Sugar Helps Medicine Go Down

Suga Talking about the effects of High Fat/High Carb meals (HFHC) on metabolic function, without considering the type of fat and type of carbohydrate involved, is as meaningful as talking about the color of cheese on Mars…it’s a reddish brown by the way.

There’s no such thing as a perfectly controlled scientific experiment, but examining diet without distinguishing between the saturated and unsaturated fats – looking at what happens when they’re ingested alone or with different amounts of glucose, fructose or sucrose – is likely to produce misleading and potentially invalid conclusions.

Regular intake of starch or glucose in combination with highly unsaturated fats can be a recipe for disaster. In fact, when it comes to the creation of inflammatory and stressful biological conditions, few things are as effective as the polyunsaturated fats.

“A majority of the studies on linoleic acid and its derivatives show a direct/indirect link with inflammation and metabolic diseases.”

“Adults with a diet rich in omega-6 polyunsaturated fatty acids (PUFAs) display increased stress reactivity…a maternal diet rich in omega-6 PUFAs during gestation and lactation produce changes in sociability consistent with those observed in ASD [autism].”

“Compounds…derived from linoleic acid, may affect adrenal steroid production in humans and mediate some of the deleterious effects of obesity and oxidative stress…”

“…a moderately high fat diet of coconut oil, either in the presence or absence of fructose, does not induce significant diabetic symptoms (elevated fasting blood glucose and glucose intolerance) while isocaloric diets with soybean oil (either with or without fructose) do.”

Consuming ‘too much’ starch or pure glucose can be problematic in its own right. The more rapid conversion of starch into glucose in the blood, can powerfully stimulate insulin, disposing of any excess sugar by turning it into fat.

“Glucose ingestion…in healthy human subjects resulted in… profound acute pro-inflammatory changes…”

“Animals fed a low-fat, high-sucrose…diet were actually leaner than animals fed a high-complex-carbohydrate diet.”

Eating starch increases glycogen stores in the liver, but often less effectively than sucrose or fructose. The potential surge in insulin from the consumption of pure glucose can be followed by a fall in blood sugar levels, causing cortisol to increase.

“…small amounts of fructose can markedly reduce hyperglycemia during…glucose infusion by increasing NHGU [net hepatic glucose uptake] even when insulin secretion is compromised.”

The catabolic effects of hypoglycemia and high cortisol can impact upon metabolic conditions in a variety of different ways, interfering with thyroid function, promoting serotonin and increased endotoxin release, driving numerous inflammatory factors.

“Chronic excessive glucocorticoid exposure results in whole-body insulin resistance and the development of abdominal adiposity in humans.”

“…mechanisms of posthypoglycemic insulin resistance induced by lipolysis include increase in endogenous glucose production, suppression of peripheral utilization and oxidation of glucose, and increase lipid oxidation…”

“…following regular exercise and CR [caloric restriction] there are GC[glucocorticoid]-induced mechanisms that promote adipose tissue mass gain and impaired metabolic control in healthy organisms…”

When a low thyroid person with slow digestion consumes under cooked starch, it can more easily become food for bacteria, irritating the intestines and encouraging higher levels of endotoxin to pass into the liver, and through to the main system, spreading inflammation.

A high fat meal in general can promote endotoxin, but starch or glucose combined with the polyunsaturated fats (PUFA) has been shown to escalate the severity of inflammatory reactions and promote the conditions of stress.

“Feeding an EFAD [essential fatty acid-deficient] diet reduces baseline inflammation and inflammatory response to endotoxin long before the development of EFAD, and added AA + DHA modifies this response…In response to lipopolysaccharide [endotoxin], the levels of tumor necrosis factor and interleukin-6 were significantly lower with HCO [coconut oil], reflecting reduced inflammation.”

The breakdown products of PUFAs interfere with blood sugar regulation in a variety of ways. They reduce the ability of the cell to properly use glucose. They cause an increase in cortisol secretion. They promote serotonin and estrogen, and they’re responsible for rising levels of toxic free radicals, cytokines, prostaglandins and other pro-inflammatory things.

