Sugar Helps Medicine Go Down
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.
“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.”
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.
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.
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.
“…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 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.
“…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.
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…”
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.
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.
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 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.”
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.
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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.