Do You Struggle to Lower Your Blood Sugar?

If you have diabetes or pre-diabetes, you have probably been told to vigilantly restrict your carbohydrate intake. And this may have worked, or it may not have. Often this strategy only helps to "manage" the condition without resolving it.

If carbohydrate restriction has not sufficiently lowered your blood sugar and reversed the insulin resistance of diabetes or prediabetes, it's not your fault because carbohydrate intake is not the whole story when it comes to blood sugar and insulin resistance.

In fact, there is so much more to the story it might just blow your mind.

Diabetes Dogma Debunked?

The current prevailing view of type 2 diabetes and pre-diabetes is based on the idea that it is caused by eating too much carbohydrate, which chronically raises blood sugar and thereby causes the insulin resistance inherent in diabetes and prediabetes. 

Although there is low-quality scientific evidence that high carbohydrate consumption promotes insulin resistance, there is no high-quality evidence that high carbohydrate consuption is actualy the cause of insulin resistance and diabetes. If the cause were simply excess carbohydrate consumption elevating blood sugar, then there would be plenty of studies showing that keeping blood sugar down would reverse type 2 diabetes. But there is no such study.

So something else is at play besides carbohydrate intake. In fact, there are cultures around the world that obtain 70-80% of their calories from carbohydrates without developing diabetes or heart disease. There is an Amazon tribe that gets 80% of calories from very well-cooked starches, and they has the lowest incidence of heart disease in the world.

Since diabetes is a major contributor to the development of heart disease, there is no way that this Amazon trible would have a very low incidence of heart disease if their predominantly carbohydrate diet were causing diabetes.

You could say that such cultures are genetically and metabolically adapted to live on such high-carb diets and that this example would not apply to people with different ancestry. And I would tend to agree that these cultures probably have adapted to that kind of diet. It certainly seems to be the case that many people, especially of European ancestry, do not seem to thrive on high-carb diets.

But the next example that decouples high-carb diets from diabetes involves people of European ancestry, living in the United States. Perhaps the strangest evidence of all that carbohydrates and sugar are not sufficient to cause diabetes involves a study conducted in the United States in the early 20th century. In this study, obese, diabetic subjects were restricted to a diet of only white rice, potatoes, and sugar. And their diabetes and obesity were reversed. It was hard as heck to keep them on the diet, and they were begging to eat something else, but yes, they reversed diabetes and obesity with a temporary diet of only sugar and starch!

How could that be possible? It has to do with whether free fatty acids are burned for energy in the mitochondria or are released from the body via sulfation or glucuronidation. More on that later in this post.

The bottom line is that carbohydrates alone are not sufficient to cause insulin resistance. Insulin resistance is actually caused by factors like the following:

• Genetic factors that promote hyperglycemia
• Polyunsaturated fatty acids (PUFAs) from seed oils in food and oxidation byproducts of PUFAs called aldehydes that damage membranes and mitochondrial function
• Environmental toxins that damage the ability of mitochondria to process glucose
• Environmental toxins that damage the function of cell membranes and insulin receptors
• "Lipolysis dominance" in which mitochondria preferentially metabolize fatty acids over glucose
• "Leaky" fat cells that dump free fatty acids into the bood stream
• Stress, and other factors that elevate cortisol and blood levels of glucose and free fatty acids
• Po-inflammatory endotoxin from "bad" bacteria in your gut
• Inflammatory cytokines like tumor necrosis factor (TNF)

Factors like the ones listed above disable the body's ability to process carbohydrates. So we should not be quite so focused on carbohydrate and more focused on the true contributors to diabetes.

Although some foods and quantities of them spike glucose more than others, with normal insulin sensivity, glucose will come back down quickly. If glucose stays elevated, something else is causing that to happen.

Genetic Factors

Genetics can play a significant role in how your blood sugar and insulin response respond to various types of carbohydrates, fats, and proteins. 

For example, some genetic variants promote a high blood sugar and high stress hormone response to the consumption of saturated fats. In people with these genetic variants, the real cause of hyperglycemia is the consumption of saturated fat.

Somewhat counterintuitively pehaps, these people can typically maintain metabolic health on a high-carb diet as long as they do not eat much saturated fat. 

Polyunsaturated Fats (PUFAs)

One of the main ways to make rats diabetic in the research world is feeding them a diet high in omega-6 polyunsaturated fats (PUFAs). So eating lots of high-PUFA seed oils (corn, canola, cottonseed, soy, etc) is a dietary route for creating insulin resistance.

And that is exactly what the processed and prepared foods of the Standard American Diet specializes in ... PUFAs from seed oils in everything. Even many seemingly healthy, alternative processed foods contain PUFAs from seed oils. For example, nearly all of the prepared foods in the fresh foods bars at Whole Foods Market contain canola oil.

