Fasting and Ketogenic Diets: The GAPS Epilepsy History

The GAPS epilepsy chapter traces dietary treatment from fasting in antiquity to the ketogenic diet developed at the Mayo Clinic in the 1920s. It presents the modern diet as an attempt to reproduce fasting’s metabolic effect without requiring a person to keep fasting.^[1]

Fasting From Antiquity to the Early 1900s

The chapter traces fasting for epilepsy to Hippocrates and Galen. In the early twentieth century, Bernard Macfadden, Hugh Conklin, Dr. McMurray and others reported that many patients had no further seizures after a 21-day fast, especially when it was followed by a low-carbohydrate diet. Their reports described better results in children than adults.^[1]

Fasting could not continue indefinitely, and the chapter says seizures returned in many cases after the fast ended. That limitation drove the search for a diet that could replace the fast.

The 1921 Ketone Discovery

In 1921, researchers found that fasting changes metabolism: the liver draws on body fat to make ketone bodies that cross the blood-brain barrier and supply the brain with energy when glucose is unavailable.^[1]

Researchers assumed ketone bodies were suppressing seizures, and that assumption led to a high-fat diet that sharply restricted carbohydrate and protein. The same chapter later says the original ketone explanation proved incomplete because ketone levels do not correlate with anticonvulsant effect.^[2]

The Mayo Clinic Results

The Mayo Clinic developed the ketogenic diet in the 1920s. Campbell-McBride reports that 95 percent of patients achieved some seizure control from the outset and 60 percent became seizure-free, with the best results again reported in children.^[1]

Anticonvulsants and the Diet’s Decline

Anticonvulsants began appearing in 1938, and the ketogenic diet gradually fell out of favor. Work continued at Johns Hopkins Hospital from the 1930s onward, and the Johns Hopkins model became the classic ketogenic diet. Interest rose again in the 1990s because medication controls seizures in about 70 percent of cases, leaving a substantial group without adequate control.^[1]

Why Old and Modern Results Differ

The chapter says modern outcome figures come largely from children offered the diet after medication has failed, while the 1920s reports came from a period when diet was used first. Campbell-McBride argues that these are different starting populations and that the comparison should be read in that context.^[1]

Her closing position on diet-first childhood epilepsy explains how she uses that history in the GAPS framework.

Read the History as History

A 21-day fast is part of the historical reports in the book, not an instruction to reproduce them with a child. The practical lesson in this history is why clinicians looked for a sustainable food-based treatment instead. The classic ketogenic-diet account explains the calculated protocol that followed.

The figures from the 1920s and later treatment-resistant groups come from different settings. Keep the date, the people treated and the outcome definition beside each percentage. “Some seizure control” and “seizure-free” do not describe the same result.

Frequently Asked Questions

Is the Ketogenic Diet a Modern Invention?

The diet was developed in the 1920s, after a much older history of fasting for epilepsy.

Did Researchers Prove Ketones Stop Seizures in 1921?

No. The chapter says researchers assumed ketones suppressed seizures and later evidence showed ketone levels did not correlate with anticonvulsant effect.

Why Did the Diet Fall Out of Favor?

Anticonvulsant drugs began appearing in 1938 and became the dominant treatment, although ketogenic-diet work continued at Johns Hopkins.

Your Next Step

Use the GAPS epilepsy overview for the wider discussion. Continue with Classic Ketogenic Diet for Epilepsy: The GAPS Account, or Diet-First Childhood Epilepsy: The GAPS Book’s Position, for the next question you want to understand.

My Care Team Log is listed in the WFLI Shop. A notebook can keep your dated observations and questions together.

References

1. Campbell-McBride N. Gut and Psychology Syndrome, expanded text represented by the second German edition (2015), “Epilepsie” (“Epilepsy”). English paraphrases checked against that text; no English page numbers are implied.
2. Campbell-McBride N. Gut and Psychology Syndrome, expanded text represented by the second German edition (2015), “Epilepsie” (“Epilepsy”). English paraphrases checked against that text; no English page numbers are implied.