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Role of Follistatin in Aging

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#1 sub7

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Posted 04 July 2016 - 08:54 PM


As you know Bioviva CEO Liz Parish has undergone vector-gene therapy, which, supposedly, does two things

1- Lengthen telomeres

2- Increase Follistatin expression

 

The potential value of 1 is obvious, but 2 really took me by surprise. The role of Follistatin is simply to block myostatin and just increase skeletal muscle strength and mass. This is of course a great way to inhibit sarcopenia and would have value for a 65 - 70 year old. But for someone of Liz Parsih's age, sarcopenia is probably a long way from setting in. Am I missing something here? What would be the reason to use Follistatin so early on? Does Follistatin do more than merely inhibit Myostatin and accomplish more than increase muscle strength and mass?

 

Thanks



#2 Rocket

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Posted 11 July 2016 - 02:27 AM

Blocking myostatin is also a great way to cause an increase in lean body mass...... Not just prevent sarcopenia in old age. Liz doesn't have to wait 20 years to know if the gene therapy worked. I imagine that like taking ghrp successfully blocking myostatin would or should cause hunger spikes as the muscles require fuel to grow.

But I highly doubt Liz took a dose to knock out myostatin activity completely, so its a big question mark about what will or is happening with the dose she took. After all there is nothing published that is worthwhile by her company.

I know a dozen gym rats that would love to try gene therapy to block myostatin.

Edited by Rocket, 11 July 2016 - 02:30 AM.


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#3 corb

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Posted 12 July 2016 - 08:31 PM

If you're interested in the role of follistatin in (rather in relation to) aging, you're lucky because I accidentally uploaded a paid paper couple of days ago which has some information about that.

 

https://www.dropbox....en2016.pdf?dl=0

 

Granted not everyone develops diabetes as they age but quite a few people have pre-diabetic symptoms and this has some implications about how much you can actually get out of exercise if you're in that group. It doesn't give a clear answer if getting extra follistatin would help - in fact like in most cases when it comes to these proteins and their quantities in there is no clear answer.

Follistatin therapy does seem to help people with muscle dystrophies though.

http://www.nature.co...mt2014200a.html

 

The problem there is completely separate from the TGF beta pathway and therefore the results aren't amazing, but it's better than nothing.


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#4 PeaceAndProsperity

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Posted 14 July 2016 - 06:35 PM

Constant telomerase expression = too many stem cells accumulating.

Follistatin overexpression = constant addition of new muscle cells from stem cell conversion = reduced stem cell count.

Follistatin therapy without telomerase therapy = stem cell depletion.

 

Both therapies need eachother. The question is, is follistatin therapy enough to deplete the stem cell count and prevent too many stem cells from accumulating? To me it seems that it's not. 



#5 corb

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Posted 14 July 2016 - 09:53 PM

Constant telomerase expression = too many stem cells accumulating.

Follistatin overexpression = constant addition of new muscle cells from stem cell conversion = reduced stem cell count.

Follistatin therapy without telomerase therapy = stem cell depletion.

 

Both therapies need eachother. The question is, is follistatin therapy enough to deplete the stem cell count and prevent too many stem cells from accumulating? To me it seems that it's not. 

 

In mice, Follistatin alone ameliorates some aging deficiencies and extends lifespan of naturally aged mice.

It's quite possible they were simply overfed and pre-diabetic though. Animal experimentation is just a guideline, it doesn't give definitive answers.
But also bare in mind mice are capable of expressing TERT in most of their tissues unlike humans - of course also bare in mind the fact long telomeres don't' help mice in any way.

So there is no easy answer, again, it's animal research and protein expression in relation to aging is not well understood, if at all.


Edited by corb, 14 July 2016 - 10:00 PM.


#6 sub7

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Posted 23 July 2016 - 09:08 AM



The problem there is completely separate from the TGF beta pathway and therefore the results aren't amazing, but it's better than nothing.

 

Awesome paper; getting ready to read it ASAP
Can you please elaborate on what you mean with the above?



