Do You Really Know It’s True?

Do you really know that it’s true that sugar – even when consumed in quantities well beyond ‘daily requirements’ – is bad for you? Before you say ‘yes’, or even after you say ‘yes’, let’s just run through it a bit because I think it’s important.

What is it you have experienced in order to come to this conclusion, or is it just that it’s been said to you so many times, in so many ways, by so many people that now you just believe it and accept it as a given. That would be understandable, although not necessarily completely reliable.

For starters, what do you mean when you say the word ‘sugar’? Are you referring to the sugar found in fruit – commonly known as fructose (or sucrose) – or are you thinking about some form of starch (or plain glucose)? Or do you have all the different kinds of sugars grouped together in your mind as one thing.

Just that little piece of information alone, can make a big difference to what you perceive is happening (when you consume a food with ‘sugar’ in it) and help you begin to untangle some of the confusion.

Very often, when people talk about the potentially negative effects of ‘sugar’ in relation to blood sugar issues (and hormonal/biochemical responses), they are actually referring to the effects of foods made mostly from starch, a carbohydrate which when consumed quickly breaks down into glucose.

“Fructose and sucrose solutions enhanced energy intake but did not increase body weight…Intake of fructose or sucrose solution did not impair insulin-stimulated glucose uptake or signaling…”

Glucose, when consumed in isolation (from starch rather than sucrose, which is glucose and fructose combined), can quickly raise blood sugar and be far more insulinogenic (promoting insulin secretion) than cane or fruit sugar (sucrose and fructose) or higher fructose sugars (honey, HFCS etc), potentially exacerbating existing blood sugar issues, promoting the release of inflammatory substances.

“Low-dose fructose improves the glycemic response to an oral glucose load in adults with type 2 diabetes…”

“Single catalytic 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 roughly threefold increase in glycogen synthesis under euglycemic hyperinsulinemic conditions in people without diabetes.”

On top of this, starch from grains, beans, legumes, certain fruits and under cooked vegetables can feed bacterial overgrowth issues. Increasing bacterial toxins combined with some chemicals found in these foods can interfere with digestion and can create sensitivities to other foods which might otherwise be easily assimilated.

“…anti-nutritional and toxic factors…are shown to be widely present in leguminous foods which are important constituents of the diet of a large section of the world’s population…”

Rising levels of bacterial endotoxin combined with a high dietary fat intake can promote many of the issues which are often attributed to sugar consumption.

“…we found that metabolic concentrations of plasma LPS [endotoxin] are a sufficient molecular mechanism for triggering the high-fat diet–induced metabolic diseases obesity/diabetes.”

Often when people say they’ve noticed the negative effects of sugar in their diet (or the positive effects of removing sugar from their diet) – when looked at more closely – it turns out that the foods they are referring to don’t actually have much in the way of actual white sugar or sucrose in them.

Sometimes they’re high in starch and other times these foods don’t have much starch or much of any form of sugar in them at all. But they’re almost always filled with a variety of harmful and toxic anti-metabolic ingredients, in particular the polyunsaturated fats.

Polyunsaturated fatty acids (PUFA) have been shown time and time again, to be responsible for directly interfering with the ability of cells to properly metabolise sugar, thereby promoting issues incorrectly blamed on fruit sugar, including chronic hyperglycemia and insulin resistance.

“…free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation.”

“Linoleic acid also dose-dependently reduced mitochondrial membrane potential…reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function…chronic exposure to linoleic acid-induced β-cell dysfunction…”

Although it might appear to the naked eye as though these issues are ‘obviously’ the result of excessive consumption of sugar, when examined properly it can become apparent that this is far from the truth.

When dietary sugars are removed from the scenario, stress hormones such as adrenalin and cortisol rise and polyunsaturated fats begin to be released out of storage into the blood, interfering with cellular function.

“…chronic periods of stress can be detrimental to health by increasing inflammation and promoting the progression of diseases including cancer.”

There will continue to be a supply of sugar into the bloodstream, but now it will be at the expense of valuable muscle and other tissue and the combination of the above conditions can gradually lead to worsening symptoms of blood sugar disregulation, eventually becoming diabetes and other stress related illnesses.

