Welcome all seeking refuge from low carb dogma!

“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Thursday, February 15, 2018

Keto Klarity Karma ~ All Aboard the Jimmy Moore Livin La Vida Low Carb Drama Express!!

You are forewarned:  

This post contains no science.  It's a bit of gossip and speculation, and simply exposing and documenting some goings on in the LLVLC and related worlds this past year and in recent times. There's no TL,DR.  But c'mon, I KNOW some of you are here at the Asylum for this stuff.  πŸ‘ΏπŸ˜ˆπŸ˜ˆπŸ˜‡πŸ˜‡

While it is possibly a royal waste of my time, I do think it is important to keep shining a light on the source of so much information on the internet.  Whether it's from Jimmy Moore directly, or through the filters of his podcasts, or the reality that he's an internationally best selling author of health and nutrition books, his level of disinformation cannot go unchecked. 

Lastly, much of this was written train of thought when it was going down.  I did my best to change tenses and edit out repetition in an effort to actually publish.  I make no promises. πŸ˜€

Friday, January 26, 2018

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


BUMPED January 26, 2018

This post was written around three and a half years ago, and through some bizarre twist of dietary fate, somehow ketogenic diets are still trending on Google for everything from weight loss to hang nails.  So I thought I'd bump this post which was my attempt at dispelling some myths regarding ketosis and the role of dietary protein in the mix.  

In the end, and some of these points are not made specifically in this post but I'll make them here:
  • Carbohydrate restriction is the greatest determinant of ketogenesis 
  • Protein (various amino acids) can feed into the Krebs Cycle and attenuate the reduction in oxaloacetate that favors ketogenesis from fatty acids.
  • Ketogenesis represents a conversion of fat energy to ketone energy but it is not evidence of the ultimate usage of that energy.  
  • Like glucose, ketones will be burned for energy before fatty acids, so ketogenesis is not an indicator of actual fatty acid oxidation ("fat burning")
  • Type 1 Diabetics have elevated ketogenesis and gluconeogenesis.  This is evidence that gluconeogenesis does not "kick one out of ketosis"!
  • The availability of gluconeogenic substrates is an unlikely cause for any elevation in blood glucose levels by stimulating gluconeogenesis.
  • Ketogenesis occurs in all of us at low levels, moreso when fasted and in caloric deficit.  But significant levels generally require significant metabolic dysregulation (e.g. Type 1 diabetes) or carbohydrate restriction.  The exception to this is high intake of MCTs.
  • Exogenous ketones are not "ketogenic" any more than eating a banana is "gluconeogenic".  Both simply directly supply the energetic substrate vs. creating it in the body.

Sunday, January 21, 2018

A quick note

I am unsure why, but I am experiencing some problems with notifications, reading and posting responses to comments.  This morning I posted one reply (I think, no notice it didn't go through) and then was unable to respond to another (kept getting some verification notice).  

In addition, I have been mostly on my phone as my computer screen cracked rendering it unusable until I managed to disable the touch screen.  With that successfully disabled, it's a crapshoot if the unit turns on for limited use.   I'm hoping Tuesday for my replacement.

I would *REALLY* love returning to more regular blogging in 2018.  

Saturday, January 13, 2018

Insulin Treatment in Diabetes ~ Why Does It Often Cause Weight Gain?


Diabetes, whether Type 1 or Type 2, is a dysfunctional, wasteful metabolic state.  As a result, an uncontrolled diabetic either uses or loses more energy than their non-diabetic selves would otherwise use.  As such, the untreated diabetic is essentially "underweight" compared with the body weight that the same energy intake would produce were they not diabetic.

There are differences in endogenous insulin production between the two types of diabetes.  In Type 1, there is effectively no insulin production.  In Type 2, there is usually elevated basal insulin production, but a relative deficiency in acute insulin secretion, specifically an impaired early insulin response to glucose (GSIS). 

The absolute or relative insulin deficiency results in the following to a greater or lesser degree:
  1. Excessive lipolysis resulting in an increased cycling of the Triglyceride/Fatty Acid cycle.  
  2. Impaired suppression of glucose production in the liver, specifically an increase in glucose production via gluconeogenesis.
  3. Glycosuria (sometimes called glucosuria) due to impaired re-uptake of glucose in the kidneys and/or hyperglycemia exceeding re-uptake capacity.
All three of these are "Calories Out" in the Calories In - Calories Out (CICO) energy balance model.   Thus to greater or lesser degrees, diabetic individuals have greater energy expenditure.  When insulin therapy corrects these, energy expenditure is reduced.  Thus if the treated diabetic continues to consume their habitual amount of food, they will gain weight accordingly.   This is in contrast to the often postulated model whereby insulin treatment either induces hunger and overeating due to hypoglycemia, or the thoroughly debunked TWICHOO (aka the Carb-Insulin Hypothesis/Model) whereby insulin magically traps fat made from carbs in the fat cells thereby starving the rest of the body and causing hunger and overeating.  

The diabetic state also increases protein turnover rate, but this post focuses on the energetics.  While protein breakdown and synthesis require energy, the difference doesn't seem to be significant compared to total energy expenditure or the contributions of the three processes listed above.

Thursday, December 7, 2017

High BMI and Risk of Cardiovascular Disease


This post discusses a few studies on BMI and body composition and CVD mortality.  It was prompted by a Twitter conversation wherein Rob made claims regarding frail obese people, and that obesity science must address body composition to move forward.  The idea being that people with BMIs up to 40 don't have a "weight" problem, they have a fat problem, and the solution is to gain more lean mass then lose fat mass whether or not there is net weight gain/loss/neutrailty in the process.  BMI is essentially a useless measure.    

There are a lot of people, particularly in the "strong women" and Healthy-At-Every-Size (HAES)/related communities putting forth a similar message, that weight doesn't matter, and the former, especially, promoting lifting heavy weights and "thickness".  A sizeable proportion of people from just about every corner of the internet is fixated on the concept of preserving and/or building lean mass.   Building lean mass -- in all contexts -- is promoted as healthy, and health protective.  At worst, lean mass is benign.   

As a BMI outlier, I have considerable skin in this game so I got curious when presented with a study that showed reduced CVD mortality for those with high muscle vs. low muscle, irrespective of fat mass.   There appears to be yet another one of those "obesity paradoxes" discussed in the literature.  I'll discuss problems with that study as well as what kind of actionable information it provides in a future post.  In short, once you have CVD and/or surgical intervention, your survival rate increases with increased adiposity and fat free mass.  Those with the lowest fat seem to fare the worst in one study, while this is improved by higher FFM in another.    

However ....

What about developing CVD (or other diseases) in the first place?  Heart disease rates are (seemingly universally?) higher among the obese (by  BMI) than the lean.  Is it ALL about just the fat though?

I think many will be shocked by, and perhaps scratching their heads over, the results here.

This study of over 60,000 subjects followed up for an average of 15 years.   They looked at BMI, %BF, FMI (fat mass to height) and FFMI (fat-free mass to height) and resultant CVD mortality. 
  • The strongest hazard ratios were found for BMI (HR=2.7) vs all other measures (BF% HR=1.6, FMI HR=2.2)
  • Very high FFMI (fat FREE mass index) had a HR of 2.2 vs. medium FFMI
  • Restricting analysis to the more accurate measures of body composition gave similar results, with the association for BMI somewhat stronger! (HR = 3.0)
This study sure gives me pause, and fits in with what I've been thinking (and doing) for going on two years now regarding total weight:  Should we worry so much about preserving "Lean Mass" in people who got obese on the SAD?

Is being heavier healthy depending on body composition?  The main study discussed in this post seems to indicate otherwise.  I share some thoughts at the end.  You can browser search on "My Thoughts" to skip to that if you like.

Thursday, November 23, 2017

Happy Thanksgiving!

I have much to be thankful for this year, and this is a day for celebration.    Wishing you all the best day, I'm thankful for all who read here!  

I'll be making an apple pie (crust from scratch too!) and there's a slice with my name on it ... it will be worth every calorie!  Also my sister makes the BEST pecan pie only once a year on Thanksgiving, so you better believe I'm having a slice of that too!  I hope you all enjoy the special foods at your celebrations, but more importantly the family and friends you celebrate with.   Have a great day!

Thursday, November 9, 2017

Diabetes Un-Funged

The Noakes Foundation has put out a new book entitled Diabetes Unpacked* , edited by Dr. Zoe Harcombe PhD.   It is a compilation of chapters written by a who's who of the low carborati.  This installment deals with Chapter 3 by Dr. Jason Fung, a nephrologist masquerading as an obesity specialist and diabetologist.  He has no formal training in either, and his grasp of some pretty basic physiology is tenuous at best.  That latter "charge" can be backed up by fact checking (or attempting to fact check that which isn't simply Fung POOP (Pulled Out Of Posterior)) any of his various blog articles, books, podcasts or YouTube videos.  

* That's my Amazon affiliate link

This post will be an evolving one of sorts that I'll bump if and when content is added.  I've avoided giving Fung much "ink" here, frankly because I never thought anyone would take him seriously enough to deserve it.  Clearly I was wrong.  There's apparently no limit as to who can become the latest #LCHF-lavor.  Jimmy Moore still has a following.  #IRestMyCase 😎

Dr. Jason Fung on Insulin Resistance and Its Causes
from:  Insulin Toxicity and How to Cure Type 2 Diabetes

Monday, October 30, 2017

FREE!!!! Carb Sanity Academy presents: Healthy for the Holidays

This mix of snarkasm and practical advice is brought to you by Facebook Memories reminding me of a post I made around a year ago -- The #LCHF Weight Loss Industry & Evangelizing Low Carb -- and the upcoming Keto Clarity Academy event featuring Melanie Miller and Jimmy Moore "influencing" people on how to stay healthy for the holidays.

The holiday season will be soon upon us, and even those who celebrate no December holidays will likely still have to navigate related social engagements. 

