Blood Sugar Beliefs.

SugarAndSpike “Glucagon, cortisol, adrenalin, growth hormone and thyroid tend to increase the blood sugar, but it is common to interpret hyperglycemia as “diabetes,” without measuring any of these factors.”Ray Peat PhD

It’s perfectly understandable for it to appear as self-evident, that sugar restriction will result in the lowering of blood sugar levels, and that this – so called improvement in the symptoms of what is often referred to as diabetes – is representative of some kind of metabolic recovery.

Unfortunately this is a potentially very misleading idea, which – when looked at from a more appropriate physiological perspective – no longer seems logical, nor does it appear to be supported by much in the way of high quality experimental evidence.

“Dietary intakes of total carbohydrates, starch, sucrose, lactose or maltose were not significantly related to diabetes risk after adjustment for confounders…fructose was inversely related to diabetes risk.. The replacement of 5 % energy intake from SFA [saturated fat] with…fructose was associated with a 30 % lower diabetes risk…” (Ahmadi-Abhari S, et al., 2014)

Although there are many things which increase blood sugar (and not all of them are harmful), chronic hyperglycemia – often a symptom of metabolic dysfunction – has been shown to be alleviated by the introduction of greater amounts of sucrose or fruit sugar in the diet, rather than by its avoidance.

“Fasting plasma glucose levels fell in all subjects and oral glucose tolerance…significantly improved after 10 days of high carbohydrate feeding. Fasting insulin levels also were lower on the high carbohydrate diet…” (John D. Brunzell, et al., 1971)

Before you get carried away, I’m not saying the only thing wrong, when someone has problems properly regulating blood sugar, is that they aren’t eating enough sugar.

However, talking about sugar dysregulation issues in a simplistic sugar-blaming manner, without looking at the impact that biological stress can have on proper metabolic function, is at the very least, unhelpful and misleading. And the assumption that high blood sugar or hyperglycemia is necessarily driving the diabetic state and associated metabolic damage, is also likely inaccurate.

“Compared with [YesBreakfast]…plasma glucose, FFA [free fatty acids], and glucagon were 36.8, 41.1, and 14.8% higher, respectively… on the [NoBreakfast] day…Skipping breakfast increases PPHG [postprandial hyperglycemia] after lunch and dinner in association with…impaired insulin response.” (Jakubowicz D, et al., 2015)

“Recent clinical studies…found that T2D patients treated to maintain glycemia below the diabetes definition threshold…still develop diabetic complications. This suggests additional insulin- and glucose-independent mechanisms could be involved in T2D progression and/or initiation…” (Moraru A, et al., 2018)

“…mortality risk did not increase with hyperglycemia unless associated with simultaneous hyperlactatemia…intensive insulin therapy may not be the most plausible approach to curtailing mortality risk….further efforts might be focused on understanding and regulating lactate metabolism as the key energy mediator and mortality risk predictor…” (Green JP, Berger T, et al., 2012)

When decisions regarding health are made on the basis of the idea that consuming too much sugar causes ‘diabetes’, it makes sense to me that the long term results would quite often be far from good. I’m not a doctor, and none of this is intended as health advice, but as far as I have been able to tell, there is little in the way of evidence, showing that sugar consumption is what is really to blame.

When sugar is restricted, and (after a little while) when glycogen stores are depleted, both cortisol and adrenalin rise in an attempt to maintain the supply of blood sugar, as well as making available an alternative fuel in the form of free fatty acids released from storage.

Cortisol maintains blood sugar – partly by blocking the use of sugar for many purposes (eg. immune cell function) and – by converting valuable muscle and other tissue into fuel for cells.

At the same time, when fats released from storage are polyunsaturated (PUFAs), they can lead to a chronic inability of cells to use glucose, further promoting hyperglycemia, and the release of more cortisol.

The by-products of oxidation of PUFAs are now known to directly stimulate cortisol synthesis.

The breakdown products of PUFAs have been found to be closely associated with the progression and severity of symptoms of type 2 diabetes.