When fat (in particular polyunsaturated fat) is combined with starch or glucose, the cells ability to use the available blood sugar is impaired, promoting hyperglycemia and insulin resistance as well as chronically high levels of disease promoting stress substances.

“These results suggest that a high-fat diet accelerated aging…by increasing liver mRNA level for Hsd11b1, increasing insulin secretion, and promoting lipid accumulation in the liver.”

“…the intake of orange juice in combination with an HFHC [high fat high carb] meal prevents an increase in ROS generation and the inflammatory response…in contrast to the increase in both of these indexes after the HFHC meal with glucose or water.”

Rapid increases in blood sugar caused by the consumption of excessive amounts of pure starch or glucose stimulates insulin release and can potentially promote fat synthesis more easily than white sugar. Even this is most likely dependent upon the existence of other metabolic issues.

“The capacity for glycogen storage…is larger than generally believed, and…Fat synthesis from CHO [carbohydrate] will not exceed fat oxidation after one high-carbohydrate meal, even if it is uncommonly large…These findings challenge the common perception that conversion of CHO to fat is an important pathway for the retention of dietary energy and for the accumulation of body fat.”

“The fat supplement…did not alter 24-h energy expenditure…and failed to promote the use of fat as a metabolic fuel…The overall energy balance was closely correlated with the fat balance…but not with the carbohydrate balance…These data indicate that substantial imbalances between intake and oxidation are much more likely for fat than for carbohydrate.”

Although the combination of fat and sugar of any kind can potentially lead to weight gain and some other issues, it is the polyunsaturated fats (particularly when consumed with starch) that are the most likely promoters of obesity and other related forms of metabolic dysfunction.

“LA [linoleic acid] induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.”

Polyunsaturated fatty acids can promote increased circulation of the stress substances – including cortisol, serotonin, estrogen and nitric oxide – and powerfully suppress thyroid energy system metabolism. The resultant rise in stress is a major factor in the development of blood sugar dysregulation and fat deposition and sugar is possibly the most powerful anti-stress substance available.

“PUFA may modulate the steroid hormone message, so that the high C20:4 [arachidonic acid] concentration…may help amplify the estrogen signal and inhibit the progesterone signal.”

“Results presented here are among the first evidence that consumption of beverages sweetened with sugar, but not the artificial sweetener aspartame, inhibits stress-induced cortisol secretion in humans…”

In order to unravel faulty thinking about ‘sugar’ and discover what is at the root of all kinds of health issues, one thing that needs to happen first is for there to be an honest look at the actual ingredients in foods being consumed.

It’s important not to blindly label things ‘high sugar foods’, particularly when they are filled with metabolism interfering fats and starches and poisonous chemicals, often not containing much in the way of actual white sugar or sucrose at all.

When metabolic issues have become chronic – perhaps due to excessive exposure to polyunsaturated fats and other toxic things – it can be easy to falsely assume that sugar is causing your issues.

“A total of 27 patients with a history of hypothyroidism demonstrated a positive result to the breath test (27 of 50, 54%), compared with two in the control group (two of 40, 5%)…Abdominal discomfort, flatulence, and bloating were significantly more prevalent in the bacterial overgrowth positive group.”

You can continue to react badly to many foods that are potentially highly therapeutic, long after you have stopped contact with what was originally responsible for the damage.

“…intake of HF [high fat] diets and chronic exposure to low levels of EDCs [endocrine-disrupting chemicals] found in foods and drinking water can lead to adverse effects on human health beyond a single generation.”

Blood sugar dysregulation, digestive distress and liver damage – all of which are known to be caused by polyunsaturated fats and chronic increases in stress substances – can take time to be reversed causing all sorts of ongoing problems including difficulties with lactose and fructose and negative reactions to sugar in general.

“Fifty two strains of…bacteria isolated from the upper gut of patients with small intestinal bacterial overgrowth were screened…Culture supernatant and deoxycholate, both alone and combined, significantly reduced lactase, sucrase, and maltase activity.”

“…lactase activity…increased by consumption of various carbohydrates, including sucrose, fructose, galactose and glycerol…the glucose diet caused a slight increase in lactase activity…”

Improving metabolic issues takes time and lots of trial and error and this process is only made more difficult and confusing when symptoms are being blamed on ingredients that weren’t the cause of the issues, were combined with many highly problematic and harmful things and in some cases were not actually even there in the first place.

