Beware of Blood Sugar Bugs in Your Belly.

FrogBlog There is a powerful relationship between issues of blood sugar regulation and bacteria, and in order to tell the story in any kind of meaningful way, the conversation needs to include the effects of sugar and the polyunsaturated fats and some of the ways in which they can be involved.

Two things which have been shown to play a causative role in the development of diabetes related blood sugar issues (as well as obesity), are insulin resistance and chronic low level inflammation.

Although as discussed in previous posts, it has been effectively demonstrated that both the polyunsaturated fats – as well as increasing amounts of cortisol secretion – are common promoters of both of the above mentioned factors, the interconnectedness between these issues and rising systemic levels of bacterial endotoxin is important to understand.

Endotoxin – technically referred to as Lipopolysaccharide (LPS) – is produced by certain types of intestinal bacteria as a part of their basic structure and when released, directly irritates cells activating defensive responses, particularly serotonin.

Under normal circumstances when metabolism is running at an optimal level, a small amount of bacterial endotoxin is generally not problematic (in fact it can have a beneficial effect, adaptively stimulating proper function of systems) and the little that passes through the intestinal wall into the blood stream can be destroyed or removed by the liver.

This is where the idea of sugar restriction – as well as the increasing consumption of fats and numerous other foods which directly interfere with digestion – becomes involved in the story.

Anything that interferes with thyroid function and energy metabolism tends to slow digestion, allowing bacteria to multiply. When insufficient sugar is consumed – and glycogen stores are depleted – cortisol and adrenalin are secreted and the polyunsaturated fats are released into the blood stream.

Apart from directly promoting inflammation – as well as insulin resistance and blood sugar disregulation – these factors then further interfere with metabolism, leading to a greater reduction in intestinal function.

In conjunction with the above scenario – and in an attempt to remove sugar from the diet – it has become increasingly popular to consume more fat as well as difficult (sometimes impossible) to digest fibers and starches.

The combination of these factors can feed bacterial overgrowth and significantly increase endotoxin (and serotonin) secretion, promoting intestinal permeability and thus allowing greater amounts of these toxins to pass into the blood stream.

If the liver eventually becomes overloaded, more and more endotoxin can get further into the system, irritating cells and gradually destabilising metabolic function.

This directly results in the activation of numerous inflammatory substances, including serotonin and nitric oxide.

At a certain point, it is possible for a vicious cycle to be created – whereby each of these factors helps to promote more of the others – further suppressing metabolic energy systems, promoting cortisol, free fatty acid release, and subsequently increasing inflammation and blood sugar disregulation.

One way of approaching these (and other connected issues) would be to attempt to reduce the factors which interfere with digestion – and which also promote the production of bacterial endotoxin – whilst at the same time providing sufficient fuel for energy systems, allowing for proper intestinal barrier function and liver detoxification capability, plus greater blood sugar stability.

This could then allow for a reduction in many of the promoters of inflammation and other related stress substances, gradually reducing symptoms of metabolic dysfunction, including improving insulin sensitivity and lessening chronic hyperglycaemia and other issues of diabetes.

Attempting to provide sufficient amounts of protein from milk or cheese or gelatin – as well as having a regular supply of sugar from easy to digest carbohydrates such as sweet ripe juicy fruits, fruit juice, honey and white sugar – whilst at the same time avoiding the polyunsaturated fats and too much in the way of fibrous, starchy grains and beans (as well as under cooked vegetable matter) is one potentially very effective approach to experimenting with the above ideas.

See more here

Endotoxemia Is Associated With an Increased Risk of Incident Diabetes

Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk.

The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression in a Mouse Model of Alcoholic Liver Disease

Bacterial endotoxin stimulates adipose lipolysis via toll-like receptor 4 and extracellular signal-regulated kinase pathway.

Association between hypothyroidism and small intestinal bacterial overgrowth.

Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.

Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis

Duodenal mucosa of patients with type 1 diabetes shows distinctive inflammatory profile and microbiota

Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice


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