Sugar Helps Medicine Go Down
Talking about the effects of a High Fat/High Carb meal (HFHC) on metabolic function, without considering the type of fat and type of carbohydrate involved, is about as meaningful as talking about the color of cheese on Mars…it’s a reddish brown by the way.
Even though there’s probably no such thing as a perfectly controlled scientific experiment, examining the impact of diet upon metabolic health, 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.
In fact, regular intake of starch or glucose in combination with the highly unsaturated fats can be a recipe for disaster, and lots of evidence suggests that when it comes to the creation of inflammatory and stressful disease promoting biological conditions, few things are as effective as the polyunsaturated fats (PUFAs).
“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].”
“…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.”
“Dietary LC n-3 PUFA are highly vulnerable to oxidation…4-Hydroxy-2-hexenal (4-HHE) and 4-hydroxy-2-nonenal (4-HNE) are major end-products derived from n-3 and n-6 PUFA peroxidation…high-fat diets containing realistically oxidized n-3 PUFA induced the highest amounts of 4-HHE and inflammatory markers in plasma.”
Consuming ‘too much’ easily digestible starch or pure glucose, can be stressful and inflammatory in its own right. Although the response to starch depends to some degree upon individual digestive and metabolic function (and upon the source of starch), the more rapid conversion of some starches into glucose in the blood, can powerfully stimulate insulin, and increase fat storage. Indigestible starches can be problematic for other reasons which I’ll discuss a little, further on.
“Glycaemia was significantly lower after the meal containing the highest amount of sugar…compared with the non-sweetened cereal…There was a significant inverse correlation between the amount of sucrose incorporated and the degree of glycaemia…plasma insulin response was significantly lower after the highest sugar meal…compared with the meal without sugar…We found a significant reduction in glycaemic and insulin responses when sugar replaced the rapidly digested starch in a processed breakfast cereal, i.e. the opposite of what is commonly believed.”
“Glucose ingestion…in healthy human subjects resulted in…an immediate increase in intranuclear NF-kappaB binding…an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha…consistent with profound acute pro-inflammatory changes…”
Eating starch increases glycogen stores in the liver, but often less effectively than sucrose or fructose. The potential rapid rise in blood sugar and surge in insulin from the consumption of pure glucose or starch, can be followed by a fall in blood sugar levels, causing cortisol to increase. The addition of some fructose or sucrose can protect against metabolic stress.
“Single…doses of fructose infused have shown a ∼30% reduction in postprandial hepatic glucose output under hyperglycemic conditions in people with type 2 diabetes and a…threefold increase in glycogen synthesis under euglycemic hyperinsulinemic conditions in people without diabetes…fructose replacement of other carbohydrates resulted in clinically significant improvements in glycemic control…”
The stress inducing, catabolic effects of low blood sugar and high cortisol can impact upon metabolic conditions in a variety of different ways, interfering with thyroid function, promoting the harmful effects of the stress substances (like serotonin and endotoxin), driving numerous inflammatory factors.
These kinds of stressful, inflammatory conditions, interfere with the use of sugar for energy production and can promote the progression of illness, including obesity.
“…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…”
When a thyroid suppressed person with slow digestion, consumes under cooked or hard to digest starch, it can in many cases more easily become food for bacteria, irritating the intestines and encouraging higher levels of endotoxin and other inflammatory things to pass into the liver, and through to the main system, spreading inflammation.
A high fat meal in general can promote systemic endotoxin circulation, but starch or glucose combined with the polyunsaturated fats (PUFAs), has been shown to escalate the severity of inflammatory reactions and worsen the conditions of stress and metabolic interference in a variety of ways. Combining the starches with the highly saturated fats, appears to make them safer.
“Baseline endotoxin concentrations…increased significantly by approximately 50% after a high-fat meal or after a high-fat meal with cigarettes but not after no meal or cigarettes alone…a high-fat meal…also significantly reduced plasma endotoxin neutralization capacity, which is an indirect measure of endotoxin exposure…Low-grade endotoxemia may contribute to the postprandial inflammatory state…”
“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.”
“…we observed a statistically significant increase in plasma levels of LPS [endotoxin]…after the intake of the CHO-PUFA meal, whereas no postprandial changes were observed after the ingestion of the Med and SFA-rich meals.”
