It’s Easy To Believe Sugar Is Unhealthy.

13335329_10153688502607336_1397235237_n It’s easy to believe sugar is unhealthy, especially when you are told that regular consumption does things within your system, like for example, helping to increase the production of cholesterol.

If you live in a world where ‘experts’ say that high cholesterol causes heart disease, and polyunsaturated fats (PUFAs) are a health food – in part because they can ‘lower’ cholesterol levels in the blood – then this idea starts to sound more legitimate.

When you add to that popular theories about PUFA being anti-inflammatory, and sugar causing ‘adrenal fatigue’ – or suggestions that ‘sugar cravings’ result from a so called ‘serotonin deficiency’ – you might even start to believe that consuming more PUFA and removing sugar from your diet is a good idea.

Unfortunately (or fortunately), a large amount of high quality experimental evidence exists which undermines the foundations underpinning these, and other related belief systems.

Many studies have shown the direct relationship between chronically high levels of cortisol and a significant number of degenerative diseases or inflammatory conditions.

“Cortisol is secreted by the adrenal cortex in response to stress…A number of studies have demonstrated that stress can disrupt neuroendocrine circadian rhythms in ways that favor tumor growth and metastasis.”

Cortisol and adrenalin tend to rise in response to stress – particularly under circumstances where there is insufficient availability of sugar – and experiments have shown that sugar (for eg. sucrose) can lower levels of cortisol and related stress substances.

Another experimentally demonstrated physiological principle relates to the way in which excessive stress – leading to rising cortisol and adrenalin – promotes an increase in the release of free fatty acids out of storage. PUFA breakdown products (in particular) powerfully promote stress.

“Oxidized derivatives of linoleic acid have the potential to alter steroidogenesis….One such derivative is…(EKODE)…EKODE stimulates corticosterone biosynthesis and amplifies the effect of ACTH…Increased levels of fatty acid metabolites may be involved in the increased glucocorticoid production observed in obese humans.”

Lots of scientific studies have shown that the release of fat into the blood stream, directly correlates with (or even causes) the onset of inflammatory states which can promote conditions – such as diabetes, cardiovascular disease and cancer – often blamed on too much consumption of sugar.

“…elevated plasma levels of FFAs are not only a major cause of insulin resistance in skeletal muscle and liver but may, in addition, play a role in the pathogenesis of coronary artery disease.”

It is more common today for free fatty acids to be highly polyunsaturated in composition, and exposure to PUFA is possibly the main cause of chronic systemic inflammation. PUFA is powerfully anti-thyroid, and a suppressed thyroid energy system is synonymous with stress, leading to the release of greater amounts of free fatty acids, promoting a potentially downward spiraling inflammatory vicious circle-like state.

“…polyunsaturated dietary lipids such as those in corn oil activate Kupffer cells. This triggers production of oxidants and activation of NF-κB leading to synthesis of mitogenic cytokines such as TNFα which increases cell proliferation in parenchymal cells, causing promotion of previously initiated cells leading to tumors.”

“Breakdown of EPA and other UFAs [unsaturated fatty acids] by COX leads to the production of prostaglandins with LOX breakdown leading to the production of leukotrienes, and breakdown by CYP450 producing epoxyeicosatrienoic acid…all of which have been associated with pathology in a range of diseases including AD [Alzheimer disease]…”

“…the anti-inflammatory effect of EFA [essential fatty acid] deficiency was more marked that that of dietary (n-3) fatty acid supplementation in acute inflammation.”

Sufficient availability of sugar is necessary to improve thyroid function and energy metabolism (and to inhibit the release of the PUFAs from storage), and this is one reason why it makes biological sense for sugar to be understood as an anti-inflammatory substance.

The suppression of thyroid metabolism causes an increase in the release of cortisol as well as other inflammatory stress substances like estrogen, serotonin and nitric oxide. Metabolic suppression also interferes with digestion in a number of ways, eventually promoting bacterial overgrowth and increased exposure to bacterial endotoxin.

Many studies have shown a relationship between increased circulation of endotoxin (LPS) and the release of other substances which promote inflammation, such as serotonin for instance. Around 95% of serotonin is produced in the intestines in response to bacterial toxins and other poisonous substances. Endotoxin in the blood has also been shown to have a direct inflammatory effect.