Environmental Toxins

In a study of obese people, only the ones that had elevated levels of toxins were insulin resistant. In other words, obesity itself does not necessarily cause insulin resistance and diabetes. And it seems that that toxins alter the function of insulin receptors, creating insulin resistance.

With insulin resistance, glucose cannot enter muscle cells (the main storage site for glucose), so glucose instead enters fat cells, most of which do not require insulin for glucose to enter them. Gucose that enters fat cells is converted to fat and stored.  But fat cells have a finite capacity to store fat. And once the capacity a person's fat cells to store fat is exceeded, the fat cells start "leaking" fatty acids back into the blood stream, which is another cause of insulin resistance.

Leaky Fat Cells and Lipolysis Dominance

As fat cells get "full", cannot store more glucose, and start leaking free fatty acids back into the blood, these fatty acids--especially if they were derived from high-PUFA seed oils--are prone to oxidation. And oxidized fatty acids promote inflammation and insulin resistance by impairing the function of insulin receptors. Oxidized PUFAs also damage cell membranes, the lining of arteries, and organs throughout the body.

When too many free fatty acids acids flood the mitochondria to be "burned" for energy (lipolysis), glucose cannot be burned for energy. This is called "lipolysis dominance". In this situation, fatty acids are out-competing glucose for entry into the mitochondria, so glucose builds up in the blood. If this becomes chronic, the body releases more insulin in an attempt to drive glucose into cells. And when insulin is chronically elevated, this causes insulin resistance and is the hallmark of insulin resistance. 

Because of differences in how mitochondria produce energy from fatty acids and glucose, lipolysis dominance lowers the ratio of NAD+ to NADH. NAD+ is needed to fully metabolize glucose. So as the ratio of NAD+ to NADH falls, instead of fully metabolizing glucose, cells can get stuck in an alternative way of processing glucose called "aerobic glycolysis", which produces lactic acid as the byproduct. When lactic acid reaches high enough levels it is called lactic acidosis, which can ultimately result in death. 

If lipolysis is inhibited in people with diabetes, their diabetes is reversed, at least temporarily. This happens with the use of the drug Acetamox or high doses of aspirin. This is NOT a recommendation to use either Acetamox or megadoses of asprin to manage diabetes, but the fact that inhibiting lipolysis reverses diabetes demonstrates that lipolysis dominance is a major factor in diabetes.

By the way,  all of this can happen even in skinny people who have few fat cells and therefore a limited ability to store fat. Their fat cells reach their fat storage capacity very quickly and start leaking fatty acids into circulation. 

Stress, Cortisol, Low-Carb Diets, PUFAs, and Estrogen

Too much lipolysis can also be caused by stress or fasting, which raise cortisol and adrenaline, which in turn flood the bloodstream with free fatty acids. Not consuming enough carbohydrates can cause this as well. Think long-term low-carb or keto dieting. Yes, long-term keto frequently creates insulin resistance, even after it initially reduced insulin resistance. 

Lipolysis is also increased by excess PUFAs because they mimic estrogen, which increases lipolysis. In contrast, saturated fatty acids (SFAs) inhibit lipolysis. Plus, the inflammatory effects of PUFAs increase cortisol, which causes the release of free fatty acids into the bloodstream, thereby promoting lipolysis and lipolysis dominance.

Free fatty acids and cortisol also interfere with the insulin receptor, thereby promoting insulin resistance. And free fatty acids increase TNF-alpha, which increases inflammation. Free fatty acids also promote high serotonin, which suprisingly increases cortisol. 

PUFAs Are Not Done With You Yet!

Some of the degradation products of oxidized PUFAs are aldehydes, including malondialdehyde, and these aldehydes have a strong anti-metabolic effect that raises blood sugar. 

In addition, these aldehydes comprise most of the substance in atherosclerotic plaques. They are a key driver of cardiovascular disease.

PUFAs from seed oils also enable you to get fat on low calorie diet. And when you gain fat while eating a diet high in PUFAs from seed, your fat will contain lots of these PUFAs. Then becoming obese can drive insulin resistance and diabetes. Or, your fat cells might reach their storage limit well before you would be considered obeste and start leaking free fatty acids. 

The safest way for the body to get rid of excess PUFAs is actually not to burn them for energy in the mitochondria but to allow the liver to sulfate or glucuronidate them. This means eating some safe carbohydrates instead of overly restricting carbohydrates.

Leaky Gut, Gut Dysbiosis, and LPS

Systemic Inflammation seems to be one of the main drivers of insulin resistance and diabetes, and perhaps the most common and potent inflammatory substance is lipopolysaccharide (LPS) from the surface of gram-negative bacteria in the gut.

