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The big fat diabetes solution

Reading time: 25 minutes

Greg Perry stared down at the hole in his left foot. A few months earlier it was just a raw blister caused by his boot, but now the wound spread like a fried egg across his sole – a hollowed pink yolk surrounded by grayish-white flesh that peeled up and crusted in burnt yellow edges.

His Toronto foot and ankle specialist, Christopher Lu, was blunt. “What’s happening out here,” he nodded to the ugly diabetic foot ulcer, “is also happening in here,” he said, tapping lightly on Perry’s chest.

“The way you’re going Greg, you’re going to die. That fat around your belly is also around your organs. It’s killing you.”

“I want to live to see my grandkids,” Perry thought afterward, as he slumped in his car and started to cry.

His older brother Roy had diabetic foot ulcers too, but they had turned dark and gangrenous. Somewhere in the world, doctors amputate a diabetic foot or limb every 30 seconds. There are 73,000 amputations of diabetic ulcers every year in the United States alone. Roy had his left leg amputated at the knee. After that, he used to use his right foot to push his wheelchair around.

Because diabetes had deadened his nerves, he hadn’t felt the pressure wound this was causing, and a blister festered and spread up his calf. Roy was scheduled to have his right leg amputated, too, but he had died of a heart attack first. He was 68. Greg was 62.

He didn’t really need Dr Lu to tell him his diabetes was out of control. He had been diagnosed with Charcot foot, a kind of degenerative foot arthritis linked to high blood sugar that causes joints to weaken, first in his right foot, then in his left.

Perry wore special ski boot-like footwear to immobilize his twisted, softened foot bones. The ulcer was a common complication. Perry weighed over 300 pounds, the bulk of which he carried in his swollen abdomen, which jutted out in front of him like an overdue pregnant belly.

Those pounds had packed on, not receded, with treatment. Every visit to the diabetes specialist nurse had resulted in more drugs and a bigger weigh-in, though he was doing everything he has been told to do: metformin pills to lower his blood sugar, more pills for high blood pressure and to lower cholesterol.

He was counting his calories and cutting his fats, but when his blood sugar spiked, he was given more metformin. When it climbed again, insulin was added to the mix. He started at 10 units a day, but the dose was upped at each visit until he was taking 74 units each day. His belly had ballooned in tandem.

The result of his last hemoglobin A1C test, which measures long-term blood sugar based on the rate of oxygen-carrying red blood cells coated in sugar, was 10 percent. Eight percent is a red flag for dangerous blood sugar levels. A healthy result is somewhere between 4 and 5.9.

Cracking the code
While he was at a conference in California a few months before this appointment with Dr Lu, Perry had run into an old friend who was looking fabulous. His friend told him that his son had lost 60 pounds and he had lost 40 pounds following the books of Toronto kidney specialist Jason Fung, author of The Diabetes Code (Greystone Books, 2018) and The Obesity Code (Greystone Books, 2016).

Perry had been to see Jason Fung, but had dismissed his advice about the benefits of intermittent fasting and eating quality fats. “I can’t fast!” he’d thought. “I’m a diabetic. I’ll die! This guy is crazy.”

Perry’s diabetes nurse had agreed that it was dangerous, quack advice. Everyone knew fat was very bad and fasting was ridiculous, she said, as she increased his insulin prescription.

Now, after Dr Lu’s devastating assessment, Perry was ready to give Dr Fung’s office another call. He enrolled in a class starting in December 2018, at the Intensive Dietary Management Program that Fung had founded with researcher Megan Ramos, who had overcome her own diagnoses (at age 12) of nonalcoholic fatty liver and, later, type 2 diabetes.

Ten months later, Perry’s transformation, like that of thousands of other diabetic and obese patients, is the reason why low-carb and high-fat ketogenic diets are the fastest-growing food phenomenon. Perry shed 50 pounds, dropping from over 300 to 252. He lost nine inches from his waist. His A1C scores plummeted from a usual of 10 or 11 to between 6 and 7 percent.

With Dr Fung’s help, he weaned himself off of insulin, until after just four months he had stopped taking it altogether. “I still take the metformin, but when I get down below six consistently, I’ll go off of that too. A photo of his foot ulcer reveals that it has healed dramatically and almost disappeared.

What the fat?
Since public health agencies have for decades cited fat as the chief villain in type 2 diabetes, how can eating more fat, rather than cutting it – along with eating fewer carbohydrates and more calories overall – result in less fat around the waist, lower blood sugar levels, and reduced need for insulin medication in people with type 2 diabetes?

Clearly, overweight must feature in the diabetes epidemic. It’s well established that being obese is the strongest risk factor for type 2 diabetes, and both of these conditions are soaring.