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#7 pone11

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Posted 29 July 2016 - 10:19 PM

If you're interested in the role of follistatin in (rather in relation to) aging, you're lucky because I accidentally uploaded a paid paper couple of days ago which has some information about that.

 

https://www.dropbox....en2016.pdf?dl=0

 

Granted not everyone develops diabetes as they age but quite a few people have pre-diabetic symptoms and this has some implications about how much you can actually get out of exercise if you're in that group. It doesn't give a clear answer if getting extra follistatin would help - in fact like in most cases when it comes to these proteins and their quantities in there is no clear answer.
 

 

Be very clear that this paper is not about your glucose levels ("prediabetes") but is rather about your *insulin* levels relative to glucagon.   The distinction is worth making because not all prediabetes is the same.   Sometimes prediabetes is about insulin resistance (so insulin levels go and stay high), but other times it may not reflect that.

 

I found an incredible rodent paper that demonstrates that during periods of starvation, when the body starts autophagy, that glucose levels *rise* while insulin continues to trend down:

https://www.ncbi.nlm...les/PMC3149698/

 

The study is fascinating because the control group is rats that are genetically disabled to do autophagy.  When they look at starvation in both groups, sometime around hours 19 to 23 for the group that can do autophagy:
 

1) Free amino acids surge

2) Glucose levels go sharply up

3) Insulin levels continue to trend down, even in face of higher glucose

4) Glucagon continues to slightly trend up

 

What appears to be happening here is autophagy releases amino acids from inside of the cells.  Autophagy is eating defective proteins, mitochondria, viruses, and bacteria, and these are producing large amounts of free amino acids.  The FAA are then feeding gluconeogenesis to produce glucose.

 

This raises the question in adult humans with "prediabetes" is the cause of the high glucose level a) insulin resistance or b) autophagy?   In my own case, I intermittent fast, and I have noticed that my glucose levels never come below 100 mg/dL during my fast.   So even though I have no food to stimulate glucose higher or raise insulin, my glucose stays high.   After I eat my first meal, glucose trends down, probably as a response to insulin going high after the meal.  I am fairly sure that if we measured my metabolites during the fast, you would see stable rising glucagon and falling (and probably very low) insulin.   

 

I am starting to wonder if much of adult prediabetes may in fact reflect a lot of collected garbage in our cells and the body being overwhelmed by trying to clean this out by autophagy in the overnight fast.


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#8 aconita

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Posted 29 July 2016 - 11:43 PM

I am starting to wonder if much of adult prediabetes may in fact reflect a lot of collected garbage in our cells and the body being overwhelmed by trying to clean this out by autophagy in the overnight fast.

 

If that was true starving people in third world should all be diabetics which doesn't seem to be the case, actually the opposite seems happening: diabetes cases are sharply rising in industrialized countries where people is constantly surrounded by something to chew on, mainly garbage full of sugar, triggering a constant need for insulin production which likely leads to insulin insensitivity.

 

Some times pre-diabetics don't reflect insulin insensitivity?

 

Well, I guess the response to such high demand might sometimes differ in some individuals but likely the trigger is the same, just a different reaction.

 

Just my thoughts, of course.

 

Interesting papers... by the way.



#9 corb

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Posted 30 July 2016 - 01:08 AM

 

If you're interested in the role of follistatin in (rather in relation to) aging, you're lucky because I accidentally uploaded a paid paper couple of days ago which has some information about that.

 

https://www.dropbox....en2016.pdf?dl=0

 

Granted not everyone develops diabetes as they age but quite a few people have pre-diabetic symptoms and this has some implications about how much you can actually get out of exercise if you're in that group. It doesn't give a clear answer if getting extra follistatin would help - in fact like in most cases when it comes to these proteins and their quantities in there is no clear answer.
 

 

Be very clear that this paper is not about your glucose levels ("prediabetes") but is rather about your *insulin* levels relative to glucagon.   The distinction is worth making because not all prediabetes is the same.   Sometimes prediabetes is about insulin resistance (so insulin levels go and stay high), but other times it may not reflect that.

