Monthly Archives: January 2013

diabulemia

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.

Yes, I think sugar and empty calories, and the associated hyperinsulinemia are the bane of anyone with obesity or any sort of hyperplastic fat tissue disorder.  And yes, this is the worst type of evidence to support such a stance, but when you’ve got lemons, well…

Make no mistake, diabulemia may as well be spelled DIE-abulemia.  It’s not a laughing matter.  But yeah, well, lemonade, etc.  So here it goes

Diabulemia

Type I diabetics have low insulin and are lean; type II diabetics have high insulin and are not.  Insulin injections in either population promotes hyperplastic fat growth.  Sounds scary, right?  It is:

insulin

This poor soul unfortunately restricted his insulin injections to only two sites.  Make all the jokes you want, but the effect is obvious…  this is happening everywhere in hyperinsulinemic heavyweights (not just two specific sites).

CHO III Picture 279

 So what do Type I’s do when they want to lose some fat mass?  Stop jabbing themselves with insulin. Unfortunately, it’s really that simple.  Type II’s and anyone with excess or hyperplastic fat tissue can do the same with low carb or keto, although this would be a great benefit to their overall health.  But for Type I’s… not so much – they need insulin to prevent the horrific manifestations of ketoacidosis, which includes but is not limited to: death.

Type I’s are hyperglycemic because of low insulin; insulin therapy prevents diabetic ketoacidosis, a deadly condition.  But for those who simply choose to selectively reduce their insulin dosage, they: 1) don’t die; 2) lose fat; and 3) get hyperglycemic and incur all the damage that ensues (retinopathy, nephropathy, neuropathy).  Furthermore, they’re walking on thin ice – DKA is lurking.  It is just as stupid yet more dangerous than using tapeworms to lose weight.

tape-worms

Type II’s are hyperglycemic because of insulin resistance; a condition that is pathologically neutered via carbohydrate restriction.  Type I’s who reduce insulin injections to decrease fat mass are doing just as much damage as Type II’s who DON’T reduce carbohydrate intake.


Diabulemia is akin to an eating disorder.  Biologically, the lack of insulin allows fat to be released from adipose tissue with gravitas, and it prevents glucose from being stored in any meaningful capacity.  You’re literally pissing calories here, burning ’em like crazy there; all of which is a helluva lot easier than “eating less moving more” … which is why diabulemics do it (because they have the option [unlike the rest of us]).  Diabulemia is good from a fat loss perspective, but will most definitely contribute to severe and possibly deadly complications down the line.   Carbohydrate restriction, however, is a win-win-win… (for everyone except The Man, so perhaps it’s a win-win-win… fail)

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.


Humans aren’t big rats, but here it is again, anyway:

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes (German et al., 2010)

I’m ignoring the brunt of this paper and only focusing on the positive control groups.  [Positive controls… meaning they were included because they would definitely exhibit the expected response.]

Force rats into a state of diabulemia, and their insulin levels plummet, blood glucose soars, and they become ravenously hungry (open squares in the graphs below).German I

But lo and behold, fat mass atrophy ->German II

Eat less move more?  Well, they certainly didn’t “eat less…” (see above) … and:German III

nor were they “moving more.”  Low insulin seems to have a way to bypass that whole “eat less move more” thing (eg, Metabolic rate per se).

 

Throwing the baby out with the bathwater works if the baby is fat and the bathwater is insulin.  (no, not a fat baby.)

 

calories proper

 

 

Insulin vs. fat metabolism FTW

Insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.

Teaser: insulin-induce hypoglycemia can get deadly quite fast, and there is no equivalent for the effects of insulin on fat.  However, the effects of insulin on fat are 100 times more powerful.

Background: Hormone sensitive lipase (HSL) responds to insulin by inhibiting lipolysis.  It halts fat burning.  It got its name because it’s THEE most hormone-sensitive lipase in the body.  The hormone about which we are speaking is of course insulin.  And the enzyme, or at least one of the enzymes as it were, is HSL.  To be clear, it takes very little insulin to inhibit HSL.  Just a dollop, in fact.

Effect of very small concentrations of insulin on forearm metabolism.  Persistence of its action on potassium and free fatty acids without its effect on glucose.   (Zierler and Rabinowitz, 1964)

Expt 1.  Since we’re all about jabbing people with insulin lately, let’s get at it again.  Jab someone with about 100 uU (/min*kg), and muscle and fat vacuum glucose out of the blood.  Same goes for potassium; and adipose gets all stingy too… it stops releasing and starts storing fat.  This is “healthy,” and its part of why people say insulin, and by extension carbohydrate, causes lean people grow fat tissue.

What do you think would happen in an insulin resistant obese crowd.  Less glucose vacuuming, but scrooge adipose will still responds with gravitas, by saving more and spending less?  Likely.  HSL is like the little piggy’s straw house.  The strong young wolf can blow it down.  The COPD emphysema wolf can blow it down…  because it’s made of straw.


Thus, insulin causes lean people to grow fat tissue, and it causes obese people to grow more fat tissue.

In other words, with regard to common obesity, being resistant to insulin means postprandial hyperglycemia; you can’t handle sugars proper.  but it’ll still make you fat(ter).

Expt 2. The interesting part.  Try jabbing healthy people with 10x less insulin.  Looks like IR obesity!  Adipose gets stingy, potassium scrams, but no effect on glucose uptake.

In the figure below: A-DV is muscle; A-SV is adipose.  Glucose uptake into fat & muscle is unaffected by a low dose of insulin.glucose on 10uU

Second figure: with the same dose, adipose goes on a budget SAVE MORE SPEND LESSFAs on 10 uU

Conclusion.  In a healthy person, (eg, healthy person), even very low doses of insulin cause fat growth.  This isn’t an issue of high vs. low glycemic issue.  The insulin dose used in this study was less than that expected from a respectable low glycemic index meal.  This is probably why the glycemic index hasn’t cured the obesity epidemic.  On the other hand, dietary fat doesn’t stimulate insulin…  just sayin’

Furthermore, perhaps glucose uptake into adipose promotes fat storage under certain conditions, but it’s clearly neither necessary nor essential.  Insulin can Miracle Grow fat mass without affecting glucose uptake one iota.  I imagine the abundance of 3C precursors simply isn’t “the limiting factor.”  And it works just as good with Whole Foods Low GI pa$ta and Wonderbread.buttressed

Translation: insulin buttresses fat growth.  and it doesn’t matter how much.  FYI this probably seems nonsensical at first: carbs stimulate insulin in order to dispose of said carbs, like a logical feedback mechanism.  Perhaps.  But said insulin cares far more about fat than said carbs.  On a scale of 1 to 10 (ie, putting things into “perspective”): insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.

 

 

Part II.

Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans (Bonadonna et al., 1990)

There are a lot of data in this paper, but here are the relevant points:

Infuse insulin at various rates.  In the lowest infusion rate, the only aspect of glucose metabolism to respond is hepatic glucose production (second line; HGP declines from 2.0 to 1.34 at the lowest dose):glc turnover

WRT low dose insulin on glucose metabolism: liver responds, not skeletal muscle.  Skeletal muscle doesn’t even look at glucose until insulin infusion reaches 250 – 500 uU, which is probably why back in ’64 they saw absolutely no effect at 10 uU.  At 100 uU they saw an effect, but according to these data, it was likely due solely to liver, because skeletal muscle doesn’t seem to care until levels exceed 250 uU (it’s an infusion rate, not an absolute concentration.  But that’s neither here nor there).  To be clear, 10 uU insulin infusion doesn’t affect glucose metabolism (1964).  period.  100 uU modestly affects it (1964), and this is probably so modest because only liver is helping out (1990).  At 500 uU, full scale attack on blood glucose.

But fatty acids are obliterated with 5 – 50 x less:FA turnover

It worked with 10 uU in ’64, and it worked just as well with 100 uU in ’90.  (FYI the first paper was published in 1964; this one in 1990).

Furthermore, in the table above glucose metabolism was progressively affected with increasing insulin concentrations.  Not so much with FAs:FA suppression

FA flux is rapidly and completely shut down with a dollop of insulin.  Indeed, it is obliterated.  Giving more insulin doesn’t do anything, because, well, when you blow down a straw house, it tends to stay down.

 

calories proper

 

Become a Patron!

 

 

Save

40 years ago a group of researchers turned ketosis into poetry.

But first, a brief primer.  In red.

“The glucose muscle-sparing effect of fat-derived fuels” 

or, the Randle Cycle 2.0.  it’s like a course in life enhancement.

Part I.  Intermediary metabolism

The glucose-fatty acid cycle
The Randle Cycle, as originally proposed, states that fatty acid oxidation inhibits glucose oxidation.  This is good because during starvation, every tissue than can survive on fatty acids instead of glucose should do so, sparing as much precious glucose as possible for the brain.

The glucose-sparing effect of fat-derived fuels
A critical vital horcrux to this is in the oh-so-humbly-disguised phrase “fat-derived fuels.”  The fat-derived fuels are ketones, and they are rescuing the brain from starvation (ie, neuroglycopenia); they do so by supplementing glucose as a fuel source.  Ketones are good at this; many tissues are happy to oxidize ketones when they are available.

The glucose muscle-sparing effect of fat-derived fuels
Ketones are derived from fat.  During prolonged starvation, glucose comes from skeletal muscle amino acids (eg, alanine).  Ketones spare glucose.  Thus, ketones spare muscle.  QED.

Continue reading

Non-sequiter nutrition IV. in vino veritas

The French Paradox is neither a paradox nor French, really.  Red wine isn’t saving the French from a saturated-fat induced heart attack epidemic….  Not to take anything away from red wine, however, as the metabolic effects of red wine (and alcohol in general) are rather interesting.

Background info: alcohol (ethanol) metabolism produces NADH (stick with me here, this article doesn’t get all technical on you I promise).

NADH inhibits gluconeogenesis (Krebs et al., 1969); as such, alcohol lowers blood glucose, regardless of whether if it’s pinot, cabernet, or straight moonshine (Harold  R. Murdock, 1971).

Continue reading