“Increased levels of fatty acid metabolites may be involved in the increased glucocorticoid production observed in obese humans.”

“…results provide evidence that LA [linoleic acid]…can trigger activation…and expression of inflammatory mediators…highly expressed during the pathology of atherosclerosis…as well as participating in inflammatory processes…”

“Linoleic acid is a direct precursor of the bioactive oxidized linoleic acid metabolites. It is also a precursor of arachidonic acid, which produces pro-inflammatory eicosanoids and endocannabinoids.”

PUFA damages thyroid function and digestion, increasing the likelihood that starch will impact upon proper blood sugar regulation, and worsening bacterial endotoxin issues.

“Several fatty acids had potent T4 to T3 [active thyroid hormone] conversion-inhibiting activity…Significant inhibition was evident with…arachidonic acid and linolenic acid…Saturated fatty acids, such as palmitic, stearic…acids, had little or no…inhibiting activity.”

This metabolic dysfunction can result in a vicious circle of stress and inflammation, which continues to be fueled by the release of polyunsaturated fats stored in tissue, for a long time, even in the absence of it being consumed.

“…results indicate that the accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress…”

PUFA disturbs many cellular functions but it directly interferes with metabolic energy production, gradually damaging the oxidizing ability of the cell. Sugar does not have this effect.

“…results indicate that…PUFA-rich soybean oil is more obesogenic and diabetogenic than coconut oil which consists of primarily saturated fat. They also show that fructose is less obesogenic than soybean oil and reveal a striking fatty liver morphology induced by soybean oil…”

“…we find that neutrophil-derived leukotrienes [PUFA breakdown product] aid the colonization of distant tissues by selectively expanding the sub-pool of cancer cells that retain high tumorigenic potential…”

“…corn oil rapidly activates NF-κB in Kupffer cells via oxidant-dependent mechanisms. This triggers production of low levels of TNFα which is mitogenic in liver and promotes growth of hepatocytes”

Sugar can be very therapeutic. Fructose stimulates metabolic performance, acting in ways similar to active thyroid hormone (T3), helping to protect against the inflammatory effects of the starches and the polyunsaturated fats.

“Subjects in the 3 groups ingested a 300-kcal drink of 75 g glucose…orange juice…or water along with a 900-kcal HFHC meal (egg-muffin and sausage-muffin sandwiches and 2 hash-brown potatoes that contained 81 g carbohydrates, 51 g fat, and 32 g protein)”

By increasing metabolism, fructose enables the cell to burn more glucose, increasing the amount of starch which can be safely consumed and protecting from some of its potentially blood sugar disregulating effects.

The saturated fats are also known to be able to protect against stress and inflammation.

“we found that a variety of saturated fatty acids significantly suppressed an increase in ACTH release induced by CRH stimulation…In contrast…unsaturated fatty acids, oleate, linolate and arachidonate effectively enhanced ACTH release”

Ongoing exposure to stress – often resulting in hypoglycemia, high cortisol and increased free fatty acids – is a common cause of metabolic energy system suppression and the inflammatory conditions which have been shown to lead to obesity.

“Greater numbers of prior day stressors were also associated with lower fat oxidation as well as higher insulin production. People with lower fat oxidation are more likely to gain weight by storing fat than those with higher fat oxidation, and thus their risk for obesity is increased. Higher levels of insulin are lipogenic, further enhancing fat storage.”

Fructose and sucrose effectively promote glycogen storage, protecting against stress, inflammation and excessive endotoxin release.

“…drinks with added fructose or galactose…were twice as effective as…glucose in restoring liver glycogen…”

“…the intake of orange juice was able to neutralize the oxidative and inflammatory stress caused by the HFHC meal and the associated increases in…endotoxin concentrations…”

It is the ongoing stresses which combine to have a major impact upon metabolism. Rather than demonizing nutritious foods, lumping together things that differ greatly, it can help to explore how the composition of fats and sugars (as well as protein and other nutrients) can relate to biological stress reduction or promotion.

