" is exactly equivalent to "empty"

You may think it is all very clever to write imprecisely... or perhaps (as I suspect) it is done on purpose to allow wiggle-room when you are shown to be wrong (hence my use of the term weasel words) but in any case a reasonable person, when confronted with others who clearly did not read what they wrote as it was intended to mean, would try to clarify their position rather than berate those others for their ignorance, while desperately trying to defend their original choice of words.

IF you cannot even be trusted to be intellectually honest over basics like the English language or word selection, then I see no reason to expect any better from you in anything you write. And so far -- from what little I have read of your comments -- you are living down to my expectations.

It is laughable that you accuse me of choosing ignorance because I do not read your blog... where you have the gall to post a critique of Gary Taubes GCBC without even having read it yourself..! instead you rely on someone elses's cliff-notes version. Again, no doubt this affords you all kinds of wiggle-room to misquote and misrepresent what you have not read.

Vasco Névoa said...

Wanna see something neat? it's the "high-resolution" graph of my blood glucose during a 6 hour home-made oral glucose tolerance test, back in the day when I had severe reactive hypoglycemia.

I took a BG sample every 15 minutes because I wasn't happy with the results from the standard OGTT that said "everything is fine". It couldn't be fine, I felt like crap when my adrenals raised hell after every meal.

I used to think the up-and-down was due to my endocrine system playing ping-pong with insulin and glucagon, but now I understand that it may very well be hyperinsulinism all the way, with acute IR stepping in. Very interesting.

Your blog is always a laugh, even though the biochemistry is mostly lost on me. But I am learning from it. Keep it up, Petro! :)

Nigel Kinbrum said...

@FrankG: See my latest blog post.

Peter said...

@Vasco, that is one very interesting line!


Unknown said...
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Vasco Névoa said...

Yep, I think so too, but unfortunately I've never seen the issue of oscillating convergence of glycemia discussed in the literature. Do you know of any docs I can read?
It's a pity I couldn't take insulin measurements as well, but I don't think there are insulin meters available to the public. Bummer. :) And doctors just don't play along with these experiments.

As another interesting aside, I found out why I was hyperinsulinemic: gut bacteria. After antibiotics I enjoyed a couple of weeks without symptoms. LAter I also did an intravenous GTT in parallel with an oral one (cool doctor), and the IV reaction to sugar was clearly normal, whereas the digestive reaction was havoc. This pretty much places the smoking gun in the gut and in the bacteria's hands.

Now I follow a primal/LCHF diet and things are just peachy. I enjoyed a slice of cake the other day in "Peter style" (with a thick slab of butter on top) but the reactions of people around me were... exaggerated. :) Oh well, their loss. :D

Peter, I have a question for you: how do you keep a healthy gut if you don't eat much soluble fibre? Aren't you afraid to lose too much flora and vilii by feeding on such high amounts of fat and so little bacteria food?

ItsTheWooo said...

@Vasco Only 66? Doesn't count. YOu don't have hypoglycemia, according to Stephen Guyenet. Going from 165 ->88 in 1.5 hrs should not make you hungry, because 88 is euglycemia.
Being 66 at the 2.5 hr mark is not hypoglycemia, in fact this is a sign you are very insulin sensitive and your blood sugar is so low all the time. Blood sugar problems are the result of fat cell expansion, of "more fat going into the fat cell than leaving" because of your hedonism disease, errr addiction, so stop eating like an unsupervised 5 year old with your constant hyperrewarding meals, and you should be alright.


On a serious note, Vasco your case is super interesting.

After antibiotics do you remain free of hypoglycemia? Have you done a repeat OGTT?

Some antibiotics can destroy insulin producing cells, streptozotocin is used in studies to mimic type 1 diabetes. Very curious what abx you were given.