Worldwide, diabetes prevalence has quadrupled in just three decades and surged to ninth place among leading causes of death. Nearly one in 10 adults around the globe now has the condition, which is well-recognized as a “lifestyle” or diet-related disease – unlike type 1 diabetes, which involves an autoimmune attack on the pancreas.

Even children are being affected. The world’s youngest type 2 diabetic – three years old – was diagnosed in Texas a few years ago. In the UK, where no children had type 2 diabetes only 20 years ago, now one in five kids is obese by age 11, and the rate of pediatric type 2 diabetes has doubled in the past five years.1

The rise of the resistance
Type 2 diabetes is diagnosed based on high blood sugar levels. The hormone insulin keeps blood sugar at a steady state within a narrow range. When you need more and more insulin to keep your blood sugar steady at the same level, that’s called insulin resistance – the key condition leading to type 2 diabetes.

In patients like Greg Perry, the medical response is to give more and more of the drug insulin to maintain a safe level of blood sugar, but that doesn’t solve the underlying problem of why a person’s blood sugar is soaring in the first place.
The public health picture that has emerged shows obesity and diabetes holding hands.

From doctors, dieticians and public health programs, we have been given the idea that if we just kick fat to the curb – eating less nasty saturated fats and more healthy vegetable fats and carbohydrates – and we exercise a lot more, not only will we ditch obesity, but diabetes will go away, too.

But recent research is throwing up problems with that picture. In the past decade, for example, Samuel Klein and his team of scientists at Washington University School of Medicine have established that not all body fat is the same when it comes to diabetes.

Just losing (or surgically removing) fat from the belly, for example, does not affect the underlying metabolic problem of insulin resistance that leads to diabetes.

Fat around the organs, called visceral fat, is more dangerous than fat under the skin, and a fatty liver is a hallmark of insulin resistance.2

The bad news we don’t hear so often: you can be thin but have a fatty liver. You can look in the mirror and think you’re fine, but be packing liver fat and be insulin resistant, which puts you at risk for all the same diseases that obese people suffer.

Forty percent of the normal-weight population have the exact same metabolic disorder and fatty liver that 80 percent of obese people have – and they are at the same risk of diabetes, according to pediatric endocrinologist Robert Lustig.

Nonalcoholic fatty liver disease, a condition that didn’t exist a generation ago, is now the leading cause of liver transplant, and its prevalence is growing faster than obesity or diabetes, increasing 700 percent between 2002 and 2017.3

“There are more thin sick people (67 million in America) than fat sick people, and the thin sick people are calling the fat sick people the problem,” Lustig told the weight loss program JumpstartMD.

Lustig said studies have shown that the blood sugar levels of apparently healthy adults have remained the same for the past 40 to 50 years, but the need for insulin in these “healthy” adults has risen two- to four-fold to keep the level of glucose the same.

Immune problem
There is growing evidence that the immune system and underlying inflammation are involved in both obesity and diabetes. It’s the oxidation of fatty acids, not the breakdown of glucose, that activates inflammation in healthy cells, according to a study published last year by researchers from Boston University School of Medicine, Massachusetts Institute of Technology and the University of Kentucky. 4

“The blood glucose paradigm seems to be slowly but surely fading away,” says one of the paper’s authors, molecular immunologist Barbara Nikolajczyk of Boston University.

She points to a landmark 2009 study in diabetic veterans, in whom intensive insulin management of their blood glucose levels did not affect cardiovascular events or deaths.5

In other words, adding insulin to the high blood glucose problem does nothing to solve the underlying disease, which the researchers found is driven by fatty acid metabolites.

“It’s not clear where those fats are coming from,” said Nikolaczyk. “Certainly, your body makes fats and changes fats. Anything you eat is going to be laundered through the liver and be changed.”

Homemade fat
Researchers do know that the fat stuffing the livers of people with insulin resistance and type 2 diabetes comes from a process called de novo lipogenesis – the creation of new fats from scratch.

The liver makes this fat chiefly from fructose, which is not just found in fruits but also in table sugar, honey, maple syrup and everything sugar is added to from candies and cookies to ketchup and salad dressings.

Liver fat and body fat are difficult to utilize compared to glycogen, which is the easily burned body fuel that the liver makes from glucose in carbohydrates.

Fung uses a freezer/fridge analogy with groceries representing the glycogen fuel. If you’ve come home with way more food than you need and stuffed your kitchen fridge (glycogen stores in the liver), you can’t leave the rest to rot on your high-traffic counter (the blood serum), so you put it in the big freezer in the basement, stored as triglycerides or body fat that is harder to get to.