Let me preface this by saying that I recognize there are a number of people who absolutely cannot, or probably should not, stray from their dietary regimen.  There are others who, when they do, have a much harder time getting "back on the wagon" compared to whatever issues staying on plan will cause.  If you are any of these people, this blog post is not for you.  This blog post is aimed at all of those who are angst-ridden going into and through the upcoming holidays and associated social occasions.  Perhaps you're currently engaged in losing weight, or you've lost weight and are working to maintain it.  This post is for you. 

Since 2007 I have been doing some form of this strategy when either losing or maintaining.  If you look around the various dietary communities, you'll see a common theme.  Of course there are always exceptions, but those who struggle with falling short of goals and/or maintaining their losses while remaining (largely) true to their dietary framework, almost invariably fall into the food substitute trap.  The problem with many of these foods is that they:

  • Remove any "magic" that eliminating certain foods or food groups has on reducing ad libitum caloric intake.
  • Can cause increased intake of foods with a "health halo" (e.g. it's fill-in-the-blank so it's "healthy" ... heck, I can even eat that for breakfast!)
  • Are rarely as good as the "real thing", ultimately leaving you with some degree of dissatisfaction and deprivation.   
  • Often contain more calories than the foods they are replacing

All of the above hold for various dietary paradigms.  The last bullet point is especially true for those following various low carb ones. 

With all of this in mind, first up, my FREE Carb Sanity Academy tips for getting through the rest of 2017 without messing with your goals.   (And then the snarkasm 😎)

Sunday, October 22, 2017

Ξ²-Cell lipotoxicity in the pathogenesis of non-insulin-dependent diabetes mellitus of obese rats: Impairment in adipocyte-Ξ²-cell relationships


I'm bumping this post due to some recent discussions on social media regarding the reversibility of Type 2 Diabetes and the role of low carbohydrate diets in the growing "curing diabetes" paradigm.  Recently Dr. Roy Taylor (the investigator I most closely associate with the crash diet, though this is an extensive group) and colleagues, who implemented a "crash diet" to cure diabetes -- by reducing pancreatic and hepatic (liver) fat concurrently with rapid weight loss -- published the following in BMJ:  Beating type 2 diabetes into remission.    The criteria are non-diabetic markers for a period following reversal of the progression.  Here is where various low carbohydrate interventions "fail", as many are able to maintain normoglycemia only by avoiding carbohydrates.  The question remains if this is effectively the same as other reversals.  I contend it is not, as normal pancreatic function -- specifically GSIS -- has not been restored.  Anecdotally (because we really don't have truly long term studies on LCHF following weight loss phase), many LCHFers see rising fasting levels, and one outspoken advocate, Tim Noakes, is among the many who remain on metformin to manage glucose levels.  The burning question, that remains unstudied by the advocates of low carbohydrate diets, is whether such diets will slow, halt or reverse the disease itself.  Here is where rodent data is NOT promising, especially when diabetes is viewed across the full metabolic milieu rather than the isolated metric of blood glucose. 


Ξ²-Cell lipotoxicity in the pathogenesis of non-insulin-dependent diabetes mellitus of obese rats: Impairment in adipocyte-Ξ²-cell relationships

Yes, this is a rat study, but it seems applicable in light of the recent Diabetes "Crash Diet" Cure and the reductions in pancreatic fat seen in the study.  The study and the pancreatic fat issue were discussed here.  Summary:  11 diabetics followed a 600 cal/day diet for 8 weeks and regained normal insulin secretion and glycemic control.  The restored glucose induced insulin secretion (GSIS) was attributed to reduction in pancreatic fat content.

The investigators in the current study had this to say in the introduction (bolded emphasis is mine):

Saturday, September 30, 2017

The Insulin Paradox

I think this post has needed a bump for a while.     I also think the data on growing animals eating a keto diet should be cause for at least caution in encouraging such diets for kids, teens or even young adults.


One of the more difficult things to sort out from the enormous amount of information out there is the actual effect, if any, of dietary composition on resulting body composition.  This is complicated from the get-go by many rodent studies that are done on reproductively mature animals that are still growing.  How to compare this to humans who cease growing vertically once they reach adulthood?  Next we have to sort through the studies that are done, and the implications of them, in the context of weight loss/underfeeding vs. those in the context of weight gain/overfeeding.  Clearly there are compensatory mechanisms at play in both situations that are drastically different.  Lastly, and here's where we probably have the least amount of information, and practically nothing in humans, what role does one's dietary composition have on their body composition over the long haul for a "normal" weight stable adult?    Verifiable science basically fails us on this last point, and we're left mostly to the "wolves" of the diet/fitness industry -- e.g. body builders,  trainers and nutritionists for elite athletes, etc. -- for their anecdotal reports.  I don't mean to disparage these folks with the term wolves (hence the quotes), but we can never separate the reports from the reality when there's money on the line in a world where ads are required to include "results not typical" disclaimers.  While I'm not saying all of these folks, or even a majority, are of the 2am infomercial variety, the claims remain largely unverifiable.  It would sure be cool if there was a privacy-sparing way to collect verifiable body composition, dietary and activity data for a large population of free-living humans, eh?