Practical Approach to High Blood Sugar After Long-Term Keto Diet

Practitioner’s Preface

There are four documented ways to put type 2 diabetes into remission: a very low-calorie diet [1,2,3], bariatric surgery (especially the use of the Roux-en-Y procedure) [4,5], a ketogenic diet [6,7], and use of GLP-1 agonists such as semaglutide, dulaglutide, and tirzepatide [8]. Each comes with advantages and limitations.

There is strong one- and two-year clinical data demonstrating that a very-low-carbohydrate/ ketogenic diet is both safe and effective for achieving remission of type 2 diabetes symptoms; however, there is limited long-term data. As outlined in a previous article titled Blood Sugar May Increase After Years on a Ketogenic Diet in Type 2 Diabetes, the five-year Virta Health data showed that the average HbA1c for those completing the study averaged ~7.3%, which was up from 6.3% at a year, and 6.7% at two years [9]. An 8-year dataset from UK-based General Practitioner Dr. David Unwin’s practice found that HbA1c tended to drift or worsen as time went on [10].

While “carb creep” (increased carbohydrate consumption) may explain the blood sugar rise for many people, these data do not account for individuals who continue to follow ketogenic carbohydrate restriction yet whose blood glucose begins to rise anyway. The rise in blood glucose results from the liver-pancreatic alpha cell axis, which is explained by Dr. Roger Unger’s bi-hormonal theory of diabetes [11,12,13]. Understanding this mechanism allows for some simple long-term strategies to help those who were previously in remission of type 2 diabetes symptoms to better control their blood sugar levels.

How Pancreatic Cells Control Blood Sugar

In healthy individuals, the pancreatic alpha cells and pancreatic beta cells exist in a tightly regulated paracrine relationship where one cell secretes chemical messengers that diffuse through the extracellular space to affect the nearby target cell. When insulin rises, glucagon release is suppressed. When healthy people eat, their beta cells secrete insulin, which is communicated to the alpha cells of the pancreas and signals them to stop secreting the hormone glucagon. The insulin that is released locally within the pancreas acts as an immediate, powerful biological “brake” that shuts down glucagon secretion from the neighbouring alpha cells.

When someone hasn’t eaten for a while, blood sugar falls, alpha cells release glucagon that binds to receptors on liver cells, and this triggers a rapid enzyme cascade (via cyclic AMP) that converts stored glycogen into glucose (glycogenolysis), releasing it into the bloodstream to fuel the brain, muscles, and organs.

If fasting is prolonged and glycogen stores run low, glucagon released from the alpha cells signals the liver to manufacture glucose from scratch using circulating amino acids from protein (gluconeogenesis), and makes glucose from the glycerol backbone of triglycerides derived from fat, via the glycerol pathway.

What Happens on a Long-Term Keto Diet?

When following a very low-carbohydrate (keto) diet over time, the body has much lower demand for insulin, which results in the pancreatic beta cells scaling back on insulin production. Without enough insulin to quiet the alpha cells, the continuous secretion of glucagon goes completely unchecked, removing the paracrine “brake” of insulin on glucagon. This tells the liver to ramp up both glycogen breakdown (glycogenolysis) and glucose creation (gluconeogenesis) from proteins and fats.

This baseline relative insulin deficiency (compared to glucagon) explains why people who were diagnosed several years ago with type 2 diabetes and who have followed a very-low-carbohydrate (keto diet) for an extended period begin to experience a glucose spike after eating a meal that is low in carbohydrate, but high in protein. The sudden influx of amino acids stimulates the uninhibited alpha cells to release glucagon. Since insulin release is too low due to long-term carbohydrate restriction, there is no countersignal to stop the liver from breaking down glycogen and overproducing glucose.

Insulin-to-Glucagon Ratio

Even in healthy individuals without type 2 diabetes, eating protein foods in the absence of carbohydrates stimulates both insulin and glucagon, but amino acids inherently favor glucagon secretion over insulin [15]. This shift creates a lower insulin-to-glucagon ratio, resulting in higher blood glucose.

Since protein triggers alpha cells much more intensely than it triggers beta cells, eating a moderate to high-protein intake without sufficient dietary carbohydrates over the long term is what results in higher blood glucose levels, shifting the body into a higher glucagon-to-insulin state.

