The Secrets to Reverse Insulin Resistance Naturally

Insulin resistance is the body’s impairment in processing insulin. But since it’s induced by diet and lifestyle, you can learn how to reverse insulin resistance naturally in this science-backed article.

Moreover, Insulin resistance is not just associated with obesity, metabolic syndrome, non-alcoholic fatty liver disease, and type 2 diabetes – it’s their primary driver.

Notably, more than 50% of the U.S. population already shows a prediabetic state (Menke et al. 2015¹).

What Is Insulin Resistance?

In brief, insulin resistance is the body’s impairment to process insulin.

It’s best explained using an analogy. Since insulin is a hormone, it acts as a messenger or key to a cell’s receptor.

If insulin cannot fully open the door to a cell anymore, the cell has developed insulin resistance.

We know that it’s the cell’s receptor that is developing insulin resistance because the amino-acid structure of insulin is always the same, in lean as well as obese people.

Given that the door to the cell didn’t open fully, less glucose than expected can enter the cell. As a result, the cell longs for more glucose.

Hence, the body reacts to the cell’s energy shortage by producing more insulin, ensuring sufficient glucose uptake.

Let’s suggest that a healthy cell just needed one key (insulin) to let in twelve glucose molecules, while one with an insulin-resistant receptor only could uptake six molecules.

In response, the body now produces two keys to fully open the cell and let in the necessary twelve units of glucose.

Hence, energy provision can be secured, but it comes at the cost of persistently elevated insulin levels (Fung 2016²).

As a result, the body adapts to insulin resistance by increasing the production of insulin.

However, that’s a standard response to deal with resistance. For example, more force, more money, more drugs, are similar responses to other kinds of resistance.

What Causes Insulin Resistance?

Nevertheless, increasing dosage seldom leads to a happy ending. Neither does it in our case. Increasing volume usually promotes resistance.

Thus, the more often a person consumes a particular drug, the lesser the effect. Similarly, the same is true for insulin.

Since insulin resistance shares the characteristics of common types of resistance, insulin itself is our primary candidate for the cause of insulin resistance.

If high insulin levels cause insulin resistance, the body needs to produce more insulin to ensure functionality. As a result, even more severe insulin resistance is developed.

And the vicious cycle fuels resistance over and over again.

For this reason, the 2011 Banting Medal Winner, Dr. Barbara Corkey, called her lecture, “Hyperinsulinemia is the root cause of insulin resistance, obesity, and diabetes (Corkey 2012³).”

And for this insight, she received the American Diabetes Association’s highest scientific award.

Likewise, here’s what the path to type 2 diabetes looks like:

1. Diet rich in fattening carbohydrates
2. Persistently high insulin levels
3. Insulin resistance
4. Higher insulin levels
5. Obesity, severe insulin resistance (pre-diabetes)
6. Even higher insulin levels fueling resistance
7. Type 2 diabetes

If insulin causes insulin resistance, we have to ask why the human body is aiming at developing insulin resistance?

The answer is simple. It’s a safety mechanism, since too high insulin levels can quickly lead to alarmingly low blood glucose levels.

As a result, hypoglycemia would most likely cause death.

Therefore, the development of insulin resistance is the biological principle of homeostasis at work, adaption of the body to enable stable, healthy levels of blood sugar (Fung 2016⁴).

Moreover, insulin-resistant people show high fasting insulin levels independent of diet. Hence, insulin resistance and metabolic syndrome, drive themselves to extremes over time.

Does Insulin Resistance Cause Weight Gain?

As far as 35 years ago, scientists have proven that hyperinsulinemia induced by insulin injection into healthy men leads to insulin resistance.

Although they only exposed subjects to high insulin levels for as little as 40 hours, researchers could conclude that hyperinsulinemia leads to “insulin-resistant states, such as obesity” (Rizza et al. 1985⁵).

Additionally, science also provides evidence for similar cases without exogenous insulin injection.

Researchers from the Diabetes Division at the University of Texas Health Science Center found that stimulation of insulin secretion causes insulin resistance.

On top of that, they summed up that high insulin levels are a compensatory response to insulin resistance and a self-reinforcing cause of the flawed insulin action (Del Prato et al. 1994⁶).

Moreover, patients showing a rare form of tumor secreting excessively high amounts of insulin called insulinoma are known to develop insulin resistance (Pontiroli et al. 1990⁷).

In cases where the tumor was surgically removed, the procedure could reverse insulin resistance too (Ghosh et al. 2008⁸).

And here’s another fantastic example. Researchers from the Department of Medicine at the University of California at San Diego set patients on intensive insulin treatment.

Likewise, the prescription of large doses of insulin to type 2 diabetes patients isn’t an unusual practice.

The results were astounding. Although the subject’s blood sugars were regulated very well, their insulin resistance became more severe with time and dosage.

As a result, the scientists observed higher insulin resistance, more significant hyperinsulinemia, and progressive weight gain.

A patient gained about 20 pounds or 9 kilograms on average, despite a caloric reduction of 300 calories per day.

In short, that’s crushing evidence. Insulin causes insulin resistance and weight gain.

Which Cells Can Begin to Exhibit Insulin Resistance?

To comprehensively understand its functioning, knowing which cells can develop insulin resistance is critical.

Because if all cells exhibit insulin resistance equally, the regulation of the body set weight, and hence weight gain, might not be affected severely.

Instead, insulin resistance targets specific areas. Since weight gain works tremendously with it, insulin resistance can’t affect fat cells.

But what about the brain? We know that the hypothalamic region in the brain regulates body fat and the body set weight.

Given that the body sensitively reacts to high levels of insulin and sets its thermostat for bodyweight too high in obese subjects, insulin resistance also can’t affect brain cells.

As a result, we only have two suspected areas of crucial insulin action left – the liver and the muscles.

In light of its significant role as the primary organ for metabolism, it might not surprise you that the liver cells can begin to exhibit insulin resistance.

Furthermore, in the area of the liver, the state is more precisely called hepatic insulin resistance.

Moreover, it’s an exciting fact that hepatic insulin resistance is isolated from insulin resistance in the muscles – the second major area of its effect.

While dietary interventions can reverse insulin resistance in the liver, they aren’t affecting muscle cells.

On the other hand, proper exercise can increase insulin sensitivity in the muscles but isn’t impacting reversing insulin resistance in the liver over time.

From a comprehensive point of view, it doesn’t matter where insulin resistance develops. Either way, it’s going to increase overall insulin levels (Fung 2016⁹).

Signs of Insulin Resistance

As we discussed the functioning of the hypothalamus and hormones to regulate body set weight, we concluded that overeating and lack of exercise are rather symptoms than causes of obesity.

As early as 1990, Dr. Walter Willett observed a significant connection between type 2 diabetes and obesity.

But the scientist, who is Professor of Epidemiology and Nutrition at Harvard’s School of Public Health until now, had a hard time spreading his word.

His research explained that weight gain after the age of 18 is the primary symptom of type 2 diabetes. Likewise, a weight gain of 35 kilograms yielded a 17,200 percent higher probability of diabetes (Colditz et al. 1990¹⁰).

But Willet also pointed out that even slightly being overweight increases diabetes risk by a factor of five (Powell 2012¹¹).

Although it’s in the healthy weight range, a body mass index of 23 can already be a symptom of insulin resistance in females (Colditz et al. 1995¹²).

In times where the public didn’t consider obesity and diabetes a primary health concern and governmental guidelines declared some weight gain as still healthy, nobody believed him.

That Willet also correctly identified a high-fat diet as an effective treatment of type 2 diabetes, didn’t help to challenge conventional thinking either (Fung et al. 2018¹³).

Since insulin resistance develops 13 years before type 2 diabetes, on average, obesity is a primary sign of insulin resistance.

It’s the same disorder as type 2 diabetes, but only on an earlier evolutionary stage (Tabak et al. 2009¹⁴).

Moreover, visceral fat is a major factor in high insulin resistance.

Given that it often accumulates before insulin resistance can be noticed, it is a significant sign of insulin resistance and metabolic syndrome development (Taksali et al. 2008¹⁵).

In this case, we need a definition – what is visceral fat?

