The Carb-Sane Asylum

S ummary: 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: Excessive lipolysis resulting in an increased cycling of the Triglyceride/Fatty Acid cycle.   Impaired suppression of glucose production in t...

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.  M...

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 diagn...

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 pa...

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.

As I have quite a few tangential thoughts going on, in search of a cohesive theme here, I've decided I'd just throw up a few short posts, and perhaps come back and put them together at some later date. The Glycemic Index is credited to Canadian researcher David Jenkins, and originated, near as I can tell, with this paper:   Glycemic index of foods: a physiological basis for carbohydrate exchange
. INTRODUCTION :   Recent work has suggested that the carbohydrate exchange lists that have regulated the diets of many diabetics for over three decades may not reflect the physiological effect of foods. Such factors as food form, dietary fiber, and the nature of the carbohydrate have been shown to have a marked influence on the postprandial glycemia and allowances cannot be made for these in lists which take into account only the available carbohydrate content of foods. Currently, very good blood glucose control has been advocated for diabetics to reduce the incidence of lo...

The cornerstone of the American justice system:  Innocent until proven guilty.  According to Wikipedia : sometimes referred to by the Latin expression Ei incumbit probatio qui dicit, non qui negat (the burden of proof lies with who declares, not who denies).  I like the first part of that Latin expression and suggest that what is truly needed in nutritional circles is to put the burden of proof on those making claims.  My point here is not a political one, it is not to argue the merits of my country's justice system or its implementation, or anything of the sort.  It is to put forth a suggestion -- that ALL who demonize foods be tasked with proving their charges.   I suggest this because it is darned near impossible to do the opposite especially in the face of baseless charges.   It is a bit of a stretch, but keep in mind that many of the compounds, such as water, can be toxic at some level of ingestion.  Furthermore, some of the chemical ...

In the next day or few, I'm going to be discussing diabetes. What it is, and what the science says causes it -- at least to the current state of knowledge and understanding.  This will serve as a prelude to  a larger discussion on hyperinsulinemia and insulin resistance in the pathogenesis of Type 2 diabetes.   Diabetes is   β-cell dysfunction. Period. This does not mean that other organs and the organism as a whole are not involved in this dysfunction developing, but diabetes is, ultimately, an insulin deficiency syndrome.   If that sounds "off" because of the hyperinsulinemia associated with T2, stay tuned! So I'm going to cobble together a few sources to introduce (or reintroduce) some terminology and basics of    β-cell function that will be used in future posts on this.   Molecular Formation of Insulin On a molecular level, the final product, insulin, starts out as preproinsulin, is converted to proinsulin and then finally to the ...

Just about every major blogger and guru in the IHC has a lengthy medical disclaimer page.  They are not providing medical advice on the internet because if they are an MD it's illegal (my understanding of the law, feel free to correct me if I'm wrong here),  and if they are not, it's illegal to practice without a license.  Same goes for nutritional advice and all that.   Right after the medical disclaimer, where you've usually been given the "I have no special training in what I'm about to convey" spiel, or, the flipside, the disclaimer is signed with a name and a litany of letters after it.  And from time to time, you get nothing more than a telling of someone's story on how they cured themselves.  The IHC is big on this.  One of the more recent trends in the IHC is the promotion of ketogenic diets for curing cancer.  I consider this to be wholly irresponsible unless there is a focus on using the diet in conjunction with medical therapies ...