“…it is well known that humans are far more prone to disease pathology in the course of endotoxemia than mice…and we speculate that the functionality of an alternative inflammasome pathway in humans might in part be responsible for this phenomenon…”

“The observation of a direct effect of such highly substoichiometric amounts of LPS on both fibrinogen and coagulation can account for the role of very small numbers of dormant bacteria in disease progression in a great many inflammatory conditions…”

Endotoxin and serotonin promote estrogen production, and all three have a tendency to interfere with liver function (interfering with proper detoxification), furthering degeneration and inflammation, and encouraging the progression of many disease states including cancer.

Cholesterol is known to play an important role in protection from infection and poison, and assists with the safe removal of endotoxin. Increased cholesterol production has been demonstrated to promote longevity and protection from disease in elderly populations. Low cholesterol on the other hand, has proven to be connected to the worsening of many conditions including depression, heart failure and cancer.

“Hypocholesterolemia is an important observation following trauma…Cholesterol levels were also adversely affected by infection or organ system dysfunction…Because lipoproteins can bind and neutralize lipopolysaccharide, hypocholesterolemia can negatively impact outcome.”

“Subjects with low TC [total cholesterol] levels…are at higher risk of dying even when many related factors have been taken into account…physicians may want to regard very low levels of cholesterol as potential warning signs of occult disease or as signals of rapidly declining health.”

Although the polyunsaturated fats interfere directly with cholesterol production, sugar consumption helps to protect against the release of PUFA from storage into the blood. Sugar also helps to directly promote the production of cholesterol. By improving thyroid energy metabolism, the sufficient availability of sugar can directly and indirectly support the conversion of cholesterol into the highly protective anti-aging hormones, pregnenolone, progesterone, dhea and testosterone.

Increasing your intake of sugar (and lowering exposure to PUFA) reduces cortisol release and protects against the breakdown of muscle and other tissue, which takes place more during stress, as a means to providing the necessary supply of sugar for the body and brain. At the same time, sugar protects against the release of inflammatory amino acids (such as tryptophan) into the blood stream, which promote degeneration and aging. High stress and greater circulation of tryptophan can increase levels of serotonin in the brain, which contrary to popular opinion, is not a good thing.

“Unlike artificial sweeteners, sugar may provide the fuel needed to meet the energetic demands of stress, which may reduce the need for glucocorticoid-driven energy catabolism and mobilization of the body’s energy stores.”

There are some who are promoting the confusing and illogical idea that ‘sugar cravings’ are the result of a deficiency of serotonin, however from a physiological perspective, sufficient availability of sugar is likely to help lower serotonin production in the intestines as well as in the brain. Blood sugar dysregulation on the other hand, is likely to do the opposite. This makes more sense in the context of experimental science which demonstrates the relationship between increased serotonin, and the onset of many inflammatory conditions, including depression and anxiety.

“Serotonin…(5-HT)…has an essential role in the regulation of emotion….Here we show that 5-HT from the dorsal raphe nucleus (5-HTDRN) enhances fear and anxiety…”

“…serotonin is the first metabolite shown to be elevated in obesity that inhibits the activity of BAT [brown adipose tissue]…Thus, inhibiting Tph1[tryptophan hydroxylase 1]-derived serotonin may be effective in reversing obesity and related clinical disorders such as NAFLD and type 2 diabetes.”

There is no conclusive evidence showing that sugar (or even fructose) consumption is responsible for the increasing incidence of NAFLD (non alcoholic fatty liver disease) and related conditions, including obesity, diabetes, cancer or cardiovascular disease.

“…our preliminary systematic review and meta-analysis does not support a NAFLD-inducing effect of fructose in isocaloric exchange for other carbohydrates at levels of exposure that are well above that found in Western diets.”

“On the basis of the current study, it cannot be concluded that a high-carbohydrate diet or increased percentage of total energy intake in the form of carbohydrates increases the odds of obesity. “

Numerous high quality studies however, explain the physiological mechanisms which connect high cortisol and excessive exposure to the polyunsaturated fats (amongst other things), to the onset of these disease states. From a biological perspective, sugar is far more likely to be protective.