Visceral Fat vs. Subcutaneous Fat

Visceral fat is deposited inside and around the intra-abdominal organs. These include, most notably, the liver, intestines, and kidneys.

Subcutaneous fat, on the other hand, is directly accumulating under the skin.

Furthermore, visceral fat can be divided into the more dangerous intra-organic fat and omental fat accumulated on the outside of organs, such as the pancreas.

Fat deposits inside the liver are most crucial to the development of insulin resistance. They are called intrahepatic fat (Fabbrini et al. 2009¹⁶).

Additionally, intra-organic fat is a major contributor to non-alcoholic fatty liver disease, type 2 diabetes, and cardiovascular disease (Bray et al. 2007¹⁷).

Conversely, omental fat’s effects are rather insignificant, since its surgical removal doesn’t result in metabolic improvements (Fabbrini et al. 2010¹⁸).

Increased waist circumference is a significant sign of visceral fat deposits. Therefore, the occurrence of obesity, where most of the fat accumulates around the abdomen, is known as central adiposity or central obesity.

Notably, it correlates very well with intrahepatic fat deposits (Jakobsen et al. 2007¹⁹).

Moreover, central obesity is an accurate predictor for metabolic issues, insulin resistance, and its progression towards type 2 diabetes independent of total weight (Matos et al. 2011²⁰; Wander et al. 2013²¹).

Hence, visceral fat reduction significantly lowers the risk of type 2 diabetes (Fujimoto et al. 2007²²).

Subcutaneous fat, on the other hand, doesn’t significantly contribute to the development of insulin resistance and diabetes.

Therefore total body fat measured through body mass index (BMI) is a suboptimal indicator.

Consequently, even type 2 diabetes often develops in people with a “healthy” BMI (Taylor et al. 2015²³).

This phenomenon is called TOFI, which stands for “thin on the outside, but fat on the inside.”

In short, it’s the visceral or intra-organic fat that makes the difference.

So how can we easily test for insulin resistance?

Testing for Insulin Resistance at Home

Well, the most accurate way to check your visceral fat would be magnetic resonance imaging (MRI).

But this method is expensive as well as time-consuming. The same is true for a blood test.

Hence, we need cheaper and faster options yielding sufficient accuracy.

The body mass index is, by far, not a perfect indicator of insulin resistance. In contrast, large waist circumference is a much better insulin resistance symptom in females and males.

It better correlates with visceral fat deposits, since it’s a measure of body mass distribution around the trunk (Fung et al. 2018²⁴).

Researchers found that your waist circumference is optimal when it equals half your height. For example, a waist size of 34 inches (86 centimeters) is ideal for a person who is 68 inches (1.72 meters) tall.

The waist-to-height ratio is easy to measure and to apply since the desirable values between 0.4 and 0.6 are independent of age.

Moreover, waist-to-height-ratio is a superior predictor of years of life lost compared to body mass index or other total weight or body fat-based measures (Ashwell et al. 2012²⁵).

For this reason, waist-to-height-ratio (WHtR) is our method of choice when it comes to testing for insulin resistance at home.

Insulin Sensitivity vs. Insulin Resistance

Insulin sensitivity is the ability of cells to respond to insulin effectively.

Hence, it’s the opposite of insulin resistance.

The higher the insulin sensitivity of a cell, the better it absorbs glucose from the bloodstream.

Accordingly, insulin sensitivity means that the key (insulin) opens the lock (cell receptor) correctly. Then blood sugar can enter the cell through the open door.

Thus, targeting its root cause high insulin levels, hyperinsulinemia, can increase insulin sensitivity naturally.

On the contrary, the standard treatment for diabetes still focuses the symptom – high blood sugar levels, hyperglycemia.

If we just lower blood sugar, the elevated insulin levels, and low insulin sensitivity remain.

When one injects exogenous insulin to lower blood glucose, insulin levels also rise. And in the long run, insulin sensitivity is reduced.

As a result, people gain weight and can develop cardiovascular disease (Herman et al. 2017²⁶).

How to Increase Insulin Sensitivity Naturally

If we can cut off the permanent supply of foods well-known to raise blood sugar, we can counteract hyperinsulinemia. Thus, we can increase insulin sensitivity naturally over time.

Because reducing the intake of fattening carbohydrates and the incorporation of intermittent fasting periods can lower insulin levels.

When glycogen stores are empty, the body preferably burns off visceral fat in the liver since it’s best accessible. Therefore, we can reduce insulin resistance in liver cells.

How do we know that this approach increases insulin sensitivity naturally?

As bariatric surgeries removing fat in and around the liver and pancreas show, type 2 diabetes can reverse within weeks.

Furthermore, a low-carbohydrate diet used to be an effective treatment for type 2 diabetes before the low-fat movement went mainstream.

Notably, low-carb diets as a standard treatment for obesity do even range back to the mid-nineteenth century (Banting 1869²⁷).

As the New York Times stated, a low-carb diet can yield the same benefits as a $26,000 surgery (Hallberg et al. 2016²⁸).

Additionally, recent studies confirm that type 2 diabetes can be reversed naturally by targeting the underlying root cause through diet (Westerman et al. 2008²⁹).

Hence, our primary targets to eliminate are highly refined carbohydrates like sugars and flours because they have the most severe impact on blood glucose and diabetes risk (Villegas et al. 2007³⁰).

Moreover, we want to reduce starchy vegetables like potatoes and rice too, since all carbohydrates are sugars. Starches, for example, are long chains of glucose, so-called polysaccharides.

But sugars aren’t just hiding in plant foods. Let’s start where we can simply increase insulin sensitivity naturally through awareness – packaged food.

1. Read Labels

Sugar is hiding everywhere to raise revenues due to its addictive nature (Lenoir et al. 2007³¹).

And the food industry is very creative when it comes to inventing different names for sugar to prevent it from being listed as the first ingredient.

Sucrose, table sugar, isn’t a monosaccharide. Besides glucose, there is a second much sweeter sugar molecule in it – fructose.

Unlike glucose, which is widely known to spike blood sugar and insulin, fructose is generally underestimated.

Nevertheless, fruit sugar directly promotes insulin resistance and fat gain (Tappy et al. 2010³²).

Like alcohol, it significantly contributes to (non-alcoholic) fatty liver disease.

For this reason, the leading endocrinology researcher Dr. Robert Lustig warns of the worldwide reckless consumption of this liver toxin (Lustig 2014³³).

Moreover, fructose encourages cravings, inhibits leptin, and stimulates the hunger hormone ghrelin (Teff et al. 2004³⁴).

Fructose metabolism’s waste product uric acid fosters insulin resistance and inhibits nitric oxide – a chemical critical for the functioning of our brain and blood vessels (Rho et al. 2012³⁵).

Although its impact on blood glucose and insulin levels is low, fructose fuels the development of insulin resistance in the liver.

How does fructose metabolism in the liver work?

The liver metabolizes 100% of fructose ingestion – there is no other pathway. Excess fructose is metabolized into fat in the liver. And fatty liver is a crucial factor in the development of insulin resistance.

Moreover, most natural sweeteners are rich in fructose and hence not a great alternative to sucrose.

For example, agave syrup can consist of up to 97% fructose.  Although artificial sweeteners aren’t an option either, don’t fall into the all-natural sweeteners and fruit sugar trap.

The direct effect of fructose on the liver, paired with the impact of glucose on insulin levels, is the perfect recipe for insulin resistance.

2. Eat Real Food

Given the uniquely fattening dual-exposure of the disaccharide sucrose, the logical next step is to dodge processed food whenever possible.

After starting with reading labels, you should already be shocked about the amounts of sugar and high-fructose corn syrup in seamlessly harmless foods like dressings or even vinegar.

What is processed food to avoid?

Shelf-stable and readily seasoned foods like bakery goods, bars, marinated vegetables, or meat will most likely contain low-quality vegetable oils, trans fats, artificial sweeteners, and other chemicals or additives.

For example, researchers have proven that the popular additive monosodium glutamate significantly elevates insulin levels and promotes weight gain (Chevassus and Renard et al. 2002³⁶).

