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Welcome all seeking refuge from low carb dogma!

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Friday, August 8, 2014

All Roads Lead Through Krebs ~ True Keto Clarity & The Truth About Fat Burning Beasts

As Jimmy Moore embarks on his whirlwind Keto Clarity tour, I've decided at this point to take a pass at reading/reviewing the book.

I do, however, think it's time to inject some biochemical facts into this discussion to combat the misinformation train wreck that is Mr. Moore.  Specifically: 
  • Excess protein is turned into glucose
  • Ketones are magic molecules
In his podcast interview with Primal Man of Science Mark Sisson, Jimmy repeated what is clearly becoming a mantra of his, is part of his now "canned" speech on nutritional ketosis, and apparently is discussed in the book.  After mentioning that "long word" -- gluconeogenesis -- Jimmy launches into his discussion of where people who are low carbing go wrong over the long term:  they are eating too much protein.  This sabotages ketogenesis, spikes blood glucose, and stalls weight loss according to Jimmy.

The entire podcast is enlightening (though not for the reasons Sisson and Moore would hope) but I excerpted this clip for you which I found to be particularly informative (direct link):


In general chemistry we learn the various factors that generally determine reaction rates, among them is the concentration of reactants.  The more reactants there are, the faster the reaction will occur.  In biochemistry, this general rule almost never holds true.  Why?  Because:

  • Most reactions are under the control of a "living catalysts" more commonly referred to as enzymes and will not occur without the enzyme in active form with all necessary co-factors.
  • Many reactions (e.g. synthesis reactions) are not thermodynamically favored.  That is they proceed in the opposite direction of that which is spontaneous, which is accomplished by coupling with another reaction with favorable energetics.
Therefore, various metabolic pathways are almost never regulated by the substrate per se.  I was recently discussing here the hierarchy of macronutrient metabolism.  This is important as it manages these energy containing molecules in such a way as to store those that are most efficient at storing, and utilizing first those which cannot be stored at all or stored efficiently.  If the presence of fatty acids meant we burned them for energy -- whether we needed that energy or not -- there would be no saving the energy for a rainy day, or even an overnight fast.  

Most who are familiar with low carb diets have long been aware of gluconeogenesis.  The liver maintains blood glucose levels in the post-absorptive state ("fasted") by producing glucose, and it does this by either breaking down glycogen or making glucose via the gluconeogenesis pathway.  In reality, likely a little bit of both occur at all times, though depending on the diet and/or nutritional status, one may rely more heavily on once source or the other.

I don't suppose Sisson has ever heard of the LoBAG diets.  (Perhaps the spy minion should read some of the posts while he/she is here).  That link is to a blog post of mine, with additional commentary added more recently, but is from the early days of the Asylum.  

LoBAG stands for Low BioAvailable Glucose and though carb content varied from 20 to 40% on different versions of the diet, protein was doubled in all, from 15% to 30%.  Furthermore, since these were not calorie restricted weigh loss diets, the absolute protein consumption effectively doubled from baseline.  As an example of where absolute amounts matter more than percentages let's say one begins on 2400 cal/day of a 50C/30F/20P diet (roughly 300g C, 80g F, 120g P).  If this person switches to consuming 1200 cal/day of a low carb diet 10C/60F/30P (roughly 30g C, 80g F, 90g P), he has actually cut carbs and protein while keeping fat intake constant.  And yet this is often described as "upping fat and protein".  So

In LoBAG studies, because they did not cut calories, they doubled the absolute amount of protein in the diet.  In diabetics no less.  And guess what?  HbA1c improved because endogenous glucose production (EGP) in the liver decreased.

These subjects, whose metabolisms are "primed" for excessive glucose production (hyperglycemia in diabetes is due to unchecked gluconeogenesis), didn't respond to protein increases with the expected increase in EGP.  Jimmy Moore can go home now ... And yet Mark questioned Jimmy (paraphrase):
Does Dr.Westman had an explanation for the body so readily making glucose when it has been so finely keto-adapted?
Perhaps he should spend his next relaxing work day actually cracking open a biochemistry text rather than worrying about whether he'll look more cool in the papasan chair or on the cabana bed for the next video.   After all, Sisson has a degree in Biology from Williams College, so presumably he is capable of researching this for himself.   That is his job, after all.  Well, that's what he told the audience repeatedly at PaleoFX this past April.

Krebs though ...


I want to back up to the title of this post.  I have been beating this drum for a very long time in the carbs vs. fat debate.  MOST of the energy produced from either one is produced from Krebs on forward (e.g. the electron transport chain), and the common entry into that pathway is acetyl-CoA.  Don't believe me, how about this opening summary quote from Chapter 20 of Marks' (obviously not Mark'S) Medical Biochemistry p. 360:
The TCA cycle (tricarboxylic acid cycle [Krebs]) accounts for over two thirds of the ATP generated from fuel oxidation. The pathways for oxidation of fatty acids, glucose, amino acids, acetate, and ketone bodies all generate acetyl CoA, which is the substrate for the TCA cycle.
I'm going to get to protein in a minute, but I have altered the diagram I often use here to show where amino acids feed into the Krebs cycle to demonstrate the point about converging pathways.  (Note that this version of the cycle is incomplete in the intermediates of the cycle shown.)

I like to liken the Krebs Cycle to a giant revolving door  with many entrances and exits about the rotation at which people can get on and off.  We can also imagine that nobody gets in the main entrance (around 2 o'clock in the diagram) unless there are some people in the compartment to help pull them in. When the "door" is filled with people in each compartment, it revolves around and the coordinated "pushing" of all the people imparts a momentum to the door itself, while any single person can pretty much be swept along and round and round without even trying.  In your "balanced metabolism", there are lots of people in each section of our imaginary door.  Glucose is converted to pyruvate which is readily converted to acetyl-CoA for entry into Krebs.  Meanwhile fatty acids are broken down more or less directly to acetyl-CoA for entry into the very same Krebs cycle.  

The "fat burns in the flame of carbohydrate" saying, that Sisson dismisses as mythology later in the podcast, actually has a basis in the biochemistry of Krebs.  When there is glucose around, the different compartments remain relatively full of passengers at every point around the rotation.  When glucose is scarce, emergency workers are dispatched to pull people out of the revolving door at the oxaloacetate opening (around 10-11 o'clock).  Biochemically, oxaloacetate gets depleted. When that section or the door comes around to 2 o'clock, there aren't enough people in the compartment to pull in new passengers.  