“Diabetic population as a whole showed higher MDA [malondialdehyde] plasma levels compared to controls…The patients with a poor metabolic control showed the highest plasma MDA concentrations…” (Noberasco G, et al., 1991)

“…our study suggests that hyperglycemia in newly diagnosed patients with Type 2 DM is associated with elevated OS [oxidative stress] through increased lipid peroxidation…” (Manohar SM, et al., 2013)

“In diabetic patients a positive correlation was found between plasma MDA levels and mean daily blood glucose…results confirm the increase of lipid peroxidation during Type 2 diabetes. The correlation with the degree of metabolic imbalance suggests a possible role for lipid peroxidation in the occurrence of glucose-induced macromolecular changes.” (Altomare E, et al., 1992)

“In both groups of type 2 D.M, serum MDA levels were significantly higher than the normal. In type 2 DM with myocardial infarction, MDA levels were significantly higher than Type 2 cases without any complications.” (Mahreen R, et al., 2010)

Adrenalin and cortisol (as well as PUFAs) can cause insulin resistance, and this – in combination with the above and other factors – encourages blood sugar dysregulation and other related degenerative and diabetogenic symptoms.

Even though it is the starches (or complex carbohydrates) which are generally recommended – often to those with chronically high blood sugar – as a ‘healthy’ alternative to sucrose or fruit sugar, they can raise blood sugar more rapidly and to a greater degree, largely because of the way in which they quickly convert to pure glucose.

As a result of this more insulin needs to be secreted, a factor which can be responsible for the exacerbation of many issues associated with high blood sugar or ‘diabetes’. The blood sugar lowering or hypoglycemic effects of raised insulin, can promote the excessive release of cortisol and adrenalin, and an increase in circulating levels of PUFAs, causing hyperglycemia as well as increased fat production and eventually obesity.

The stress promoting effects of chronically raised insulin are a significant cause of metabolic illness and the degenerative symptoms that go along with the so called diabetic state.

Contrary to popular opinion, the fructose component of fruit sugar or sucrose, not only slows the rate at which glucose enters the blood stream, but also significantly reduces the insulinagenic effects of glucose, improving or preventing many of the above reactions.

Fructose by itself, does not require insulin for it to be metabolized, and as such has been shown to effectively promote the replenishment of glycogen stores, protecting against the stress effects that often lead to the diagnosis of diabetes.

“…low dose fructose improves the glycemic response to an oral glucose load in normal adults without significantly enhancing the insulin or triglyceride response. Fructose appears most effective in those normal individuals who have the poorest glucose tolerance.” (Moore MC, et al. 2000)

“…analyses of short-term controlled feeding trials showed that isocaloric fructose replacement of other carbohydrates resulted in clinically significant improvements in glycemic controlwithout significantly affecting insulin in diabetic individuals.” (Cozma AI, et al., 2012)

It’s possible that replacing sugar with starch or ‘complex carbohydrates’ might initially provide the illusion of improvement with regards to hyperglycaemia, by increasing exposure to insulin, and temporarily giving the impression that lower blood sugar readings are the result of disease remission and an overall improvement in health.

It is long term consumption of PUFAs, that is one of the most potent promoters of stress and systemic inflammation, creating the conditions that are so often wrongly blamed on too much white sugar in the diet.

Under circumstances such as these, chronic and excessive exposure to stress of many different kinds, particularly when sugar is restricted – or in combination with over consumption of the starchy glucose producing carbohydrates – can promote the factors (insulin resistance, high cortisol and adrenalin, and rising levels of polyunsaturated free fatty acids) which worsen blood sugar regulation capability.

Confusion can arise as a result of the ability of cortisol (and other stress substances) – at least in the short term – to suppress symptoms and provide a certain amount of improvement in the way a person feels.

Removing all forms of sugar (including starches) from the diet, can sometimes create the illusion of an improvement in blood sugar regulation issues, by temporarily lowering readings, giving a false impression of health improvement by suppressing a number of metabolic requirements.

High protein intake – in the absence of enough sugar – can also reduce blood glucose levels when insulin (which is secreted as a necessary part of protein absorption and synthesis) removes sugar from the blood. This kind of diet over a period of time, can advance diabetes related problems, whilst also being able to appear at first like a metabolic improvement.

The potentially hypoglycemic effects of this scenario, when stress and exposure to PUFAs is already an issue, can set in motion a vicious circle of low and high blood sugar, and associated problems.

A high fat low sugar diet – particularly when high in PUFAs – interferes with thyroid energy systems, slowing liver function. A sluggish, under active liver, is a cause of low blood sugar and stress, and even though it is becoming more and more common for indicators of stress to be seen as if they were a sign of the effectiveness of a dietary approach, the long term results are often faster aging, chronic inflammatory illness, and degeneration.