Moreover, if you can limit your carbohydrate intake to whole foods, you can make use of the protective effects of fiber. Fiber is the carbohydrate proportion of plant foods the human body can’t digest.

Therefore, fiber reduces carbohydrate absorption and dampens blood glucose and insulin responses.

Furthermore, it bulks up foods, forms a gel, which decreases energy density, and supports satiety.

Avocados are among the best low carb foods high in soluble fiber. Hence, they are nutrient-dense and rich in electrolytes, vitamins, and monounsaturated fatty acids.

Moreover, they help to absorb fat-soluble nutrients from other food sources (Mercola 2017³⁷).

As a diabetes study shows, a higher proportion of fiber in meals significantly lowers blood sugar and insulin spikes (Chandalia and Garg et al. 2000³⁸).

For this reason, nature has foreseen fiber in raw food. Hence, it’s the processing, which is removing protective factors and causing harm.

Moreover, nutrient-dense whole foods add minerals to your meal, slow down digestion, and counteract insulin secretion.

Choosing real over fake foods reduces the number of empty calories consumed.

3. Stop Snacking

Our grandparents had it right. This advice for weight loss used to be common sense. Moreover, it is another excellent way to reduce the amounts of sugar and other additives, since snacks are mostly processed foods.

If you think that one is obvious, we have to take a look at what conventional wisdom nowadays includes:

• Eat six times a day
• Eat more often to lose weight
• Never skip breakfast
• Eat more snacks

Countless campaigns have brainwashed us with contradictory diet advice during the last decades. And the saddest thing is that even health professionals fell for those myths and started to promote snacking too.

Eating more frequently to lose weight is as stupid as it sounds. Studies confirm that people who snack generally eat more throughout the day (Stubbs et al. 2001³⁹).

Moreover, it’s a fact that snacking doesn’t support weight loss (Cameron et al. 2010⁴⁰). The only thing snacking supports is the revenue of highly processed foods.

The reason why snacking is bad for you is that it inhibits longer periods of low insulin levels. Furthermore, snacks substantially spike insulin levels since they often contain sugar and refined carbohydrates.

You might have heard that we lose weight while sleeping. This is based on the absence of insulin due to a lack of ingestion. But if we eat six times a day, that’s also the only period left in which insulin levels can drop.

Compared to the 1960s, where three meals a day were regular, we created an imbalance between feeding and fasting.

Since fasting is the most effective natural treatment for insulin resistance, we have to bring it back to everyday life (Fung 2016⁴¹).

Indeed, that means the absence of sodas, juices, smoothies, or any other sugary beverages between mealtimes. Instead, stick to plain water, tea, or coffee.

4. Skip Breakfast

This tip to increase insulin sensitivity with little effort might sound hard but isn’t. Just skip the least important meal of the day.

As so often, breakfast is just essential to the food industry. Many people opt for packaged food due to lack of time in the morning.

Notably, there’s nothing wrong with breaking your fast at noon.

It’s important to realize that skipping breakfast extends the most natural intermittent fasting period of the day and, therefore, is so valuable.

We have learned morning hunger over the decades, but it’s not natural. In my experience, morning hunger usually disappears with the forced habit of breakfast in as little as a week or two.

But where do I get the energy from to start the day if I skip breakfast to lose weight?

Fortunately, nature has foreseen a hormonal cocktail called the dawn phenomenon to get us ready for an upcoming day.

Before we wake up, the body increases adrenaline, glucagon, human growth hormone (HGH), and cortisol levels.

The stress hormone cortisol is at its daily peak level when we wake up. Adrenaline and cortisol mobilize energy for activity. Glucagon supports by moving glucose from the liver’s glycogen stores into the blood.

And helping to repair and synthesize new protein is what HGH does after waking up. Our bodies secrete these hormones in a pulsatile manner.

It’s part of the circadian rhythm. In the absence of dysfunction, they decrease throughout the day (Fung 2016⁴²).

Most people even report a gain in productivity before noon after successfully unlearning the breakfast habit. This step comes with little effort, but it is hard to get over.

But if you mastered it, you already implemented the most effective treatment to reverse insulin resistance naturally just by skipping breakfast – intermittent fasting.

5. Use Apple Cider Vinegar

Diluted apple cider vinegar has a history as a weight loss drink. And according to studies, it still helps you lose weight today (Kondo et al. 2009⁴³).

Although it is not a panacea, apple cider vinegar helps to increase insulin sensitivity naturally. Because similar to dietary fiber, apple cider vinegar has protective effects on carbohydrate absorption.

For this reason, vinegar is added to sushi rice, potato chips, or French fries.

Likewise, adding apple cider vinegar to white rice reduces the relative blood sugar spike by almost 40 percent and thus helps with weight loss (Sugiyama et al. 2003⁴⁴).

If you take apple vinegar shortly before a meal, it’s particularly useful (Johnston et al. 2010⁴⁵).

Correspondingly, a study on apple vinegar for weight loss showed that two teaspoons of vinegar lower the resulting blood sugar and insulin levels by 34 percent.

Moreover, apple cider vinegar also helps to lower blood pressure (Kondo et al. 2001⁴⁶).

But even more interesting, apple cider vinegar increases insulin sensitivity by helping to reduce critical visceral fat inside the liver (Kondo et al. 2009⁴⁷).

More than two teaspoons of ACV aren’t a problem either since acetic acid increases satiety and lowers calorie intake throughout the day (Johnston et al. 2005⁴⁸).

Therefore, consume at least one tablespoon or three teaspoons of apple vinegar a day to reap the health benefits.

But it’s entirely up to you whether you consume it as a shot, diluted with water, or as natural dressing.

Moreover, you can combine apple cider vinegar as a vinaigrette with healthy fats such as extra virgin olive, avocado, or coconut oil. This way, you can increase insulin sensitivity even more naturally.

And read the label!

Apple cider vinegar should be produced naturally and not exceed 1.5 grams of sugar per 100 grams.

Can Insulin Resistance Be Reversed?

In times where countless ads promise to lose weight fast, we often forget that weight gain didn’t happen overnight.

With this in mind, metabolic syndrome and insulin resistance as its driving force are developing step-by-step, pound-by-pound over years.

Therefore, that you can’t reverse insulin resistance in a week should be common sense, but isn’t.

While conventional caloric reduction suggest that time doesn’t matter, insulin resistance is very time-dependent (Fung 2016⁴⁹).

Moreover, there is evidence that reversing insulin resistance and metabolic syndrome can take just as long as their development took.

Therefore, French scientists observed different subjects from non-obese over recently obese to long-term obese.

And they found that insulin sensitivity decreases with duration of obesity and age. As a result, time is a significant factor for insulin resistance.

While non-obese subjects didn’t show high levels of insulin, recently and long-term obese participants exhibited high insulin levels (Le Stunff et al. 1994⁵⁰).

In other words, hyperinsulinemia comes first and the severity of insulin resistance develops over time. But everything starts with persistently high insulin level.

In other words, the fat are getting fatter more easily and losing weight harder.

So, if you ask yourself: Can I reverse insulin resistance?

The answer is yes. But it may take a severe amount of time as it did for your cells to exhibit insulin resistance.

Moreover, a dietary change might not yield immediate results. Why?

Because severe insulin resistance keeps insulin levels high by itself. Therefore, the body set weight stays high initially too.

Nevertheless, according to studies, proper diet and fasting are even more effective against insulin resistance than bariatric surgeries (Lingvay et al. 2013⁵¹).

And these have proven that removal of visceral fat in and around the liver can reverse type 2 diabetes (Schauer et al. 2017⁵²).

Insulin Resistance and Exercise

Exercise has many positive effects. It improves strength, endurance, blood pressure, blood sugar, and insulin sensitivity. And all this without medication.

Although exercise can help to lose weight, its effect is less than people expect.

Accordingly, diabetes studies show that the effects of exercise are greatly overestimated (O’Gorman et al. 2006⁵³; Boulé et al. 2001⁵⁴).

Nevertheless, it is no secret that sport brings health benefits.

So why doesn’t exercise reveal itself as the panacea?

With this in mind, there are the following reasons:

• Exercise increases appetite
• Exercise reduces other physical activities
• It needs a regular basis
• Illness or ailments are hindering
• Visible results are widely overestimated

First, exercise has compensatory mechanisms. Hence, those who exercise more will eat more. When I prepare for a marathon, I have more appetite.

