Can Type-2 Diabetes Be Reversed?

Feb 16, 2024
A clipboard with a form titled "Blood Glucose Testing Record", a stethoscope and a blood glucose meter sit on top of the clipboard.

Type-2 diabetes (T2D) has long been considered a progressive and irreversible disease. For many people, a T2D diagnosis means taking anti-T2D drugs for life. Over half of T2D patients wind up dependent on insulin injections within 10 years.1 

But more recently, many studies and reports have shown reversal of T2D can be possible.1 In this article, we’ll see what it takes to reverse this chronic condition, as we examine: 

  • The role of HbA1c
  • How anti-T2D medications work
  • Insulin resistance and T2D
  • Fatty liver and insulin resistance
  • The role of fructose

When it comes to T2D, the words “reversal” and remission are often used interchangeably. There’s a difference between the two though.1 Let’s start by seeing what that difference is.

 

The role of HbA1c

If you have T2D, your blood glucose (a.k.a. blood sugar) levels are persistently high.2 

To achieve reversal, your blood sugar must return from diabetic to normal levels. Meanwhile, remission is defined when you sustain normal levels over time.1 

A key factor in the diagnosis of T2D is your results on the hemoglobin A1c (HbA1c) test. 

Hemoglobin is a protein in your red blood cells that transports oxygen throughout your body. Glucose in your bloodstream sticks to hemoglobin. So, the higher your blood glucose levels, the more glucose-coated hemoglobin you’ll have.3,4 

The HbA1c test measures the percentage of your red blood cells with glucose attached to hemoglobin. It’s usually considered to provide a good indicator of your average glucose level for the past three months. That’s because red blood cells live for about three months on average.3,4 

An HbA1c result of 6.5 percent or higher on two separate tests will cause you to be diagnosed with T2D. In remission, your HbA1c remains below 6.5 percent for at least 3 months after you’ve stopped anti-T2D medications.3,5 

 

How anti-T2D medications work

All oral drugs for T2D work to reduce your blood glucose and HbA1c. They do this in different ways though.6 

The most common medicine for T2D is called Metformin. This medication and others like it work to decrease the amount of glucose released into your blood from your liver. It makes your muscles more responsive to insulin as well, so more glucose is absorbed from your blood.6 

Some medicines work to prevent carbohydrates from breaking down in your intestines. Carbs, which include starches and sugars, raise your blood glucose more than other food nutrients do.6 

Other drugs help excess glucose exit your body through your urine. That is, they block your body from reabsorbing glucose after it passes through your kidneys.6 

There are also meds that stop the breakdown of GLP-1. This chemical, which naturally lowers blood glucose levels, breaks down fast. But the drugs make GLP-1 stay active in your body for a longer time. They make you feel full longer after eating too.6 

Medications for T2D can also make your fat tissues more sensitive to insulin. Or they can boost insulin production by your pancreas.6 

 

Insulin resistance and T2D

Insulin is a hormone produced by your pancreas. It helps your cells take up glucose for energy use. It also triggers your muscles and liver to store glucose as glycogen.7,8 

As glucose enters your cells, your blood sugar levels fall. In turn, this drop should cause a decrease in your blood insulin levels. Lower insulin in your blood then signals your liver to release glycogen and turn it into glucose. This finely tuned feedback loop ensures that your body has energy all the time even if you haven’t eaten for a while. But this system can get out of whack when you regularly consume too much sugar.7 

Your pancreas has to release a lot of insulin when large amounts of sugar consistently enter your bloodstream. The overdrive makes insulin less effective over time. This condition is known as insulin resistance.7 

Your pancreas will try to compensate by secreting even more insulin, but its capacity to produce insulin isn’t unlimited. Eventually, it’ll begin to wear itself out, and then your blood sugar levels will stay high.7 

Having a lot of insulin in your blood also signals your muscles and liver to store glucose. The problem is, these sites can only store a limited amount of glucose. Once those storage sites are full, your liver sends the extra glucose to fat cells, leading to weight gain.7 

Insulin resistance is considered a precursor to T2D. People who’ve had insulin resistance for a while nearly always wind up diagnosed with T2D eventually.2,9 

 

Fatty liver and insulin resistance

Both genetic and lifestyle factors contribute to insulin resistance. A key lifestyle factor is excess fat, especially in your liver.10 

You have a fatty liver if fat makes up between 5 and 10 percent of your liver weight. This fat buildup mainly results from drinking too much alcohol or eating too much of the wrong foods.11

Studies show that excess fat can lead to overproduction of reactive oxygen species (ROS) in your liver, which causes inflammation and injures your liver cells. As a result, insulin signaling in your liver becomes impaired, leading to insulin resistance.12,13 

The liver has an amazing ability to heal and repair itself after damage. Normal liver cells can grow and multiply to replace injured ones. Your liver isn’t invincible though, so it’s a good idea to avoid certain foods while the healing process is happening.14 

 

The role of fructose

Fructose is a simple sugar that’s found naturally in fruits. It’s also the main ingredient in high-fructose corn syrup (HFCS) — a cheap, highly processed sweetener.15 

HFCS is widely used for prolonging the shelf life of processed foods. Examples are candies, cookies, cereals, crackers, breads, jams, sauces, ice cream, and fast food. Common drinks like soda and many juice products contain HFCS too.15 

Most of the fructose you consume is processed by your liver. Specifically, it breaks down fructose into glucose, lactose, and glycogen. But remember that your liver has a limited capacity for storing glucose (as glycogen).15

When you consume a lot of fructose — especially as HFCS — the excess, unprocessed fructose drives the production of fatty acids in your liver. Fructose also promotes the buildup of triglycerides (a type of fat) in that organ. This means that a high fructose intake is a major contributor to fatty liver.15,16,17 

 

Conclusion

Consuming too much fructose can give you a fatty liver, which can then cause insulin resistance. In turn, insulin resistance drives the development of T2D. 

But contrary to conventional belief, T2D reversal and remission are possible. Considering the role of fructose in fatty liver and insulin resistance, the most effective starting point for reversal is eliminating fructose from your diet. 

Fortunately, we’ve done all the hard work already, and we’re here to guide you every step of the way. Ready to be free of T2D? Learn more about the Diabetes Diet Solution now.

 

References

  1. Reversal and Remission of T2DM – An Update for Practitioners - PMC (nih.gov)
  2. Type 2 Diabetes: What It Is, Causes, Symptoms & Treatment (clevelandclinic.org) 
  3. Hemoglobin A1C (HbA1c) Test: MedlinePlus Medical Test
  4. A1C: What It Is, Test, Levels & Chart (clevelandclinic.org)
  5. International Experts Outline Diabetes Remission Diagnosis Criteria | ADA
  6. Diabetes & Oral Medication: Types & How They Work (clevelandclinic.org)
  7. Insulin Resistance and Diabetes | CDC
  8. Glycogen: What It Is & Function (clevelandclinic.org)
  9.  Pathophysiology of Type 2 Diabetes Mellitus - PMC (nih.gov)
  10. Hepatic insulin resistance, metabolic syndrome and cardiovascular disease - ScienceDirect
  11. Fatty liver — symptoms, causes and treatment | healthdirect
  12. Fatty liver as a consequence and cause of insulin resistance: Lessons from type 2 diabetic liver
  13. Oxidative stress as a crucial factor in liver diseases - PMC (nih.gov)
  14. Cells that maintain and repair the liver identified | National Institutes of Health (NIH)
  15. Fructose and the Liver - PMC (nih.gov)
  16. Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects - PubMed (nih.gov)
  17. JCI - Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans