las

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!)

Tuesday, January 26, 2016

Announcing my 40 Day Lenten Lentil Fast and Mark Hyman's Fat Summit

BUMP - and due to time constraints but lots of comments already here, I've changed my mind on starting a Fat Summit thread and retitled this one.  I hope to put a "best of" video together in response to this tentatively titled The Fact Summit.  Thanks for all your participation!





Lent begins on February 10th this year, so I have decided to engage in a 40 day fast beginning today, January 15th.   The fast officially ends on Valentine's Day at which point I will return to eating like 99% of humans on the planet. What will I be consuming during this fast?  Well I wouldn't want to kill my gut flora or get my electrolytes outta whack, so I have decided to include 1 cup (which might be two if my body tells me it needs it) of The Faker Foodie's organic, paleo, vegan, non-GMO, unicorn horn free lentil gelatin broth (see non-affiliate link below).  Also, since I'll be in ketosis anyway I will boost my ketones by drinking one ounce of pure acetone (not the lemon flavored stuff from Walgreens, but the real organic stuff from the paint department at the Home Depot) for extra energy #MentalClarityRocks.  That tastes terrible and I don't want to ruin my daily lentil poop fix so I will mix it with gluten free maple syrup, aka tree water from maples certified grown at least 100 miles from a dwarf wheat plant.   Oh, and I plan to pause my fast for 1 hour each day.

Wish me and my pancreas luck!  40 days of fasting is going to be rough, but my health is worth it!!  Also follow me -- @nailpolishremoverandbeans -- on narcissisteevee.com.  Don't forget to make lots of buttery fingerprints on the screen of your electronic device to send me lots of love!  #FastingClarity

Thursday, January 14, 2016

Thirty Years of Glycemic Index Dogma, and The American GI Man


Sixteen post bumps for 2016 ... No. 3

I think this post from around a year ago, in light of the new book by David Ludwig is a necessary bump.

It's not every diet guru that is a principal investigator on a "groundbreaking" study that directly debunks the thesis of their book.  In this regard, Ludwig is, if not one of a kind, the leader of the pack.




Originally published on January 19, 2015

The former British colonies/territories may be known for a lot of things, but in the nutrition world, I'm going to go out on a limb here and state that the Glycemic Index - GI - is the trifecta.

In Canada, David Jenkins pioneered the concept, for applications in diabetes treatment.  This cause was picked up and concurrently championed in Australia by Janette (Jenny) Brand-Miller.  A little late to the party, in one of the original Thirteen, David Ludwig took up the cause in the USofA.  Are these the men and woman who made us fat?

Adapted from Adele Hite's Eathropology
image link
Yes, that's pretty silly ... but no more so than Adele Hite and others like her, who in the same breath decry the error in equating correlation with causation as they point to plots like the one above to indict the low fat diet.

Thursday, January 7, 2016

Ketones: Not Hippocrates' Food

If you've circulated in the realms of nutritional science or sorcery for any length of time, you've probably heard the phrase ...

Let food be thy medicine

and medicine be thy food


... enough for it to have long past turned to the point of cliché.   Whether or not it was actually said by Hippocrates notwithstanding, you've probably seen it misused as often as it is appropriately applied.   This post is about its misuse in the image below.

Starving cancer:  Dominic D'Agostino at TEDx TampaBay
Screenshot

Tuesday, January 5, 2016

MAD about Atkins for Epilepsy!

Hello all!  A short detour in the sporadic blogging as I came across this 2013 paper yesterday:  A decade of the modified Atkins diet (2003–2013): Results, insights, and future directions   Eric H. Kossoff, Mackenzie C. Cervenka, Bobbie J. Henry, Courtney A. Haney, Zahava Turner

The acronym in my title has been used to denote the Modified Atkins Diet, and as the title of the paper implies, it has been utilized clinically in the treatment of epilepsy for over a decade now.  The lead author of the paper is Eric Kossoff, and here are some relevant bio points for him:
  • Associate Professor of Neurology and Pediatrics at Johns Hopkins Children's Center, Director of the Pediatric Neurology Residency Program. 
  • Coauthor of Treatment of Pediatric Neurologic Disorders and the 5th edition of The Ketogenic Diet (Amazon affiliate link).
  • Wrote the foreward to The New Atkins for a New You (2010) written by Eric Westman, Stephen Phinney and Jeff Volek.
  • Member Science Advisory Board for Atkins Nutritionals
  • Has received funding from The Dr. Robert C. Atkins Foundation (see paper) which was funded by proceeds from Atkins Nutritionals products.
  • Has received funding from Nutricia, makers of KetoCal supplement/foods used with both KD and the MAD.