Your prior blood sugar patterns suggest insulin overproduction to any increase of sugar in the blood; first 166->88 (from oral glucose), then 104->66 (from endogenous glucose), and then a small oscillation between 90s and 80s. It appears the problem is directly a sort of "internal overdose" of insulin as the trigger is always an increase of blood sugar. This is precisely what is (or was) wrong with my glucose regulation. Lustig would define this state as "insulin hypersecretion" and sometimes it occurs as a nervous system / brain insult with excessive vagal tone and deficient SNS underlying it. Extreme/significant insulin resistance may not be involved, basal hyperinsulinemia may not be involved.

I am also really curious that the IV test was normal but the Oral test was FUBAR. Were the conditions exactly equal: rate of glucose infusion, total carb intake, diet the days preceding, etc?

ItsTheWooo said...

@Makro Rant produced!

I did not magically become hyperactive and energetic the moment I started a low carb diet.
It took months and years to gain this degree of energy/health. The earliest observation on low carb was that my sugar stopped crashing constantly and I felt full/not hungry like everyone else. Increased energy was very slight at first. It was a gradual change and I had to lose most of my body fat for it to occur.

Saying that your pathological fatigue is normal because the LC diet didn't produce energy right away is like saying depression is normal because antidepressants take a few days or weeks or months to resolve depression entirely.

Oh, and one more thing: I would point out the state of gluttony and sloth does not require the qualifier of conscious vs unconscious.

Here is another example of you kind of randomly making stuff up and assuming your definition is universal. Even amongst those who will admit to believing in the sins of gluttony and sloth (almost no one will admit this) there is not necessarily the expectation that someone is consciously choosing to be bad. They might be possessed by spirits, or they might just be innately a bad person and that is why they demonstrate the immortal behavior (so choice need not even figure in ).

blogblog said...


I must have been asleep during all those exercise physiology lectures and laboratory sessions I attended at university.

Brisk walking won't even get a reasonably fit person into the cardiac training zone. I once monitored my heart rate during an hour long very brisk (8km/h)walk up and down some reasonably steep hills - my heart rate never exceeded 100bpm. An Olympic distance runner would probably have a heart rate of 60-70bpm for the same activity level.

To get an elite athlete to the Anaerobic Threshold is a brutal experience. At university we tested an elite distance runner on a treadmill. It took over four minutes and a heart rate of 213bpm before he reached his AT.

js290 said...

@Theresa, have you tried some resistance training to dump out the glycogen stored in your muscles?

Vasco Névoa said...

@Wooo, @Peter
Well, since you really seem interested, I think I'll write up a "case report" of sorts in my blog, with all the juicy details. :)
I'll come back and link it for you guys when I'm done. I'm very curious as to what insights and interpretations you will derive.
Cya around! :)

Nigel Kinbrum said...

@Woo: Your blood sugar used to crash regularly. Mine didn't. I've always been a laid-back "yeah, whatever" kind of person, whereas you're a highly-strung "OMG! WTF!" kind of person. My work life involved many hours a day on a computer and my retired life involves many hours a day (but not quite as many) on a computer arguing with you lot! ;-p

We'll have to agree to disagree over conscious vs unconscious. You do write some weird stuff!

@blogblog: As I mentioned in the blog post that I linked to, the less fit somebody is, the lower the % of max exercise intensity they start burning glycogen and the more glycogen is burned. This is reflected in the higher fasting RER of unfit people relative to fit people. Don't do a Woo and project your personal experience onto the rest of the population. I can assure you that my HR goes over 120bpm when I'm walking briskly. I can easily get my HR up to 180bpm (my MHR is ~167bpm based on the formula 220-age)!

@js290: You'd better not use the phrase "dump out" when referring to muscle glycogen. It implies total depletion and you'll have FrankG on your case!

For the record, when I wrote "As cells are emptied (of glycogen)...", I meant "As cells are depleted (of glycogen)...". But hey! I'm only human. I used the wrong word. I'm so, so sorry. I'll try harder next time. Was that sarcastic enough for you, FrankG?

