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…”

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…”

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.”

“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…”

“…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…”

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 biologist or a doctor, but as far as I have been able to tell, there is no physiological evidence which effectively shows 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 PUFA oxidation are now known to directly stimulate cortisol synthesis.

The PUFA breakdown products 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…”

“…our study suggests that hyperglycemia in newly diagnosed patients with Type 2 DM is associated with elevated OS [oxidative stress] through increased lipid peroxidation…”

“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.”

“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.”

Adrenalin and cortisol (as well as PUFAs) 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, in reality they often raise blood sugar more rapidly and to a greater degree, largely because of the way in which they can 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 PUFA levels, 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, in actuality 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.”

“…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.”

It’s possible that replacing sugar with starch or ‘complex carbohydrates’ might initially provide some with 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.

Long term consumption of PUFA is one of the most potent promoters of stress and systemic inflammation, which create 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 perhaps in combination with over consumption of the starchy glucose producing carbohydrates – can promote the very common factors (insulin resistance, high cortisol and adrenalin, and rising levels of polyunsaturated free fatty acids) which worsen blood sugar regulation capability.

Confusion can often 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 false impression of improvement in blood sugar regulation issues, by temporarily lowering readings, and can give the 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 easily advance diabetes related problems, whilst also being able to appear at first like a metabolic improvement.

The potentially hypoglycemic effects of these scenarios, when stress and PUFA exposure is already an issue, can set in motion a vicious circle of low and high blood sugar and many associated problems.

A high fat low sugar diet – especially if the fat is high in PUFA – can interfere with thyroid energy systems, slowing liver function. A sluggish, under active liver is a common cause of low blood sugar and stress, and even though it is becoming more and more common for indicators of stress to be viewed as if they were a sign of the effectiveness of popular dietary approaches, the long term results are faster aging, chronic inflammatory illness and degeneration.

It’s true that the avoidance of starchy carbohydrates can be genuinely helpful as a means to reducing metabolic dysfunction (including improvement in blood sugar regulation) and this is partly because of a potential reduction in exposure to bacterial endotoxin. It’s important to ensure there is still sufficient energy available to fuel thyroid metabolism, effective digestion and detoxification. Sugar is a great candidate for this position.

Insufficient sugar suppresses thyroid function, inhibiting digestion and intestinal barrier function, increasing exposure to endotoxin, and endotoxin (LPS) has been shown to promote 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.”

“…data suggest that metabolic endotoxemia could be involved in the pathogenesis of insulin resistance in obese and T2DM subjects…”

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

“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…”

“…it was established that NIDDM…patients have significantly greater plasma 5-HT concentrations…”

“Increased expression of iNOS induced hepatic insulin resistance and hyperglycemia at least in part by impairing insulin signaling at multiple levels…”

“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.”

To put it another way, sugar is a basic anti-stress pro-thyroid substance, and a fundamental factor protecting against rising levels of stress. Furthermore, sugar plays a crucial role in the production of the anti-stress cholesterol, and subsequent conversion of cholesterol into the anti-inflammatory protective hormones such as pregnenolone and progesterone, 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 the many related metabolic problems – there is an overwhelming number of biologically rational reasons to avoid that trap.

The relationship between increased lactate production, and diabetes and cancer progression, is a good example of what is at stake if the oxidative metabolism interfering (carbon dioxide lowering) effects of greater exposure to PUFA and the substances of stress, are ignored in favour of a sugar demonising ideology. This is particularly shocking once you become aware of the impact that restricting sugar can have in relation to the many promoters of 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.”

A far more rational method seems to call for removing PUFA 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 (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, as well as possibly cyproheptadine, methylene blue, activated charcoal and a number of other stress and inflammation lowering things.

Although I am not claiming to have all (or even any) of the answers with regards to how to deal with worsening metabolic conditions, my own personal experience (and the experiences of others I have been in contact with) have led me to the conclusion that unless one has experimented enough with some of the above concepts, and actually experienced what improved metabolism can achieve, no claims would provide much confidence.

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

See more here

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

Fructose vs. glucose in total parenteral nutrition in critically ill patients.

Skeletal muscle lipid peroxidation and insulin resistance in humans.

Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles.

Effects of acute progesterone administration upon responses to acute psychosocial stress in men

Fructose and dietary thermogenesis.

Prevention of fat-induced insulin resistance by salicylate

Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults.

Links between thyroid hormone action, oxidative metabolism, and diabetes risk?

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

Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.

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

Dietary intake of carbohydrates and risk of type 2 diabetes: the European Prospective Investigation into Cancer-Norfolk study

Effect of glycine in streptozotocin-induced diabetic rats.

Paracrine Interactions within the Pancreatic Islet Determine the Glycemic Set Point

Lactate, a Neglected Factor for Diabetes and Cancer Interaction

High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial.

Progesterone modulates diabetes/hyperglycemia-induced changes in the central nervous system and sciatic nerve.

High fat diet-induced hyperglycemia: prevention by low level expression of a glucose transporter (GLUT4) minigene in transgenic mice.

Amelioration of high-fat feeding-induced insulin resistance in skeletal muscle with the antiglucocorticoid RU486.

Minocycline Attenuates Severe Hyperglycemia in Patient with Lipodystrophy

Hyperlactatemia Affects the Association of Hyperglycemia with Mortality in Nondiabetic Adults With Sepsis

Improved Glucose Tolerance with High Carbohydrate Feeding in Mild Diabetes

Methyldopa blocks MHC class II binding to disease-specific antigens in autoimmune diabetes.