 

I found an incredible rodent paper that demonstrates that during periods of starvation, when the body starts autophagy, that glucose levels *rise* while insulin continues to trend down:

https://www.ncbi.nlm...les/PMC3149698/

 

The study is fascinating because the control group is rats that are genetically disabled to do autophagy.  When they look at starvation in both groups, sometime around hours 19 to 23 for the group that can do autophagy:
 

1) Free amino acids surge

2) Glucose levels go sharply up

3) Insulin levels continue to trend down, even in face of higher glucose

4) Glucagon continues to slightly trend up

 

What appears to be happening here is autophagy releases amino acids from inside of the cells.  Autophagy is eating defective proteins, mitochondria, viruses, and bacteria, and these are producing large amounts of free amino acids.  The FAA are then feeding gluconeogenesis to produce glucose.

 

This raises the question in adult humans with "prediabetes" is the cause of the high glucose level a) insulin resistance or b) autophagy?   In my own case, I intermittent fast, and I have noticed that my glucose levels never come below 100 mg/dL during my fast.   So even though I have no food to stimulate glucose higher or raise insulin, my glucose stays high.   After I eat my first meal, glucose trends down, probably as a response to insulin going high after the meal.  I am fairly sure that if we measured my metabolites during the fast, you would see stable rising glucagon and falling (and probably very low) insulin.   

 

I am starting to wonder if much of adult prediabetes may in fact reflect a lot of collected garbage in our cells and the body being overwhelmed by trying to clean this out by autophagy in the overnight fast.

 

 

After a quick search I found these:

 

 

Glucose-starved Cells Do Not Engage in Prosurvival Autophagy*

 

In response to nutrient shortage or organelle damage, cells undergo macroautophagy. Starvation of glucose, an essential nutrient, is thought to promote autophagy in mammalian cells. We thus aimed to determine the role of autophagy in cell death induced by glucose deprivation. Glucose withdrawal induces cell death that can occur by apoptosis (in Bax, Bak-deficient mouse embryonic fibroblasts or HeLa cells) or by necrosis (in Rh4 rhabdomyosarcoma cells). Inhibition of autophagy by chemical or genetic means by using 3-methyladenine, chloroquine, a dominant negative form of ATG4B or silencing Beclin-1, Atg7, or p62 indicated that macroautophagy does not protect cells undergoing necrosis or apoptosis upon glucose deprivation. Moreover, glucose deprivation did not induce autophagic flux in any of the four cell lines analyzed, even though mTOR was inhibited. Indeed, glucose deprivation inhibited basal autophagic flux. In contrast, the glycolytic inhibitor 2-deoxyglucose induced prosurvival autophagy. Further analyses indicated that in the absence of glucose, autophagic flux induced by other stimuli is inhibited. These data suggest that the role of autophagy in response to nutrient starvation should be reconsidered.

 

http://www.ncbi.nlm....les/PMC3798503/

 

 

Glucose induces autophagy under starvation conditions by a p38 MAPK-dependent pathway.

 

Autophagy is a natural process of 'self-eating' that occurs within cells and can be either pro-survival or can cause cell death. As a pro-survival mechanism, autophagy obtains energy by recycling cellular components such as macromolecules or organelles. In response to nutrient deprivation, e.g. depletion of amino acids or serum, autophagy is induced and most of these signals converge on the kinase mTOR (mammalian target of rapamycin). It is commonly accepted that glucose inhibits autophagy, since its deprivation from cells cultured in full medium induces autophagy by a mechanism involving AMPK (AMP-activated protein kinase), mTOR and Ulk1. However, we show in the present study that under starvation conditions addition of glucose produces the opposite effect. Specifically, the results of the present study demonstrate that the presence of glucose induces an increase in the levels of LC3 (microtubule-associated protein 1 light chain)-II, in the number and volume density of autophagic vacuoles and in protein degradation by autophagy. Addition of glucose also increases intracellular ATP, which is in turn necessary for the induction of autophagy because the glycolysis inhibitor oxamate inhibits it, and there is also a good correlation between LC3-II and ATP levels. Moreover, we also show that, surprisingly, the induction of autophagy by glucose is independent of AMPK and mTOR and mainly relies on p38 MAPK (mitogen-activated protein kinase).