Saturday, January 2, 2016

What is Diabetes?

Sixteen Post Bumps for 2016 ...  No. 2

Update Notes & Summary


This post discusses the section entitled INCREASED PROINSULIN AS THE MAIN BETA CELL SECRETORY DEFECT in the following 2007 article:  PROINSULIN, PROAMYLIN AND THE BETA CELL ENDOPLASMIC RETICULUM: THE KEY FOR THE PATHOGENESIS OF DIFFERENT DIABETES PHENOTYPES.    

This is but one of the papers that turned up as I was delving deeper into the progression of Type 2 diabetes and what it really involves.  It was this work that began the research and blogging journey into sorting out what insulin resistance is, if indeed it does exist as it is commonly "understood" from the standpoint of peripheral tissue glucose metabolism.   In the words of the authors of the paper:
... for three decades, the beta cell dysfunction has been shaded by the theoretical construction of peripheral insulin resistance.
These researchers have access to roughly 170,000 records of everyone diagnosed with diabetes since 1942 in the jurisdiction of the Bucharest Registry of Diabetes.  This post discusses the common defect found in all forms of diabetes:  β-cells dysfunction.  A breakdown of the insulin assembly line resulting in reduced secretion of biologically active fully formed insulin, and increased secretion of inactive proinsulin precursor.





Originally Posted 2/17/2013



"the proinsulin disorder in diabetes is not 
only ubiquitous but it is also precocious"



As a second post setting up for future discussions on insulin resistance and it's role in diabetes (especially type 2)  I wanted to share the following paper with you here:


It is a long paper, almost 18 full pages of text, and more than 9 to list the 298 (yikes!) references. I will by no means attempt to address it in its entirety here, rather I shall focus on the section entitled "INCREASED PROINSULIN AS THE MAIN BETA CELL SECRETORY DEFECT".  But first, the abstract of this 2007 paper:
Based on our clinical and epidemiological data, we have sustained for a long time the unitary character of the various phenotypes of the diabetic syndrome. In this paper, we add several arguments sustaining that the unitary character of diabetes is related to a common primary defect in the function of the beta cell endoplasmic reticulum, leading to an inadequate processing of the two main secretory molecules: pre-proinsulin and pre-proamylin. The post-translational changes of these molecules might explain the main proapoptotic and anti-regenerative pathogenic mechanisms leading to a progressive decrease in the β cell mass/function. In our view, the increased proinsulin levels encountered in various diabetes phenotypes could be not only a marker of beta cell dysfunction but also could indicate the main β cell defect, suggesting also its location.

Friday, January 1, 2016

The Cause of Hyperglycemia in Type 2 Diabetes


Sixteen Post Bumps for 2016 ...  No. 1

Post Summary

  • The main role of insulin in the body is to inhibit processes that release energy substrates into circulation on an otherwise "always on" continual basis. 
  • Insulin plays a stimulatory role in the clearance of glucose from circulation, but this is secondary to its inhibitory role, and may not even be physiologically important. 
  • The generally accepted progression of "insulin resistance" -- beginning with impaired uptake of glucose in response to insulin stimulation, leading to a "backing up" of glucose into circulation, and requiring more and more insulin to clear the glucose -- is almost certainly incorrect.
  • Radiolabel studies have demonstrated that in both T1 and T2 diabetics, glucose uptake is not impaired, and indeed may even be greater than normal.
  • Hyperglycemia is due to relative insulin deficiency even if overall insulin levels are high.  This deficiency is due to failure of the pancreas to secrete insulin in both sufficient quantities and in a timely manner.
  • Endogenous glucose production is supposed to be suppressed when dietary (exogenous) glucose is added.  The failure to suppress this is responsible for the hyperglycemia.
  • Rather than hyperinsulinemia, the critical "event" is impaired or an almost complete lack of early glucose stimulated insulin secretion (GSIS).  This "defect" is accompanied by a lack of suppression of glucagon secretion.
  • Subsequent hyperinsulinemia in those capable of secreting substantial amounts (early T2s) is due to endogenously produced hyperglycemia.





