Insulin Can Be Irresistible.

FriendlyBugs  Although it’s an understatement to say many are recommending sugar restriction as a means to improving health, evidence – relating to inflammatory conditions like insulin resistance, obesity and diabetes – suggests that this approach is unsafe and can end up powerfully driving worsening inflammation, stress and disease.

“Central to metabolic diseases is insulin resistance associated with a low-grade inflammatory status…we looked for a molecule involved early in the cascade of inflammation and identified LPS (bacterial endotoxin)…LPS is a strong stimulatory of the release of several cytokines that are key inducers of insulin resistance.”

When sugar intake is restricted – and glycogen stores are depleted – the hormones cortisol and adrenalin tend to rise as part of a process necessary for providing alternative sources of fuel.

Adrenalin helps get the remaining glycogen out of storage and releases fat from tissue in the form of free fatty acids. Cortisol converts muscle and other tissue so that it can be used for the provision of more energy.

If fatty acids released into circulation are made up of high levels of polyunsaturated fat (PUFA), they have an impact upon numerous factors known to be involved in the development of insulin problems.

The breakdown products of the polyunsaturated free fatty acids can provoke a chronic inflammatory state responsible for insulin dysfunction in a manner which can be difficult to reverse.

“Oxidized derivatives of linoleic acid…may be involved in the increased glucocorticoid production observed in obese humans.”

“…insulin resistance…correlates with enhanced oxidative stress.”

“…lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil in a dose dependent fashion…PUFA-mediated suppression of the mRNA…was partially restored by pioglitazone treatment…effects…seem to be due to increased insulin sensitivity.”

“…JNKs…can interfere with insulin action…and are activated by inflammatory cytokines and free fatty acids, molecules…implicated in the development of type 2 diabetes.”

“…accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.”

Many of the substances released under conditions of stress have been shown to have a negative impact upon insulin and blood sugar regulation.

PUFA stimulates the ongoing release of the ‘stress hormones’ – cortisol, adrenalin, serotonin, prolactin and estrogen – and directly damages thyroid function, suppressing energy metabolism. This tends to dysregulate blood sugar utilization and engender inflammation, very often slowing or impeding proper digestion.

“Obesity is associated with several metabolic and endocrine disorders…several mechanisms have been proposed including…the presence of thyroid hormones resistance, chronic low-grade inflammation, and insulin resistance.”

“Cortisol counteracts…insulin activation of glycogen synthase…insulin inhibition of hepatic glucose production and the insulin inhibition of lipolysis…leading to…systemic insulin resistance…exaggerated by increased free fatty acid mobilization…”

A sub optimal digestive system generally allows for bacteria to feed and grow in quantity, promoting the release of harmful byproducts like LPS (endotoxin). Endotoxin causes serotonin secretion to increase.

“…the gut microbiota plays a key role in promoting levels of colon and blood 5-HT (serotonin)…select microbes and their metabolic products can be used to promote endogenous, localized 5-HT biosynthesis…”

Increased circulating serotonin levels have been shown to be responsible for reducing insulin sensitivity and effectiveness.

“SERT-deficient mice exhibit hyperglycemia and insulin resistance, both of which are characteristic features of diabetes.”

Serotonin and endotoxin have both been demonstrated to promote inflammation and interfere with mitochondrial energy metabolism and blood sugar regulation.

“Latest evidence suggests…bacterial LPS (endotoxin) deriving from the gut microbiota may trigger inflammation and oxidative stress in response to diets…This “metabolic endotoxemia” has been shown to initiate or promote obesity, insulin resistance, metabolic syndrome, and finally diabetes.”

A suppressed and under active thyroid system impacts upon intestinal barrier capability, which can allow for more of the toxic byproducts of bacterial overgrowth to pass through to the liver.

“…high-fat feeding dramatically increased intestinal permeability…gut bacteria are involved in the control of intestinal permeability and furthermore in the occurrence of metabolic endotoxemia.”

If the liver becomes stressed and overloaded, this can interfere with detoxification, which means that potentially harmful substances produced in the intestine (such as bacterial endotoxin and serotonin) pass into the main system where they promote further inflammation and aggravate problems associated with insulin function and diabetes.

