Type 1 diabetes is a condition in which the pancreas secretes too little insulin to clear glucose from the blood leading to chronically elevated blood glucose. From Wikipedia on T1D (highlights mine):
Diabetes mellitus type 1 (also known as type 1 diabetes, or T1D; formerly insulin-dependent diabetes or juvenile diabetes) is a form of diabetes mellitus that results from the autoimmune destruction of the insulin-producing beta cells in the pancreas. The subsequent lack of insulin leads to increased glucose in blood and urine. The classical symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger) and weight loss.
The cause of diabetes mellitus type 1 is unknown. Type 1 diabetes can be distinguished from type 2 by autoantibody testing. The C-peptide assay, which measures endogenous insulin production, can also be used. Administration of insulin is essential for survival.
Type 2 diabetes (T2D) is quite a bit different:
Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue. In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood. The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.
Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system. However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.
While medical researchers, nutritionists, and health writers go to great lengths to explain diabetes by looking at insulin resistance, lack of insulin, and other factors no one describes what I think seems to be an even bigger problem, and quite possibly the root cause of T2D: a leaky gut.
It's not quite like it sounds. Leaky gut is not a perforated gut, but a malfunctioning gut. All guts are leaky, by design. The leakiness is referred to as "intestinal permeability." The small intestine has two important jobs:
- Bring nutrients into the body
- Keep toxic substances out of the body
A good review of gut permeability can be found here: Alterations in intestinal permeability (Arrietta, 2006).
From the lower oesophageal sphincter to the anus, the gastrointestinal tract has a single contiguous layer of cells that separates the inside of the body from the external environment. Separation is important as there are a wide variety of environmental agents in the lumen of the bowel that can initiate or perpetuate mucosal inflammation if they cross the epithelial barrier. While the epithelial lining of the intestine plays a critical role in preventing access of these agents, it is not the only component of what is termed barrier function. Also important are secreted products such as immunoglobulin, mucous, defensins, and other antimicrobial products.
One mechanism that controls the passage and blockage of nutrients or toxins between the small intestine and the bloodstream are tight junctions (TJ). Often shown as a very simplistic structure, as this discussion on celiac disease and TJs:
Tight Junctions are not quite as simple as shown in the graphic above, they involve some complex protein structures and permeable membranes:
A description of the figure above explains:
The main barrier function of the epithelium is thought to depend on tight junctions, which are connected with the actin cytoskeleton (left panel). Three types of transmembrane proteins are part of tight junctions: occludin, claudins and junctional adhesion molecules (JAMs), and they are connected to adaptor proteins such as zona occludens 1 (ZO1), ZO2 and ZO3. Many additional proteins are also essential, including PAR6, atypic Ca2+- and diacylglycerol-independent protein kinase C (aPKC), and PAR3. This complex, which is important for cell polarity, is regulated by Cdc42, as is the CRUMBS3–PALS1–PATJ-complex, which is essential for tight junction assembly. The precise role of RhoA and Rac in tight junction regulation has still to be elucidated. Recently, it was suggested that RhoA-dependent phosphorylation of occludin is crucial for tight junction function.
Tight Junctions communicate with each other, with the body, bacteria, fungi, and with the foods or toxins they come into contact with. It's an immensely elaborate biological marvel that scientists are just beginning to understand. The important takeaways here are:
- Tight Junctions can and do malfunction
- Things get into our blood that should not be there
- Tight Junctions allow the passage of glucose from food to bloodstream.
Glucose, salt, emulsifiers, organic solvents, gluten, [Microbial transglutaminase] mTG, and nanoparticles are extensively and increasingly used by these industries to improve the qualities of the food (as claimed by manufacturers and some consumers). However, all these food additives increase intestinal permeability by bringing about TJ paracellular transfer. In fact, TJ dysfunction is common in multiple [auto-immune disease] AD and the central part played by the TJ in AD pathogenesis has been extensively described. It is hypothesized that commonly used industrial food additives abrogate human epithelial barrier function, thus, increasing intestinal permeability through the opened TJ, resulting in entry of foreign immunogenic antigens and activation of the autoimmune cascade.
Conclusion to Part 2:
I am not trying to solve the Leaky Gut disease phenomenon, I am just laying the groundwork to show that malfunctioning TJs can result in high blood glucose. There are lots of papers, like the two or three linked above, that explore leaky gut if you are interested.
T2D is a disease in which chronically elevated blood glucose leads to loss of insulin sensitivity. The elevated blood glucose then damages cells and entire organs as it circulates through the body. The usual explanation is that we simply eat too much glucose-containing foods, ie. sugar, potatoes, and this leads to chronically high gluocose levels and/or a worn-out pancreas. Yet, a high carb diet can cure some cases of diabetes. How can this be?
Next...a description of how glucose gets from food to blood, and blood to cells, under normal circumstances. Also, why high blood glucose is so dangerous.