Originally Published 10/3/2013

Thursday, December 17, 2015

On Therapeutic Treatments and Outcomes

This Blog's been awfully quiet and boring lately!






This post is another backgrounder for the upcoming post revisiting ketogenic diets and the treatment of cancer:  Ketones are NOT the End of Cancer. Tim Ferriss & Dominic D'Agostino Should Be More Responsible  (link will work when published).   The whole topic of ketone therapy for epilepsy provides a great example with which to discuss various concepts of therapies, and what can or cannot be extrapolated to non-therapeutic contexts.

Saturday, November 28, 2015

Therapeutic Safety: Context is Everything


I'm working on some posts on "the list" from a recent one, and find myself in need of a few backgrounders for the upcoming Ketones are NOT the End of Cancer. Tim Ferriss & Dominic D'Agostino Should Be More Responsible (link goes live when it's published) post.  Recently I tweeted out the following:  



My tweets are auto-posted to Facebook (including to my mostly-private page) where a friend responded to the statement that "a ketogenic diet is [...] safe". The comment basically challenged how we know this, or even if we know this to be true, My response is essentially the impetus for this post, but it was, in a nutshell:

CONTEXT


Thursday, November 12, 2015

My Gut Feeling on Microflobesity Was Right


This post brought to you by Duck Dodgers' arrogance.  If there ever were an example of what is wrong with science in the Incestral Health Community, it is the phenomenon that is "Duck Dodgers" and his comments here.    A seemingly non-controversial post -- on how the US Dietary Guidelines were never any radical departure from the way humans around the globe have eaten for thousands of years -- went viral, at least in part because of Duck's return.   What rubs me personally the wrong way about this person (or persons, though I've been told it is only one person who posts with that ID in comments here so I operate on that assumption) is his response to any challenge to "How Food Enrichment Made Us Fat, Diabetic, and Chronically Diseased" otherwise known as the "Iron Food Enrichment Hypothesis".  Despite doubling down on the whole fortification thing at the off-the-grid web rental only around a month ago, this guy comes on here and plays word games regarding whether it is even a theory or hypothesis.   Duck behaves as if I somehow owe it to him and the internet to take his unscientific self seriously, and if I don't take him and his ideas seriously it can only be that I find them inconvenient to my comfortable mindset.  

I have wasted enough time on this whole nonsense, if anyone wants at it they know full well where they can go to discuss it.  I don't dabble in non-scientific mumbo jumbo and I laid out some general thoughts on this in this post:  Science ... .   


Wednesday, November 11, 2015

Science ...


... it's called that for a reason.  



This post was prompted by the discussions in this seemingly non-monumental post -- Are the Dietary Guidelines REALLY So Radical? -- that erupted to over 750 comments. The discussion somewhat culminated in this comment, and there are a few posts forthcoming that require this "backgrounder" on thoughts.


I like to blog about science.  I like to deal in science.  I consider myself a scientist in much the same way that formerly practicing MDs still consider themselves doctors.   I used to conduct primary research, which some of today's "scientists" have never even done outside of the classroom environment if that  (as opposed to folks like Gary Taubes, Zoe Harcombe and James DiNicolantonio to name a few).  I studied science (a few disciplines, and some engineering too), and I had a career in scientific research (again a few differing fields and applications).  I "can't help myself" whenever I read a scientific study but to analyze it.  There is a lot of good research going on.  There is a lot of crappy research as well.  I'm hopeful that some find what I write about here helpful, though usually the more scientific the topic, the less interest a post seems to garner.  This doesn't bother me, because in writing a blog post on something I'm looking into, I learn a lot myself, and as geeky as it sounds, this is something that is as personally rewarding or just plain enjoyable as some may find their own favored hobbies.