Insulin is like a traffic cop that will direct the excess glucose to the fat freezer in the basement. So long as insulin is hanging around, though, all traffic is flowing to the freezer, and you can’t take anything out. You have to wait for insulin to retreat before you can unpack your stored fat.

Wrong villain
Public health has not only wrongly vilified traditionally consumed saturated fats found in things like animal meat, butter, cream, cheese and coconut oil while promoting insulin-spiking carbohydrates, thinks Fung, but he traces the origins of the diabetes epidemic to the “infamous” 1980 dietary guidelines in which “the fattening carbohydrate was reborn as a healthy whole grain.”

Carbohydrates break down into glucose, which is met by a high spike of insulin that packs excess sugar away to the inaccessible deep freezer of fat. It is carbohydrates that get turned into highly saturated fat in the liver through de novo lipogenesis and are the real culprits behind triglyceride body fat.

“Eating dietary carbohydrates, not dietary saturated fat, increases saturated fat levels in the blood,” according to Fung. “Saturated fat levels in the blood, not the diet, are associated with cardiovascular disease.”

The trouble with high-carbohydrate diets and the success of low-carbohydrate diets have become apparent enough that even the American Diabetes Association 2019 dietary guidelines, for the first time in decades, give a nod to low-carb eating.

They hasn’t wavered on saturated fats yet, but dietary saturated fat has been repeatedly shown to be protective against metabolic diseases.

Fung points to the Tokelau Migrants study as an example, where eating lots of coconut as part of their traditional diet led to a population of islanders having extremely high saturated fat levels.6 “There was virtually no obesity or diabetes,” said Fung. “When they changed to a Western diet, they got fat and diabetic. So, no, saturated fats in humans are unlikely to cause type 2 diabetes.”

A 2016 study also found that perhaps the most protective fats are mono-unsaturated fats, which are found at high levels in red meat, whole dairy, nuts, avocados and olives.7

It’s really the processing of fats that has made them dangerous. It turns out the fatty acid with the least benefit is the one recommended most by public health agencies: polyunsaturated fats (PUFAs) from vegetable oils.

Balancing fatty acids
Studies have shown that omega-3 fats like those found in oily fish have an anti-inflammatory effect. In contrast, the omega-6 fats in the polyunsaturated seed oils like corn and sunflower oil that are recommended by public health guidelines tend to fuel inflammation because of the processing they’ve undergone.

They are oxidized and rendered to a rancid state that promotes the chronic low-grade inflammation underlying diabetes and other diseases.

Because of their abundance in cooking oils, omega-6 oil consumption has increased dramatically. The omega-6 to omega-3 ratio of roughly 1:1 estimated in traditional diets has risen to 20:1 or higher, in parallel with astronomical rises in obesity and diabetes.

Research has shown that lowering that ratio from 18:1 to 3:1 reduces this disease-causing inflammation. The goal, then, should be to consume no more than twice the amount of omega-6 as omega-3 fats to lower the ratio to an optimal 1:1 to 2:1.1

In clinical studies, lowering the ratio of omega-6 to omega-3 fats from 18:1 to 3:1 led to a reduction in markers of inflammation

Public health enemy: fructose
Trans fats, or industrial oils, have also been identified as metabolic disasters. Starting in the 1950s, they were synthesized and commonly added to things like margarine to make it spreadable and to crackers and cookies to give them a long shelf-life.

Research established their link to obesity and cardiovascular disease, and they were shown to fuel the liver’s de novo lipogenesis fat-making machine.

These days, no one is denying the role of trans fats in disease. Both the United States and Canada banned their use by the food industry in 2018, for example.

But public enemy number two is proving much harder to eradicate. As Robert Lustig eloquently illustrated to the masses a decade ago, sugar is fueling the obesity crisis. Table sugar, or sucrose, is one molecule of burnable glucose and
one molecule of fructose, which our liver can do nothing with but pack away as fat through de novo lipogenesis.

“It’s long been known that both ‘lipotoxicity’ and ‘glucotoxicity’ are associated with inflammation leading to diabetes,” he explains. “But it wasn’t clear which, when and how, resulting in different factions battling for supremacy. The science of this controversy is now beginning to come into focus.”

He points to a recent paper in Cell Metabolism showing how fructose impairs the function of mitochondria, the cell’s powerhouses that burn fuel to produce energy.8

Combine that with the work of Nikolajczyk’s team showing that fat burning is impaired in type 2 diabetes, and Lustig thinks the villain is obvious.

“Apart from its calories, sugar is bad for two reasons: it turns into fat in the liver, and it mucks up the mitochondria, the little energy burning factories inside each cell. Both of these result in a process known as insulin resistance, which leads to chronic disease.”