For Those Previously Diagnosed with Type 2 Diabetes

For individuals previously diagnosed with type 2 diabetes, the pancreatic beta cells release insufficient amounts of insulin due to beta cell dysfunction. As outlined in a previous article, in 10-15% of those diagnosed with type 2 diabetes, the beta cells have crossed a “point of no return” and can not secrete a rapid burst of local insulin anymore, and typically have lower baseline fasting insulin levels, indicating more exhausted beta-cell function. 

When dietary carbohydrate is restricted, the daily demand for insulin drops, which results in a low insulin-to-glucagon ratio.

• The lack of a robust localized insulin surge from the pancreatic beta cells removes the “paracrine brake” on the pancreatic alpha cells, and over an extended period of time on a very low-carbohydrate, moderately high-protein diet, there is insufficient insulin release from the pancreatic beta cells to inhibit glucagon release from the alpha cells, leaving the alpha cells uninhibited.
• When the amino acids from dietary protein enter the bloodstream, they stimulate these unmoderated alpha cells to hypersecrete glucagon, and when the liver is exposed to a wave of glucagon, it is strongly signaled to ramp up gluconeogenesis, turning those amino acids directly into glucose.
• The solution is not to restrict carbohydrates further, or to adopt a carnivore diet. Eliminating carbohydrates floods the body with more amino acids from protein, amplifying the uninhibited glucagon release and worsening the problem.

• The key is to restore the pancreatic paracrine “brake” and calm down the unregulated glucose production coming from the alpha cells.

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How high can blood sugar rise from eating only protein and low-carb veggies?

Everyone’s blood glucose response to foods is different, but having eaten low-carb for years and having previously put type 2 diabetes into remission (March 2019-March 2021) and continuing to eat low-carb, this is the blood glucose response I had on May 26, 2026, after eating 6 oz. of coho salmon with asparagus and mushrooms, without eating any carbs. My blood sugar before the meal was 5.2 mmol/L (94 mg/dl) and rose to 9.3 mmol/L (167 mg/dL) after 2 hours.  My mistake was thinking that coho salmon was a ‘fatty fish’ (see below for explanation).

 

I recently made the same meal, except this time I ate 1 tbsp. cold, cooked barley 10 minutes beforehand, and my blood sugar was 5.7 mmol/L (103 mg/dl) 2 hours afterwards. The explanation as to why this worked is below.

 

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Practical Dietary Strategies

To counteract relative insulin deficiency of type 2 diabetes and long-term carbohydrate restriction, below are a few practical dietary strategies that can help. 

1. Simulate the “First-Phase Insulin Response”

Healthy individuals have what is called “the first-phase insulin response,” which is a rapid, intense burst of pre-stored insulin within the first 5 to 10 minutes of glucose entering the bloodstream. This pre-stored insulin released from the beta cells acts as a metabolic brake on the alpha cells, suppressing glucose production in the liver, preventing a sharp spike in blood sugar.

Individuals diagnosed with type 2 diabetes lack a first-phase response because their pancreatic beta cells release insufficient amounts of insulin due to beta cell dysfunction. Even when dietary carbohydrate is restricted over a long period of time, this first-phase insulin response is not restored, and daily demand for insulin is further suppressed. 

Simulating the “first-phase insulin response” seen in healthy individuals can help restore the pancreatic paracrine brake and calm the unregulated glucose production coming from the alpha cells before a protein-containing meal is eaten, and the timing of this targeted carbohydrate intake is critical.

The 10-Minute Rule

Eating a small amount of slowly metabolized carbohydrates 10 minutes before eating a meal that contains protein coaxes the pancreatic beta cells to release a small pulse of insulin before the meal. This inhibits the pancreatic alpha cells, quieting glucagon hypersecretion. 

Forcing the beta cells to release insulin before eating a protein-containing meal prevents the liver from overproducing glucose and reduces post-meal blood sugar spikes, reducing unregulated liver gluconeogenesis over time.