On the other hand, exercise compensates for physical activities in general. Since I am sitting in my apartment all day due to coronavirus lock-down, I feel like running.

On the other hand, a nurse who walks a few kilometers at work will feel less inclined to run.

Moreover, the 125 kilometers in April gained me seven kilograms. And the last marathon preparation did too.

A reason for concern? No, since the gain was mainly lean mass and it’s an excellent method for stress reduction.

Accordingly, exercise is not the magic formula for weight loss that has been marketed to us. And the results are rather demoralizing.

Finally, not lack of exercise but excess glucose and fructose – also known as table sugar – cause insulin resistance.

If you don’t turn off the sugar tap, you won’t achieve much with or without exercise.

Nevertheless, exercise can only help against insulin resistance in skeletal muscle. However, the core of the disease lies in the liver (Fung et al. 2018⁵⁵).

Fatty Liver and Insulin Resistance

Fat deposits in and around organs are a significant factor in insulin resistance. And the first place where this visceral fat accumulates is in the liver (Taksali et al. 2008⁵⁶).

Accordingly, a fatty liver develops before symptoms of insulin resistance become apparent.

Although the liver is essential for metabolism, excess dietary fat passes it by. Therefore, it can be stored in the whole body.

Since this subcutaneous fat accumulates directly under the skin, it’s less dangerous. While it is visually unattractive, subcutaneous fat doesn’t impact metabolism.

However, the metabolic pathway for carbohydrates and proteins is different. Firstly, they are stored in the liver as glycogen.

Once glycogen stores are full, the liver converts excess glucose into fat. Thus, energy can be stored throughout the body and in and around organs.

When this “de novo lipogenesis” produces more fat than can be transported away, it accumulates in the liver.

As a result, central obesity develops.

In short, at some point, the liver cannot absorb any more glucose and develops insulin resistance.

Therefore, too much sugar and insulin cause fatty liver in the long run (Bawden et al. 2017⁵⁷).

Once liver cells developed insulin resistance, fasting insulin levels rise. And voila, the vicious circle is established:

• Insulin resistance increases insulin secretion
• Higher insulin levels cause increased insulin resistance

Thus, fatty liver is the foundation for insulin resistance and type 2 diabetes.

In contrast to popular belief, people who develop fatty liver are predominantly not alcoholics.

Although its discovery is comparatively recent, non-alcoholic fatty liver disease (NAFLD) is the western world’s primary factor in liver disease (Angulo et al. 2002⁵⁸).

And you cannot exercise a fatty liver away.

Therefore, one has to reverse insulin resistance with diet, since that’s the way it developed.

How to Reverse Insulin Resistance With Diet

If we want to reverse insulin resistance naturally by burning off sugar and visceral fat with the help of intermittent fasting, we need to shut down the supply of insulin-secreting foods.

In this way, you can enable to tackle intra-organic fat to reverse insulin resistance in the liver.

But which foods raise insulin levels and support hyperinsulinemia?

Different macronutrients cause different insulin responses. And it’s widely known that carbohydrates have the most significant impact.

Since they are chains of sugar, carbohydrates break down into glucose.

And as we already know from sucrose, the fruit sugar fructose has a unique metabolic pathway directly promoting insulin resistance in the liver. While glucose is generally spiking blood insulin levels.

With this in mind, conventional sugar has a dangerous dual effect:

• High blood sugar and insulin levels
• Insulin resistance in the liver (fatty liver)

So, which foods raise insulin levels, and to what extent?

Glycemic Index vs. Glycemic Load

A first attempt to measure insulin elevating carbohydrates is the glycemic index. It helps to distinguish high glycemic index foods like starchy potatoes from options rich in dietary fiber like broccoli.

But the glycemic index only measures carbohydrate-containing foods.

Moreover, it describes the effect of a 50-gram portion of the carbohydrates in a specific food on blood glucose, while neglecting other macronutrients.

With this in mind, glucose sets a reference value of 100. While potatoes, for example, score an 80, broccoli’s value is about 10. And here’s the problem.

Watermelons also scored an 80 on the glycemic index. But to ingest 50 grams of carbs out of watermelons, you need to eat a whole kilogram.

Therefore, the glycemic load tries to address this issue by adjusting for serving size. In our example, the difference is drastic.

The glycemic load vs. index comparison of watermelons results in a tiny glycemic load value of 5 compared to the glycemic index score of 80.

While the glycemic load seems more practical, we still encounter an issue. In short, the measure is just aimed at foods causing high blood glucose levels.

But it’s not only blood sugar that spikes insulin. Furthermore, all meals, not just carbohydrates, cause insulin secretion.

For this reason, we instead need a measure that considers all macronutrients.

Insulin Index of Food

The insulin index measures the effects of foods on the blood insulin level during a period of two hours after ingestion.

Therefore, it’s a better measure when fighting insulin resistance than the glycemic load or index (Holt et al. 1997⁵⁹)

It was unknown for quite a while and is still often neglected, but protein and fat can stimulate insulin secretion too (Nuttall et al. 1991⁶⁰).

On the contrary, pure fats like extra virgin olive oil aren’t causing an insulin or blood glucose response.

But seldom they are ingested exclusively. Nevertheless, the effect of fatty acids on insulin is mild.

Amino acids, on the other hand, can have a medium impact on blood insulin. For this reason, many low-carb diets don’t work for weight loss.

So, how do fat and protein increase insulin levels without affecting blood glucose?

The stomach secretes two hormones that increase insulin production – glucagon-like peptide one (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), the incretin hormones.

The incretin effect is triggered by oral intake of glucose, too, where it is responsible for 50 to 70 percent of its overall insulin response.

Moreover, the insulin index considers all foods. Hence, even non-caloric sweeteners like sucralose are significantly raising insulin levels through the incretin effect (Pepino et al. 2013⁶¹)

But there are various glucose-independent pathways to increase insulin. For example, the artificial sweetener saccharin around your mouth raises insulin even if you spit it out (Just et al. 2008⁶²)

Amino acids from dairy, meat, and seafood stimulate the incretins. Therefore, they raise insulin more significantly than most plant proteins, but also support satiety by slowing stomach emptying substantially.

Consequently, animal proteins make you stay full longer. Although the satiety effect may outweigh the insulin and weight gaining impact, we have to be careful with protein intake.

Foods That Lower Insulin Resistance List

The severe impact of lean protein on insulin levels used to be a missing fact in low-carbohydrate diets, like the Atkins diet.

Consequently, substituting carbohydrates with lean cuts of meat, low-fat dairy, or even protein shakes and bars doomed them to fail.

So what should we eat to prevent and reverse insulin resistance naturally?

Fat, since substituting carbohydrates with all-natural dietary fat is a simple and natural treatment for insulin resistance (Masharani et al. 2015⁶³).

Remember, fat is the macronutrient that affects insulin production the least. Hence, dietary fat can counteract hyperinsulinemia.

But which are foods with healthy fats we should eat?

Therefore, here’s a list of foods with healthy fats:

• coconut oil
• coconut milk
• MCT oil
• extra virgin olive oil
• olives
• avocado (oil)
• cod liver (oil)
• fish roe
• mackerels
• sardines
• salmon
• anchovies
• herring
• grass-fed or pastured meat
• grass-fed butter
• ghee
• lard
• tallow
• pastured eggs
• walnuts
• macadamia nuts
• flaxseeds

In contrast to conventional wisdom, saturated fat doesn’t promote cardiovascular diseases, whereas carbohydrates do (Mozaffarian et al. 2004⁶⁴).

Moreover, various studies suggest that eating saturated fat protects against stroke (Siri-Tariano et al. 2010⁶⁵).

Besides fatty fish low in mercury like mackerels or sardines, flaxseed oil is an excellent and plant-based source of omega-3 fatty acids.

Highly refined and industrially processed vegetable oils, on the other hand, are rich in omega-6 fatty acids, are inflammatory and support coronary heart disease as well as cardiovascular disease (Ramsden et al. 2013⁶⁶).