Some do well with starches in their diet but this is more likely to be true when metabolism and digestion is functioning in closer to optimal fashion. Potatoes are a highly nutritious starch for those who can handle them well.

If you don’t remove polyunsaturated fats from your diet (and eventually from storage in tissue) and if you continue to lump every carbohydrate together, it’s possible to have problems no matter what you try to do, as you go on talking about fat and sugar as if all types are exactly alike.

On top of all this, sugar restriction itself can lead to high cortisol and rising levels of stress substances which can, for periods of time improve certain symptoms, sometimes even making a person feel quite euphoric. In many cases it can be hard to distinguish between what is helping long term health and what is actually causing harm.

“…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.”

Understanding different ways of measuring energy system function, like for instance the use of pulse and temperature tracking, can be very helpful in these circumstances.

Until one has spent quite some time experimenting with avoiding toxic anti-metabolic substances in order to heal the liver and digestion – gradually increasing the consumption of simple sugars as the body starts to be able to better handle them – it can be difficult to understand how much difference this can make to metabolism and how many symptoms can improve or be completely resolved.

Many people today are not really open to talking about the importance of simple sugar for metabolic health and it’s not surprising. The scare tactics and fear mongering campaigns have been relentless.

“when sucrose was substituted, resting metabolic rate rose toward baseline values even though total caloric intake was unchanged and weight loss continued. The sucrose-induced rise in resting metabolic rate was accompanied by a rise in serum triiodothyronine values, but not plasma insulin or norepinephrine concentrations.”

Unfortunately belief systems today are supported by ‘science’ which very regularly fails to distinguish between (or even understand) the biological significance of the different carbohydrates and many other nutrients, almost always disregarding the damaging impact of the polyunsaturated fats whilst somehow miraculously placing the blame upon evil white sugar and a few other popular villains.

It is becoming more and more unlikely that the majority will partake in the self-experimentation necessary to be able to experience the metabolic improvements and health benefits which can be achieved with the addition of simple sugars from milk, sweet fruit, fruit juice, honey and white sugar.

The environment is becoming increasingly stressful, dogmatic and full of confusion and misinformation and this is especially true in relation to conversations about what ‘sugar’ actually is and how much might truly be required to achieve closer to optimum metabolism.

See more here

Long-term exposure of INS-1 rat insulinoma cells to linoleic acid and glucose in vitro affects cell viability and function through mitochondrial-mediated pathways.

Free fatty acids and insulin resistance.

Free fatty acids-the link between obesity and insulin resistance.

Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate meal in man.

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse.

Does high polyunsaturated free fatty acid level at the feto-maternal interface alter steroid hormone message during pregnancy?

Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose.

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

Effects of an enteric anaerobic bacterial culture supernatant and deoxycholate on intestinal calcium absorption and disaccharidase activity.

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

Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis.

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

Carbohydrate metabolism and de novo lipogenesis in human obesity.

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

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

Free Fatty Acids Block Glucose-Induced β-Cell Proliferation in Mice by Inducing Cell Cycle Inhibitors p16 and p18

Antinutritional properties of plant lectins.

Failure of dietary fat intake to promote fat oxidation: a factor favoring the development of obesity.

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body

High-fat or ethinyl-oestradiol intake during pregnancy increases mammary cancer risk in several generations of offspring

Dietary carbohydrates enhance lactase/phlorizin hydrolase gene expression at a transcription level in rat jejunum.

Increase in Adipose Tissue Linoleic Acid of US Adults in the Last Half Century

Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes.

Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination

Association between hypothyroidism and small intestinal bacterial overgrowth.

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

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

Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse.

Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis

Low calorie dieting increases cortisol.

The effect of feeding different sugar-sweetened beverages to growing female Sprague-Dawley rats on bone mass and strength.

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

Anti-nutritional and toxic factors in food legumes: a review.

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.

Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism

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

Sugars and Health Controversies: What Does the Science Say?

Metabolic Endotoxemia Initiates Obesity and Insulin Resistance

Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial.

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

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

Dietary fats and cancer.

Resting Metabolic Rate and Respiratory Quotient in Human Longevity



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