The benefits of nothing
The fastest way to correct the problem of too much glucose and too much insulin, says Fung, is to fast. Going without food, rather than just low-calorie, puts insulin to rest, so fat in the freezer can burn.

Intermittent fasting, be it skipping breakfast, eating one meal a day, fasting five or six 16-hour periods a week or two or three 24-hour periods or longer, switches the body to fat-burning mode.

Low-calorie diets eventually fail because metabolism slows to match the decreased energy intake, as illustrated in a study of Biggest Loser contestants, all but one of whom regained most of the weight they lost on camera within six years.9 In contrast, studies of alternate-day fasting show that basal metabolism stays steady even after 22 days.10

Short-term fasting corrects the underlying cycles of excess by ridding the body of those excesses, not merely masking the symptom of high blood sugar. Plus, unlike other diets, fasting is free: it requires no food shopping, special meal preparation, or calorie or carb counting.

Whether you eat low carb or keto to keep insulin levels down between fasts is up to you, but allowing the body time to recover without digesting is key.

On the first day Greg Perry went to Dr Fung’s clinic, he decided to fast and went 27 hours without food or sugary drinks. “I was surprised,” he says. “I felt really good.”

His Charcot feet keep him from the benefits of vigorous exercise, but he has narrowed his eating to just once a day and fasts longer from time to time. Every weigh-in and every blood test result has been in the right direction.

Now, along with the crowds of people that are flouting public health’s advice, ditching their Diet Cokes and pastas, fasting but also enjoying prohibited fatty foods when they feast, he’s celebrating. “There’s no way I’m going back,” Perry says. “I can’t even picture it.”

Toxic insulin
Mainstream medicine’s answer for type 2 diabetes, as Greg Perry discovered, consists of insulin and more insulin, while treating complications like foot ulcers, kidney problems and heart disease as they arise.

Nephrologist Jason Fung is a rare doctor who has questioned what all this insulin is actually doing in the diabetes picture. When a patient has consumed a lot of sugar, a lot of insulin is released to deal with it. High insulin levels cause insulin resistance in a vicious loop of high sugar, high insulin, more resistance and so on.

Medicine has merely relied on injected insulin to force cells to accept more glucose in order to lower the glucose levels in the blood – without thought to the consequences.

Fung asks a question doctors seldom do: “If this high glucose level was toxic in the blood, why wouldn’t it also be toxic inside the cells?”

“Insulin doesn’t eliminate glucose from the body; it merely shoves the excess out of the blood and forces it into the cells, anywhere: eyes, kidneys, nerves, heart,” Fung explains. “Over time, all the organs simply start rotting from too much glucose.”

Unlike people with type 1 diabetes, who have high blood sugar because they have no natural insulin production and need it, type 2 diabetics already have too much insulin, and doctors prescribe them more, making them sicker still.

High insulin itself triggers other problems. Both high blood sugar and high insulin force the body to excrete magnesium, for example. Since magnesium is essential for insulin and blood sugar regulation, the depletion can trigger a downward spiral of deficiency linked to high blood sugar.1

Leptin is the hormone that regulates appetite, and high insulin can also cause leptin resistance, so your brain thinks you’re starving. “The higher your insulin goes, the more weight you gain and the hungrier you get,” explains Lustig.

And remember the analogy of insulin as a one-way traffic cop, directing glucose to the glycogen freezer? When insulin is around, you can’t burn stored fat. “The reason insulin resistance develops in all the organs and in all peoples of the world is precisely to shield against this toxic sugar load.”

A calorie is not a calorie
In a key 2015 experiment by Lustig’s team, 43 obese children with at least one other chronic metabolic disorder, such as hypertension, high triglycerides or a marker of fatty liver, were given nine days of food that restricted sugar but substituted starch to maintain the same fat, protein, carbohydrate and calorie levels as their previously reported home diets.

Whole fruit was permitted, because the fiber in fruit offsets the ill effects of fructose, which is why high fiber is a benefit to diabetics. But the rest of the non-sugar calories came from processed foods like hot dogs, potato chips and pizza – just no sugary cereals, soda, pastry or sweetened yogurt.

The children were weighed daily, and if they started to shed weight they were told to eat more. Interestingly, some said it felt like too much food.

At the end of the nine days on the sugar-restricted diet, the children’s metabolic health had vastly improved without a change in weight. Their blood pressure dropped, triglycerides fell 33 points, LDL “bad” cholesterol decreased by 10 points, and liver function tests improved. Fasting blood glucose dropped five points, and insulin levels were cut by one-third.