The  "empty compartment" (oxaloacetate depletion) causes two things to happen.  
  1. Pyruvate is diverted to the left towards gluconeogenesis, and 
  2. Acetyl-CoA (now from fats mostly) is diverted into ketogenesis.
As fewer passengers are taken on as acetyl-CoA, and lost to oxaloacetate with each turn, the Krebs cycle "door" slows.  The cycle is never just one molecule that goes along for the ride throwing off reducing equivalents and ATP.  It is always a bunch of each species around the loop that keeps the revolving door turning, pulling people in from various doorways and generating energy as it churns around.

So, first things first:  there is no real "elaborate metabolic machinery" involved in producing ketones.  And as you can see, the biochemistry (in a physiological context) is quite simple.  Most importantly, gluconeogenesis and ketogenesis go hand in hand.  They don't really compete!   Oh ... and they are both unequivocally associated with "starvation" metabolism.  

In the liver, when glucose is scarce, other sources of pyruvate are shuttled into the gluconeogenesis pathway rather than acetyl-CoA production.  When fat is metabolized  in this metabolic condition, there is no "carb flame" to ensnare it into the Krebs "revolving door", thus this acetyl-CoA is shunted to acetoacetate rather than a spin around the cycle.  Here's an interesting little biochem tidbit given recent discussions as well (the note about ethanol toxicity):   


 The AA can be converted back to acetyl-CoA as we'll see, or ...

The NAD+/NADH status of the liver cell, which is governed by the sum total of metabolic activity in the cell, is what really determines the fate of the acetyl-CoA to Krebs vs. "ketone 1" (acetoacetate) and then subsequently to BHB or acetone.  By the way, all of these "ketone bodies" are in various body fluids, it is simply that different tests measure different species (urine is AA, breath is acetone, and blood testers measure BHB).


Primary Metabolism thus far ...


Carbohydrate ► Glucose ► Pyruvate ► Acetyl CoA ►►► CO2 + H2O + ATP
Fatty Acids ► Acetyl CoA ►►► CO2 + H2O + ATP
There are some differences in the production of ATP and reducing equivalents (NADH or FADH2) up until the point of Acetyl-CoA, but after that we're talking about the same metabolic pathways for the majority of energy production.


How Does Protein Factor In?  


If you read some of my older blog entries, you will see my understanding "evolve" a bit.  It is easy to fall into the trap that protein is only used for energy after first being converted to glucose.  Although I took two biochemistry classes in college -- one in the bio department, and one in chem -- I honestly don't recall either spending much time on how protein fits into the picture for energy production.  In bio, we focused on the cycles themselves more, the regulation of the various pathways and how this integrated into physiology.  In the chem course, we focused tediously on the mechanisms of the various reactions and the chemical structures of intermediates and enzyme active sites.



But, just because we didn't focus on it doesn't mean it wasn't all there in the textbooks or ignored entirely.  So, as it turns out, amino acids feed into Krebs and associated pathways at various places.  I've referred to this diagram many many times.

It seems odd to talk about "protein" being glucogenic and anti-ketogenic, when in fact some amino acids (in the white boxes) are ketogenic, while others are solely glucogenic, and many can be either depending on the situation and where they are fed into the cycle.

So one of the roles amino acids play in metabolism is in keeping the revolving Krebs door filled with people so that it keeps going around.   It is this, preventing "oxaloacetate drain", that is the most likely mechanism by which dietary protein blunts ketosis by allowing fatty acid derived acetyl-CoA to enter the cycle and be metabolized to completion.  In the process, the amino acids that feed into Krebs produce ATP and/or reducing equivalents depending on their points of entry.  

Some (actually only a few!) can provide substrate directly for the gluconeogenesis pathway.  It should also be pointed out that other substrates for this pathway include glycerol (from the backbone of dietary triglyceride fats) and lactate from anaerobic respiration, and also some short chain fatty acids.   

It is not gluconeogenesis, however, that puts the brakes on ketogenesis.   Look at the pathways above again, and realize that it is a deficiency of oxaloacetate that favors ketogenesis rather than processing of acetyl CoA through Krebs.  Gluconeogenesis "drains" OAA.  Protein puts the brakes on ketogenesis because it keeps the Krebs revolving door going around and generating energy the old fashioned way.   If amino acids fill the revolving door, fatty acid derived acetyl CoA is going into Krebs!   

Ketones in Starvation ...


I am including this screenshot from Cahill & Veecht to show the adaptation in starvation to a fat and ketone burning metabolism.  


The free fatty acids rise almost immediately but rise only slightly more after a few days.  (Note that the y-axis can be misleading as these are concentrations of the number of molecules, fatty acids contain much more energy per molecule than glucose,  AA or BHB).  The ketones rise sharply for a bit longer before leveling off, and it would appear that the BHB formation is the "adaptation" that "preserves" this energy.    Below are also from C&V and demonstrate how ketogenesis is glucose sparing mostly for fueling the brain.  

I would note the use of the thickness of the arrows to denote the relative contributions of the fuels for energy.  Obviously, stored fat is the major fuel but the body effectively converts some to a glucose substitute to fuel the brain while sparing lean muscle mass (protein).

Perhaps I'm missing something, but can someone please point out to me how minimizing dietary protein so as to supposedly prevent gluconeogenesis, is a good idea for fat loss and lean mass retention???



What Becomes of the "Ketone Bodies"?  


Here is where I can't help but remind the low carb hucksters of what the man himself claimed.  Yes, the "late great" one.  Dr. Robert Atkins.    Atkins' claim was that ketones were the result of incomplete metabolism of fatty acids, and that they were excreted unused in the urine.  A CICO man through and through.  

It is also why Jimmy's desperate attempts to claim that Atkins wasn't a ketogenic diet are disingenuous at best.  Most folks went to the diabetic supply section of their pharmacy to purchase ketostix when they tried Atkins for the first time.  And the reason why being knocked out of ketosis elicited despair was that Atkins made it sound like ketosis really was the magic pathway so that you could eat endless fat and pee out most of the calories.  Indeed as you "climbed the rungs" after induction, you were to add in 5g/day at a time of carbs until you could figure out how many carbs you could "get away with" and remain in this magical metabolic state.    It's all right there in the original 1972 book.  

I don't know why, with my background, I never thought to do the math on this back when, but they've looked into these claims (and one can do rough calcs using average urine volumes and ketone levels for estimates) and we're talking like 20 cal/day tops here.  Over the long term such "energy leakage" could really add up, but this most certainly cannot be the reason for greater short-term weight loss on Atkins or other low carb plans.

As it turns out, the ketones ... drumroll please ... feed into Krebs!  

So the above biochemistry is from the same link as given previously and you can find more detailed reactions here.  
And lastly, though redundant (and I had to switch up the missing intermediates from the original diagram), I've worked ketone metabolism for energy into the cycle below.   My point in bothering with this is to show that acetoacetate basically gives the Krebs revolving door a push in the process of creating the precursor of acetyl CoA to feed in as usual for energy production.

