Via Spanish Caravan, a frequent commenter with let’s just say a “medical background.”
Physiological Insulin Resistatnce (PIR) results from glucose deficiency the same way mucin deficiency induces dry eyes, nostrils, colon and anemia like symptoms. They’re both ways of preserving glucose for your brain.
When you VLC, your muscles become insulin resistant to preserve your glucose for the brain. So while your muscles are running on fatty acids, they become insulin resistant. This leaves glucose for your brain but the net result is your BG going up as you’re “physiologically” insulin resistant. There doesn’t really seem to a problem with this state, as there is with mucin deficiency; it’s not known to induce diabetes or make prediabetics diabetic. At least not according to those who advocate VLCing. I have a feeling however, that this is a disease-prone state.
The effects of low carbohydrate diets on insulin sensitivity depend on what is used to replace the dietary carbohydrate, and the nature of the subjects studied. Dietary carbohydrates may affect insulin action, at least in part, via alterations in plasma free fatty acids. In normal subjects a high-carbohydrate/low-GI breakfast meal reduced free fatty acids by reducing the undershoot of plasma glucose, whereas low-carbohydrate breakfasts increased postprandial free fatty acids.
Why is it disease-prone? Because high serum free fatty acids are implicated in various disease states, especially immune related (and also diabetes in some cases). High serum FFA and very low trigs that we see among those who VLC are associated with nascent autoimmunity, especially rheumatic autoimmunity.
We’re talking about triglycerides as low as 10-20 in some of these guys who are in long-term ketosis; you can only attain those levels in long-term ketosis or in starvation. And starvation is ipso facto ketogenic, a point which most people miss. That’s why the immune related problems that people who undergo starvation apply directly to those who’re in long-term ketosis.
Why do you think antibody-positive hypothyroidism is rampant in those who VLC? I used to think these people were hypothyroid to begin with but began VLCing to relieve their symptoms. The opposite is happening: healthy people are developing hypothyroidism (either euthyroid or later Hashimoto’s) upon going on ketosis or undertaking autoimmune protocols. Why? That’s because antithyroid antibodies like TG and TPO are markers for abnormal T-lymphocyte function. T-lymphocyte dysfunction, as I’ve mentioned elsewhere, can be induced in long-term VLCing through either thymus atrophy or starvation-like immunodeficiency. There is a correlation of something like 70% between thyroid antibodies and rheumatic autoimmunity; that’s why most people develop RA or other diseases after contracting Hashimoto’s or vice versa.
Jaminet made a connection between mucin and stomach cancer; he should have made a larger connection between mucin, secretory igA, which is immunoglobulin A found as secretions in tears, saliva, and secretions from the gastrointestinal tract and other epithelium layers. IgA plays an important immune function and could be behind many of the immune problems being encountered by those VLC, along with obviously gut dysbiosis which eviscerates immune-aiding microbes:
Secretory IgA (SIgA) serves as the first line of defense in protecting the intestinal epithelium from enteric toxins and pathogenic microorganisms. Through a process known as immune exclusion, SIgA promotes the clearance of antigens and pathogenic microorganisms from the intestinal lumen by blocking their access to epithelial receptors, entrapping them in mucus, and facilitating their removal by peristaltic and mucociliary activities. In addition, SIgA functions in mucosal immunity and intestinal homeostasis through mechanisms that have only recently been revealed. In just the past several years, SIgA has been identified as having the capacity to directly quench bacterial virulence factors, influence composition of the intestinal microbiota by Fab-dependent and Fab-independent mechanisms, promote retro-transport of antigens across the intestinal epithelium to dendritic cell subsets in gut-associated lymphoid tissue, and, finally, to downregulate proinflammatory responses normally associated with the uptake of highly pathogenic bacteria and potentially allergenic antigens. This review summarizes the intrinsic biological activities now associated with SIgA and their relationships with immunity and intestinal homeostasis.
We keep triangulating this thing: long-term ketosis and VLCing => glucose deficiency symptoms like dry eyes, constipation, anemia symptoms, PIR + immunodeficient symptoms like unexplained food allergies, allergic rhinitis, sinusitis, respiratory infections, runny nose ==> disease state for T lymphocyte dysfunction and low immunoglobulins ==> pathogenesis of immunodeficiency + autoimmunity ==> then, and this is the reason why it’s hard to connect the dots, years down the road, clinical immunodeficiency and autoimmunity. Some people never get diagnosed because these are crypto disease states that are normally referred to specialists only when symptoms become severe. You’ll never suspect you have selectively immunodeficiency; your only symptom might be a mildly runny nose, especially if you supplement with Vit D.
Hopefully the notion that maintaining very low levels of carbohydrate and persisting in a state of ketosis long term will soon be a thing of the past.