The PUFAs and their breakdown products are associated with blood sugar regulation issues. Evidence shows that they reduce the ability of cells to properly use glucose, and they also cause an increase in cortisol secretion. They promote the stress substances like serotonin and estrogen, and they’re responsible for rising levels of toxic free radicals, cytokines, prostaglandins and other pro-inflammatory things. They have been associated with the development and progression of many kinds of inflammatory diseases, including diabetes and cancer.
“Oxidized derivatives of linoleic acid have the potential to alter steroidogenesis…One such derivative…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.”
“…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…A majority of the studies on linoleic acid and its derivatives show a direct/indirect link with inflammation and metabolic diseases.”
“…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…sustained stimulation of cell proliferation is most likely a key step in the ultimate development of cancer in liver…”
PUFAs damage thyroid function and digestion, increasing the potentially harmful impact of starch (or sugar in general) upon metabolic function and proper blood sugar regulation, worsening the severity of bacterial endotoxin and other inflammation 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.”
“…the production of pro-inflammatory cytokines and chemokines, and the induction of oxidative reactions by activated leukocytes and epithelial cells represent the main event in the intestinal inflammation…Polyunsaturated fatty acids…are…principal targets of oxidative modifications. These lipids…readily undergo non-enzymatic oxidation to form chemically-reactive species that can induce a wide range of biological effects including inflammation…
“…diabetes associated with dyslipidemia, even in well-controlled patients, was associated with increased lipid peroxidation. Furthermore, dyslipidemia and increased lipid peroxidation were strongly correlated with higher levels of systemic inflammation.”
This metabolic dysfunction can result in a vicious circle of stress and inflammation, which can continue to be fueled by the release of PUFAs stored in tissue, for a reasonably long time, even in the absence of excessive fat consumption.
PUFAs disturb many cellular functions, but they have been shown to be able to directly interfere with metabolic energy production, damaging the oxidizing ability of the cell. Suppression of energy production, can then further increase oxidative stress. I’m unaware of evidence showing that sugar consumption itself is responsible for this kind of effect.
“…ratios of lactate dehydrogenase to citrate synthase and beta-hydroxyacyl coenzyme-A dehydrogenase to citrate synthase were increased, indicating myocardial reduction of tricarboxylic acid cycle…PUFAs increased oxidative stress in the heart by providing cardiac susceptibility to lipoperoxidation and shifting the metabolic pathway for energy production.”
“…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…”
“…oxidative stress produced…progressive ATP depletion…Besides demonstrating a close relationship between lipid peroxidation and haemolysis, these data…strongly indicate…a profound modification of erythrocyte energy metabolism during oxidative stress.”
Sugar can be very therapeutic. Both fructose and sucrose stimulate metabolic performance, and help to limit stress induced thyroid energy system suppression, which can protect against some of the inflammatory effects of 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)…the intake of glucose and a HFHC meal are profoundly and rapidly proinflammatory…at the cellular and molecular level…”
“Fructose virtually abolished the fasting induced…fall in glucose and insulin and rise in glucagon…fall in triiodothyronine…ketosis and acidosis…increased ammonia excretion…hyperuricemia (and hypouricosuria), and…fall in plasma alanine and rise in branched chain amino acids. Fructose also significantly reduced urinary sodium loss…fructose exerted a prominent protein-sparing action…low-dose fructose infusion essentially abolishes the entire hormone-substrate response to fasting, and spares body protein without raising insulin…”
By helping to stabilize blood sugar and improve overall metabolic function, fructose can enable the cell to burn glucose more effectively, possibly increasing the amount of starch which can be safely consumed, protecting from some of its potentially inflammatory, stress promoting, blood sugar dysregulating effects.
The saturated fats are also known to be able to protect against some of the damaging effects of the PUFAs, and reduce 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 – encouraging hypoglycemia and high cortisol – is a common cause of metabolic energy system suppression and the inflammatory blood sugar dysregulated conditions which have been shown to promote obesity and disease.
“…depression and stress elevate cortisol production…insulin secretion rises as cortisol increases…Persistent hypercortisolemia and higher insulin enhance visceral fat accumulation…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, and improved glycogen availability can help protect against stress and improve metabolism, reducing inflammation from free fatty acid release and excessive endotoxin exposure.