Bottom line:  ketones are a "detour" in the fat burning path -- like getting off the wrong exit on the highway, and going round the loop-d-loop and getting back on going in the same direction.  [FWIW, as far as calories go, yes, you waste a little "gas" accounted for in calories out. ]   IF Atkins had been correct about peeing out quantitatively significant acetoacetate molecules, although the fatty acids were completely oxidized to make acetyl CoA, excreting AA would represent incomplete extraction of energy from the fatty acids, or "incomplete fat burning".  Major calories out (see Marks' Med Biochem quote above) .  Too bad it's not true ... and equally bankrupt of the current bearers of the Atkins torch to make up new (unfounded) ideas to replace the disproven.


And just to beat that horse but good and dead and kill it again.  From Marks'






So now here's a thought regarding dietary protein ...


If we "starve" Krebs in the liver so as to promote ketogenesis, what does that do to Krebs in all of the other cells?   These cells rely on Krebs processing the acetyl CoA from all substrates to generate the bulk of the energy needed to live.  Is it any wonder that these keto-obsessed athletes -- like Ben Greenfield -- resort to supplementing with oxaloacetate when they need to actually burn fat or ketones for energy?


Fat Burning or Ketone Fueling?


I'm going to finish the biochemistry and metabolism part of this post with this discussion, and it relates to a common misconception perpetuated by the likes of Jimmy Moore.   Being in ketosis is NOT an indicator of overall fat burning.  

Fat burning is the break down of fatty acids all the way down to CO2 and H2O.  This happens all the time in the unstarved state.  

Being in ketosis is NOT an indicator of net BODY fat burning.

Case in point, the medium chain triglycerides, aka MCTs.  Coconut oil and CO derived MCT oil (the shorter of the MCTs) are favorites for the ketogenic crowd.  For good reason, because if ketones are the objective, these will force your liver to make them, pretty much regardless of one's nutritional status.  MCTs are metabolized preferentially in the liver as we have no mechanisms to elongate these for storage from this starting length.  This rapid acetyl-CoA production exceeds the capacity of Krebs and ketones are produced and sent out into circulation for use elsewhere.  When this happens, long chain fatty acid oxidation -- aka from body fat or other dietary fats -- is reduced.

Furthermore, if someone is eating hundreds of grams of dietary fat, there is no net body fat burning going on.  And don't look now, but Jimmy Moore has inadvertently demonstrated via his second nutritional ketosis experiment (e.g. May 2013 to present) that it is indeed possible to be a fat burning beast and gain substantial amounts of body fat.


Because calories matter ...



Which Leaves Us With Therapeutic Uses:


The only proven uses for ketogenic diets that I am aware of, have been with neurological diseases.  Let's go back to the Cahill & Veech paper.  It is entitled Ketoacids?  Good Medicine?  In the abstract they write:
Recent studies have shown that D-ß-hydroxybutyrate, the principal "ketone", is not just a fuel, but a "superfuel" more efficiently producing ATP energy than glucose or fatty acid. 
That's because it's not a fair fight!  These ketoacids are but a redox step plus one from acetyl CoA -- the primary "fuel" our metabolic power plants.  They also have an advantage over glucose and pyruvate in that they do not require transporters into cells or the mitochondria where most of the neuronal issues seem to arise.  They are therefore a ready source of acetyl-CoA from which to produce energy.  Peter Attia spoke hopefully of development of ketone precursors as an alternative to ketogenic diets.

Aside from this, and the less promising possibility that diet can manipulate cancer at a metabolic level (the results of these have been way overhyped, and in a short time here we'll have Jimmy leading a panel at #AHS14 discussing this for sure), we're left with ketosis for weight management.  Although some experience appetite suppression -- especially in the early going -- from ketosis, this is not universal or necessarily lasting.

Jimmy Moore has claimed that the calories will work themselves out when you're in nutritional ketosis.  He, himself, has demonstrated this not to be true.  


Meanwhile ...


  • There are no examples of human cultures in chronic ketosis
  • There are no examples of human cultures consuming upwards of 60% fat for any length of time (e.g. lifelong and all members)
  • There is no evidence that the few human cultures consuming high fat diets are ever in ketosis except during periods of famine
  • There are no long term RCTs in humans of the effects of THIS diet (not Atkins, not "low carb") at weight maintaining caloric levels.
  • We only have the n=1 examples .....

But this guy says it's backed by the science!




This was 2004.  Back when Jimmy Moore was eating lean meats on his Atkins diet, hitting the treadmill/elliptical daily, losing 180 lbs, and actually improving his health in the process.



73 comments:

CynicalEng said...

"how minimizing dietary protein so as to supposedly prevent gluconeogenesis, is a good idea for fat loss and lean mass retention" - I think the line of thought is that dietary protein intake increases insulin and glucagon release. Insulin impairs fat release and ketogenesis - as per http://www.ncbi.nlm.nih.gov/pubmed/749914 - hence excess protein isn't conducive to running high blood ketones and losing fat ?

carbsane said...

This is the other line of reasoning against protein, except that I've never seen the insulin angle proffered for protein -- more like ignored! The main thrust of this post was this new mantra that excess protein turns to glucose and that is the problem. Thus a "proper" keto diet is uber high fat, rather low protein.

The other point, perhaps I neglected to stress, is that if the acetyl CoA goes into Krebs, that IS fat burning. Ketosis is not synonymous with fat burning.

charles grashow said...

Jimmy et.al. might want to do some research on Dr M Judah Folkman and anti-angiogenesis with regard to starving cancer.




http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891166/


Natural
health products that inhibit angiogenesis: a potential source for
investigational new agents to treat cancer—Part 1





http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891180/


Natural
health products that inhibit angiogenesis: a potential source for
investigational new agents to treat cancer—Part 2





http://www.ted.com/talks/william_li


Can we eat to starve
cancer?





http://www.pbs.org/wgbh/nova/cancer/folkman.html


Dr. Folkman Speaks






http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2268723/


Judah
Folkman, a pioneer in the study of angiogenesis






http://www.aao.org/publications/eyenet/200711/feature2.cfm


Interview With Judah
Folkman






http://www.scientificamerican.com/article/quiet-celebrity-interview/


Quiet
Celebrity: Interview with Judah Folkman






http://www.pbs.org/wgbh/nova/body/folkman-cancer.html


Cancer
Warrior Judah Folkman





http://www.youtube.com/watch?v=mDXb4I8ZzOk


NOVA
scienceNOW : 45 - Phoenix Mars Lander, Brain Trauma, Mammoth Mystery,
Profile: Judah Folkman


Profile: Judah Folkman
- 38:30


Dr. Judah Folkman, who died in 2008 at age 74, was a giant in
the field of cancer research. He wasn't always considered a trailblazer,
however. In the 1970s, when he first proposed that cancer depends critically
on new blood vessel growth, or angiogenesis, other medical researchers
ridiculed his ideas. But Folkman proved his theory of angiogenesis, and today
it has led not just to cancer therapies but also to treatments for other
diseases of abnormal blood vessel growth






http://www.pbs.org/wgbh/nova/body/cancer-warrior.html


Transcript/Video


Cancer
Warrior


PBS
Airdate: February 27, 2001






http://www.hindawi.com/journals/jcr/2013/895019/


Tumour
Angiogenesis: A Growth Area—From John Hunter to Judah Folkman and Beyond






http://jnci.oxfordjournals.org/content/82/1/4.full.pdf


What Is the Evidence
That Tumors Are Angiogenesis Dependent?