The avoidance of starchy carbohydrates can sometimes be helpful as a means to reducing metabolic dysfunction (including improvement in blood sugar regulation), partly because of a reduction in exposure to bacterial endotoxin. But it’s important to ensure there is still sufficient energy available to fuel thyroid metabolism, digestion, and detoxification. Sucrose and fructose are great candidates for this position.

Insufficient sugar suppresses thyroid function, inhibiting digestion and intestinal barrier function, increasing exposure to endotoxin, and endotoxin (LPS) can cause inflammation, hyperglycemia, and insulin resistance.

“Lipopolysaccharides (LPS) of the cell wall of gram-negative bacteria trigger inflammation, which is associated with marked changes in glucose metabolism. Hyperglycemia is frequently observed during bacterial infection and it is a marker of a poor clinical outcome in critically ill patients.” (Nguyen AT, et al., 2014)

“…data suggest that metabolic endotoxemia could be involved in the pathogenesis of insulin resistance in obese and T2DM subjects…” (Liang H, et al., 2013)

Suppression of thyroid energy systems, and increased endotoxin circulation, can also lead to a rise in other substances of stress, like estrogen, serotonin, nitric oxide, and lactate, and these substances are associated with high blood sugar, and other diabetes related issues. Dealing with stress, and improving thyroid/oxidative metabolism, moves functioning away from overreliance on the stress systems.

“The data suggest that estrogen…may relate to deterioration of glucose tolerance. Longer duration of estrogen use among current users may relate to an increased risk of type 2 diabetes.” (Zhang Y, et al., 2002)

“The enterochromaffin cells of the gastrointestinal tract produce peripheral serotonin postprandially….it induces a decrease in the concentration of circulating lipids as well as hyperglycemia and hyperinsulinemia…” (Watanabe H, et al., 2011)

“…it was established that NIDDM…patients have significantly greater plasma 5-HT concentrations…” (Barradas MA, et al., 1988)

“Increased expression of iNOS induced hepatic insulin resistance and hyperglycemia at least in part by impairing insulin signaling at multiple levels…” (Shohei Shinozaki, et al., 2011)

“In line with experimental evidence, we could demonstrate in humans that poor glycemic control is related to higher NO activity and hyperperfusion of the kidney.” (Schneider MP, et al., 2013)

To put it another way, sugar is a basic anti-stress pro-thyroid substance, and a fundamental factor protecting against rising levels of stress. Sugar plays a crucial role in the production of the anti-stress cholesterol, and the subsequent conversion of cholesterol into the anti-inflammatory protective hormones, such as pregnenolone, progesterone and testosterone, also shown to protect against symptoms associated with diabetes.

Even though the idea of removing white ‘processed’ sugar from the diet has been made to sound appealing, as a very simple solution to chronic hyperglycemia or blood sugar dysregulation issues (and related metabolic problems), there are a number of biologically logical reasons to avoid that trap.

The relationship between increased lactate production, diabetes, and cancer progression, is one example of what can be at stake, if the oxidative metabolism interfering (carbon dioxide lowering) impact of too much exposure to PUFAs and other substances of stress, are set aside, in favor of a sugar demonizing ideology. This can be shocking, once you become aware of the impact that excessive restriction of sugar can have in relation to stress, inflammation, and disease.

“…data indicate that chronical hyperlactatemia might indicate the early stages of insulin resistance and contributes to the onset of diabetes…A common feature of primary and metastatic cancers is increase in glycolysis rate, leading to augmented glucose uptake and lactate formation, even under normal oxygen conditions.” (Wu Y, et al., 2016)

A far more rational method seems to call for avoiding PUFAs, in the context of a diet that aims to promote thyroid metabolism and lower cortisol, adrenalin, as well as free fatty acid release, by providing sufficient protein and other nutrients (from milk, cheese, or gelatin) and plenty of simple sugars, from sweet ripe juicy fruits, fruit juice, honey, and white sugar.

Some other things that have been shown to improve blood sugar regulation, include aspirin, biotin, thiamine, glycine, minocycline, coffee and caffeine, taurine, famotidine, niacinamide, cyproheptadine, methylene blue, activated charcoal, and a number of other stress and inflammation lowering things.

Have you experienced the long term effects of the removal of PUFAs, on the ability to effectively and efficiently metabolize sugar?

See more here

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