How about arguing the point instead of my choice of words? My guess is that you have no argument, which is why you used a crude diversionary tactic. Intellectual dishonesty at its finest!

Dr. N said...


Sounds like you have some bacterial overgrowth. Surprisingly common in my patients. Supplementing with some prebiotic fiber such as Inulin on a daily basis can really help straighten out your sugars as well as symptoms of "low blood sugar".

Sanjeev said...

Hey Frank - don't let Nigel con you; Nigel is actually Carbsane in drag.

You know how those brits love dressing in drag

xxxxxxxxxxxx said...

LOL@ Sanjeev .........LOL

Vasco Névoa said...

@Dr. N
Yes, thanks Dr. N. I realized that myself, with some interesting reading at Art Ayers' blog.
I've been taking pro and prebiotics, both commercial and natural, including home-made yogurt and sauerkraut, and milk kefir, for a few months. It gets better, then it gets worse, then better again... the LCHF diet, with very little carbs and lots of soluble fibre (green leaves and the occasional tomato) makes it a lot easier to navigate, but I'm working on eradicating the problem. A supplement of apple fibre every night seems to be helping. But it's work in progress, and I don't know how long it's going to take to fully recover. But at least I know exactly what is wrong with me and have a handle on how to fix it. ;)
However, this hyper-insulinism turns me into a walking experiment when it comes to diet-metabolism relationship. :)

Say, do all your patients with bact. overgrowth become hyper-insulinic?

blogblog said...


stop washing with soap and kiss a few strangers. This will fix your gut flora ASAP.

Vasco Névoa said...

Yeah, I noticed that at Art's blog. :)
I became much more selective when it comes to hygiene - I wash my hands thoroughly after messing with the chemicals of bike mechanics, but not so after messing with the dirt in the greenery. ;)
However, there's a fundamental question here: how can eating bacteria repopulate the necessary diversity in the gut, if the stomach acids perform their function of disinfection? I suppose only extremely acid-adapted species like H. Pylori are capable of resisting the stomach and passing down to the small intestine, so it kind of makes it pointless to eat bacteria... right? How does this work?

Lori Miller said...

I'd like to know the answer to Vasco Nevoa's question about bacteria getting into the gut, too.

Eva said...

Given this scenario of insulin resistance in diabetic dogs as being the cause of somogyi rebound, how fast could the blood sugar rise be expected to work if it was only from insulin resistance? SOme years ago, my dog was diagnosed diabetic and put on insulin. At first, I left it to vets to balance him but he was doing really badly, losing weight (don't get me started about that crap Science Diet food they wanted me to give him), etc, so I turned to google research, bought a blood glucose monitor and started blood testing A LOT.

I found the dog was getting food/insulin and then dropping from about 300 to under 100 blood sugar in 15 minutes! 15 MINUTES!!! Sometimes the meter would catch a read as low as 50. Understanding this was a human bg monitor, it was not totally accurate for dogs, but the pattern was clear that he was going for a hypo at record speed.

Then, sometimes, he would act weird for a bit, eyes would roll back a bit or sometimes not, then his blood glucose would reverse rapidly and rise fast. He survived. THis would happen every 2 days. I even tried blocking the hypo by giving him pure sugar but could not stop it even with that. The insulin was just slamming him too hard.

In between hypos, blood glucose would be high but slowly normalize. I assumed insulin resistance caused that. After 2 days, resistance would lesson and on the next insulin shot, he would go hypo again, weird eye thing, and then the pattern started all over.

I showed my numbers/graphs to the vet and they said, give MORE insulin! I said, no give LESS! Big argument, me very pissed off, and I had to switch vets. My discovery, most vets are dangerously stupid at diabetes control.

