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!)

Monday, March 12, 2018

The Manhattan Project of Nutrition That Wasn't

With publication of the results of the second of the "Original 3" NuSI funded studies, I'm finally getting around to publishing up this post (and perhaps a second one shortly) regarding the Nutrition Science Initiative (NuSI), founded in 2012 by Peter Attia, MD and "science journalist" Gary Taubes. Bottom line ... for NuSI, it was "all over but the crying" a couple of years ago now. 

Monday, March 5, 2018

Dietary Energy Density and Incidence of Diabetes in the Women's Health Initiative


In the Women's Health Initiative, a 2017 analysis of the energy density of baseline diets, stratified to quintiles, revealed several correlative components of an energy dense diet (comparing the top quintile (Q5) to the bottom (Q1).  The energy density, in kcal/gram of food, nearly doubled in Q5 vs. Q1 corresponding to a nearly 50% increase in caloric intake.  The dietary components correlating with this are:

  • Fat:  Fat content is by far and away the greatest contributing factor to consuming an energy dense diet.   Absolute intake more than doubled (2.5X) from Q1 to Q5, and comprised roughly 90% of the increased caloric intake.
  • Animal Protein:  As protein intake from plant sources remained relatively constant, animal protein intake increased by 40% resulting in an increase in total protein of 25%.  Therefore animal foods are a considerable contributor to increased energy density of the diet.
  • Added Sugars:  Added sugar comprised 11% of caloric intake across the quintiles, however absolute added sugar increased almost 50%.  
  • Carbohydrate:  Total carbohydrate intake is not associated with increased energy density of the diet.  Increases in added sugars were offset by reduction in other carbohydrates so that absolute intake remained constant.  Thus as a percentage of the caloric intake, carbohydrate declined significantly.
  • The macro percent composition of the least energy dense diets was P/F/C of 18/26/59, while the percents were 16/45/41 for the most energy dense diets.
The near doubling of energy density is associated with an (adjusted) roughly 25% increase in the risk of developing diabetes.

Monday, February 26, 2018

Maybe the Solution Lies in Making the Food Industry Our Friends

In our current times of rising obesity and chronic disease rates in the developed world (and spreading globally), I see a handful of "usual suspects" upon which the phenomenon is blamed:

  • The food industries
  • Governments and guidelines
  • The entertainment industries 
  • The general health and beauty industries
  • The diet and fitness industries 
By far and away, in no particular order, the two at the top of the list shoulder most of the blame.  You know the story by now.  Ancel Keys .... McGovern Committee ... Low fat dietary guidelines ... we got fat because CARBS and INSULIN!!!

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