“…ingested in the form of glucose–fructose mixtures (or sucrose), not only is this ingestion rate more tolerable due to lower gut discomfort but total body glycogen status can also be enhanced over glucose…alone, due to greater liver glycogen repletion.”
Incessant exposure to a variety of stress promoting factors can combine to have a major impact upon metabolism. Rather than demonizing nutritious foods (lumping together many things that differ greatly in effect), it makes more sense, for starters, to explore some of the finer details regarding how the composition of fats and sugars can either promote, or help reduce biological stress.
I’m not saying don’t eat starch if you like to eat starch, nor am I saying you must eat lots of sugar and have no fat in your diet. In fact, I’m not saying what to do or what not to do at all. I’m not a doctor or a scientist, and I eat lots of potatoes. This is just ideas and information to consider, and there is plenty of information in the studies included. Do with it what you will.
The relationship between stress and sugar is well documented, as is the relationship between the PUFAs and inflammatory metabolic illness. A consistently low supply of sugar can often mean that cortisol stays high, and that there will be a greater level of exposure to polyunsaturated free fatty acids and other promoters of inflammation and metabolic suppression. This can create a situation where an inflammatory stress state becomes chronic, sometimes with a virtual 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…Chronic excessive glucocorticoid exposure results in whole-body insulin resistance and the development of abdominal adiposity in humans.”
Consumption of sugar can sometimes be enough to switch off the stress response, significantly limit fatty acid exposure, and create the conditions required for improved 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 improved thyroid performance) can help divert away from the inflammation and the stress promoting substances, including endotoxin, serotonin, estrogen, nitric oxide, lactate and histamine. Orange juice has many beneficial and protective ingredients, including sugar.
Improved glycogen storage and supply helps to lower cortisol, and protects against the inflammatory by-products of the excessive breakdown of muscle tissue, which often results from stress, low blood sugar and exposure to PUFAs.
It is potentially very misleading to refer to the inflammatory effects of high sugar or fatty foods, when the actual ingredients of these foods can vary so greatly. The real issues are metabolic suppression, blood sugar dysregulation, inflammation and stress. Some kinds of ‘sugar’ and ‘fat’ are better than other kinds at causing or encouraging these issues. 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, by grouping things inappropriately, and misrepresenting the significance of findings, they can end up adding to the confusion.
Foods listed as being high in saturated fats are very often made up of high levels of MUFAs and PUFAs, which are not accounted for when discussing outcomes. Extreme quantities of the different kinds of carbohydrates are sometimes used to cause unrealistically harmful results. High fat or carb, versus low fat or carb meal percentage differences are often insignificant. Other potentially metabolism interfering ingredients in meals being used for studies, are commonly ignored. Short term symptom reduction due to stress can be treated as though it is representative of long term beneficial effects, when the opposite can be true. The combined effects of inflammatory and protective foods, potentially draw attention away from the dangers of the problematic ingredients.
“…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 genuinely to discover the truth and promote awareness, there are many effective ways to approach an experiment, which can be enlightening, however, many studies appear as though they are working towards predetermined objectives.
Comparing a group being fed a high sucrose or fructose/saturated fat meal, with a second group being fed a high PUFA/starch meal, and other groups being fed fat free/sucrose or glucose meals is one possible way. There are many ways to tweak studies in order to get more informative and useful results.
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. It is interesting that this part of the story is often ignored.
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.”
Unfortunately, many studies are less than optimally designed, performed or interpreted. It’s possible that ulterior motives, agendas, or cognitive bias play a part. It is not popular to state that white sugar, fructose, or the saturated fats can provide protection against the inflammatory disease promoting things, even if results imply this to be the case.
Perhaps nobody wants to admit that it’s okay to have dessert before dinner, or for that matter, instead of dinner.
Replacing oils high in PUFAs, like soy, safflower, sunflower, canola, corn and fish oils, with coconut oil, butter, ghee and other highly saturated fats, can be 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 is one potential way to help improve metabolic function and protect against stress and inflammation.
This is not so much a question of belief or non-belief. Experimentation and experience matter most. It’s better to find out for yourself.
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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.