MacSmiley said...

Does Keto Clarity even mention Krebs Cycle?

The whole thing makes me dizzy, but I do get the point that Jimmy is wrong, of course.

MacSmiley said...

Shhhh. No one in LC wants to admit that protein is I insulinogenic.

Nigel Kinbrum said...

1) Minimising dietary protein starves the liver & kidneys of gluconeogenic precursors.

2) Blood glucose level drops.
3) The pituitary gland secretes ACTH.
4) ACTH stimulates the adrenal cortex to secrete cortisol.
5) Cortisol cannibalises LBM to create gluconeogenic precursors.

This doesn't sound like a good idea to me.

CynicalEng said...

As others don't want to admit that there is negligible blood sugar impact due to the accompanying glucagon release. No extra glucose for the insulin to store, homeostasis cruises along.

CynicalEng said...

Eating *adequate* protein avoids that. How much protein is required per day for a Jimmy Moore to feed his gluconeogenesis of say 140 grams/day ?

carbsane said...

?? Glucagon stimulates EGP

carbsane said...

Jimmy has just admitted to weighing 260 lbs but he looks a bit heavier than that. It's possible that he's quite a bit, let's say, "differently composed" than he was at that weight after he first lifted weights back in 2007-8.

EJ said...

"Perhaps I'm missing something, but can
someone please point out to me how minimizing dietary protein so as to
supposedly prevent gluconeogenesis, is a good idea for fat loss and lean
mass retention???"

It depends what you mean by "minimizing dietary protein". Unfortunately the low-carb crowd has a tendency to not measure anything but carbs, because measuring anything else might be that evil "calorie counting", "CICO", "deprivation" "eat less move more" "Food Pyramid" "conventional wisdom" nonsense advocated by Ancel Benjamin Keys.

Near as I can tell, when Jimmy Moore "moderates" his protein, he's probably eating around 80 grams per day or so. This is the amount which would be found in about 16 eggs or 12 ounces of beef. It's not "minimized" except when compared to the insane amounts of protein some people think they're supposed to eat on the Atkins diet. I've seen sedentary people try to get in 150, 200, 300 grams of protein per day. This is more than Arnold Schwarzenegger would have consumed during his Mr Universe days.

From what I've seen, most men can get by just fine with 50 to 120 grams of protein per day. Jimmy Moore's consumption is probably in the middle of that range, and is probably perfectly adequate.

One question that probably should be asked is, "if fat is so satiating, why do you need to eat so much of it?". A stick of butter contains about as many calories as a quart of cooked oatmeal, or 5 bowls of breakfast cereal or 9 slices of bread. But even the most dedicated carb addict could probably get by with 2 eggs, 2 strips of bacon, 2 slices of toast, and a cup of black coffee. (or if they really insist on sweetener, 10 grams of sugar added to the coffee).

George said...

Enjoyable discussion of Krebs. Ketosis is good, as you say, for neurological disorders. It may well be that appetite dysregulation under Western diet conditions - addiction or whatever - is not only hormonal but also has a neurological aspect that can be medicated successfully by ketogenic diets. Whether it takes lifelong adherence or stays fixed after a while is another question. Whether or not one finds this post convincing in its disputational aspect, it is certainly informative and one of your best.

carbsane said...

He says he's eating 80-100g protein per day -- closer to 80 most days, 100 on the days he works out. Considering that he is eating less than 30 total carbs, the only real ones likely from dairy and chocolate, his protein requirements would be more than that. He is pretty tall and 80g is probably more in line with a minimum he should be consuming on a regular diet that didn't force reliance on gluconeogenesis.


Surely ketosis reduces the need for gluconeogenesis, but he's been at this for two years now and at one time lost almost 80 lbs. Nobody (well maybe Fat Head) was fooled by the DEXA games, and below 15% protein not to mention the IF up to like 36 hours, he lost at least the usual lean mass. Regaining on low protein it's likely been all or mostly fat gain. Even though 80 g isn't low per se, it is in the context of his diet.

As to fat being satiating, that's a bugaboo with Jimmy that's been going on for YEARS!!! He is on the book podcast tour saying that you need to find carb tolerance, moderate down protein and then eat sat fat to satiety and the rest will settle out. Ummmm ... it's not! Again!!


Several years back when he had the menus blog he wrote of eating 25 chicken wings. Even small ones, that's a lot. He said he didn't feel satisfied until the 25th and blamed it on chicken being notorously low in fat (which he remedied with butter and a boatload of ranch dressing). When I pointed out what he would have had to eat in drumsticks or thighs to match the calories he responded as if I agreed with his assertion that chicken was low fat. There's a screw loose there somewhere.

EJ said...

According to Buffalo Wild Wing's nutritional data, a Buffalo wing contains 5 grams fat and 6 grams protein. They clock in at 72 calories each (47 calories from fat), so about 67% of calories from fat. 25 restaurant Buffalo wings would total about 1800 calories, 125 grams fat, 150 grams protein, and zero carbs.

http://www.nutrition-charts.com/buffalo-wild-wings-nutrition-information/

I remember the first time I even heard of Atkins he was on the Oprah Winfrey Show, and he exclaimed that Buffalo wings were one of the best restaurant options available for a low-carb diet.

If someone eats 25 Buffalo wings and doesn't feel full, they probably have problems understanding their body's hunger and satiety signals. It would be a really good idea to learn some mindfulness practices.



For example, they could take a small bite of chicken wing, put the wing down on the plate, let go of the wing. Then they could chew slowly at least 20 times, paying close attention to the sight, smell, flavor, texture. then swallow. Then wait a few seconds. Then think about all of the work that people had to do to put the chicken on the plate, and about the sacrifice of the chicken. Then, they could ask their self if they are at least 80% full. If not, they could ask their body what it's hungry for. If it's chicken wings, they could take another bite.


Or, it could be that their body is screaming for carbohydrates, and so it sends out hunger signals, and makes the person eat 25 chicken wings, when 1/2 a cup of cooked rice would have done the trick.

carbsane said...