Those seed oils can release harmful chemicals – aldehydes – when heated.

For this reason, stay away from deep-fried foods and hydrogenated trans fats like margarine. Moreover, there are seed oils you should generally avoid:

• Canola
• Corn
• Cottonseed
• Grapeseed
• Peanut
• Safflower
• Soy
• Sunflower
• Partially hydrogenated vegetable

What to Eat With Insulin Resistance

Furthermore, refined grains and sugars promote heart disease. Due to their processing, foods like flour and added sugar are very high in glycemic load and therefore spike blood glucose and insulin tremendously.

Consequently, we generally want to replace them with green vegetables and natural fats.

But aren’t green vegetables like broccoli sources of carbohydrates?

Yes, but their main carbohydrate proportion is the anti-nutrient fiber. The body does not absorb fiber. Therefore, fiber can be subtracted from total carbohydrates to get a more reliable measure “net carbs.”

With this in mind, we can determine the residual proportion of non-refined net carbs of our diet to reverse insulin resistance naturally. They should ideally stay within a range of 5 to 10 percent of total daily caloric intake.

Why so little?

Because there are simply no essential carbohydrates, and they have the most significant impact on insulin levels.

But there are essential fatty acids and amino acids our bodies need to thrive and survive in the long run. For this reason, we should not eliminate protein from our diet, although it is impacting insulin levels.

Therefore, we want to eliminate concentrated proteins in the form of processed bars, powders, and shakes. Natural proteins, on the other hand, are mostly accompanied by natural fats or fiber.

But over the last decades, we forgot about traditional cuisine, applying the principle of whole foods to animal products as well.

Instead we began to focus on muscle meat and egg whites while discarding the more nutritious organ meats and egg yolks. And with them we discarded natural fatty acids, vitamins, and other minerals.

Correspondingly, I appeal to bring back an approach to animal products that is more nose to tail.

Insulin Resistance and Keto Diet

Bone broth, liver, kidneys, and even blood used to be part of traditional diets for a reason. Those are the fattier parts of meat.

And a diet rich in natural fats is the foundation to increase insulin sensitivity naturally.

It’s the focus on lean meat, unnatural feed, and antibiotics that can have adverse impacts on our health. Animal products per se are not harmful.

Contrarily, eating wild game and seafood is among the best you can do to your body.

Nevertheless, the ideal value of dietary protein to increase insulin sensitivity is 20 to 25 percent of total caloric intake. The proportion can be slightly higher if you are doing a lot of resistance training.

Due to its low impact on insulin and positive effects on satiety, we aim for at least 70 percent of natural dietary fats.

As a result, we get a low-carb high-fat diet (LCHF) – also referred to as a low-carb healthy-fat or ketogenic diet.

For the devotees of the keto diet, ketosis is the ultimate goal.

In essence, ketosis is a fancy term for burning fat for energy.

And that’s only possible if insulin levels are low. Therefore, keto is suitable for reversing insulin resistance naturally.

Since keto mimics the effects of fasting and depletes glycogen stores, you can tap into body fat for fuel.

To reverse of insulin resistance we focus on visceral fat in the liver and insulin levels. Hence, this corresponds to the effect of a ketogenic diet.

However, the package of natural remedies for insulin resistance rests on two pillars:

• Ketogenic diet to not constantly stimulate insulin production
• Intermittent fasting to burn visceral fat when insulin levels are low

Nevertheless, studies show that LCHF and keto diets can reverse insulin resistance naturally (Westman et al. 2008⁶⁷).

Fasting and Insulin Resistance

Fasting is an all-natural way to get rid of the excess sugar in our bodies.

And one of the most remarkable diabetes specialists, Dr. Elliot Joslin, already knew this in 1916.

The records of the effect of fasting against insulin resistance in modern times go back as far as 1969 (Jackson et al. 1969⁶⁸).

Additionally, recent studies suggest intermittent fasting is a safe treatment for insulin resistance and more effective in burning visceral fat than a low-carb diet (Catenacci et al. 2016⁶⁹).

In short, fasting helps to reverse insulin resistance in the liver.

Exercise may support insulin sensitivity, but it’s limited to skeletal muscle, while intermittent fasting addresses the underlying issue, fatty liver.

To enable an effective burning of the hepatic fat in the liver by fasting, an LCHF or keto diet lays the foundation. Given that, these diet interventions prevent excessive production of insulin.

Moreover, prolonged and intermittent fasting for weight loss and cure of ailments has been a health tool for centuries. Religions incorporate fasting customs for a reason. But, sadly, we forgot about these traditions.

Fasting is the most effective strategy to consistently lower insulin levels.

This effect is vital for people suffering from hyperinsulinemia and insulin resistance because it helps them to burn off excess glucose and finally tap into body fat for energy.

Can Fasting Reverse Insulin Resistance?

As research shows, regular 16/8 intermittent fasting directly improves insulin sensitivity. Therefore it doesn’t just reduce high insulin levels.

Furthermore, fasting can reverse insulin resistance, which most diets can’t (Halberg et al. 2005⁷⁰).

Additionally, a fasting detox yields lots of health benefits like the removal of unnecessary or dysfunctional components from cells.

The 2016 Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for the discovery of this mechanism known as autophagy (Levine et al. 2017⁷¹).

However, there are many myths about the drawbacks of fasting. For example, a sticky myth ist that it will overwhelm you with hunger.

But Viennese researchers have shown that the hunger hormone ghrelin gradually decreases after the peak on the first day of fasting (Natalucci et al. 2005⁷²).

According to research, blood glucose levels also remain stable when switching to burning body fat for energy (Merimee et al. 1974⁷³).

Therefore the intake of carbohydrates is simply not necessary. And isn’t it the body fat that generally worries us? Consequently, the breakdown of body fat will not harm us in any way.

In contrary to conventional wisdom, fasting also doesn’t cause muscle loss, as you will see when we compare intermittent fasting and calorie restriction.

Intermittent Fasting vs. Calorie Restriction

The primary difference between eating less but frequently and intermittent fasting for weight loss is a hormonal change.

Notably, insulin drops.

As observed in a randomized trial in young overweight women, intermittent fasting shows a stronger decrease in fasting insulin levels and insulin resistance compared to conventional calorie restriction.

The intermittency makes the difference.

Why?

It’s a survival mechanism. Nature designed humans to use the stored energy in times of food scarcity. And that’s why we are storing body fat in the first place.

For this reason, the human growth hormone rises while fasting too. It preserves the lean mass to assure agility in the absence of food.

Additionally, the hormone noradrenaline increases to keep the basal metabolic rate up (Zauner et al. 2000⁷⁴).

Compared to intermittent fasting, conventional calorie restriction leads to loss of lean mass. Moreover, the basal metabolic rate decreases when you eat less but frequently.

Intermittent Fasting Reverses Insulin Resistance Naturally

Do you remember the body set weight? Hormones set the weight thermostat in your brain. And your body targets to adjust to it in the long run. Therefore, it suppresses the resting metabolic rate.

For this reason, people are regaining weight after the eat less, move more regime – from “The Biggest Loser” to even bigger gainer. We better know this effect as yo-yo dieting.

Moreover, the metabolic adaption as the body’s response to chronic calorie restriction doesn’t even recover after six years.

And that’s what a study involving the participants of the T.V. show “The Biggest Loser” suggests.

Furthermore, those who lost the most weight during the competition showed a greater persistence of metabolic adaption (Fothergill et al. 2016⁷⁵).

Hence, this compensatory effect of a lower metabolic rate coupled with constant cravings due to small snacks seals the widely proven failure of conventional calorie reduction.

Accordingly, an empirical study from the U.K. showed that 99.5 percent of overweight women and men could not successfully lose weight through calorie restriction (Flides et al. 2015⁷⁶).

In contrast to calorie restriction, intermittent fasting changes the hormone balance positively.

Since it is hormones that control our body, intermittent fasting is the most effective natural remedy for insulin resistance.

Due to it’s fighting both primary and secondary causes of insulin resistance, fasting is that effective:

• High insulin levels
• Visceral fat

Hence, intermittent fasting can reverse insulin resistance naturally.