 

http://www.ncbi.nlm....pubmed/23116132

 

 

So it seems like it's the other way around. You need the glucose for autophagy to function if we go by these papers.

In aging autophagy is generally impaired, supposedly by inflammaging. Maybe the the amount of glucose produced doesn't change, but there's less autophagy so more glucose is left unused.

Of course that's just one factor.



#10 pone11

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Posted 30 July 2016 - 07:48 AM

 

I am starting to wonder if much of adult prediabetes may in fact reflect a lot of collected garbage in our cells and the body being overwhelmed by trying to clean this out by autophagy in the overnight fast.

 

If that was true starving people in third world should all be diabetics which doesn't seem to be the case, actually the opposite seems happening: diabetes cases are sharply rising in industrialized countries where people is constantly surrounded by something to chew on, mainly garbage full of sugar, triggering a constant need for insulin production which likely leads to insulin insensitivity.

 

Some times pre-diabetics don't reflect insulin insensitivity?

 

Well, I guess the response to such high demand might sometimes differ in some individuals but likely the trigger is the same, just a different reaction.

 

Just my thoughts, of course.

 

Interesting papers... by the way.

 

 

Several points on this:

 

* You aren't following the hypothesis.  Prediabetes does not always reflect insulin sensitivity.    Sometimes it reflects autophagy.   That's what the mouse study shows.   The autophagy-driven type of prediabetes NEVER BECOMES DIABETES.  The rate limiting factor for gluconeogenesis is the amount of free amino acids in the blood created by autophagy.   So the prediabetes of insulin resistance gives the same high fasting glucose symptom of autophagy, but the underlying causation is totally different.   To really get at this issue measure the insulin and glucose and free amino acids over the course of a long fast and see the behavior.   Autophagy driven high fasting glucose will be displayed with low insulin and a surge in free amino acids.   High fasting glucose associated with insulin resistance will show high insulin and high glucose, and presumably the free amino acids will not surge because autophagy never starts up in high volume (due to the high insulin levels).   That's just an approximation of the idea....

 

* I don't think a culture in which starvation is the norm is comparable to western societies that overeat all the time.   The point is an adult in a culture that has constant starvation has gone into autophagy constantly and most of the cellular malaise of badly folded proteins, mitochondria, viruses, and bacteria that can be easily "eaten" has been eaten.  In Western society, we eat around the clock, to the absurd extent that some people have six small meals a day and then get a snack in the middle of the night on top of it.  This complete lack of fasting means they rarely get into long periods of autophagy and have tremendous amounts of accumulated "muck" in their cells that never gets cleaned.   I read a book on autophagy as a strategy to beat neurological diseases recently named the "Protein Cycling Diet":

https://proteincycli...s3nmvrwklbxs-1/

 

In this book he makes educated estimates about the amount of time it would take the body to get rid of accumulated protein damage for an aged adult, assuming different amounts of time in autophagy.   His most aggressive autophagy plan takes 1.3 YEARS to clear the cellular debris.   The typical autophagy plan takes about seven YEARS.   He argues pretty persuasively that people in western cultures never spend much time in autophagy, so they simply keep accumulating badly folded proteins.   His argument for why many of these protein-based diseases like Alzheimer's have taken off in the last 50 years is because of the change in eating habits shutting down time in autophagy.

 

This is an area of intense interest for me.   I wish I could afford to do some extensive testing of my insulin and free amino acids over time in a fast, to try to confirm how my own prediabetes is behaving.   Because I am thin and have very little body fat I am fairly convinced that my own prediabetes is reflecting autophagy rather than true insulin resistance.