I highly doubt it. Not sure that it needs to, but the idea that excess protein is turned to sugar *should* require some substantiation. I didn't have time to dig up the citations, but research has been done to directly test this. Somehow I doubt it's in the book :p

carbsane said...

Thank you George.

John Smith said...

Dedicated low carbers do not have to exercise as frequently as carb addicts to stay shredded, once every ten years is more than sufficient. In fact he may need to cut back on the weight lifting so as to avoid overtraining.

Nigel Kinbrum said...

Another thing that long-term ketosis is good for...http://nigeepoo.blogspot.co.uk/2014/08/ketogenic-diets-and-sudden-cardiac-death.html

Nigel Kinbrum said...

"There's a screw loose there somewhere."
I'm starting to think that it's chronic hypercortisolaemia damaging the hippocampus etc. :-/

Nigel Kinbrum said...

Without blood glucose, we're dead. So why go to all of the trouble of making it out of expensive protein which then produces expensive urine, when you can get it from natural carbohydrate foods?

Also, http://nigeepoo.blogspot.co.uk/2012/04/how-eating-sugar-starch-can-lower-your.html It's not even very accurate. Don't do it.

Nigel Kinbrum said...

Eating *adequate* protein often results in high blood glucose, as the counter-regulatory loops to generate blood glucose in the absence of dietary carbs aren't very accurate. See http://nigeepoo.blogspot.co.uk/2012/04/how-eating-sugar-starch-can-lower-your.html

charles grashow said...

According to Jimmy his latest diet is 80-85% fat, 30 gram carbs and 80-100 grams protein/day.

If we assume 90 grams protein (15%) and 80% fat then he's consuming 2400 calories/day

1920 calories fat (80%)
360 calories protein (15%)
90 calories carbs (5%)

Question - if he's in ketosis all of the time and he's regained at least 30 lbs then his theory/mantra that CICO doesn't matter has to be wrong. Or am I in error?

Also - per his last posted DEXA scan he's got problems.

newbie said...

"I like to liken the Krebs Cycle to a giant revolving door with many entrances and exits about the rotation at which people can get on and off" - this is the best imagery I have ever encountered for visualizing the Krebs Cycle - LOVE IT!

In response to your query - "?? Glucagon stimulates EGP"
From wikipedia - http://en.wikipedia.org/wiki/Glucagon
When glucagon binds to the glucagon receptors, the liver cells convert the glycogen into individual glucose molecules and release them into the bloodstream, in a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis.

Onto the reason I am commenting - actually a question - from Peter Attia's blog - http://eatingacademy.com/nutrition/ketosis-advantaged-or-misunderstood-state-part-ii - "The second important point to recall is that ketone bodies bypass this process (i.e., glucose to pyruvate to acetyl CoA), as B-OHB enters the mitochondria, converts into acetoacetate, and enters the Krebs Cycle directly (between succinyl CoA and succinate, for any biochem wonks out there)." Doesn't that mean that B-OHB can bypass the slowdown at Acetyl coA and run Kreb's from a different entry door? And does that make a difference - I'm not sure?? HELP in understanding this!

newbie said...

I brought up the bottleneck at acetylCoA (which ends up favouring ketogenesis) as it is part of the discussion by Chris Masterjohn -- http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html - I'm just trying to piece it all together. Thanks again for your attempts at clarification of the issues involved.

MacSmiley said...

Just spell it out, Nigel: Sudden Cardiac Death! 😧

Great eye-opening blog post, though. 👀

MacSmiley said...

Tongue, meet cheek. 😜

carbsane said...

Thank you! The analogy is not perfect, but I do think it gets the general idea of Krebs instead of thinking about single molecules going through a series of reactions.

As to your main question -- I should label my figures! LOL . This one demonstrates that B-OHB does NOT bypass the process. Acetoacetate -- from BOHB or remaining, gives Krebs a "push" at the succinyl-CoA/succinate "entry", but the result is good old fashioned acetyl CoA that must go through Krebs as all acetyl CoA does. Marks' summary diagram shows ketones ultimately feeding in at acetyl CoA.



More in a bit ...

Sanjeev Sharma said...

a large fraction of those on the national weight control registry regularly weigh and/or tape measure themselves. lots of the research on executive function points to self-monitoring as an important tool for adherence.

if (a BIG if) ketosis "works" I would first look to explain the effectiveness via these established mechanisms (self regulation, monitoring, feedback, sense of agency, executive function) before mighty keto-metabolism mouse mechanisms.

Sanjeev Sharma said...

back in the day when I followed eating disorder research there was a fairly long-lived theory that high cortisol during certain sensitive windows was a contributing factor.


Next time I trawl for updates on my pet theories I'll have to check if anything ever came of that.

John Smith said...

A man in his 40's with a lot of fat around the middle is tempting fate to begin with, throw in the weird diet and he'd better carry around a four leaf clover and a rabbit's foot.

Puzzling why people do this, I changed my evil ways in my mid-40's because I looked like Jimmy and recognized the risk of a myocardial infarction. He is my "before" picture.

carbsane said...

More on Attia's post. The diagram he used is similar to the one I highlighted in this post: http://carbsanity.blogspot.com/2012/08/ketone-and-fat-burning-are-not-same.html


From the diagram in that post and Fig 20.1 from Marks in this post, what is bypassed or diverted or whatever when ketones are metabolized is the GDP→GTP conversion (ultimately coupled to ATP) that is coupled to the succinylCoA→succinate step in Krebs. But the product of this (acetoacetyl CoA) goes back to "start" with acetyl-CoA.


What I did with Attia's diagram in yellow is show where transporters are involved in the metabolism of glucose. In the brain we're talking non-insulin stimulated GLUT1s, which is why keto helped this little girl: http://www.nydailynews.com/life-style/health/girl-3-finally-speaks-thanks-cream-cheese-heavy-diet-article-1.1402730


Pyruvate also enters the mito matrix with the help of a carrier protein: https://www.rpi.edu/dept/bcbp/molbiochem/MBWeb/mb1/part2/krebs.htm


BHB and AA require no such assistance to getting into the mitochondrial matrix and this is why ketones are therapeutic in certain conditions.



In the paper about Parkinsons and Alzheimers, I think they also identify an issue with the pyruvate dehydrogenase enzyme activity. Don't have the time to delve there today. Bottom line is that ketones basically bypass either the need for transporters or metabolic steps where there may be deficiencies and provide acetyl-CoA to Krebs. Hope that makes sense.

carbsane said...

Sanjeev stole my response :-)


Wheat Belly has had some success stories by having folks monitor BG and never letting it get over 100 or 110 after a meal. This is a very effective way of ensuring compliance with a very low carb diet (whether diabetic or not) coupled with a heavy dose of inappropriately instilled paranoia about non-compliance = amputation down the road.