A chronically low supply of sugar can mean that cortisol stays high and there is continuous exposure to polyunsaturated free fatty acids. This can create a situation where an inflammatory stress state is ongoing with an inability to revert back to proper metabolic function.

“Glucocorticoids…are critical in the regulation of energy homeostasis, and liberate energy substrates for mitochondrial oxidation during stress by enhancing muscle protein breakdown, adipose tissue lipolysis, hepatic gluconeogenesis, and reducing glucose utilization, all of which elevate circulating glucose concentrations.”

Greater consumption of sugar can help switch off the stress response, prevent fatty acid exposure and directly provide the requirements for mitochondrial energy production.

“…carbohydrate restriction may be the predominant factor responsible for the decreases in resting metabolic rate observed with the hypocaloric diets…sucrose replacement increase the resting metabolic rate by 200 to 250 kilocalories per day…sufficient to accelerate the loss of body fat by nearly 1kg per month.”

Sugar and thyroid help divert away from the inflammation and stress promoting substances, including serotonin, estrogen, and histamine.

“Caloric intake in the form of orange juice or fructose does not induce either oxidative or inflammatory stress…”

An improved glycogen supply lowers cortisol, and protects against the inflammatory by-products of the excessive breakdown of muscle tissue, which often results from stress and PUFA exposure.

It is potentially very misleading to refer to the inflammatory effects of high sugar or fatty foods. The real issues are metabolic suppression, blood sugar disregulation, inflammation and stress. Some kinds of ‘sugar’ and ‘fat’ are better than other kinds at causing or encouraging these things. Some kinds are better at protecting against and reversing them.

Scientific experiments often fall short of providing useful information capable of improving clarity of understanding. Instead they can end up adding to the confusion.

“…there may be food products that may be noninflammatory and protective against the proinflammatory effects of other foods. These observations are relevant to the role of postprandial inflammation in the pathogenesis of atherosclerosis, cardiovascular disease, and insulin resistance.”

When the intention is to discover the truth or reinforce awareness, there are many ways to approach an experiment which can be enlightening.

Comparing a group being fed a high sucrose or fructose/saturated fat meal with a second group being fed a PUFA/starch meal is one possible way. There are lots of good ways to tweak studies in order to find out more.

“…the intake of orange juice in combination with an HFHC meal prevents…the inflammatory response…”

The fact that orange juice can have an anti-inflammatory effect when consumed with very inflammatory foods is important to know. Knowing what is making the foods inflammatory in the first place is equally, if not more important.

If the study results were to show that a saturated fat, high sucrose meal is protective in its own right, surely that would make the potential conclusions more meaningful and useful.

“…dietary MCFAs/MCTs [coconut oil] suppress fat deposition through enhanced thermogenesis and fat oxidation in animal and human subjects…several reports suggest that MCFAs/MCTs offer the therapeutic advantage of preserving insulin sensitivity in animal models and patients with type 2 diabetes.”

“If a massive amount of glucose is consumed in the brain during stress, therefore, it is possible that feeding a high-sucrose diet contributes to counteracting stress.”

“…we observed a 21 percent reduction in resting metabolic rate after institution of a hypocaloric carbohydrate-free…diet…almost entirely reversed by isocaloric substitution of sucrose.”

Unfortunately, many studies are less than optimally designed and performed.

Often powerful agendas are at play. It may not be acceptable to suggest that white sugar, fructose, or the saturated fats can provide protection against the inflammatory disease promoting things.

Perhaps nobody wants to admit that it’s ok to have dessert before dinner, or for that matter, instead of dinner.

Replacing high PUFA oils like soy, safflower, sunflower, canola, corn as well as fish oils, with coconut oil, butter, ghee and other highly saturated fats, is a good starting point. A diet with enough protein from milk, cheese and gelatin and plenty of sugar from sweet fruits, fruit juice and white sugar can help improve metabolic function and protect against stress and inflammation.

