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 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 idea is misleading, and also – when looked at from an appropriate physiological perspective – illogical, as well as being unsupported by high quality experimental evidence.

Although there are many things which increase blood sugar (and not all of them are harmful), chronic hyperglycaemia – 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.

When sugar is restricted, and – after a little while – glycogen stores are depleted, both cortisol and adrenalin rise in an attempt to maintain the supply of blood sugar, as well as providing 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 (for eg. immune cell function) and – by converting valuable muscle and other tissues into fuel for cells.

At the same time, when fat released from storage is polyunsaturated, it can lead to a chronic inability of cells to use glucose, further promoting hyperglycaemia as well as the release of more cortisol.

Adrenalin and cortisol (as well as the polyunsaturated fats) cause insulin resistance, and this – in combination with the above and other factors – worsens
blood sugar disregulation 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 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 is secreted, a factor which – particularly when polyunsaturated free fatty acids are high – is responsible for the exacerbation of many of the issues related to diabetes, including increasing cortisol and adrenalin, as well as both hyperglycaemia and hypoglycaemia, increased fat production, and eventually obesity.

Contrarily, 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.

One way in which replacing sugar with starch might initially provide the illusion of improvement with regards to hyperglycaemia, can be the result of insulin’s ability to rapidly dispose of blood glucose, as such temporarily lowering sugar readings.

In the long run, by promoting many of the factors discussed above – including insulin resistance and high cortisol – and in the presence of increased amounts of polyunsaturated fats, this only worsens blood sugar regulation issues, helping to advance many of the symptoms, the causes of which are often incorrectly blamed on white sugar.

This can become even more confusing as a result of cortisol’s ability – 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 however, can also – for a period of time – create the false impression of improvement in blood sugar regulation by temporarily lowering readings, thus seemingly reducing hyperglycaemia.

The consumption of increased amounts of protein – in the absence of sufficient sugar – can temporarily reduce blood glucose levels as a result of insulin, which when secreted as a necessary part of protein absorption and synthesis, simultaneously removes sugar from the blood.

This can (regrettably) lead to blood sugar levels falling too low, once again resulting in the promotion of cortisol, adrenalin and free fatty acid release, which can eventually cause high blood sugar and many of the related issues of diabetes.

The increased consumption of fat (when sugar is restricted) – in combination with rising amounts of polyunsaturated fats released from storage – is known to directly interfere with thyroid energy systems, significantly slowing liver function. As a result of the fact that a sluggish under active liver is a very common cause of hypoglycemia, this is then another way in which what might appear at first to be a metabolic improvement, can in actual fact eventually prove to be something all together different.

It is true that the removal of starch from the diet can be genuinely helpful as a means to reducing metabolic dysfunction (including blood sugar regulation) partly because of potentially significant bacterial and subsequent endotoxin reduction. This approach however, is likely to be far more effective in the context of the provision of sufficient sugar for energy to enable proper digestion as well as detoxification via a well fueled liver.

As simple and appealing as it might seem, the most appropriate approach to chronic hyperglycaemia – and the many related metabolic problems which interfere with the proper regulation of blood sugar, does not unfortunately appear to involve the removal of sucrose or fruit sugar from the diet.

A far more rational method seems to call for removing polyunsaturated fats in the context of a diet suppressing cortisol, adrenalin and free fatty acid release, by providing sufficient protein – from milk, cheese or gelatin – and increasing amounts of simple sugars from sweet ripe juicy fruits, fruit juice, honey and white sugar.

Have you experienced the effects of the removal of polyunsaturated fats on your ability to effectively and efficiently metabolise sugar?

See more here

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

Skeletal muscle lipid peroxidation and insulin resistance in humans.

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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.

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

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

High levels of lipid peroxidation in semen of diabetic patients

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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.

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

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

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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

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

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

Increased lipid peroxidation in type 2 poorly controlled diabetic patients.

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

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

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


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