Ketosis is even more difficult to maintain than this, and requires vigilance. The diet for epilepsy is no ad libitum free for all either. If -- as with Jimmy -- protein must be limited as well, you can be assured some lean mass is lost in the process despite his gaming of the DEXA several months in.


However since ketosis is no guarantee of weight loss (neither is glycemic control), it's unlikely to work in the long run.

Jane Karlsson said...

This field is in an interesting state right now. Last year it was discovered that BOHB is a histone deacetylase inhibitor, which means it activates transcription of antioxidant genes. I think this is HUGE.

'Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor'
http://www.ncbi.nlm.nih.gov/pubmed/23223453

We already knew that BOHB scavenges hydroxyl radicals.
'Antioxidant capacity contributes to protection of ketone bodies against oxidative damage induced during hypoglycemic conditions'
http://www.ncbi.nlm.nih.gov/pubmed/18339375

Muata Kamdibe said...

Hey Evie and my other Asylum inmates ;) It's been a while since I've posted a comment, but I've been lurking. It never amazes me how some things never change in the LC/Paleo world. It kinda makes me glad that I've found more interesting things to do with my life that's not connected to being on the internet. Anyways, I've been watching a lot of debates with Creationists and Evolutionists on YouTube lately, and I couldn't help but see a striking similarity with the arguments (if you want to call them that) that Evolution deniers make with those of Calorie deniers. On the one hand, the Evolution deniers say, "Evolution is just a theory." And then they do a Cuba Gooding-esque chant of "Show me the transitional fossil records!". Then, we have the Calorie deniers say, "Calories don't count! It's all about eating (or not eating) _______ (fill in the macro)". What is insane is that there is an abundance of evidence contradicting both illogical positions, yet here we are. (sigh!)


Quick question guys, has there ever been an RCT overfeeding study in which a person either lost weight or gained zero weight? Also, has there every been a RCT weight loss study in which the participants either gained weight or remained the same weight?

charles grashow said...

Jimmy Moore at AHS14 - look at how health he looks

https://www.youtube.com/watch?v=QoJJ_N7FCZM&list=PLbhWKPDKXIEAhNzG0GiCw7jE59KS6WH5w&index=13

Pinky Artichoke said...

You know, my male companion (mid-30s, 6'1", a hair under 200lb) routinely eats 20-25 wings at a sitting. It's not really that much for a bigger guy if he missed a meal earlier in the day or something.

newbie said...

It makes so much more sense! I did not get what the point of ketone production was, since it is supplying acetylCoA, of which there is plenty from beta oxidation of FAs in peripheral tissues. BUT, there are no FAs entering the brain (actually not true, there are, but not many - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927939/ and http://www.hindawi.com/journals/bmri/2014/472459/), so ketones are the brain's energy source when glucose is scarce - ketosis is all about the brain (and RBCs, kidney cells, etc which are mostly glucose users), not the peripheral tissue - they have lots of acetylCoA - you made it so clear - again a multitude of "thank you"s:).
OK, so in the LBAG state, you are releasing FFAs from adipocytes, the FFAs are carried by albumin - NEFAs in the plasma. These end up in the mitochondria of your average peripheral cell, and by beta-oxidation, give you loads of acetylCoA, and the incorporation of this molecule is the rate limiting step of the TCA cycle....ketones bodies just ultimately adding to the traffic jam in the peripheral tissue's mitos. The only point of the ketone bodies is to feed the tissues that don't use FFAs well. So why all the hype about the "advantaged" state of ketosis? I am serious in this question - I don't get it. Peter Attia's posts led me to believe that ketones have a very special entry point into the Krebs Cycle, but in fact they don't "enter" it between succCoA and succ, they just give it a shove by accepting the CoA.
You don't have to post this if I am stating the obvious points that so many others have already understood.

Steve G said...

25 wings = approx. 1800 cals, 120g fat http://www.fatsecret.com/calories-nutrition/buffalo-wild-wings/chicken-wings. That's not counting add on stuff (scientific terminology) like fries and beer. by the time he walks out the door he has more than likely consumed 3000+ calories mostly fat. Better off just drinking the beer.

EJ said...

No doubt a normal person could eat 25 chicken wings. Professional Competitive Eater Joey Chestnut once at 182 chicken wings in 10 minutes. The question is, are they doing it out of hunger? In Chestnut's case, there's no doubt he's ignoring his body's hunger signals and pushing through.


A common assertion in the low carb religion is that fat and protein are so satiating, so satisfying, that it isn't possible for a human being to overeat the stuff. Thus, there is no reason for anyone to count calories or monitor portion sizes or even moderate their food intake as long as they aren't eating more carbs than their body can tolerate.


Suppose a scientist invented a machine that could tell whether or not you were hungry and an eccentric millionaire made you a bet - you start with a plate of 25 chicken wings and you can eat as many as you like until you are no longer hungry. You can take as much time as you want. You will get paid $100,000 for each chicken wing you leave uneaten, but if the machine says you are still 'hungry', you get nothing.


You decide to take your time, take small bites, chew thoroughly, wait a few moments between bites, and ask yourself if you're really hungry before going for the next wing. Heck, you might even eat the carrots and celery they always serve with the wings.


At the end of this challenge, how much cash will you get from the millionaire? $1 million? 1.5 million? More?


Or would you eat all 25 wings and still be "hungry" because 125 grams of fat isn't enough and 175 grams of protein will cause an insulin spike through gluconeogenesis? Plus it's high in Omega-6 and the chicken was probably corn fed or something.

MacSmiley said...

LOL!!

Kade Storm A.K.A. Hedonist said...

Spot on!

carbsane said...

Hi Muata!!!! Sorry for the belated reply here. It's good to see you around!


What has been getting to me in the discussions is this notion that to acknowledge the role of calories is tantamount to believing that 3500 cal = exactly 1 lb of fat tissue, and somehow if you can't demonstrate this, then all things calories are wrong. And yet the alternatives have not a shred of evidence to support them per your last paragraph. Temporary fluid shifting/retaining/shedding happens and can seemingly stall a person to where it can mess with ones motivation, etc. But everyone gains in the overfeeding studies, everyone loses in the underfeeding studies when caloric intake is closely monitored and verified.

And cortisol can't make fat out of thin air ;-)

carbsane said...

Actually RBCs (and I think kidney) can't use ketones b/c they rely on anaerobic glycolysis and lack mitochondria.


In many circumstances, infused ketones have been shown to have powerful effects. It is ridiculous IMO to extrapolate that to physiological conditions.


To me it is only an advantaged state compared to the alternative (mass muscle breakdown and death). But it can be exploited to treat some neurological disorders.