Next tried dropping insulin dosage, no more hypo but the insulin was not seemingly lasting longer than about 5 hours. Solution, which I came up with myself, was to switch to super long acting insulin called Lantus (usually used more for cats). Success! My dog was more sensitive than average to insulin. Long acting insulins for him acted like short acting insulins for other dogs and short acting insulins were deadly fast. (also, many dogs do badly on the insulin supposedly made for them, which is really just a failed human insulin that has been remarketed for the pet industry and it still sucks) So dog became balanced on Lantus, gained back normal weight, recovered.

(continued next)

Eva said...

(continued from previous)
Point is, could insulin resistance account for his initial violent descent and ascent of blood sugars in the course of half an hour? I suspect the ascent was true somogyi response, ie internal organs slamming out sugar to save him from near death. Later, then he truly did have insulin resistance for about 48 hours. The initial threat had been dealt with but he was insulin resistant for 2 days after. The next shot of insulin after a somogyi was almost useless in effect.

And if you did a bg curve during that time for only 12 hours, during his time of insulin resistance, you would most surely assume the dog needed MORE insulin, like tons more. But if I had went with more, the dog would likely have died once that insulin resistance wore off 2 days later. As it was, I think he was barely surviving those hypos. 48 hours of intermittant blood testing and some intense testing around the time of the hypo was the only way I was able to figure it out, no thanx to the vets who seemed sure that all dogs do well on the same dosages as their other few diabetics.

Also confounding the matter was although my dog seemed calm on the outside, not a typical assumed candidate for stress induced high blood glucose, my own testing over time revealed that his at the vet bg numbers were always way way higher than at home. He was very stressed at the vet, even though he didn't act it. I even brought my own bg tester to the vet and did it there with my own device, to make sure the diff could not be accounted for by the using of diff meters. SO again, vet tendency was to always want to give more insulin, because when he was at the vet, his numbers made it look like he needed more.

I was also joined a mailing list for diabetic dogs and my experience was, for dogs that would not balance easily, home testing often revealed something similar was happening in other people's dogs. The hypos were not 'hidden,' as you could catch them in the numbers if you figured out the pattern and tested really often at the right time. But if you only tested once every 2 hours, both the descent and ascent might hardly show at all as you could easily miss them both. This somogyi pattern, we found in many dogs that were not getting balanced easily.

Plus the somogyi only happens maybe once every 48 hours because in the middle, the insulin resistance blunts/blocks it. Home testing saved so many of these dogs that would probably have been killed otherwise by too much insulin. Sensitive dogs need longer/slower acting insulins. You get to understand it better if you start dealing with say 200 diabetic dogs like were on our mailing list, instead of just one or two here and there like most vets. My dog was on the extreme end of insulin sensitivity but there were others like him that had to have either just less insulin or a longer acting insulin to prevent violent blood sugar descent often missed by widely spaced (2 hour spacing can totally miss it) bg tests.

I am not disputing the overall concept of insulin resistance you present, but I can tell you one thing and that is those hypos are often truly there and if you test often enough, you can catch them. But you have to be testing at the exact right time so it's tricky.

Sanjeev said...

I don't know how well established this is ... looks pretty new, but it appears that gut ecosystems (with perhaps hundreds of species) gravitate towards one of a limited number of types.

google up (include the quotes).

"gut flora" "3 types"

Some of the older research showed that taking those probiotics doesn't change anything, and it's been suggested the existing ecosystem resists change via competition, not much via stomach acid.

I think some earlier research showed some beneficial effects too, so again this field's in a state of flux.

Peter said...

Hi Eva,

Correct in large part. But I would comment that a relative insulin overdose does two things, first is it causes hypoglycaemia. Second it causes insulin resistance. What determines whether there is a hypo or a Somogyi overswing WITHOUT hypo (as per continuous blood glucose monitoring) is which kicks in first and what the background level of insulin resistance is. Think of a dog which develops hyperinsulinaemic insulin resistance at a blood insulin concentration of, say 400microiu/ml. This may occur at a blood glucose of 6mmol/l, 2mmol/l or 0.5mmol/l.