Sugar dysregulation seems to be commonly misunderstood to be the result of the consumption of too much sugar but this is not accurate. There is plenty of good science explaining how the metabolic effects of ongoing stress – thyroid dysfunction, high cortisol, increased exposure to endotoxin, serotonin, estrogen, and the polyunsaturated free fatty acids – powerfully promote chronic hyperglycemia and other symptoms of diabetes.

“…interrelationships between adipose tissue, inflammation, and insulin resistance appear key to understanding type 2 diabetes risk…low-grade chronic systemic inflammation contributes to this risk…endotoxin may act as a mediator of inflammation…”

“Impaired glucose tolerance and type 2 diabetes affect ∼40% of all Americans over the age of 65, yet the pathogenesis of this age-associated deterioration in glucose metabolism is poorly understood…aging is also associated with a marked inability of mitochondria to switch from lipid to glucose oxidation on insulin stimulation, which may further contribute to dysregulated glucose and lipid metabolism…”

“…free fatty acids (FFA) are one important link between obesity, insulin resistance, and type 2 diabetes. Plasma FFA levels are elevated in most obese subjects, and physiological elevations of plasma FFA inhibit insulin-stimulated glucose uptake…which…will result in hyperglycemia and eventually in type 2 diabetes.”

Insufficient availability of sugar promotes greater exposure to PUFA, and taken together this is a powerful driver of hypothyroidism, bacterial endotoxin circulation and exposure, as well as rising levels of the other substances of stress. Real science examining the biochemical changes that occur during the progression of NAFLD show these things to be central factors.

“Oxidative stress plays an important role in the pathogenesis of chronic liver diseases. The plasma level of 8-isoprostane, a product of lipid peroxidation…8-Isoprostane values are elevated in patients with NAFLD…increased lipid peroxidation is involved in the pathogenesis of NAFLD…”

“Thyroid hormones are crucial for hepatic lipid and glucose metabolism. Nonalcoholic fatty liver disease (NAFLD), a very common and potentially serious disease of modern society, shares common clinical features with hypothyroidism, such as obesity, insulin resistance and dyslipidemia.”

“Endotoxin levels were considerably increased in NAFLD patients, with marked increases noted in early stage fibrosis compared with controls…As endotoxin may promote insulin resistance and inflammation, interventions aimed at reducing endotoxin levels in NAFLD patients may prove beneficial in reducing inflammatory burden.”

It has become popular to claim that sugar is to blame, because blood sugar dysregulation often goes hand in hand with the stress state. This of course, is not accurate, and the fact that sugar is not being used effectively is not the fault of sugar. In fact, limiting sugar consumption exacerbates all of this.

There is some evidence which suggests that excessive intake of starch (or pure glucose) as well as the consumption of a variety of difficult to digest fibers can promote bacterial issues, inflammation and thyroid dysfunction, although this is far more likely in combination with PUFA. If anything the combination of PUFA and starchy carbs is probably responsible for many of the problems which are mistakenly blamed on sucrose or fructose.

“…current findings indicate that sugary foods contribute minimally to ‘food dependence’ and increased risk of weight gain.”

Of course, there are numerous ways to set up (or misinterpret) an experiment, in such a way as to suggest that sugar or fructose is the culprit for disease. Alternatively, it has become common to just ignore the studies that say otherwise, and continue to make these claims. Unfortunately, people listen and believe.

A diet avoiding PUFAs (as well as possibly limiting fat in general) and restricting intake of starches and fibers – particularly many kinds of under cooked vegetables, grains, beans and legumes – and providing sufficient protein from milk, cheese and gelatin, and plenty of sugar from sweet ripe juicy fruits, fruit juice, honey and white sugar, is a physiologically rational approach to improving the metabolic conditions which have been unfairly blamed on sugar.

See more here

Sucrose ingestion normalizes central expression of corticotropin-releasing-factor messenger ribonucleic acid and energy balance in adrenalectomized rats: a glucocorticoid-metabolic-brain axis?

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

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

Hypocholesterolemia in sepsis and critically ill or injured patients

The importance of the gastrointestinal tract in the control of bone mass accrual.

Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis

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Serotonin receptor type 3 antagonists improve obesity-associated fatty liver disease in mice.