Conclusion

Persistently high insulin levels (hyperinsulinemia), are the root cause of insulin resistance and many other modern diseases.

Insulin resistance is the body’s impairment to respond to insulin – a safety mechanism counteracting hyperinsulinemia.

Furthermore, it’s the primary driver of metabolic syndrome and type 2 diabetes.

When the insulin resistance ball starts rolling, it’s difficult to stop it since insulin resistance causes more insulin secretion. It’s a vicious cycle.

Since it’s a disorder introduced by diet and lifestyle, it needs diet and lifestyle interventions to stop and eventually reverse insulin resistance.

On the other hand, bariatric surgery is an alternative often executed when diabetes has developed. But it’s unnatural and expensive.

However, research suggests that all the benefits of surgery can be achieved naturally with superior effectiveness.

Since both treatments target to eliminate the underlying root causes hyperinsulinemia and visceral fat in the liver, they yield similar effects.

Therefore, a LCHF or ketogenic diet and intermittent fasting can reverse insulin resistance naturally.

On the one hand, these methods lower insulin levels, and on the other hand, they help to burn off the intrahepatic fat.

Conversely, treating the symptom, high blood sugar, through medication is not the answer.

Moreover, exogenous insulin increases risk of insulin resistance, obesity, diabetes, cardiovascular disease, cancer, and even death (Smooke et al. 2005⁷⁷; Johnson et al. 2010⁷⁸; Stoekenbroek et al. 2015⁷⁹).

Studies

#1-10

¹Menke A, Casagrande S, Geiss L, Cowie CC. Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. JAMA. 2015 Sep 8;314(10):1021-9. doi: 10.1001/jama.2015.10029. PubMed PMID: 26348752.

²Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

³Corkey BE. Banting lecture 2011: hyperinsulinemia: cause or consequence?. Diabetes. 2012 Jan;61(1):4-13. doi: 10.2337/db11-1483. PubMed PMID: 22187369; PubMed Central PMCID: PMC3237642.

⁴Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

⁵Rizza RA, Mandarino LJ, Genest J, Baker BA, Gerich JE. Production of insulin resistance by hyperinsulinaemia in man. Diabetologia. 1985 Feb;28(2):70-5. doi: 10.1007/bf00279918. PubMed PMID: 3884419.

⁶Del Prato S, Leonetti F, Simonson DC, Sheehan P, Matsuda M, DeFronzo RA. Effect of sustained physiologic hyperinsulinaemia and hyperglycaemia on insulin secretion and insulin sensitivity in man. Diabetologia. 1994 Oct;37(10):1025-35. doi: 10.1007/bf00400466. PubMed PMID: 7851681.

⁷Pontiroli AE, Alberetto M, Capra F, Pozza G. The glucose clamp technique for the study of patients with hypoglycemia: insulin resistance as a feature of insulinoma. J Endocrinol Invest. 1990 Mar;13(3):241-5. doi: 10.1007/BF03349549. PubMed PMID: 2195099.

⁸Ghosh S, Roychowdhury B, Mukhopadhyay S, Chowdhury S. Clearance of acanthosis nigricans associated with insulinoma following surgical resection. QJM. 2008 Nov;101(11):899-900. doi: 10.1093/qjmed/hcn098. Epub 2008 Jul 31. PubMed PMID: 18669553.

⁹Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

¹⁰Colditz GA, Willett WC, Stampfer MJ, Manson JE, Hennekens CH, Arky RA, Speizer FE. Weight as a risk factor for clinical diabetes in women. Am J Epidemiol. 1990 Sep;132(3):501-13. doi: 10.1093/oxfordjournals.aje.a115686. PubMed PMID: 2389754.

#11-16

¹¹Powell A. Obesity? Diabetes? We’ve been set up. Cambridge, MA: The Harvard Gazette, 2012.

¹²Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med. 1995 Apr 1;122(7):481-6. doi: 10.7326/0003-4819-122-7-199504010-00001. PubMed PMID: 7872581.

¹³Fung J, Teicholz N. The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally. Vancouver: Greystone Books, 2018.

¹⁴Tabák AG, Jokela M, Akbaraly TN, Brunner EJ, Kivimäki M, Witte DR. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet. 2009 Jun 27;373(9682):2215-21. doi: 10.1016/S0140-6736(09)60619-X. Epub 2009 Jun 8. PubMed PMID: 19515410; PubMed Central PMCID: PMC2726723.

¹⁵Taksali SE, Caprio S, Dziura J, Dufour S, Calí AM, Goodman TR, Papademetris X, Burgert TS, Pierpont BM, Savoye M, Shaw M, Seyal AA, Weiss R. High visceral and low abdominal subcutaneous fat stores in the obese adolescent: a determinant of an adverse metabolic phenotype. Diabetes. 2008 Feb;57(2):367-71. doi: 10.2337/db07-0932. Epub 2007 Oct 31. PubMed PMID: 17977954.

¹⁶Fabbrini E, Magkos F, Mohammed BS, Pietka T, Abumrad NA, Patterson BW, Okunade A, Klein S. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15430-5. doi: 10.1073/pnas.0904944106. Epub 2009 Aug 24. PubMed PMID: 19706383; PubMed Central PMCID: PMC2741268.

#17-21

¹⁷Bray GA, Jablonski KA, Fujimoto WY, Barrett-Connor E, Haffner S, Hanson RL, Hill JO, Hubbard V, Kriska A, Stamm E, Pi-Sunyer FX. Relation of central adiposity and body mass index to the development of diabetes in the Diabetes Prevention Program. Am J Clin Nutr. 2008 May;87(5):1212-8. doi: 10.1093/ajcn/87.5.1212. PubMed PMID: 18469241; PubMed Central PMCID: PMC2517222.

¹⁸Fabbrini E, Tamboli RA, Magkos F, Marks-Shulman PA, Eckhauser AW, Richards WO, Klein S, Abumrad NN. Surgical removal of omental fat does not improve insulin sensitivity and cardiovascular risk factors in obese adults. Gastroenterology. 2010 Aug;139(2):448-55. doi: 10.1053/j.gastro.2010.04.056. Epub 2010 May 7. PubMed PMID: 20457158; PubMed Central PMCID: PMC2910849.

¹⁹Jakobsen MU, Berentzen T, Sørensen TI, Overvad K. Abdominal obesity and fatty liver. Epidemiol Rev. 2007;29:77-87. doi: 10.1093/epirev/mxm002. Epub 2007 May 2. Review. PubMed PMID: 17478441.

²⁰Matos LN, Giorelli Gde V, Dias CB. Correlation of anthropometric indicators for identifying insulin sensitivity and resistance. Sao Paulo Med J. 2011 Jan 6;129(1):30-5. doi: 10.1590/s1516-31802011000100006. PubMed PMID: 21437506.

²¹Wander PL, Boyko EJ, Leonetti DL, McNeely MJ, Kahn SE, Fujimoto WY. Change in visceral adiposity independently predicts a greater risk of developing type 2 diabetes over 10 years in Japanese Americans. Diabetes Care. 2013 Feb;36(2):289-93. doi: 10.2337/dc12-0198. Epub 2012 Sep 10. PubMed PMID: 22966093; PubMed Central PMCID: PMC3554282.

#22-28

²²Fujimoto WY, Jablonski KA, Bray GA, Kriska A, Barrett-Connor E, Haffner S, Hanson R, Hill JO, Hubbard V, Stamm E, Pi-Sunyer FX. Body size and shape changes and the risk of diabetes in the diabetes prevention program. Diabetes. 2007 Jun;56(6):1680-5. doi: 10.2337/db07-0009. Epub 2007 Mar 15. PubMed PMID: 17363740; PubMed Central PMCID: PMC2528279.

²³Taylor R, Holman RR. Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond). 2015 Apr;128(7):405-10. doi: 10.1042/CS20140553. PubMed PMID: 25515001.

²⁴Fung J, Teicholz N. The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally. Vancouver: Greystone Books, 2018.

²⁵Ashwell M, Gunn P, Gibson S. Waist-to-height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta-analysis. Obes Rev. 2012 Mar;13(3):275-86. doi: 10.1111/j.1467-789X.2011.00952.x. Epub 2011 Nov 23. Review. PubMed PMID: 22106927.