If the value of 400microIU/ml was scheduled to be reached at 0.5mmol/l the dog would seizure or die before Somogyi kicked in. The dog just hypo'ed. Hypos, as we all know, really do happen. Somogyi will not save them all. If it did diabetes would be a doddle!

If the value of 400microIU/ml was reached at 2mmol/l we would assume the hypo triggered the Somogyi effect, when it was really just the insulin hitting 400microIU/ml concurrently with the hypo.

If the insulin hit 400microIU/ml at a BG of 4mmol/l or even 6mmol/l, checked on a continuous BG meter, where is the hypo?

This exactly the argument that appears to have gone back and forth in the medical field. It's why I put this section in:

"The temporal association with hypoglycaemia, which misled Somogyi, comes from the time course of switching sources of glucose oversupply. The hypoglycaemia is not causative, it is just common for it to occur at around the same time that insulin/GLUT4s oversupply substrate to the mitochondria and they say no to it, using insulin resistance."

BTW I agree completely that the effect is occasionally very random and any hypreglycaemic event messes up any sort of control for some days afterwards.

I also have to agree that you have to look hard to find a vet who understands any of the subtleties of diabetes control. The usual approach is lente bid, feed bid, book the cataract surgery for 12 months post-diagnosis. This is current "state of the art".


Dr. N said...


Too many variables going on at once to say all my patients with bacterial overgrowth syndrome (BOS) have IR. Studies have demonstrated BOS can lead to obesity, and diabetes in mice. BOS can also alter autonomic functioning via the vagus nerve.

My practical experience with probiotics is rather hit or miss and I personally think most is from the inhibitory effects of stomach acid on the ingested probitotic. A brand called Culturelle has good laboratory data behind it and clinically works far better than most.

Better yet is a regular dosing of Inulin (5-10 grams) twice daily. Seems to out perform the probiotics.

Unfortunately, many patients often need to remain on probiotics or Inulin or their symptoms come back.

blogblog said...

@Vasco and Lori,
bacteria are far tougher than we think. Many (soil) bacteria produce spores which are practically indistructible. The spores simply revert to being normal bacteria once they pass through the stomach.

Vasco Névoa said...

@blogblog & Dr. N
Thanks for the clarifications.

It had to be that bacteria somehow pass through the stomach acid trap, otherwise we wouldn't have them. :)

Regarding inulin, isn't this fibre going to feed all of the bacteria in the gut? how come people get better just by throwing food at gut flora, independently of species selection or reinforcement? Aren't pathogenic bacteria going to be just as happy as symbiotic bacteria?

Peter, I'm sorry to be hijacking the comment thread, but it's hard to find this kind of wisdom out there. Hope I'm not disturbing. :)

gallier2 said...

Vascó, you might search in Peter's archive about FIAF which handles mostly about gut bacteria and their effect on the metabolism. It's from 2007 or 2008, the keyword is FIAF.

Vasco Névoa said...

Fascinating stuff, thanks!

Now I know why Peter hasn't replied my question about killing off gut bacteria with so much fat intake. He seems to think we have very little use for them, if we eat a high fat diet... am I wrong?

Asim said...

As Dr. Ayers points out, prebiotics and probiotics don't do much good in the context of re-establishing gut flora, quite simply because the diversity of flora is limited in them.

If you have gut flora issues, and your providing the same limited species of flora, it's not going to help much and in fact, a probiotic or prebiotic may excacerbate an existing issue.

The only way to introduce the DIVERSE flora is either through, as blogblog points out, less hygiene and playing in 'dirt'. Further, one needs to avoid excessively washing of food from the garden. At the same time, re-introducing a diverse gut flora requires persistence. It is more of a lifestyle change.

The other option is one can have a fecal transplant done, but even then, the effects would be limited if one goes back to the same habits as previously, for the same lifestyle will most likely lead to the same ratios which causes the issues in the first place.