“Compelling evidence supports the concepts that gut microbiota actively promotes weight gain and fat accumulation and sustains, indirectly, a condition of low-grade inflammation, thus enhancing the cardiovascular risk.”

The liver is also responsible for the detoxification of estrogen for excretion. Excess estrogen inhibits thyroid and promotes serotonin, and both of these things increase cortisol levels and encourage a general state of metabolic suppression and blood sugar dysregulation.

Because estrogen can get trapped inside tissue, actual levels aren’t necessarily reflected in blood test results. High prolactin, which promotes cortisol release (and is connected to insulin resistance) is an accurate measure of tissue estrogen status.

As estrogen levels increase and liver function is lowered, thyroid hormone is less able to be turned into the metabolically active form, T3, further adding to stress and suppressing energy systems, leading to greater release of the polyunsaturated free fatty acids, and worsening inflammation and insulin resistance.

Rising levels of endotoxin, serotonin and estrogen in combination with a high PUFA diet cause inflammation and insulin resistance and exacerbate bacterial issues, increasing the likelihood of obesity, diabetes, and cardiovascular disease.

“…evidence suggests that changes in intestinal microbial composition could be responsible for increased endotoxemia in response to a high-fat diet, which in turn would trigger the development of obesity and diabetes.”

“Experiments…have shown that endotoxin is associated with cardiometabolic abnormalities including obesity, insulin resistance, and diabetes….Importantly, a high-fat diet increased the proportion of…LPS-containing microbiota in the gut.”

Carbohydrate consumption – in particular the difficult to digest starchy and fibrous foods – can promote bacterial overgrowth and endotoxemia, but this is especially the case in combination with PUFA consumption, and when stress is high and metabolism and digestion are no longer optimal.

“HFHC (high PUFA high carb) meal…induces an increase in plasma LPS (endotoxin)…relevant to the pathogenesis of postprandial oxidative and inflammatory stress, insulin resistance, and atherosclerosis…”

Orange juice – and sugar from fruit in general – can protect against stress and inflammation, lowering exposure to endotoxin, estrogen, serotonin and cortisol.

“The combination of glucose…and the HFHC meal induced oxidative and inflammatory stress and an increase in…endotoxin….orange juice intake with the HFHC meal prevented meal-induced oxidative and inflammatory stress…”

The consumption of any kind of fat can lead to a temporarily insulin resistant state, however it is only the PUFA which stimulates a chronic rise in the inflammatory substances which can prevent the return to normal function when stress is lowered and fuel is available.

“Our findings provide evidence for early biological adaptations to high fat feeding that proceed and possibly lead to insulin resistance.”

Any excess sugar consumed can either be stored as glycogen for later use or converted into the predominantly saturated fats which are able to keep inflammation down when stress is high.

A diet with enough protein from milk, cheese and gelatin, and plenty of sugar from sweet ripe fruits, fruit juice, white sugar and honey, can help to protect against stress and promote thyroid function and energy metabolism.

Avoiding the consumption of PUFA can reduce the harmfulness of bacterial toxins and go a long way towards lowering inflammation and improving blood sugar regulation and insulin issues.

“Endotoxin caused a less severe change in permeability index in…EFAD (essential fatty acid deficient) rats than in normal rats…”

When stress is lowered, there is likely to be less exposure to the polyunsaturated free fatty acids, a reduction in levels of the stress substances – cortisol, serotonin and estrogen – and a gradual lowering of inflammation and improvement in blood sugar regulation.

The ease of digestion of the above foods (as well as their pro-metabolic effects) helps to reduce bacterial issues, lowering endotoxin circulation and insulin resistance, and protecting against obesity and the onset of diabetes symptoms.

“…gut bacteria are involved in…metabolic endotoxemia…inflammation, and metabolic disorders. This effect could be mediated by a mechanism that could increase gut permeability and enhance LPS absorption. Antibiotic treatment significantly lowers plasma LPS levels, gut permeability, and the occurrence of…inflammation, oxidative stress…and metabolic disorders.”

Some other things which have the potential to protect against bacterial issues and improve insulin function include magnesium, biotin, coffee and caffeine, activated charcoal, coconut oil, niacinamide, thyroid hormone, aspirin, cascara, taurine, minocycline, certain antihistamines and pregnenolone.