²⁶Herman ME, O’Keefe JH, Bell DSH, Schwartz SS. Insulin Therapy Increases Cardiovascular Risk in Type 2 Diabetes. Prog Cardiovasc Dis. 2017 Nov – Dec;60(3):422-434. doi: 10.1016/j.pcad.2017.09.001. Epub 2017 Sep 25. Review. PubMed PMID: 28958751.

²⁷Banting W. Letter on corpulence, addressed to the public. 1869. Obes Res. 1993 Mar;1(2):153-63. doi: 10.1002/j.1550-8528.1993.tb00605.x. PubMed PMID: 16350571.

²⁸Hallberg S, Hamdy O. Before You Spend $26,000 on Weight-Loss Surgery, Do This. New York, NY: The New York Times, 2016.

#29-35

²⁹Westman EC, Yancy WS Jr, Mavropoulos JC, Marquart M, McDuffie JR. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond). 2008 Dec 19;5:36. doi: 10.1186/1743-7075-5-36. PubMed PMID: 19099589; PubMed Central PMCID: PMC2633336.

³⁰Villegas R, Liu S, Gao YT, Yang G, Li H, Zheng W, Shu XO. Prospective study of dietary carbohydrates, glycemic index, glycemic load, and incidence of type 2 diabetes mellitus in middle-aged Chinese women. Arch Intern Med. 2007 Nov 26;167(21):2310-6. doi: 10.1001/archinte.167.21.2310. PubMed PMID: 18039989.

³¹Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS One. 2007 Aug 1;2(8):e698. doi: 10.1371/journal.pone.0000698. PubMed PMID: 17668074; PubMed Central PMCID: PMC1931610.

³²Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23-46. doi: 10.1152/physrev.00019.2009. Review. PubMed PMID: 20086073.

³³Lustig RH. Fat Chance: The Bitter Truth About Sugar. London: Fourth Estate, 2013.

³⁴Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. doi: 10.1210/jc.2003-031855. PubMed PMID: 15181085.

³⁵Rho YH, Zhu Y, Choi HK. The epidemiology of uric acid and fructose. Semin Nephrol. 2011 Sep;31(5):410-9. doi: 10.1016/j.semnephrol.2011.08.004. Review. PubMed PMID: 22000647; PubMed Central PMCID: PMC3197219.

#36-42

³⁶Chevassus H, Renard E, Bertrand G, Mourand I, Puech R, Molinier N, Bockaert J, Petit P, Bringer J. Effects of oral monosodium (L)-glutamate on insulin secretion and glucose tolerance in healthy volunteers. Br J Clin Pharmacol. 2002 Jun;53(6):641-3. doi: 10.1046/j.1365-2125.2002.01596.x. PubMed PMID: 12047489; PubMed Central PMCID: PMC1874333.

³⁷Mercola J. Fat for Fuel: A Revolutionary Diet to Combat Cancer, Boost Brain Power, and Increase Your Energy. Carlsbad, CA: Hay House Publishing, 2017.

³⁸Chandalia M, Garg A, Lutjohann D, von Bergmann K, Grundy SM, Brinkley LJ. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N Engl J Med. 2000 May 11;342(19):1392-8. doi: 10.1056/NEJM200005113421903. PubMed PMID: 10805824.

³⁹Stubbs RJ, Mazlan N, Whybrow S. Carbohydrates, appetite and feeding behavior in humans. J Nutr. 2001 Oct;131(10):2775S-2781S. doi: 10.1093/jn/131.10.2775S. Review. PubMed PMID: 11584105.

⁴⁰Cameron JD, Cyr MJ, Doucet E. Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet. Br J Nutr. 2010 Apr;103(8):1098-101. doi: 10.1017/S0007114509992984. Epub 2009 Nov 30. PubMed PMID: 19943985.

⁴¹Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

⁴²Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

#43-47

⁴³Catenacci VA, Pan Z, Ostendorf D, Brannon S, Gozansky WS, Mattson MP, Martin B, MacLean PS, Melanson EL, Troy Donahoo W. A randomized pilot study comparing zero-calorie alternate-day fasting to daily caloric restriction in adults with obesity. Obesity (Silver Spring). 2016 Sep;24(9):1874-83. doi: 10.1002/oby.21581. PubMed PMID: 27569118; PubMed Central PMCID: PMC5042570.

⁴⁴Kondo T, Kishi M, Fushimi T, Ugajin S, Kaga T. Vinegar intake reduces body weight, body fat mass, and serum triglyceride levels in obese Japanese subjects. Biosci Biotechnol Biochem. 2009 Aug;73(8):1837-43. doi: 10.1271/bbb.90231. Epub 2009 Aug 7. PubMed PMID: 19661687.

⁴⁵Sugiyama M, Tang AC, Wakaki Y, Koyama W. Glycemic index of single and mixed meal foods among common Japanese foods with white rice as a reference food. Eur J Clin Nutr. 2003 Jun;57(6):743-52. doi: 10.1038/sj.ejcn.1601606. PubMed PMID: 12792658.

⁴⁶Johnston CS, Steplewska I, Long CA, Harris LN, Ryals RH. Examination of the antiglycemic properties of vinegar in healthy adults. Ann Nutr Metab. 2010;56(1):74-9. doi: 10.1159/000272133. PubMed PMID: 20068289.

⁴⁶Kondo S, Tayama K, Tsukamoto Y, Ikeda K, Yamori Y. Antihypertensive effects of acetic acid and vinegar on spontaneously hypertensive rats. Biosci Biotechnol Biochem. 2001 Dec;65(12):2690-4. doi: 10.1271/bbb.65.2690. PubMed PMID: 11826965.

⁴⁷Kondo T, Kishi M, Fushimi T, Kaga T. Acetic acid upregulates the expression of genes for fatty acid oxidation enzymes in liver to suppress body fat accumulation. J Agric Food Chem. 2009 Jul 8;57(13):5982-6. doi: 10.1021/jf900470c. PubMed PMID: 19469536.

#48-54

⁴⁸Johnston CS, Buller AJ. Vinegar and peanut products as complementary foods to reduce postprandial glycemia. J Am Diet Assoc. 2005 Dec;105(12):1939-42. doi: 10.1016/j.jada.2005.07.012. PubMed PMID: 16321601.

⁴⁹Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Vancouver: Greystone Books, 2016.

⁵⁰Le Stunff C, Bougnères P. Early changes in postprandial insulin secretion, not in insulin sensitivity, characterize juvenile obesity. Diabetes. 1994 May;43(5):696-702. doi: 10.2337/diab.43.5.696. PubMed PMID: 8168647.

⁵¹Lingvay I, Guth E, Islam A, Livingston E. Rapid improvement in diabetes after gastric bypass surgery: is it the diet or surgery?. Diabetes Care. 2013 Sep;36(9):2741-7. doi: 10.2337/dc12-2316. Epub 2013 Mar 25. PubMed PMID: 23530013; PubMed Central PMCID: PMC3747905.

⁵²Schauer PR, Bhatt DL, Kirwan JP, Wolski K, Aminian A, Brethauer SA, Navaneethan SD, Singh RP, Pothier CE, Nissen SE, Kashyap SR. Bariatric Surgery versus Intensive Medical Therapy for Diabetes – 5-Year Outcomes. N Engl J Med. 2017 Feb 16;376(7):641-651. doi: 10.1056/NEJMoa1600869. PubMed PMID: 28199805; PubMed Central PMCID: PMC5451258.

⁵³O’Gorman DJ, Karlsson HK, McQuaid S, Yousif O, Rahman Y, Gasparro D, Glund S, Chibalin AV, Zierath JR, Nolan JJ. Exercise training increases insulin-stimulated glucose disposal and GLUT4 (SLC2A4) protein content in patients with type 2 diabetes. Diabetologia. 2006 Dec;49(12):2983-92. doi: 10.1007/s00125-006-0457-3. Epub 2006 Sep 26. PubMed PMID: 17019595.

⁵⁴Boulé NG, Haddad E, Kenny GP, Wells GA, Sigal RJ. Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus: a meta-analysis of controlled clinical trials. JAMA. 2001 Sep 12;286(10):1218-27. doi: 10.1001/jama.286.10.1218. Review. PubMed PMID: 11559268.