Nigel Kinbrum said...

Not everybody gains in overfeeding studies. See http://www.endocrine-abstracts.org/ea/0029/ea0029s70.5.htm

Sanjeev Sharma said...

addendum: if one's "reward system"[0] is not activated by this type of food, losing weight is _almost_ a foregone conclusion.

[0] which drives behaviour and provides NEITHER reward nor satisfaction;
that comes later as emotional/explanatory/cognitive dissonance circuitry
tries to explain the behaviour; google Olds and Milner to see how "reward system" came to be another misleading historical-baggage moniker

Muata Kamdibe said...

Thanks Nigel, I wasn't aware of this condition; however, this actually helps to show that in the majority of folks (whom I'm assuming doesn't have CT), calories, ultimately still matter. I wonder what would have happened if the study was for 8 weeks instead of 4.

Muata Kamdibe said...

No worries Evie! I'm just at the point that I believe calorie deniers are either arguing from ignorance, are delusional, or flat out snake oil men and women. You know that I find it interesting that folks will use the Jewish Holocaust as an example in all types of situations (e.g., political, religious, etc.), except for arguing for the primacy of the calorie; however, from my understanding, and brief readings, there were no obese Jews who lived in the concentration camps. "Oh, that's just an extreme example; they were starved!" is what one calorie denier once told me. Of course my response was just to sigh. Now, I treat calorie deniers as the "creationists" of the nutrition-sphere. That's right, whether a person believes that earth is only 6000 years old or they believe that calories don't count, I won't engage in any serious debate or discussion with any of them. So, I take my hat off to you guys here who must wear "pudding helmets" to lessen the force of banging your heads against the wall ;)

StellaBarbone said...

I tried the low carb, high fat diet for about two months. I was ravenous every single morning no matter how much I ate (admittedly, I'm an olive oil fan rather than magic coconut oil). Fortunately I only gained 2-3 lbs over the period, but I was really, really uncomfortable. It tasted good, though!

Nigel Kinbrum said...

Naturally-skinny people are in the minority (my ex-G/F and all of her family are naturally-skinny). They are slowly gaining weight with increasing age, but over 8 weeks there is no significant change.

Energy balance still applies, as if Eout tracks Ein, there is no energy excess when food intake is increased, therefore there is no increase in weight. ItsTheWoo cited the above study as evidence to support her opinion that Calories don't count.

carbsane said...

http://www.nature.com/nutd/journal/v4/n7/pdf/nutd201417a.pdf



I believe this is a longer study that is similar in nature about 630 cal/day over feed.


Out patient, self-report ... Baseline TDEE really needs to be measured in some reasonably accurate way or baseline is meaningless. I hate to say it but met ward study or it didn't happen ;-)


Nobody has ever doubted that different people react to overeating or deficit differently.

One other thing though ... Most people don't overeat by one day adding a significant surplus to their diet and keeping it that way. The compensatory "burn off" that might occur for 500 cals on a single day may not occur for 100 cal/day over 5 days.


There's definitely something to cycling that can be helpful beyond the psychological, but that response can't be predicted any better than CICO -- actually I think it's probably a lot more variable, but that's speculation on my part.

Muata Kamdibe said...

I watched this BBC Documentary "Why Skinny People Aren't Fat" a couple of years ago, and I think there's a lot we can learn from watching these skinny folks literally force themselves to reach their calorie allotment every day: http://youtu.be/dAQr77QMJiw

Muata Kamdibe said...

I agree Evie, and I think what gets "consciously" lost in this debate is that with CICO, you're talking about an overall framework of how a person physically gains/loses body mass. If pretty much every met ward over and underfeeding study, has shown CICO to be true, then we're talking about something that's considered a fact, right? And, haven't most of the mechanisms involved in CICO been worked out? Of course, there's still stuff to discover, but it's not like scientist haven't been working on this diligently for more than 25 years. Wasn't their darling hormone, cortisol, just discovered not too long ago? But, again, this has nothing to do the with overall framework of CICO.


If calorie deniers want to "disprove" CICO, it's pretty simple. Find obese people living in famine stricken areas. Oh yeah, and one or two peer reviewed met ward studies wouldn't hurt either ;)

StellaBarbone said...

My sisters-in-law are skinny 50 year olds. They forget to eat, but when they remember, they eat absolutely nothing that Woo would touch. My college roommate, OTOH, was obese. She was unbelievably efficient in her movements and she consistently ate somewhat more than our normal weight friends and me. I have three poodles; one fat, two thin. The fatty loves to eat and inhales every meal. If we give the three too many treats during the day, the skinnies skip their dinners, but the chubby one falls on her meal as if she has been starved. If the chubby one were human and had ready access to all the food that she could eat, I have no doubt that she would become obese.

My three dogs are the perfect example. They eat exactly the same macronutrients, they're the same size and one of the skinnies is actually a half-sister of the chubby girl. The eat the same, but one of them just has a defective appetite sensor while the other two refuse to overeat.

StellaBarbone said...

Several months ago the chubby dog had a skin infection for which she received an antibiotic that upset her stomach and caused her to lose weight. At her new, thinner weight she became more physically active. My husband was so pleased that he stopped passing out treats all day and now, with lower CI, she has increased CO. I realize that this is both a different species and anecdotal, but it all runs quite contrary to the claims of the "calories don't count" crowd.

John Smith said...

It's fun to try to figure out which psychiatric disorders they suffer from, in the case of the Libel Queen, I have managed to narrow it down to "All of them."

NS said...

MP: Eat real food, mostly plants, not too much.
JM: Eat real fat, mostly butter, as much as you want (as long as your ketometer numbers are good.)
Woohoo!!!

EJ said...

Ben Greenfield will take branch chain amino acids and greens powder when 'fasting', which seems reasonable. Though I'm not sure you wouldn't get roughly the same effect from, say, a bowl of chicken broth with some wilted spinach leaves.


What I really don't get is stuffing 1,000 calories worth of butter and MCT oil into a cup of coffee and calling that a "fast" because it doesn't have any carbs.

Nigel Kinbrum said...

Have you seen https://www.youtube.com/watch?v=xf-LuBCFINs ?

This is how you really do it. :-D

carbsane said...

My apologies for not having the time to respond fully (to be honest, there's a lot here and I'm somewhat confused). But to the cause of hyperglycemia, you may find this post helpful: http://carbsanity.blogspot.com/2013/10/the-cause-of-hyperglycemia-in-type-2.html

Greta Carbo said...

A perfect link, much material and lots of confusion for me. The Sonksen x2 PDF is entertaining as well as packed with thought-provoking metabolism. I am digesting the first reading but will have to reread a time or two again before I can make some domb ass comments. All in all, a good place to start to go along that line of thinking. Thanks.

