#9 – HuffPost, The Lie That’s Killing Us: Pre-Diabetes

Continuing with posting my top 10 articles from the Huffington Post, I think this one captures a novel and provocative idea. No, more than that, an idea that can truly change behavior.

If we talked about pre-diabetes as Stage 1 of Type 2 Diabetes do you think people would take it more seriously? I do. Full article here.

3 thoughts on “#9 – HuffPost, The Lie That’s Killing Us: Pre-Diabetes

  1. Hi Riva,
    I read your article and am generally sympathetic. But I have a few comments.
    1. A much better indicator (than serum glucose) of “pre-diabetes” or metabolic syndrome seems to be the fasting serum insulin. This blood/lab test is commercially available but more expensive than it might be if it were to be adopted as preventative by insurance companies, as you are likely aware.
    2. Genetic research and other studies (including an early classic by G. Boden) seem to indicate that roughly one half or more of the population will never achieve clinical T2DM despite a lifetime of metabolic syndrome and hyperinsulinemia. Those who do not become overt diabetic manage to avoid the loss of beta cells (via apoptosis) and beta-cell functionality that is a sine qua non of T2DM — in other words, they retain compensatory insulin secretion capacity indefinitely.
    3. Nevertheless, chronic hyperinsulinemia is associated with many other degenerative conditions besides T2DM, and is unhealthy to varying degrees in anyone.
    4. An interesting characteristic of T2DM, at least until beta-cell loss becomes advanced, is the preservation of normal (i.e. nondiabetic) amino-acid stimulation of insulin secretion (AASIS). This is unlike both T1DM and also the HNF forms of monogenic diabetes (I myself am HNF1-alpha, and use insulin) at any stage of these conditions. Hence, an earlier T2D can achieve normal blood sugars using (low-carb) diet alone. This has not been seriously studied since the 1970s, but I think would be key to better
    understanding of T2DM specifically.
    5. Other than MODY2 (glucokinase monogenic diabetes), it is the hyperglucagonemia of diabetes resulting from insulin-secretion deficiency (particular in response to meals) and the paracrine islet regulation of alpha cells that fundamentally causes hyperglycemia. This has been strongly established since the 1970s, if nevertheless much ignored by most.
    Is hyperglucagonemia an element of metabolic syndrome? Probably not at this early stage — excess serum fatty acids and ectopic fatty-acid derivatives certainly are. Saturation of subcutaneous adipose capacity is too. But during this same stage true insulin resistance of the alpha cells may be developing:
    https://www.ncbi.nlm.nih.gov/pubmed/25157166
    https://www.physiology.org/doi/10.1152/ajpendo.00175.2011
    The above two studies and others are very suggestive of this as an early stage often leading to T2DM.

  2. P.S. So the takeaway from the comments above are:
    1. Serum glucose is a much less reliable and more latent indicator than serum insulin. But I suspect the reason serum insulin will never be tested regularly by GPs is that a majority of middle-aged patients would test positive for fasting hyperinsulinemia, and this would create a crisis requiring the government. academia and industry to acknowledge dietary and evolutionary realities. Implicitly, this might also lead to almost limitless class-action lawsuits and similar sequelae.
    2. I don’t like the term “pre-diabetes” because such a large number of people have the condition but will never develop overt diabetes. For the same reason HgA1c test results are misinterpreted because many utterly different conditions can generate equivalent moderately elevated results. For example, I am a diabetic with HbA1c between 5.0 and 6.0 (closer to 5 using insulin, and closer to 6 previously) but have very high insulin sensitivity (this is a uniform characteristic associated with HNF diabetics), I am lean and fit, and I maintain a diet with almost no plant foods (and hence no carb’s) at all. By the clinical guidelines I am not quite even pre-diabetic (e.g. my intrinsic fasting BG is 95mg/dL if I do not use basal insulin — 100mg/dL to 125mg/dL is the clinical pre-diabetes range for FBG). But I was born an overt diabetic, and have been so for 60 years now. This becomes clear only in examing postprandial response to a typical mixed meal. An OGTT is too artificial, and as conventionally performed in the US now would not catch my diabetes. At most it might flag me as a pre-diabetic, quite incorrectly — my diabetic condition has nothing to do with metabolic syndrome or pre-diabetes. My glycemic response is completely stable — there is absolutely NO progressivity whatsoever, and I have been and will remain with ~40% beta-cell function for life.
    3. I also hate the term “insulin resistance”. It is used as a substitute for “hyperinsulinemia”, and it is misused in context more often than not. For example, most think that T2Ds do not have insulin deficiency but only IR (whatever they falsely imagine that this means). This is completely ignorant, and NEVER true of a clinically-diagnosed (i.e. overt) T2D. Diagnosis only occurs when beta-cell function (measured as the so-called “disposition index”) falls to 20% of normal! Only at this stage do the symptoms of polyuria and polydipsia and severe hyperglycemia manifest.
    4. In T1DM there are too few living beta cells in the islets. In HNF monogenic diabetes there is underexpression of insulin-secretion proteins/genes due to autosomal-dominant homeobox mutations. In neither of these two conditions are the beta cells deranged or degenerated and inflamed as they are in T2DM. While there is progressive beta-cell loss over time in T2DM (due to excessive rates of apoptosis), the cells present are dysfunctional with degenerated and inflamed organelles (e.g. mitochondria, endoplasmic reticula). This status is always associated with ectopic FA metabolities in the beta cells.
    Progression from metabolic syndrome to overt T2DM is a gradual continuum when it occurs.
    5. It is almost surely the alpha cells and glucagon that are the key to T2DM. The excessive focus upon IR and beta cells is non-productive.

    • Thanks Ken for the trouble you took to respond with so much information. The bottom line appears to be diabetes is such a complex variety of conditions that using our catch-call word “diabetes” and “pre-diabetes” could never define anyone’s diabetes with any accurate specificity. I am glad to know you are doing so well. I also maintain a low carb diet but since I believe vegetables are essential nutrition, I dose for those.

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