#55-60

⁵⁵Fung J, Teicholz N. The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally. Vancouver: Greystone Books, 2018.

⁵⁶Taksali SE, Caprio S, Dziura J, Dufour S, Calí AM, Goodman TR, Papademetris X, Burgert TS, Pierpont BM, Savoye M, Shaw M, Seyal AA, Weiss R. High visceral and low abdominal subcutaneous fat stores in the obese adolescent: a determinant of an adverse metabolic phenotype. Diabetes. 2008 Feb;57(2):367-71. doi: 10.2337/db07-0932. Epub 2007 Oct 31. PubMed PMID: 17977954.

⁵⁷Bawden S, Stephenson M, Falcone Y, Lingaya M, Ciampi E, Hunter K, Bligh F, Schirra J, Taylor M, Morris P, Macdonald I, Gowland P, Marciani L, Aithal GP. Increased liver fat and glycogen stores after consumption of high versus low glycaemic index food: A randomized crossover study. Diabetes Obes Metab. 2017 Jan;19(1):70-77. doi: 10.1111/dom.12784. Epub 2016 Sep 29. PubMed PMID: 27593525.

⁵⁸Angulo P, Lindor KD. Non-alcoholic fatty liver disease. J Gastroenterol Hepatol. 2002 Feb;17 Suppl:S186-90. doi: 10.1046/j.1440-1746.17.s1.10.x. Review. PubMed PMID: 12000605.

⁵⁹Holt SH, Miller JC, Petocz P. An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr. 1997 Nov;66(5):1264-76. doi: 10.1093/ajcn/66.5.1264. PubMed PMID: 9356547.

⁶⁰Nuttall FQ, Gannon MC. Plasma glucose and insulin response to macronutrients in nondiabetic and NIDDM subjects. Diabetes Care. 1991 Sep;14(9):824-38. doi: 10.2337/diacare.14.9.824. Review. PubMed PMID: 1959475.

#61-66

⁶¹Pepino MY, Tiemann CD, Patterson BW, Wice BM, Klein S. Sucralose affects glycemic and hormonal responses to an oral glucose load. Diabetes Care. 2013 Sep;36(9):2530-5. doi: 10.2337/dc12-2221. Epub 2013 Apr 30. PubMed PMID: 23633524; PubMed Central PMCID: PMC3747933.

⁶²Just T, Pau HW, Engel U, Hummel T. Cephalic phase insulin release in healthy humans after taste stimulation?. Appetite. 2008 Nov;51(3):622-7. doi: 10.1016/j.appet.2008.04.271. Epub 2008 May 10. PubMed PMID: 18556090.

⁶³Masharani U, Sherchan P, Schloetter M, Stratford S, Xiao A, Sebastian A, Nolte Kennedy M, Frassetto L. Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. Eur J Clin Nutr. 2015 Aug;69(8):944-8. doi: 10.1038/ejcn.2015.39. Epub 2015 Apr 1. PubMed PMID: 25828624.

⁶⁴Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84. doi: 10.1093/ajcn/80.5.1175. PubMed PMID: 15531663; PubMed Central PMCID: PMC1270002.

⁶⁵Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46. doi: 10.3945/ajcn.2009.27725. Epub 2010 Jan 13. PubMed PMID: 20071648; PubMed Central PMCID: PMC2824152.

⁶⁶Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707. PubMed PMID: 23386268; PubMed Central PMCID: PMC4688426.

#67-72

⁶⁷Westman EC, Yancy WS Jr, Mavropoulos JC, Marquart M, McDuffie JR. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond). 2008 Dec 19;5:36. doi: 10.1186/1743-7075-5-36. PubMed PMID: 19099589; PubMed Central PMCID: PMC2633336.

⁶⁸Jackson IM, McKiddie MT, Buchanan KD. Effect of fasting on glucose and insulin metabolism of obese patients. Lancet. 1969 Feb 8;1(7589):285-7. doi: 10.1016/s0140-6736(69)91039-3. PubMed PMID: 4178981.

⁶⁹Catenacci VA, Pan Z, Ostendorf D, Brannon S, Gozansky WS, Mattson MP, Martin B, MacLean PS, Melanson EL, Troy Donahoo W. A randomized pilot study comparing zero-calorie alternate-day fasting to daily caloric restriction in adults with obesity. Obesity (Silver Spring). 2016 Sep;24(9):1874-83. doi: 10.1002/oby.21581. PubMed PMID: 27569118; PubMed Central PMCID: PMC5042570.

⁷⁰Halberg N, Henriksen M, Söderhamn N, Stallknecht B, Ploug T, Schjerling P, Dela F. Effect of intermittent fasting and refeeding on insulin action in healthy men. J Appl Physiol (1985). 2005 Dec;99(6):2128-36. doi: 10.1152/japplphysiol.00683.2005. Epub 2005 Jul 28. PubMed PMID: 16051710.

⁷¹Levine B, Klionsky DJ. Autophagy wins the 2016 Nobel Prize in Physiology or Medicine: Breakthroughs in baker’s yeast fuel advances in biomedical research. Proc Natl Acad Sci U S A. 2017 Jan 10;114(2):201-205. doi: 10.1073/pnas.1619876114. Epub 2016 Dec 30. PubMed PMID: 28039434; PubMed Central PMCID: PMC5240711.

⁷²Natalucci G, Riedl S, Gleiss A, Zidek T, Frisch H. Spontaneous 24-h ghrelin secretion pattern in fasting subjects: maintenance of a meal-related pattern. Eur J Endocrinol. 2005 Jun;152(6):845-50. doi: 10.1530/eje.1.01919. PubMed PMID: 15941923.

#73-78

⁷³Merimee TJ, Tyson JE. Stabilization of plasma glucose during fasting; Normal variations in two separate studies. N Engl J Med. 1974 Dec 12;291(24):1275-8. doi: 10.1056/NEJM197412122912404. PubMed PMID: 4431434.

⁷⁴Zauner C, Schneeweiss B, Kranz A, Madl C, Ratheiser K, Kramer L, Roth E, Schneider B, Lenz K. Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine. Am J Clin Nutr. 2000 Jun;71(6):1511-5. doi: 10.1093/ajcn/71.6.1511. PubMed PMID: 10837292.

⁷⁵Fothergill E, Guo J, Howard L, Kerns JC, Knuth ND, Brychta R, Chen KY, Skarulis MC, Walter M, Walter PJ, Hall KD. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity (Silver Spring). 2016 Aug;24(8):1612-9. doi: 10.1002/oby.21538. Epub 2016 May 2. PubMed PMID: 27136388; PubMed Central PMCID: PMC4989512.

⁷⁶Fildes A, Charlton J, Rudisill C, Littlejohns P, Prevost AT, Gulliford MC. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015 Sep;105(9):e54-9. doi: 10.2105/AJPH.2015.302773. Epub 2015 Jul 16. PubMed PMID: 26180980; PubMed Central PMCID: PMC4539812.

⁷⁷Smooke S, Horwich TB, Fonarow GC. Insulin-treated diabetes is associated with a marked increase in mortality in patients with advanced heart failure. Am Heart J. 2005 Jan;149(1):168-74. doi: 10.1016/j.ahj.2004.07.005. PubMed PMID: 15660049.

⁷⁸Johnson JA, Gale EA. Diabetes, insulin use, and cancer risk: are observational studies part of the solution-or part of the problem?. Diabetes. 2010 May;59(5):1129-31. doi: 10.2337/db10-0334. PubMed PMID: 20427699; PubMed Central PMCID: PMC2857892.

#79-80

⁷⁹Stoekenbroek RM, Rensing KL, Bernelot Moens SJ, Nieuwdorp M, DeVries JH, Zwinderman AH, Stroes ES, Currie CJ, Hutten BA. High daily insulin exposure in patients with type 2 diabetes is associated with increased risk of cardiovascular events. Atherosclerosis. 2015 Jun;240(2):318-23. doi: 10.1016/j.atherosclerosis.2015.03.040. Epub 2015 Mar 30. PubMed PMID: 25864162.

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