This is not a question of belief or non-belief. Experimentation and experience matter most. Find out for yourself.

See More Here

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

Orange juice or fructose intake does not induce oxidative and inflammatory response.

Glucose ingestion induces an increase in intranuclear nuclear factor kappaB, a fall in cellular inhibitor kappaB, and an increase in tumor necrosis factor alpha messenger RNA by mononuclear cells in healthy human subjects.

Potential role of endotoxin as a proinflammatory mediator of atherosclerosis.

Short term essential fatty acid deficiency in rats. Influence of dietary carbohydrates.

Mechanisms of Glucocorticoid-Induced Insulin Resistance

12/15-Lipoxygenase Inhibition Reverses Cognitive Impairment, Brain Amyloidosis, and Tau Pathology by Stimulating Autophagy in Aged Triple Transgenic Mice.

TLR4 links innate immunity and fatty acid-induced insulin resistance.

Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets.

A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation.

The health implications of changing linoleic acid intakes.

Inhibition of nuclear T3 binding by fatty acids.

Resistance of essential fatty acid-deficient rats to endotoxic shock.

Structural and functional rejuvenation of the aged brain by an approved anti-asthmatic drug

Polyunsaturated fatty acids influence neonatal monocyte survival.

Arachidonic acid as a possible modulator of estrogen, progestin, androgen, and glucocorticoid receptors in the central and peripheral tissues.

Isoprostanes, Novel Eicosanoids That Produce Nociception and Sensitize Rat Sensory Neurons

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Lipid peroxidation products are elevated in fish oil diets even in the presence of added antioxidants.

Human Monocytes Engage an Alternative Inflammasome Pathway

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

Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and A/J mice.

Fructose and galactose enhance postexercise human liver glycogen synthesis.

Saturated fatty acids suppress adrenocorticotropic hormone (ACTH) release from rat anterior pituitary cells in vitro.

Neuroendocrine perturbations as a cause of insulin resistance.

Glucocorticoid antagonism limits adiposity rebound and glucose intolerance in young male rats following the cessation of daily exercise and caloric restriction

Epoxy-keto derivative of linoleic acid stimulates aldosterone secretion.

Essential fatty acid-deficient diet modifies PAF levels in stomach and duodenum of endotoxin-treated rats.

Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB.

Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver

Linoleic acid induces proinflammatory events in vascular endothelial cells via activation of PI3K/Akt and ERK1/2 signaling.

Effects of a high-sucrose diet on body weight, plasma triglycerides, and stress tolerance.

Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

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

Increase in intranuclear nuclear factor κB and decrease in inhibitor κB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect

Linoleic acid: between doubts and certainties.

Maternal diet rich in omega-6 polyunsaturated fatty acids during gestation and lactation produces autistic-like sociability deficits in adult offspring.

Evidence for an inhibitor of extrathyroidal conversion of thyroxine to 3,5,3′-triiodothyronine in sera of patients with nonthyroidal illnesses.

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Daily Stressors, Past Depression, and Metabolic Responses to High-Fat Meals: A Novel Path to Obesity

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects.

Pregnenolone protects mouse hippocampal (HT-22) cells against glutamate and amyloid beta protein toxicity.

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

11β-HSD1 reduces metabolic efficacy and adiponectin synthesis in hypertrophic adipocytes.

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog.

Marital Discord, Past Depression, and Metabolic Responses to High-Fat Meals: Interpersonal Pathways to Obesity

Neutrophils support lung colonization of metastasis-initiating breast cancer cells

Inhibition of chymase activity by phosphoglycerides.

Effect of long-chain fatty acids on the binding of thyroxine and triiodothyronine to human thyroxine-binding globulin.

Selective Inhibitors of 11β-Hydroxysteroid Dehydrogenase Type 1 for Patients With Metabolic Syndrome

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

High rates of exogenous carbohydrate oxidation from a mixture of glucose and fructose ingested during prolonged cycling exercise.

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

Low Calorie Dieting Increases Cortisol

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

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

Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis.



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