Beware Blood Sugar Bugs in Your Belly.

FrogBlog There’s a powerful relationship between blood sugar regulation issues and bacteria, and in order to tell the story in a meaningful way, the conversation has to include sugar, and the polyunsaturated fats (PUFAs), and some of the ways they can be involved.

Two things which are known to play a role in the development of diabetes related blood sugar dysregulation issues (including obesity), are insulin resistance and chronic low level inflammation.

Excessive exposure to the PUFAs – as well as rising cortisol secretion – promotes insulin resistance issues and inflammation, and all of this is interconnected with metabolic stress and increasing circulation of bacterial endotoxin.

Endotoxin – or Lipopolysaccharide (LPS) – is produced by certain types of intestinal bacteria, and when released into the system, directly irritates cells, activating defensive responses (including serotonin secretion), which over time can suppress metabolic performance, and promote many health issues.

When metabolism is functioning well, small amounts of bacterial endotoxin are not necessarily that problematic (and can even have a beneficial effect, stimulating digestive function), with the little that passes into the blood stream being dealt with by the liver. In fact, most of the substances of stress (including serotonin and cortisol), have a basic physiological role, and can be helpful up to a point.

Ongoing exposure to stress however, when combined with sugar restriction and increased consumption of the anti-metabolic polyunsaturated fats (and other foods which inhibit metabolism and digestion), can be a big part of what is able to change this story, increasing stress and bacterial endotoxin exposure, and eventually harming metabolism and promoting blood sugar related diseases.

Chronic metabolic stress and thyroid disorders, are known to promote each other. Anything that interferes with thyroid function and energy system metabolism, can increase the impact of stress exposure, and also has a tendency to further inhibit digestive function, giving bacteria more opportunity to multiply, increasing endotoxin levels.

When stress is high (and sugar supply is reduced), glycogen stores are eventually depleted, greater amounts of cortisol and adrenaline are generally secreted, endotoxin issues increase, and more of the polyunsaturated free fatty acids are released into circulation in the blood stream. All of this can be significantly anti-metabolic.

Apart from directly promoting inflammation – as well as insulin resistance and blood sugar dysregulation – both endotoxin and the PUFAs further interfere with metabolism, potentially leading to a greater reduction in intestinal function and a vicious circle like effect.

It has in recent times, become popular to attempt to deal with health issues by trying to remove sugar from the diet, increasing consumption of fat (including much more of the PUFAs) and difficult to digest fibers and starches.

The combination of these factors can greatly damage metabolism and feed bacterial overgrowth, significantly increasing endotoxin (and serotonin) secretion, promoting intestinal permeability, thereby allowing greater amounts of the inflammatory things to pass into the blood stream.

This can cause the liver to eventually become overloaded, leading to more endotoxin and other stressful inflammatory substances getting into the main system, irritating the cells and destabilizing metabolic function.

This can then directly result in a rise in the release of numerous inflammatory substances, including serotonin, nitric oxide and lactic acid, all of which can promote metabolic stress and further interference with proper blood sugar regulation.

Each of these things can help to promote more of the others, creating what can be referred to as a chronically stressed metabolism, which ends up relying upon the stress system in an excessive and ‘unnatural’ manner, as a means to survival. The long term impact of this is potentially very serious.

One way of approaching these kinds of issues, would be to attempt to reduce the factors causing stress and interfering with metabolism and digestion (which promote excess exposure to endotoxin and PUFAs), whilst at the same time gradually providing more fuel and the right nutrients for improved energy system function, lowering inflammation, and improving insulin function and intestinal barrier and liver detoxification capability.

As exposure to the substances of stress and inflammation (in particular endotoxin and the PUFAs) goes down, blood sugar issues, including insulin resistance and chronic hyperglycemia, can start to lessen.

The provision of sufficient protein from milk, cheese and gelatin, as well as plenty of sugar from easy to digest carbohydrates like sweet ripe juicy fruits, fruit juice, honey and white sugar, whilst avoiding the PUFAs and too many fibrous, starchy, grains, beans and under cooked vegetables, is one potential approach to avoiding harm from bugs in the belly and other inflammatory things.

If you like what I have to say, and you want more information (including lots of studies), showing ways that endotoxin and the PUFAs promote stress, inflammation and blood sugar dysregulation, please check out some of my other articles, including ‘Blood Sugar Beliefs’. And please share this and sign the email list up top.

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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