The antibiotic effects of a daily raw carrot salad and some occasional well cooked mushrooms can also help protect against bacterial overgrowth and related insulin dysregulating effects.

See more here

Endotoxemia Is Associated With an Increased Risk of Incident Diabetes

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

Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

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

Free fatty acids, insulin resistance, and type 2 diabetes mellitus.

JNK and tumor necrosis factor-alpha mediate free fatty acid-induced insulin resistance in 3T3-L1 adipocytes.

The potential usefulness of taurine on diabetes mellitus and its complications

Chronic caffeine intake reverses age-induced insulin resistance in the rat: effect on skeletal muscle Glut4 transporters and AMPK activity

Taurine prevents free fatty acid-induced hepatic insulin resistance in association with inhibiting JNK1 activation and improving insulin signaling in vivo.

Intracellular magnesium and insulin resistance.

A central role for JNK in obesity and insulin resistance.

Increase in Plasma Endotoxin Concentrations and the Expression of Toll-Like Receptors and Suppressor of Cytokine Signaling-3 in Mononuclear Cells After a High-Fat, High-Carbohydrate Meal

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability.

Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB.

Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes.

Reduced Serotonin Reuptake Transporter (SERT) Function Causes Insulin Resistance and Hepatic Steatosis Independent of Food Intake

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

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

The Inflammatory Syndrome: The Role of Adipose Tissue Cytokines in Metabolic Disorders Linked to Obesity

Early Skeletal Muscle Adaptations to Short-Term High-Fat Diet in Humans Prior to Changes in Insulin Sensitivity

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial.

Transient receptor potential M3 channels are ionotropic steroid receptors in pancreatic β cells

Is hyperprolactinemia associated with insulin resistance in non-obese patients with polycystic ovary syndrome?

Serotonin-mediated acute insulin resistance in the perfused rat hindlimb but not in incubated muscle: a role for the vascular system.

Thyroid Function in Human Obesity: Underlying Mechanisms

Resistance of essential fatty acid-deficient rats to endotoxic shock.

The influence of endotoxemia on the molecular mechanisms of insulin resistance.

Obesity, Insulin Resistance and Free Fatty Acids

Polyunsaturated fatty acid-mediated suppression of insulin-dependent gene expression of lipogenic enzymes in rat liver.

Oxidative stress is closely associated with insulin resistance in genotypes 1 and 3 chronic hepatitis C

Prevention of fat-induced insulin resistance by salicylate

Free Fatty Acids Produce Insulin Resistance and Activate the Proinflammatory Nuclear Factor-κB Pathway in Rat Liver

Executive functioning and diabetes: The role of anxious arousal and inflammation.

Antidepressants induce cellular insulin resistance by activation of IRS-1 kinases.

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease.

Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes

Direct effects of prolactin on corticosterone release by zona fasciculata-reticularis cells from male rats.

11β-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice

Activation of Pregnane X Receptor by Pregnenolone 16 α-carbonitrile Prevents High-Fat Diet-Induced Obesity in AKR/J Mice

Oral taurine but not N-acetylcysteine ameliorates NEFA-induced impairment in insulin sensitivity and beta cell function in obese and overweight, non-diabetic men.

Neuroendocrine perturbations as a cause of insulin resistance.

An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.

Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass

Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats.

High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes.

Minocycline Attenuates Severe Hyperglycemia in Patient with Lipodystrophy

Association between serum prolactin levels and insulin resistance in non-diabetic men

Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse.

Changes in blood glucose and insulin responses to intravenous glucose tolerance tests and blood biochemical values in adult female Japanese black bears (Ursus thibetanus japonicus).

Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice.

How does brain insulin resistance develop in Alzheimer’s disease?

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle.

Mammalian hibernation: a naturally reversible model for insulin resistance in man?

Adipose tissue function in the insulin-resistance syndrome.

Inflammation and insulin resistance

Mechanism of free fatty acid-induced insulin resistance in humans.

Effects of Aromatase Inhibition and Androgen Activity on Serotonin and Behavior in Male Macaques

Alterations of the volatile metabolome in mouse models of Alzheimer’s disease

Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences.

#sugarsaves
#thatpufafilm
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Image: FoodsMatter: “Probiotics – the ‘friendly’ bacteria:” John Scott

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