I have found that 2-3 blackberries, or a tablespoon of cold, cooked barley (a resistant starch), provide just enough complex structure, fiber, or resistant starch to gently nudge the beta cells to release a small amount of insulin without causing an independent blood sugar spike. Other examples are one tablespoon of cold cooked lentils or chickpeas, or 3 to 4 pods of cooked edamame (soybeans). The key to these examples lies in their physical matrix (fiber and resistant starch) and a micro-dose quantity.

2. Optimize Macronutrients

For individuals who were previously diagnosed with type 2 diabetes and who have been experiencing a rise in blood glucose after years on a very-low-carbohydrate (ketogenic) diet (30-50 g of carbohydrate/day), changing the types of proteins and amount of carbohydrate can help control blood sugar spikes.

• Moderate Protein Intake: Keep protein to a moderate intake of 0.80 g/kg/day, and if a higher protein intake is required, such as in the case of older adults to prevent sarcopenia, distribute protein intake evenly throughout the day in meals not above 30g of protein per day, while limiting protein sources that are high in the amino acids arginine, alanine, glycine which trigger gluconeogenesis the most of any amino acids [14-20].
• Prioritize Real, Whole Foods: Prioritize eating real, whole-food sources of protein over rapidly digested protein powders or amino acid isolates.

• Avoid Quickly Digested Protein: Avoid protein foods that are quickly digested, such as egg whites, lean white fish like cod, tilapia, haddock, and skinless chicken breast. Reach for protein foods that naturally come with fat, including whole eggs, fatty fish like king salmon, mackerel, and sardines, and cuts of meat that include fat.

• Don’t Eat Protein “Naked”: Most people diagnosed with type 2 diabetes have been taught not to eat carbs “naked”, but when alpha cells are over-reactive, it is important not to eat protein naked, either. Intentionally pair protein foods with healthy fats and fiber, which significantly slows down the absorption rate of amino acids into the bloodstream.
• Increase Overall Carbohydrates: Gradually transition from 30–50 grams of carbohydrate per day to a low-carbohydrate threshold between 80 and 100 grams of slowly digested carbohydrates per day.

Clinical Application

There is ample clinical data to support using significant dietary carbohydrate restriction for the first year or two to put the symptoms of type 2 diabetes into remission; however, maintaining long-term glucose control often requires a change in the types of proteins and the amount of carbohydrate eaten to counteract the effect of alpha cells driving unrestrained glucose production due to the suppressed and delayed insulin release.

More Info

If you would like dietary support to better manage your blood sugar levels after following a low-carb or very low-carb (keto) diet, please reach out. You can learn about me and the Comprehensive Dietary Package that I offer, along with specialized nutrition education teaching to help you know what to eat and when.

To your good health.

Joy

You can follow me on:
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Quick Clinical Summary

Q: What is a first-phase insulin response and why is it a problem in people with type 2 diabetes?

A: A first-phase insulin response is the rapid, intense burst of pre-stored insulin that occurs in healthy people when they start to eat. Pre-stored insulin is released from the beta cells of the pancreas and acts as a metabolic “brake” on the pancreatic alpha cells and suppresses glucose production in the liver. People with type 2 diabetes lack a first-phase response because their pancreatic beta cells are dysfunctional.

Q: Why does a keto diet work for the first few years to control blood sugar in type 2 diabetes, but then blood sugar starts to rise again?

A: A keto (very-low-carbohydrate) diet works very well for the first few years to reduce blood glucose by significantly reducing dietary intake of carbohydrate. The problem is, type 2 diabetes is not only due to dysfunctional beta cells of the pancreas, but also alpha cells. In a long-term keto diet, eventually there is insufficient insulin released from the beta cells to suppress the oversecretion of glucagon from the alpha cells, which drives increasing blood glucose.

Q: What are some dietary strategies that can help calm overactive alpha cells in type 2 diabetes?

A: Two key dietary strategies to counteract overactive alpha cells include mimicking a first-phase insulin response by eating a small amount of slowly metabolized carbohydrates 10 minutes before eating a meal that contains protein, and changing the types of proteins that are eaten, and slightly increasing the amount of carbohydrate. 

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Found this article of interest? Be sure to read: Alpha Cell Dominance: What Is It and How to Address It

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References

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