“This study demonstrates that ‘a calorie is not a calorie.’ Where those calories come from determines where in the body they go,” said Lustig. Sugar calories are the worst, because they turn to fat in the liver, driving insulin resistance and, in turn, upping the risk for diabetes, heart and liver disease.1

Kinder, gentler keto

Dr Arthur Agatston, originator of the low-carb South Beach Diet, has modified the diet to be ‘keto-friendly’ after discovering that it can help reverse insulin resistance and diabetes, and wipe out belly fat to boot.

The Keto-Friendly South Beach Diet is not just low carb. It’s definitely not low fat. And it’s not a strict ketogenic diet.

This new approach includes the best of the original South Beach Diet (good carbs, good fats) as well as some of the best practices of the keto diet – including low carb/high “full” fat and a longer initial phase to reverse sugar addiction and become “fat adapted.”

And it incorporates additional science-backed recommendations that promote fat burning and numerous health benefits such as controlling or reversing signs of diabetes, reso
lution of insulin resistance, weight loss, increased energy and mental clarity.

Unlike strict ketogenic diets, this plan does not require that you be in ketosis – a metabolic state where your body is burning only fat (no carbs) for fuel – to reap these benefits.

The Keto-Friendly South Beach Diet allows a higher level of carbohydrates than strict keto, but it is still solidly low carb and fat burning.

It recommends higher amounts of healthy fats, including full-fat dairy, than the original South Beach Diet. It also includes more protein than strict keto diets, which is especially important as you get older and is one of the keys to feeling satisfied after a meal.

On a strict keto diet, carbohydrates are typically restricted to fewer than 5 percent of total calories, with fat providing around 75 percent and protein accounting for the remaining 20 percent.

The keto-friendly approach
This diet falls into the category of a less strict, “keto-friendly” low-carb option. The plan allows roughly 20 to 50 grams of net carbs per day to start, increasing to as much as 100 grams after you are fat adapted and have lost your belly and your insulin resistance.

This diet does not require you to monitor ketone levels.When you lower the insulin levels in your bloodstream, the resulting hormonal effect on the cells in your body allows you to essentially “unlock” your fat stores, and your belly fat melts away without being in full ketosis.

This has been demonstrated in many clinical trials of low-carbohydrate diets. In one major study, people with insulin resistance who followed a similar low-carb diet burned up to 478 more calories per day than those on a higher-carb diet – while eating the same number of daily calories.1

Phase 1
Phase 1 is the more stringent “low-carb” phase. You’ll stay on this phase for as long as you wish to continue more rapid weight loss and until your cravings are truly under control. You can always come back to Phase 1 if you feel that you’ve gotten carried away with additional starches. Often after a vacation with some expected refined carb indulgences, you will want to return to Phase 1.

On Phase 1, your goal is to keep your net carbohydrate intake at 50 grams per day or less. Carbohydrates are not just found in sugars, starches and grains, but also in healthy foods such as vegetables, nuts and dairy products.

That’s where you’ll be getting most of your carbohydrates in this phase, but they will make up a small percentage of your daily intake, with filling protein and fat providing the rest.

When you’re on Phase 1, you’ll eat a lot of non-starchy vegetables, including broccoli, asparagus, cauliflower and zucchini, as well as healthy fats such as full-fat dairy and olive oil.

You’ll also be consuming fat contained in high-quality protein-rich foods such as fish, meat, poultry and eggs. Ultimately, you will be able to incorporate a small amount of higher-carbohydrate foods, such as lentils and black beans, into your diet.

Phase 2
Phase 2 is the lifestyle phase, although you may continue to lose weight, depending on your food selections. You’ll transition to Phase 2 once you reach your weight loss goals or whenever you feel you need a little more flexibility. Depending on your level of insulin resistance, blood test results and personal preferences, you may find that slower weight loss with the additional food options in Phase 2 is most sustainable. If you have subcutaneous fat to lose beyond your belly fat, be aware that this is a slower process and can be accomplished over a longer period on Phase 1or Phase 2.

When on Phase 2, you’ll be able to slowly increase your net carbs until you find what works best for you.

Most people find their sweet spot between 75 grams and 100 grams of net carbs per day, but if you are still insulin resistant after Phase 1, or a postmenopausal woman, you may benefit from keeping your net carbohydrates at 50 grams or less on most days, indefinitely.

Phase 2 allows for slightly more carbs than Phase 1, but your diet should still remain high in protein – don’t let carbohydrates push other food sources off your plate. The basics will be the same, but you will add whole fruits with a lower glycemic index, high-protein and high-fiber grains and a wider variety of beans, along with higher-starch veggies such as sweet potatoes.

In many ways, Phase 2 is very similar to Phase 1, just more relaxed and friendly for life.

When to transition from Phase 1 to Phase 2
How can you tell when it’s time to move on from Phase 1 to Phase 2? If most of the following statements are true for you, you are likely ready to transition.