This LPS (also called "endotoxin") can then get into the blood, causing the body to launch an inflammatory immune response because it believes it has been invaded by bacteria. The systemic inflammation impairs insulin receptors, thereby contributing to insulin resistance, diabetes, and obesity. Inflammation also raises cortisol, which also promotes insulin resistance and fat storage.

LPS-producing gram-negative bacteria can overgrow when beneficial bacteria have been depleted by factors like antibiotics, a diet of processed food, glyphosate residues in food, other environmental toxins, or chronic stress. This imbalance between beneficial and not-so-beneficial bacteria is generally referred to as "dysbiosis". And dysbiosis can cause the gut lining to become inflammed and "leaky", allowing even more LPS to enter the body.

These gram-negative bacteria can overgrow further if they are fed too much, which can happen even with "healthy" diets that include slow-digesting carbohydrates called "resistant starch", which is starch that is not easily digested by our enzymes. Soluble fiber can also feed gram-negative bacteria. So once you have dysbiosis, certain aspects of a "healthy" diet can worsen dysbiosis and even cause or worsen insulin resistance.

If you have dysbisis and/or leaky gut, you could be better off choosing easily-digested, high-glycemic carbohydrates in order to minimize the production of LPS. Think well-cooked white rice or potatoes that have not been cooled because cooling causes resistant starch to form.

This sounds crazy, right? You've been taught to avoid easily-digested, high-glycemic carbs and instead use slow-digesting starches that are high in fiber.. And that is perfectly reasonable advice if you do not have dysbiosis and instead have a microbiome that turns undigested carbs and fibers into short chain fatty acids (very good) instead of LPS / endotoxin (very bad).

But if you have dysbiosis, you have to be careful to not increase LPS / endotoxin production in your gut. The state of your microbiome determines whether soluble fiber and resistant starch are benefiicial or dangerous.

Remember the study described earlier in this post in which people reversed diabetes and obesity with a diet of white rice, potatoes, and sugar? The most likely reasons that worked is that it minimized the production of LPS / endotoxin, and it interruped "lipolysis dominance", allowing glucose metabolism to dominate mitochondrial energy production.  

This would allow excess free fatty acids to be elminated via sulfation and glucuronidation instead of causing lipolysis dominance or being oxidized into aldehydes that damage cell membranes, blood vessels, organs, etc.

Non-Alcoholic Fatty Liver Disease

In recent years, a condition called non-alcoholic fatty liver disease (NAFLD) has become strongly associated with insulin resistance, diabetes, and obesity. 

We have been taught that NAFLD is just one more manifestation of chronically-high glucose levels caused by excess consumption of starches and sugars, especially fructose. But the evidence does not conclusively show that starches, sugar, or fructose cause NAFLD. And some studies show that NAFLD can be reversed by high doses of starch, sucrose, (which is 50% fructose), or honey (typically at least 50% fructose). 

High glucose in diabetics is not necessarily from dietary sources of glucose but rather from inappropriate gluconeogenesis (synthesis of glucose) in the liver. This happens because the liver is insulin resistant, usually as a result of high cortisol and/or excess free fatty acids leaking out of over-stuffed, leaky fat cells.

In order to prevent gluconeogenesis in diabetics, diabetics should probably not decrease carb intake below 100 grams per day. Otherwise, they run the risk of high cortisol, additional inflammation, lipolysis dominance, insulin resistance in the liver, and excess gluconeogenesis in the liver.

Not only is NAFLD not caused by high carbohydrate consumption, it can be caused by a high fat diet or by chronic fasting, due to the high quantity of fatty acids released from fat cells during fasting without much glucose available to compete with the fatty acids for entry into the mitochondria.

Once you have NAFLD, you lose your primary defense against damage from circulating PUFAs because the liver will be less able to get rid of them via sulfation and glucuronidation. So one of the main things to keep the liver healthy is to limit PUFAs, thereby limiting its burden of sulfating and glucuronidating PUFAs.

Since sulfation and glucornidation are key pathways for eliminating environmental toxins, it's important to avoid burdening these pathways so that you don't reduce your liver's ability to sulfate and glucuronidate other things like toxins.

Does Avoiding PUFAs Make You Harder to Kill?

Animals in a study that were made "EFA deficient", meaning deficient in omega-6 and omega-3 PUFAs, were remarkably resilient to all kinds of assault. They were able to tolerate 7x the lethal dose of radiation and withstand 20 times the LD50 of endotoxin / lipopolysaccharide (LPS). The LD50 is the dose that would normally kill half of the animals.

And carbon tetrachloride could not create liver cancer in these animals. They were also very resilient to neurodegenerative disease.