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#11 pone11

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Posted 30 July 2016 - 08:31 AM

After a quick search I found these:

 

 

 

Glucose-starved Cells Do Not Engage in Prosurvival Autophagy*

 

In response to nutrient shortage or organelle damage, cells undergo macroautophagy. Starvation of glucose, an essential nutrient, is thought to promote autophagy in mammalian cells. We thus aimed to determine the role of autophagy in cell death induced by glucose deprivation. Glucose withdrawal induces cell death that can occur by apoptosis (in Bax, Bak-deficient mouse embryonic fibroblasts or HeLa cells) or by necrosis (in Rh4 rhabdomyosarcoma cells). Inhibition of autophagy by chemical or genetic means by using 3-methyladenine, chloroquine, a dominant negative form of ATG4B or silencing Beclin-1, Atg7, or p62 indicated that macroautophagy does not protect cells undergoing necrosis or apoptosis upon glucose deprivation. Moreover, glucose deprivation did not induce autophagic flux in any of the four cell lines analyzed, even though mTOR was inhibited. Indeed, glucose deprivation inhibited basal autophagic flux. In contrast, the glycolytic inhibitor 2-deoxyglucose induced prosurvival autophagy. Further analyses indicated that in the absence of glucose, autophagic flux induced by other stimuli is inhibited. These data suggest that the role of autophagy in response to nutrient starvation should be reconsidered.

 

http://www.ncbi.nlm....les/PMC3798503/

 

 

Glucose induces autophagy under starvation conditions by a p38 MAPK-dependent pathway.

 

Autophagy is a natural process of 'self-eating' that occurs within cells and can be either pro-survival or can cause cell death. As a pro-survival mechanism, autophagy obtains energy by recycling cellular components such as macromolecules or organelles. In response to nutrient deprivation, e.g. depletion of amino acids or serum, autophagy is induced and most of these signals converge on the kinase mTOR (mammalian target of rapamycin). It is commonly accepted that glucose inhibits autophagy, since its deprivation from cells cultured in full medium induces autophagy by a mechanism involving AMPK (AMP-activated protein kinase), mTOR and Ulk1. However, we show in the present study that under starvation conditions addition of glucose produces the opposite effect. Specifically, the results of the present study demonstrate that the presence of glucose induces an increase in the levels of LC3 (microtubule-associated protein 1 light chain)-II, in the number and volume density of autophagic vacuoles and in protein degradation by autophagy. Addition of glucose also increases intracellular ATP, which is in turn necessary for the induction of autophagy because the glycolysis inhibitor oxamate inhibits it, and there is also a good correlation between LC3-II and ATP levels. Moreover, we also show that, surprisingly, the induction of autophagy by glucose is independent of AMPK and mTOR and mainly relies on p38 MAPK (mitogen-activated protein kinase).

 

http://www.ncbi.nlm....pubmed/23116132

 

 

So it seems like it's the other way around. You need the glucose for autophagy to function if we go by these papers.

In aging autophagy is generally impaired, supposedly by inflammaging. Maybe the the amount of glucose produced doesn't change, but there's less autophagy so more glucose is left unused.

Of course that's just one factor.

 

 

The known major inducers of autophagy are low insulin and low protein.   Even a single amino acid will largely take the body out of autophagy.  Your second reference acknowledges this when it says "Autophagy is highly sensitive to the levels of nutrients, hormones, and growth factors and cytokines, among which amino acids and insulin have been the most extensively studied (see e.g. [10])."

 

The first study is simply bizarre.  If you remove glucose from cells, they die.  What was the point of that proof?   The whole point of autophagy is to provide a substrate to provide amino acids and also drive gluconeogenesis during periods of starvation.  If the glucose does not come from the free amino acids, then it comes from free fatty acids.  No body in starvation goes without glucose.   So the first study looks like a bizarre in vitro experiment.  What applicability does that have to anything in vivo?

 

The second study is fascinating, and it largely agrees with the mouse study I published.   In the mouse study, during the period when free amino acids from autophagy surge, glucose surges too.   This then raises a chicken or egg problem:  did the body create a surge of glucose from some other substrate, to drive autophagy, or did the body use the free amino acids from autophagy to drive glucose production?  Maybe it is actually some combination of the two?  The induction of autophagy might be associated with a rise in glucose, but then the free amino acids from autophagy also end up driving gluconeogenesis?   In the mouse study, pay attention to the fact that free fatty acids do NOT surge during the period where free amino acids and glucose do surge.   If the additional glucose did not come from the free amino acids, then wouldn't that have required some other substrate like additional free fatty acids?   By definition the mice were in starvation so there was no glucose coming into the body or starch in process of digestion.  