Another problem is quite simply the heavy use of antibiotics in the last 100 years. Floras are constantly disrupted, which lead to improper development of the immune system, especially among the young. One should avoid antibiotics, unless the situation is extreme and requires it.

Asim said...

"Aren't pathogenic bacteria going to be just as happy as symbiotic bacteria?"

The following article explains the latest findings.

"One surprise: It turns out that nearly everybody harbors low levels of some harmful types of bacteria, pathogens that are known for causing specific infections. But when a person is healthy - like the 242 U.S. adults who volunteered to be tested for the project - those bugs simply quietly coexist with benign or helpful microbes, perhaps kept in check by them."

It is most likely that the good batceria keep the bad bacteria in check.

Asim said...

Think about the amount of species of bacteria that lie in the gut, over 10,000, coupled by the amount of genes that are present and then think about the limitations of pro and prebiotics in providing the wide diversity of strains.

It seems that it just can't be mimicked.

This issue of gut flora is almost always ignored when taking into account traditional societies and their lack of 'metabolic' diseases and the 'paleo' versus 'carb' debate wars. These cultures ate straight from the plants with little washing, moved in all sorts of terrains.

Traditional cultures also practiced geophagy, which is the licking of earth and soil substances, and it was used especially by pregnant woman in some cultures.

Further, geophagy is practiced all throughout the wild, by various animals. Galen records that it was often done by animals that were sick and injured.

Vasco Névoa said...

Thanks for the clarifications. :)
So, a lot more dirty veggies and a bit of inulin to boost it. ;)
Just gotta be careful about potential sources of parasite eggs - those should be washed thoroughly.

Asim said...

Pectin, found in apples, is another fiber that promotes bacteria.

Remember though, and I often see people making the same mistake in the comments on Dr. Ayer's blog depsite his clarity, one should re-establish a sound flora through diversity, otherwise the implementation of inulin and pectin would not do other than cultivating what already exists in the gut.

Your right as well, parasites may be the trade-off. Of course, certain parasites may also have benefit in light of the hygiene hypothesis as well.

It's the trade-off between the industrial versus traditional culture. When humans began to settle, because of the close quarters, they exposed themselves to communicable diseases and lack of public sanitation, which caused full-blown epidemics. The burden seems to have shifted to extremism in the other way, with over-use of antibiotics, purell, constant cleansing, over-washing of fruits and vegetables and the like.

It's a tight balance.

Peter said...

Sorry all for poor response to comments. It's that eternal comments vs the next post competition.

Re Fiaf; even on the sort of LC diet I eat I have to admit to consuming the occasional disgusting plant and even more disgusting fibre. I still have gut bacteria and they do still function, but my suspicion is that they are less in control than when I used to feed them on a mix of bananas, whole meal bread and Weetabix...


Lori Miller said...

Thanks for the responses on gut bacteria.

While researching a cure for a sinus infection a few months ago, I learned that healthy people have "bad" bacteria in their sinuses as well--it's overgrowth that's the problem. (A huge dose of vitamin D and some Mucinex and salt fixed the problem where antibiotics failed.)

My dog likes to lick my mouth. Maybe she's trying to keep her host healthy and able to get food for her. ;)

Vasco Névoa said...

Thank you all for for all the info you've given here, I've learned more about gut flora in the last 3 days than the last 3 years. :)

Before Peter replied, I was wondering if there was any gain in a diet that almost eradicates gut flora, but I expect this would have negative effects sooner of later. Even if one is able to ingest all the vitamins and minerals in enough quantity and bioavailable form to compensate for inexistent flora, I suppose either the immune system or gut permeability will be serious issues. So, in the end, it's best to protect at least a minimum level of gut flora.

I expect that a non-invasive but effective way to deal with BOS would be to execute a full-throttle ketogenic diet to kill off the excess bacteria, then have some probiotics and inulin to restore the main known simbiotic species, and then continue forever with eating unwashed veggies as a source of diversity along with a low carb diet to avoid BOS relapse.