• You have been on Phase 1 for at least one month
• You are fat adapted, with increased energy and endurance
• Cravings, frequent hunger throughout the day and sugar addiction have all resolved
• Weight loss has slowed because your belly fat and waist circumference have substantially decreased
• You have evidence of metabolic improvements on blood testing: your blood triglycerides are below 75, liver enzymes are normal and hemoglobin A1C has decreased to no higher than 5.7
• You have reached your weight-loss goal

12 rules for keto-friendly eating
1) Minimize sugars
2) Strictly avoid refined carbohydrates
3) Limit snacking
4) Favor fewer, larger meals over frequent small meals
5) Maximize the healthiest fats
6) Consume full-fat dairy
7) Limit omega-6 vegetable oils
8) Eat a variety of non-starchy vegetables
9) Enjoy a wide variety of meats, poultry and seafood
10) Eat primarily whole foods

11) Eat slowly
12) Be flexible

Phase 1: Breakfast
Coffee and hazelnut muffins
Yields 6 large muffins (1 muffin per serving)
These gorgeous nutty muffins taste as good as they look. They will get you started in the morning and also make a great pick-me-up snack to pack in your lunch box.

For the muffins
3 large eggs
¼ cup strong coffee
¼ cup powdered erythritol sweetener
¹⁄³ cup unsalted butter, softened to room temperature
2 Tbsp hazelnut oil (or substitute more butter)

2 Tbsp ground flaxseed or ground chia seeds
¼ cup coconut flour
¹⁄³ cup plus 2 Tbsp lightly toasted hazelnuts, ground (reserve 2 Tbsp for garnish)
½ tsp baking soda
½ tsp baking powder
¼ tsp Himalayan pink salt
1 tsp cinnamon (optional)
For the frosting
½ cup heavy cream
¼ cup powdered erythritol sweetener
½ cup full-fat cream cheese
2 Tbsp instant coffee, mixed with 2 Tbsp water
1 tsp vanilla extract

1) Preheat the oven to 350°F/177°C. Line a 6-cup muffin tin with silicone cups or paper cupcake liners (or grease them with butter) and set aside.
2) Whisk the eggs, coffee and powdered erythritol sweetener together in a large bowl. Add all the remaining muffin ingredients to the bowl and whisk until thoroughly mixed.
3) Divide the batter among the prepared cups and bake for about 18 to 20 minutes, or until a toothpick inserted in the center of the cup comes out clean.
4) Transfer the muffins to a wire rack and let them cool to room temperature.
5) Whisk together all the frosting ingredients until creamy and smooth and frost the cooled muffins. Sprinkle the muffins with the remaining 2 Tbsp of
ground toasted hazelnuts and serve.

The muffins will keep in an airtight container in the refrigerator for up to 3 days, or you may freeze the muffins – without the frosting – for up to 2 months.

Phase 2: Breakfast
Blueberry waffles with lemon cream cheese frosting
Yields 2 large waffles (half a waffle per serving)

To make the frosting, you’ll need powdered erythritol sweetener, which has a texture similar to powdered sugar. If all you have is granulated erythritol, you can turn it into powder by processing it in a blender or a food processor for about 20 to 30 seconds.

3 large eggs
½ cup unsweetened vanilla almond milk
5 Tbsp unsalted butter, melted
1 tsp vanilla extract
¾ cup almond flour
¼ cup tapioca flour
½ cup unflavored whey protein powder
½ tsp baking soda
1 tsp baking powder
¼ tsp sea salt
1 Tbsp granulated erythritol sweetener
½ cup frozen wild blueberries
For the frosting
2 Tbsp unsalted butter, softened
3 Tbsp cream cheese, softened
1 tsp vanilla extract
2 tsp lemon juice
¼ tsp lemon zest
¾ cup powdered erythritol
1-2 Tbsp unsweetened vanilla almond milk

1) Preheat a waffle iron to medium-high heat.
2) Separate the egg yolks from the whites and place in separate bowls. Add the egg yolks to a bowl with the milk, butter and vanilla. Whisk until combined. Set the mixture aside.
3) In a separate bowl, combine the flour, whey protein powder, baking soda, baking powder, sea salt and erythritol.
4) Fold the dry ingredients into the wet ingredients, stirring just enough to combine them.
5) Beat the reserved egg whites with a handheld mixer until stiff peaks form, about 3 minutes. Fold the egg whites into the batter.
6) Gently stir in the blueberries.
7) Use a ¼ cup measure to pour the batter into the center of the waffle iron. Bake according to your waffle iron’s instructions. Repeat with the remaining batter.
8) While the waffles are cooking, make the frosting by combining the butter and cream cheese in a bowl and beating them with a handheld mixer for 1 minute or until smooth.
9) Add the vanilla, lemon juice and lemon zest and beat until combined, about 20 seconds. Beat in the powdered erythritol until incorporated.
10) Beat in the almond milk, 1 Tbsp at a time, until the frosting reaches the desired consistency.
11) Spread the frosting evenly over the waffles. Serve them immediately.