 

So the second study is fascinating, but I'm not sure it contradicts anything here.   The bottom line is up until I read that study, I had believed the myth that all humans who are prediabetic are suffering from some form of insulin resistance.  The mouse study clearly shows a different case, where high fasting glucose is associated with LOW INSULIN and high autophagy.   I can't help but notice that most adult humans develop prediabetes as aged adults over the age of 40.   That at least forces the question how many of these prediabetic adults are simply doing autophagy because their aged bodies have accumulated a lot of junk, and modern diets do not give them enough time in starvation to ever complete the job of clearing the cells of that junk.  It seems to me it would be fairly easy to measure insulin, glucose, glucagon, and free amino acids in a group of adults in the overnight fast, and then continuing the fast for - say - the next 48 hours.  I'm pretty sure if you did that on a wide age range of adults, you might see a pattern develop that suggests a lot of the adults are in autophagy and not insulin resistance.   I'm also guessing that developing an extended fasting habit might completely resolve the prediabetes over an extended number of years, as the cellular debris eaten by autophagy gradually clears out.


Edited by pone11, 30 July 2016 - 08:42 AM.


#12 corb

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Posted 30 July 2016 - 10:25 AM

The first study is simply bizarre.  If you remove glucose from cells, they die.  What was the point of that proof?

 

Both papers have the same conclusion with slightly different arguments:

 

How can this discrepancy with previous reports be explained? Most experiments showing that deprivation of glucose induces autophagy and, therefore, that glucose inhibits autophagy, were carried out in cells incubated in culture medium in the presence of serum, and/or using low concentrations of glucose or hyperglycaemic conditions
...
Therefore we conclude that glucose is an activator of autophagy under starvation conditions and that this activation is mediated by p38 MAPK.

 

Glucose deprivation is thought to be a macroautophagy-inducing stimulus. We present data here that demonstrates that glucose depletion does not induce autophagy in a variety of cell lines and that it can actually inhibit basal autophagy and autophagic flux induced by a drug

 



#13 aconita

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Posted 30 July 2016 - 09:23 PM

Prediabetes is not an appropriate term at this point since we are talking about two very different conditions which only have in common two parameters: low insulin and high glucose.

 

Prediabetes is a condition that develops into diabetes and needs to be corrected before more damage is done, a totally different scenario than someone with low insulin and high glucose because fasting.

 

If the point is to not be so fast in jumping to the conclusion someone is prediabetic just because one test shows high glucose and low insulin I totally agree.



#14 pone11

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Posted 05 August 2016 - 04:56 AM

Prediabetes is not an appropriate term at this point since we are talking about two very different conditions which only have in common two parameters: low insulin and high glucose.

 

Prediabetes is a condition that develops into diabetes and needs to be corrected before more damage is done, a totally different scenario than someone with low insulin and high glucose because fasting.

 

If the point is to not be so fast in jumping to the conclusion someone is prediabetic just because one test shows high glucose and low insulin I totally agree.

 

I understand and agree with the spirit of your point.  The problem is there is no word for a person who has "low insulin and high glucose because of fasting".   Moreover:

 

* We live in a crazy system that will never measure your insulin responses over time and graph those, thus there will be no detection that you are low insulin while high glucose.

 

* Since the standard of care diagnoses diabetes on glucose alone, a person with low insulin and high glucose because of fasting will be labeled by his own doctor as a prediabetic.

 

If you want to create a new word I don't have a problem with trying to use it.  Just understand that this is your private language and no one in the medical community would use it.



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#15 aconita

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Posted 05 August 2016 - 08:04 AM

I agree with you, the point is just to underlay how the medical standard procedures are limiting without any good reason to be so shortsighted.

 

Anyway diabetes itself is greatly misunderstood by the majority of the medical community and standard protocols on regard are totally inappropriate.

 


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