Insulin Can Be Irresistible.
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.
“…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.”
“…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.
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.
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.
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.
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.
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Image: FoodsMatter: “Probiotics – the ‘friendly’ bacteria:” John Scott