Greta Carbo said...

Glucagon. If insulin gets out of whack, beta cell damage e.g., then maybe it is glucagon that is the renegade factor in unchecked gluconeogenesis and elevated BS?


Sorry ab't the confusion, I still ramble on too much at times, I lose focus homing in too much on detail so that I lose relevance.


Great post in the link above. I am rereading the pdf therein, interesting on many levels.

carbsane said...

I'm quite surprised that that paper came from Feinman. Then again, I'm not that surprised as he has been driven by dogma and a quest for glory for the "other" Richard Feinman perhaps? He cites SonksenX2 in that new paper and w/o misstating it. Then goes on about carb restriction.

carbsane said...

Yes, in the progression of diabetes papers, it is noted that the glucagon suppression is muted -- it doesn't look as pronounced as an insulin spike but it's considerable and certainly factors into the mix. I remember reading keto causing alpha-cell demise in rats on keto. I wonder if it's demise or dysfunction or downregulation so that a long term reduction in insulin is not accompanied by runaway gluconeogenesis.


Add to the mix that there is such a thing as starvation diabetes where diabetes develops after lengthy starvation.

Greta Carbo said...

Reading Stephan Guyenet's blog, a commentator made some unusually commonsense statements so I found her blog and a post on The Glucagon Connection:

I quote:
Insulin and glucagon are like the accelerator and brake on your car. And it's the ratio of the two, rather than the absolute amount, that is important. If you have almost no insulin, you might be able to have normal BG levels if you also had almost no glucagon.

In fact, a study done in 1981 in a man who had no pancreas, showed that BG levels could be maintained at about 100 without insulin as long as they didn't give the man glucagon.

The problem is that when the beta cells give out, the alpha cells don't give out as well. In fact, they often secrete even more glucagon than they would in a nondiabetic. Glucagon tells the liver to produce and secrete glucose, so the BG levels stay high even when you don't eat.

Most diabetes researchers focus on beta cells and insulin production, but some are studying the alpha cells and glucagon production as well. A recent study found that hyperglucagonemia (too much glucagon in the blood) actually precedes the decline in insulin secretion seen in diabetes. /endquote

http://wildlyfluctuating.blogspot.com/



This is in accord with what I am learning about hormone balances and I am curious as to what you think.


It's always wrong to demonize a natural food or chemistry of the body (thinking of the big bad Nosferatu evil that is insulin ha ha), isn't it?


Nosferatu had a way of lowering blood sugar.

Greta Carbo said...

(Second try)


Reading Stephan Guyenet's blog, a commenter made some unusually commonsense statements, so I found her blog:

I quote:

Insulin and glucagon are like the accelerator and brake on your car. And it's the ratio of the two, rather than the absolute amount, that is important. If you have almost no insulin, you might be able to have normal BG levels if you also had almost no glucagon.

In fact, a study done in 1981 in a man who had no pancreas, showed that BG levels could be maintained at about 100 without insulin as long as they didn't give the man glucagon.

The problem is that when the beta cells give out, the alpha cells don't give out as well. In fact, they often secrete even more glucagon than they would in a nondiabetic. Glucagon tells the liver to produce and secrete glucose, so the BG levels stay high even when you don't eat.

Most diabetes researchers focus on beta cells and insulin production, but some are studying the alpha cells and glucagon production as well. A recent studyfound that hyperglucagonemia (too much glucagon in the blood) actually precedes the decline in insulin secretion seen in diabetes. /endquote



This is in accord with what I am learning about hormones of metabolism balance. I am curious what you think.


It is becoming increasingly clear to me, that it is unwise to demonize any natural food or metabolic molecule (I am thinking this time it's the big bad way too evil Nosferatu insulin! ha ha). Isn't it? Unwise to demonize, that is.


Nosferatu had a way of lowering blood sugar.

Greta Carbo said...

Uh oh, I forgot something.

The blogger is a Gretchen Becker and her website is:

http://wildlyfluctuating.blogspot.com/

And the quote is from The Glucagon Connection:

http://wildlyfluctuating.blogspot.com/2011/12/glucagon-connection.html

Greta Carbo said...

(Third try, going up a level)

Reading Stephan Guyenet's blog, a commenter made some unusually commonsense statements, so I found her blog:

I quote:

Insulin and glucagon are like the accelerator and brake on your car. And it's the ratio of the two, rather than the absolute amount, that is important. If you have almost no insulin, you might be able to have normal BG levels if you also had almost no glucagon.

In fact, a study done in 1981 in a man who had no pancreas, showed that BG levels could be maintained at about 100 without insulin as long as they didn't give the man glucagon.

The problem is that when the beta cells give out, the alpha cells don't give out as well. In fact, they often secrete even more glucagon than they would in a nondiabetic. Glucagon tells the liver to produce and secrete glucose, so the BG levels stay high even when you don't eat.

Most diabetes researchers focus on beta cells and insulin production, but some are studying the alpha cells and glucagon production as well. A recent studyfound that hyperglucagonemia (too much glucagon in the blood) actually precedes the decline in insulin secretion seen in diabetes. /endquote

This is in accord with what I am learning about hormones of metabolism balance. I am curious what you think.

It is becoming increasingly clear to me, that it is unwise to demonize any natural food or metabolic molecule (I am thinking this time it's the big bad way too evil Nosferatu insulin! ha ha). Isn't it? Unwise to demonize, that is.

Nosferatu had a way of lowering blood sugar.

Greta Carbo said...

Uh oh, I forgot something. (second try)

The blogger is Gretchen Becker and her website: http://wildlyfluctuating.blogspot.com/

And the reference link is: The Glucagon Connection: http://wildlyfluctuating.blogspot.com/2011/12/glucagon-connection.html

Greta Carbo said...

Interesting stuff. I can see how acetoacetate might scavenge hydroxyl radicals, but not BOHB which is fully reduced. However, your link says all three ketone bodies scavenge, so I am probably wrong about that. If AcAc nabs two hydrogens it will be fully reduced to BHOB but will create free o2 in the process which will now require catalase to neutralize. I sure would like to see the chemistry of BHOB scavenging though.

carbsane said...

Sorry about the slow moderation. I'm dealing with lots of stuff here and am not always on top of Disqus. You have been Whitelisted, though sometimes links will still hold you in moderation. You can blame Razwell if you know who that is :-)

Greta Carbo said...

I will go back to just waiting as I usually do in these situations. That usually works, and would have here too. The message of "hold on some moderation going on" (paraphrase) and the subsequent "disappearing" of my post confused me.


Razwell? The Flying Saucer Diet? Naw, I can't blame someone I don't know, but another annoyance is the slow updating of Latest Comments, can I blame the Raz for that? And, come to think of it, more than just the last four comments would be helpful.

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