Does this sound right?

ItsTheWooo said...

Our immune systems support healthy flora. When abnormal GI flora take over our intestines it's usually because one is immunocomprimised at baseline (e.g. diabetic/elderly), or alternatively you did something abnormal to kill the healthy flora that regulates the pathogenic ones, such as taking antibiotics. Give antibiotics to a patient particularly an elderly or diabetic or steroid treated one, observe very shortly they develop a GI infection called c. difficile. This is purely a result of having killed off the healthy regulatory gut flora with the antibiotic therapy so that this opportunistic pathogen goes wild.
You treat the c.diff with vancomyacin or flagyl orally, and you support the healthy GI with probiotics to prevent recurrence; if you recolonize the GI with probiotics the c.diff should not reoccur.

So to ansewr your question, our immune system favors the proper balance of GI flora, opportunistic infections and overgrowth of bad bugs is a result of good flora suppression, which can be treated with probiotics. The pathogenic ones will not reproduce as easily as the symbiotic kind because the symbiotic kind suppresses pathogenic.

blogblog said...

when I was in the army in the early 1980s I had no gut problems at all. Spending a few weeks at a time litterally living in the dirt and avoiding soap does wonders for the gut flora.

Vasco Névoa said...

@Wooo: thanks. :)

@blogblog: LOL!... ok, I get it. thx.

I've got 2 small kids (2 and 6 yo), I'll make sure to spend more time making mud pies and avoiding mom's demands to wash up before dinner. ;)

Unknown said...
This comment has been removed by the author.
Peter said...

Daytona, sorry I missed this one: Insulin resistance in ADIPOCYTES limits weight gain. This is normally a late development secondary to obesity when adpocytes are too stretched to respond to insulin. But a chronic insulin infusion down regulates insulin sensitivity in ALL tissues, PDQ. Everything then adapts and the process of weight gain restarts at a higher insulin level, with all tissues ignoring 99% of the insulin from the pump and functioning fairly normally on the sensitivity that they maintain to the other 1%... There is more on this in the next post.


blogblog said...

you get (far) better results by weight training only once a week for 30-60 minutes.

Vasco Névoa said...

@Theresa & blogblog
I agree somewhat with blogblog. If you do it everyday you will be overtaxing your body and disabling many of the benefits. If you allow for at least 48 hours of total rest between workouts, your body responds much more. Rest is just as important as exercise, be sure to use both together.
I did 14 weeks of 3 days per week weight training (with a day of rest in between) and this got me to an unbelievable strength after just 6 weeks.
I also have the negative example of younger jujitsu practitioners who, at 18 years of age, think they are supermen. They will do JJ 5 or 6 days a week, and on the weekends run a few miles and/or go to the weightlifting gym. Result: muscle and resistance loss, not gain, and chronic stress and fatigue.
The body simply does not have time to repair and grow if you do it everyday. Get at least a couple of nights sleep in between intense efforts, and eat enough to grow muscle. Muscle is protective of general health.

blogblog said...

it can easily take 2-3 weeks to fully recover from a single bout of high intensity exercise. In the most extreme cases (eg running a marathon)it takes months to recover.

Many exercise physiologists now believe that long-term high-intensity training simply teaches the body to ignore pain (due to injury) rather than improving fitness.

blogblog said...

Dietary prebiotics: current status and new definition.

Vasco Névoa said...

I guess it all depends on the dosage.
I limit my HIIT sessions to 45 minutes, rest 48h in between, and rest on weekends.
This allowed me to put on 2kg (4lbs) of lean muscle (had to buy new pants, my legs wouldn't fit in the old ones!) without ever breaking a sweat.
I always aimed for hormonal signalling, not metabolic punishment. ;)

Vasco Névoa said...

Very nice paper on biota, thanks! :D