Special tip: low-carb sugars
Some sugar alcohols do have an impact on blood sugar, including maltitol, the most commonly used sugar alcohol. They’re also known to cause digestive upset in many people. Erythritol is the only sugar alcohol that seems to have minimal to no impact on blood sugar and does not cause digestive issues for most people. For that reason, it’s the only sugar alcohol we recommend.

Phase 1: Lunch or dinner
Chicken fajita bowl
Yields 4 servings

Enjoy a fiesta in a bowl! Juicy pieces of chicken are coated in a flavorful fajita sauce and tossed with perfectly sautéed veggies and black beans. Serve over cauliflower rice and top it all with Monterey Jack cheese.

1 Tbsp olive oil
1 pound boneless skinless chicken breast
1 tsp paprika
¼ cup sliced onions
1 medium bell pepper, sliced
2 Tbsp tomato paste
2 Tbsp lime juice
1 tsp chipotle chili powder
¼ cup chicken broth
½ cup canned black beans, rinsed and drained
1½ cup cooked cauliflower rice
½ cup Monterey Jack cheese
2 Tbsp chopped cilantro (coriander)

1) Heat the olive oil over medium-high heat in a large skillet.
2) Pat the chicken dry. Dice it into ½-inch (1-cm) pieces and season it with paprika and salt and pepper to taste. Place it in the hot skillet and brown it for 3 to 4 minutes per side. Remove the chicken and set it aside, reserving the grease in the pan.
3) Reduce the heat to medium. Add the onion and bell pepper and cook for 3 to 4 minutes, until the onion is translucent.
4) Whisk together the tomato paste, lime juice, chipotle chili powder, chicken broth, salt and pepper to taste in a small bowl.
5) Add this mixture along with the cooked chicken and the black beans to the veggies in the pan and cook for 3 to 4 minutes, until the sauce is slightly thickened.
6) Divide the cauliflower rice into 4 bowls, then top with the mixture from the pan. Garnish with cheese and cilantro.

This dish may be stored in an airtight container in the refrigerator for 3 to 4 days. For long-term storage, freeze individual portions. Defrost them overnight in the refrigerator and then reheat them over medium heat until heated through, about 5 to 6 minutes.

Phase 1: Lunch or dinner
Pepperoni and goat cheese pizza
Yields 8 slices (1 slice per serving)

Who says pizza is off limits when you’re eating low carb? Once you try this version of your favorite comfort food, you won’t even want to go back to delivery.

Ingredients for the crust
1½ cups shredded whole-milk mozzarella cheese
2 oz full-fat cream cheese
1½ cups almond flour
1 large egg
1 tsp minced garlic

½ cup pizza sauce (no sugar added)
1 cup whole-milk mozzarella cheese
32 thin slices of pepperoni (2 to 3 oz)
½ cup crumbled goat cheese
2 Tbsp grated Parmesan cheese

1) Place an oven rack at the bottom of the oven and preheat it to 425°F/218°C. Take out a baking sheet and cut two pieces of parchment paper the same size. Set these aside.
2) Combine 1½ cups of shredded mozzarella and cream cheese in a saucepan over low heat and stir until melted and smooth. Remove from the heat, allow the mixture to cool slightly and then transfer it to a food processor.
3) Add the almond flour and egg to the cheese mixture and pulse until a dough forms, about 2 minutes.
4) Remove the dough from the food processor and transfer it to a piece of parchment paper. Cover the dough with the other piece of parchment paper and use a rolling pin to roll the dough into a rectangle about the size of your baking sheet, approximately a quarter-inch thick.
5) Remove the top piece of parchment paper and transfer the dough along with the bottom piece of parchment paper to a baking sheet.
6) Use a fork to poke holes all over the dough. Spread the minced garlic evenly on top.
7) Place the baking sheet in the preheated oven. Bake for 9 minutes or until the dough starts to turn golden.
8) For the topping, spread the pizza sauce evenly over the dough. Sprinkle 1 cup of mozzarella evenly on top, followed by the pepperoni and crumbled goat cheese. Sprinkle the Parmesan over the other toppings.
9) Bake for 10 to 15 more minutes or until the cheese melts and starts to bubble. Remove the pizza from the oven and allow it to cool before serving.

