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!)

Saturday, April 16, 2016

That "New" Old Study on Saturated Fat ...

Firstly, the idea that any single RCT would change history -- given that the likes of Nina Teicholz, Zoe Harcombe and others have drilled into us the fact that RCTs in this area were scarce (and will remain so) -- truly does border on the pathological at this point.    An appropriate RCT, of adequate size and duration, conducted with suitable compliance and verification, could conceivably turn any number of hypotheses on their heads.   But such a trial would be next-to-impossible.  Besides, even if this RCT-to-end-all-RCTs-&-nutritional-unknowns were to begin tomorrow, there would be no more-certain answers than we have today for at least a decade, better yet two or three.  And that right there is the monumental frustration.  EVERYBODY KNOWS THIS.  The current revisionist revisitation of studies from almost a half century ago does nothing for anyone.

Saturday, March 26, 2016

Insulin Caused Cerebral Stress - And THANK YOU! I'm baaaaack :-)

Dateline:  March 26, 2016

Helloooo Inmates!!

A quick update, but first a sincere thank you to each and every one who participated in my 40 Day Lenten Lentil Fast post.  As of this morning -- two months after publication -- we stand at just over 2700 comments.  No that's not a typo.  Who knew all I had to do was stop blogging?    It fills my heart to have such great interaction here at any time.  It especially filled it these past two months, months that have been more tumultuous than time-constrained, and some of the most difficult of my life.  So THANK YOU, and especially for much needed laughter along the way!  What more is there to say?

I may or may not elaborate further on some unintended blog-related whys for the unplanned hiatus, but surely one of them has to be that old saying "the more things change, the more they stay the same".    While there are many examples of low carb antics I could use, there seems to be something about the almighty potato that folks just don't want to see the obvious -- you know that Occam's Razor deal we hear so much about -- about, and instead must construct ever intricate explanations for why people tend to drop weight like a conscientious objector enlisted in an A. Ben Keys study when they eat nothing but potatoes.

To every fraudulent hypester out there -- I'm looking at you Dr. David S. Ludwig, and I'm looking at you too Dr. Mark Hyman -- blaming obesity on "high glycemic" refined carbs while tossing the potato onto that list at every chance ... You need to stop lying to people.  If you did that. ... if you tested your whole potato in an honest fashion, and reported the results without spin, you might get some credibility back.  But you won't, because there's no money in that game, so instead you will go on lying to people, and using the response to (not even potato chips) Pringles and lactase-treated milk & oat dust to further your agendas.   The reality is that when people consume potatoes -- perhaps with some vegetation for added texture/flavor -- without dousing them in "satiating fat", they find they have a hard time eating enough to meet their caloric needs.  Then they lose weight.  Magic I tell ya!

Here is my 2016 Potato Miracle Diet:  Go out and purchase a 5 lb bag of potatoes.  Some additional items might include a head of cabbage, a bag of sauerkraut, a can of diced tomatoes, or a few bags of steam in bag broccoli, green beans or spinach.  (I'm going for quick and easy here, feel free to substitute fresh, organic, non-GMO whatever).  Cook those potatoes up as you see fit with a minimum (if any) of cooking fat.  Eat as much, whenever you are hungry.  That's it.

But this little stunt has taken on a life of its own, and it's the gift that keeps on giving apparently.  The original here was dated over FIVE years ago!  In the interim there was the potato starch version and then back to more potatoes, and now potatoes again.  I'm bumping this because Peter D has become increasingly uncoupled from reality in his attempts to explain what cannot be explained in his world where physiological insulin resistance is somehow a prefered metabolic state and insulin is still somehow the cause of obesity.  And so, five years after his first attempt at this, he's back trying to explain the results of a recent study in  Boiled mashed potatoes for miracle satiety?  This time with protons.  I can't even ...

New posts set in the queue!  Happy Easter to all who celebrate.  See you on Monday!

Friday, February 26, 2016

Bump: The Diabetes "Crash" Cure & Pancreatic Fat

Sixteen post bumps for 2016 ... No. 5

This post has been bumped before! To read original content use browser search for "Original Publication"

The original posting of this was shortly after the first papers published on the success of a very low calorie diet -- essentially a 6-800 calorie protein-sparing-modified-fast, protein shakes + non-starchy veggies -- in curing diabetes in relatively short order.  You may also be interested in the following posts:

The Diabetes "Crash" Cure Revisited (a follow-up to this one)
Diabetes "Crash" Cures: VLCal vs. VLCarb

Check Featured Comment (if any) for further updates from me.

Saturday, February 20, 2016

Insulin Doesn't Regulate Fat Mass

Sixteen post bumps for 2016 ... No. 4

While I'm way beyond behind in my post bumping for the new year, I still plan to finish out a total of sixteen at some point.

This one doesn't need much in the way of summary, but quick points:
  • In terms of energy homeostasis, the main role of insulin in the body is as a signaling molecule in the regulation of the circulating levels of energy substrate, the two primary ones being glucose and free fatty acids.
  • This post models this for just the fatty acids using a room temperature/thermostat feedback analogy.
  • In the case of fatty acids, circulating levels are controlled mainly at the release point from the fat tissue.  
  • The role of insulin is to keep total amount of circulating free fatty acids at appropriate levels, and not to regulate the amount of fatty acids stored in the fat cells, and thus overall fat tissue mass.

Original post date: 12/13/14

Insulin doesn't regulate fat mass.  This is a bold statement.  My wording is specific.  Hear me out.

A little over three years ago, I wrote:  What Does Insulin Regulate Anyway?  Yesterday a blast from that past showed up in comments on the "new" Gary Taubes YouTube video.  I use the quotation marks around new, because Taubes has been delivering some version of this talk for seven years now, and the most significant changes have been to delete (and delete and delete some more) the most blatantly erroneous parts (some of which yours truly has had a hand in exposing).  It's amazing, really, that he still manages to fill an hour with the pared down version.  It's even more amazing that there's anyone left buying his schtick, but ... well ... I'll just leave it at that. 

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!

EDIT:  As of 2/16/16 we're at over 1200 comments (fun times!!) and for me, Disqus is slow to load in blogger.  To engage, you may wish to read/comment using this link which goes directly to disqus.

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  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

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 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.