The essentially became harder to kill by reducing PUFAs.

It's important to keep in mind that these were animals, not people. And this study did not compare restriction of high-quality PUFAs (EPA, DHA, and arachidonic acid) to restriction of low-quality PUFAs (linoleic acid from seed oils), but the study demonstrates something profound that should be further investigated.

Keto and Fasting

It probably comes as a big surprise that a ketogenic diet and fasting can actually create problems for diabetics. Yet the fact is that in most cases (but not all), three to six months on  a ketogenic diet makes a person insulin resistant. And when they come off of the diet they gain weight.

Intermittent fasting can also cause problems. A researcher at UCSF stopped recommending intermittent fasting because he was seeing loss of lean muscle mass at alarming rates. And lean muscle mass is an important defense against insulin resistnce because lean muscle mass is the main consumer of glucose and storage site for extra glucose.

The loss of muscle mass observed by the researcher with intermitten fasting is probably a result of both reduced overall intake of calories and protein and a rise in cortisol, which causes muscle tissue to be catabolized (broken down) to produce glucose. The less muscle mass you have for storing glucose, the more glucose gets converted into fat and stored in fat cells.

The greatest benefits of fasting are seen in people who are young and lean, but people who are overweight and older (over 50) often do not do as well with fasting as younger people. And people over 50 are also more likely to develop an infection as a result of fasting.

Some evidence suggests that the benefits of fasting actually have to do with reducing levels of LPS / endotoxin by providing less food to gram-negative bacteria in the gut. You may be able to replace at least some of the benefits of fasting by taking insoluble fiber or other means of binding LPS, as well as reducing soluble fiber and resistant starches in your diet.

Bye Bye Metformin?

No discussion of insulin resistance and diabetes would be complete without at least mentioning the metformin, a drug commonly prescribed to treat diabetes. Metformin inhibits Complex I in the mitochondria. And this tricks the cell into thinking that it does not have enough glucose, so it allows more glucose into the cell. Or at least that is supposed to be how it goes.

But excess glucose in the cell that is not getting fully metabolized in the mitochondria because Complex I is impaired can instead be metabolized into lactic acid via glycolysis. In fact, metformin carries a warning that it can create lethal metabolic lactic acidosis. It also poses a high risk of dementia. And it leads to B12 deficiency..

And since all cancers have impaired Complex I in their mitochondria, do we really want to use a drug that causes that condition?

In addition to all of that, although metformin lowers blood glucose, it is not considered a "disease modifying" therapy because it does not fully address diabetes. Metformin may lower lipolysis, which gives cells more opportunity to burn glucose, but lipolysis can also be lowered with aspirin, niacinamide, or even sucrose to raise insulin which lowers lipolysis.

In Summary

The bottom line is that diabetes seems to start with environmental toxins, high stress, inflammation caused by factors like leaky gut and dysbiosis. diets high in easily-oxidized PUFAs from seed oils, fat cells reaching and exceeding their storage capacity and leaking free fatty acids into circulation, and anything that causes chronic stress.

Even this may be an oversimplification as other mechanisms have been implicated in the development of diabetes, such as the following:

• Circadian rhythm disruption
• A sedentary lifestyle
• Low lean body mass
• Deficiencies of vitamin D, vitamin K, vitamin A, long-chain omega-3 fatty acids, magnesium, chromium, molybdenum, and other nutrients
• Imbalance of omega-3 and omega-6 fatty acids
• Artificial sweeteners
• Statin drugs

And this is by no means a complete list of other causal factors. Type 2 diabetes and pre-diabetes are far more complex than we thought.

So What's Next?

At this point, you're might be thinking "Whaaaaat? Is any of this true?" This all departs so much from what you have been taught.

But the evidence is getting increasingly clear that diabetes is not all about the carbs. However, we do not necessarily need throw out everthing we thought we knew about insulin resistance and diabetes. Yet in many cases we need to look more closely at what we need to do to reverse it.

We need to identify toxic load, inflammatory factors like a high-PUFA diet, high stress, other causes of high cortisol, dysbiosis and a leaky gut, etc. Once these have been identified, we can customize an approach that makes sense for the unique set of factors contributing to your metabolic dysfunction. 

You also have some additional dietary options. Although fasting or going on a very low-carb diet has worked, at least short-term, for many people, these approaches are not necessary. And used too much, they can be counterproductive.

This is how I approach insulin resistance, Metabolic Syndrome, and diabetes, using the Bio-Individual Blueprint system. It begins by thoroughly assessing the factors that could be driving your insulin resistance, then strategically addressing them in a way that works for your unique body.

If you'd like to learn more about the system, download the Bio-Individual Blueprint Roadmap and watch the walkthrough video.