Phase 1: Treats
Almond flour tortilla chips with homemade guacamole
Yields: 4 servings

These low-carb tortilla chips are made with almond flour and flaxseed for a crispy, crunchy chip that’s perfect for scooping up freshly made guacamole.


¾ cup almond flour
¼ cup ground flaxseed
1 large egg white
¼ tsp sea salt
¼ tsp baking powder
Olive oil
For the guacamole
2 large ripe avocados, pitted
Juice from 1 lime
¼ cup roughly chopped fresh cilantro (coriander)
½ tsp sea salt
¼ tsp garlic powder

1) Preheat the oven to 350°F/177°C. Cut two pieces of parchment paper to the size of a baking sheet and set them aside.
2) Place the almond flour, flaxseed, egg white, salt and baking powder into the bowl of a food processor and pulse until a dough forms.
3) Turn the dough out onto one of the pieces of parchment paper and then top it with the second piece of parchment paper. Use a rolling pin to roll the dough out into a large oval, about the same length and width as the parchment – this dough should be very thin.
4) Slide the parchment-covered dough onto a baking sheet and then carefully remove the top piece of parchment paper. Using a pizza cutter, cut the dough into 2-inch squares. Then cut each square diagonally into two triangles.
5) Spray the top of the dough with the olive oil and bake for 12 to 15 minutes, or until the chips are golden.
6) Meanwhile, scoop out the ripe avocado and place it in a large bowl. Add the lime juice, cilantro, salt and garlic powder. Mash with a fork to combine. Taste and add more salt, if needed.
7) Serve immediately, or divide the chips and guacamole into four separate containers for a pre-portioned snack to enjoy throughout the week.

Phase 2: Treats
Peanut butter cups
Yields 6 cups (1 cup per serving)

This sugar-free take on the classic candy couldn’t be easier to make and is filled with a thick layer of creamy peanut butter!

¹⁄³ cup cocoa powder
½ cup coconut oil, melted
2 Tbsp granulated erythritol sweetener
¼ tsp vanilla extract
6 Tbsp unsweetened natural peanut butter
Coarse sea salt, for topping (optional)

1) Line a 6-cup muffin tin with paper cupcake liners.
2) Whisk together the cocoa, coconut oil, erythritol and vanilla extract in a small bowl. Scoop 1 rounded Tbsp of the cocoa mixture into the bottom of each muffin cup.
3) Place the muffin tin in the freezer and leave it for 5 minutes to allow the chocolate to solidify.
4) Scoop 1 Tbsp of peanut butter into each muffin tin, spreading it into an even layer. Top with another 1 Tbsp of the cocoa mixture.
5) Freeze the peanut butter cups for another 5 minutes. Top each with a pinch of coarse sea salt (if desired). Serve immediately or transfer to a container in the refrigerator to store for up to one week

Working out net carbs
To calculate net carbohydrates, subtract grams of fiber and grams of sugar alcohol (specifically erythritol) from total carbohydrates. For example, if a food item contains 14 grams of carbohydrates per serving, but 5 grams come from fiber and 4 grams come from erythritol, you would end up with 5 grams of net carbohydrates per serving.

Total carbs 14 g
Fiber -5 g
Erythritol -4 g
Net carbs 5 g

Note that subtracting the total grams of sugar alcohol only applies to erythritol. When it comes to sugar alcohols other than erythritol, such as maltitol, sorbitol or xylitol, there’s not yet a standard for how these sugar alcohols are calculated, but the Diabetes Education Center at the University of California, San Francisco, suggests that half the carbs in these sugar alcohols can be subtracted from total carbs when calculating net carbs. So in this case, if a food has 14 total carbs, 5 grams of fiber and 4 grams of maltitol, the net carbs would be 7 grams.

Excerpted from The New Keto-Friendly South Beach Diet by Arthur Agatston (Hay House, 2019)

0Toxic Insulin

1 World J Diabetes, 2015; 6: 1152-7

Balancing fatty acids

1 Nutrients, 2016; 8: 128

Main article

1 Royal College of Paediatrics and Child Health, National Paediatric Diabetes Audit annual reports, 2017/18 and 2013/14.
2 Proc Natl Acad Sci U S A, 2009; 106: 15430-5
3 Clin Gastroenterol Hepatol, 2019; 17: 748-55.e3
4 Cell Metab, 2019; 30: 447-61.e5
5 N Engl J Med 2009; 360:129-139
6 N Z Med J, 1980; 92: 417-21
7 Lipids, 2016; 51: 507-17
8 Cell Metab, 2019; 30: 735-53.e4
9 Obesity (Silver Spring), 2016; 24: 1612-9
10 Am J Clin Nutr, 2005; 81: 69-73

A calorie is not a calorie

1 Obesity (Silver Spring), 2016; 24: 453-60

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