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Fatty liver induced by free radicals and lipid peroxidation.

Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis

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High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects

Increased lipid peroxidation in patients with non-alcoholic fatty liver disease and chronic hepatitis C as measured by the plasma level of 8-isoprostane.

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Effect of aging on muscle mitochondrial substrate utilization in humans

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In situ detection of lipid peroxidation and oxidative DNA damage in non-alcoholic fatty liver diseases.

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

Prevention of dietary fat-fueled ketogenesis attenuates BRAF V600E tumor growth

Prevention of fat-induced insulin resistance by salicylate

Impact of stress on cancer metastasis

Serotonin Mediates Oxidative Stress and Mitochondrial Toxicity in a Murine Model of Nonalcoholic Steatohepatitis

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

Relationship between Hypothyroidism and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis

Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation.

Effect of canola oil consumption on memory, synapse and neuropathology in the triple transgenic mouse model of Alzheimer’s disease

Thyroid dysfunction and nonalcoholic fatty liver disease.

Associations of Omega-3 Fatty Acid Supplement Use With Cardiovascular Disease Risks

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Indigenous Bacteria from the Gut Microbiota Regulate Host Serotonin Biosynthesis

Human Monocytes Engage an Alternative Inflammasome Pathway

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

Pathogenesis of hypothyroidism-induced NAFLD is driven by intra- and extrahepatic mechanisms.

Gene pathways associated with mitochondrial function, oxidative stress and telomere length are differentially expressed in the liver of rats fed lifelong on virgin olive, sunflower or fish oils.

Glucose substitution prolongs maintenance of energy homeostasis and lifespan of telomere dysfunctional mice

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

Elevated endotoxin levels in non-alcoholic fatty liver disease.

Low carbohydrate diets may increase risk of neural tube defects

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Significant positive association of endotoxemia with histological severity in 237 patients with non-alcoholic fatty liver disease.

Adipose tissue ATGL modifies the cardiac lipidome in pressure-overload-induced left ventricular failure

Colonic Microbiota Encroachment Correlates With Dysglycemia in Humans

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

Brain metabolism is significantly impaired at blood glucose below 6 mM and brain glucose below 1 mM in patients with severe traumatic brain injury

Effects of free fatty acids (FFA) on glucose metabolism: significance for insulin resistance and type 2 diabetes.

Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model

Fast food, soft drink and candy intake is unrelated to body mass index for 95% of American adults

Vascular effects of a low-carbohydrate high-protein diet

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

Targeting metastasis-initiating cells through the fatty acid receptor CD36.

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

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

The lipolysis pathway sustains normal and transformed stem cells in adult Drosophila.

Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala

Low-Carbohydrate Diets and All-Cause Mortality: A Systematic Review and Meta-Analysis of Observational Studies

Sugar for the brain: the role of glucose in physiological and pathological brain function

Fasting as a metabolic stress paradigm selectively amplifies cortisol secretory burst mass and delays the time of maximal nyctohemeral cortisol concentrations in healthy men.

Maternal intake of high n-6 polyunsaturated fatty acid diet during pregnancy causes transgenerational increase in mammary cancer risk in mice

Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction

Polyunsaturated lipid diet lengthens torpor and reduces body temperature in a hibernator.

Energy metabolism in trauma and sepsis: the role of fat.

Eating dependence and weight gain; no human evidence for a ‘sugar-addiction’ model of overweight.

Corn oil rapidly activates nuclear factor-κB in hepatic Kupffer cells by oxidant-dependent mechanisms

Suppressed sympathetic outflow to skeletal muscle, muscle thermogenesis, and activity energy expenditure with calorie restriction

Inhibition of Fatty Acid Metabolism Reduces Human Myeloma Cells Proliferation

Ketone body utilization drives tumor growth and metastasis

A high-fat diet rich in corn oil reduces spontaneous locomotor activity and induces insulin resistance in mice.

Associations of egg and cholesterol intakes with carotid intima-media thickness and risk of incident coronary artery disease according to apolipoprotein E phenotype in men: the Kuopio Ischaemic Heart Disease Risk Factor Study

#sugarsaves
#thatpufafilm
#raypeat

Image: sweet666heart: “L and His Love For Sugar Cubes”

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