Taurine ameliorates hyperglycemia and dyslipidemia by reducing insulin resistance and leptin level in Otsuka Long-Evans Tokushima fatty (OLETF) rats with long-term diabetes

Plasma AGE-peptides and C-peptide in early-stage diabetic nephropathy patients on thiamine and pyridoxine therapy.

Relationship between insulin resistance and lipid peroxidation and antioxidant vitamins in hypercholesterolemic patients.

Hepatocyte-secreted DPP4 in obesity promotes adipose inflammation and insulin resistance

Elevated Levels of the Reactive Metabolite Methylglyoxal Recapitulate Progression of Type 2 Diabetes.

Fluctuations of Hyperglycemia and Insulin Sensitivity Are Linked to Menstrual Cycle Phases in Women With T1D

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.

Effect of chronic coffee consumption on weight gain and glycaemia in a mouse model of obesity and type 2 diabetes

Lipopolysaccharides-mediated increase in glucose-stimulated insulin secretion: involvement of the GLP-1 pathway.

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

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

UCP2 regulates mitochondrial fission and ventromedial nucleus control of glucose responsiveness

Glycine treatment decreases proinflammatory cytokines and increases interferon-gamma in patients with type 2 diabetes.

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

High-dose thiamine supplementation improves glucose tolerance in hyperglycemic individuals: a randomized, double-blind cross-over trial.

Lipid peroxidation and resistance to oxidation in patients with type 2 diabetes mellitus.

Effect of Lipopolysaccharide on Inflammation and Insulin Action in Human Muscle

Neuroendocrine perturbations as a cause of insulin resistance.

Decreased total antioxidant levels and increased oxidative stress in South African type 2 diabetes mellitus patients

Lipid peroxidation and antioxidant enzyme activities in erythrocytes of type 2 diabetic patients.

Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

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

Lipid peroxidation alterations in type 2 diabetic patients.

Epoxy-keto derivative of linoleic acid stimulates aldosterone secretion.

Malondialdehyde (MDA) level in diabetic subjects. Relationship with blood glucose and glycosylated hemoglobin.

Blood lipid peroxidation (superoxide dismutase, malondialdehyde, glutathione) levels in Egyptian type 2 diabetic patients.

High levels of lipid peroxidation in semen of diabetic patients

Famotidine inhibits glycogen synthase kinase-3β: an investigation by docking simulation and experimental validation.

The lipid peroxidation by-product 4-hydroxy-2-nonenal (4-HNE) induces insulin resistance in skeletal muscle through both carbonyl and oxidative stress.

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

Blood Viscosity, Lipid Profile, and Lipid Peroxidation in Type-1 Diabetic Patients with Good and Poor Glycemic Control

Role of peripheral serotonin in glucose and lipid metabolism.

Increased plasma concentration of nitric oxide in type 2 diabetes but not in nondiabetic individuals with insulin resistance.

Role of Pro-Inflammatory Cytokines and Biochemical Markers in the Pathogenesis of Type 1 Diabetes: Correlation with Age and Glycemic Condition in Diabetic Human Subjects

Effect of Peripheral 5-HT on Glucose and Lipid Metabolism in Wether Sheep

Serotonin as a New Therapeutic Target for Diabetes Mellitus and Obesity

Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects.

Oxidative stress, insulin resistance, dyslipidemia and type 2 diabetes mellitus

Diabetes and increased lipid peroxidation are associated with systemic inflammation even in well-controlled patients

Executive Functioning and Diabetes: The Role of Anxious Arousal and Inflammation

Hyperglycaemia Enhances Nitric Oxide Production in Diabetes: A Study from South Indian Patients

Distribution of serotonin and its effect on insulin and glucagon secretion in normal and diabetic pancreatic tissues in rat.

An association of hyperglycemia with plasma malondialdehyde and atherogenic lipid risk factors in newly diagnosed Type 2 diabetic patients

The effect of estrogen use on levels of glucose and insulin and the risk of type 2 diabetes in american Indian postmenopausal women : the strong heart study.

Study of lipid peroxidation, nitric oxide end product, and trace element status in type 2 diabetes mellitus with and without complications

Serotonin potentiates high-glucose-induced endothelial injury: the role of serotonin and 5-HT(2A) receptors in promoting thrombosis in diabetes.

Nitric oxide levels in response to the patients with different stage of diabetes.

Increased lipid peroxidation in type 2 poorly controlled diabetic patients.

Liver-specific Inducible Nitric-oxide Synthase Expression Is Sufficient to Cause Hepatic Insulin Resistance and Mild Hyperglycemia in Mice*

Association of Antidepressant Medications With Incident Type 2 Diabetes Among Medicaid-Insured Youths

Significantly increased levels of serum malonaldehyde in type 2 diabetics with myocardial infarction

Effects of growth hormone on glucose metabolism and insulin resistance in human

Poor Glycemic Control Is Related to Increased Nitric Oxide Activity Within the Renal Circulation of Patients With Type 2 Diabetes

Increased plasma concentration of nitric oxide in type 2 diabetes but not in nondiabetic individuals with insulin resistance.

Intraplatelet serotonin in patients with diabetes mellitus and peripheral vascular disease.

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


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