The Gerson Diet as a Cancer Starving Strategy

An argument in favor of HCLF over LCHF cancer diets

2/28/23

Max Gerson (1881-1959) developed a successful cancer therapy that employed a low-fat, low-protein, high-carbohydrate diet that emphasized juices from fresh fruit, vegetables, and calf liver, along with a solid diet of oatmeal, potato, rye bread, the Hippocrates soup, raw and stewed fruits and vegetables, and after six to twelve weeks, some dairy. His high-carbohydrate diet is thought by some to be at odds with the work of Otto Warburg, who showed that a key feature of cancer cells is their abnormal fermentation of glucose even in the presence of oxygen. However, Gerson was well aware of the Warburg Effect:

“The malignancies in human beings continuously fall back deeper and deeper into fermentation.”

“The fermentation is vital for the life of the cancer cell.”

“Otto Warburg demonstrated that the cancer cell has good living conditions in blood serum… [he] showed that when the sugar level sinks to 20 mg. per cent, the lactic acid production falls to half.”

The main objective of Gerson’s therapy was to restore the conditions for proper metabolic oxidation, which was thought to make the body inhospitable to the fermenting cancer cells. But Gerson was also aware of the importance of restricting cancer’s fuel source. He reported that his nutrition protocol “regularly lowers the blood sugar considerably, so that the diet increased the effect of the liver enzymes, increased the effect of insulin, and decreased the adrenalin effect to a great extent. According to Ernst Leupold, the lowering of the blood sugar level is of great significance in cancer patients”.

Both high-carb/low-fat and low-carb/high-fat diets are used to reduce elevated blood sugar in Type 2 diabetics by helping to create more tolerable calorie deficits that increase cellular glucose uptake. However, non-diabetic people on eucaloric low-carb or ketogenic diets often witness moderate increases in their baseline glucose levels, a phenomenon termed “pseudo-diabetes”. Meanwhile, a high-carb/low-fat diet has the opposite effect, reducing the baseline glucose even when given at 2600-3200 calories as Gerson did. It is clear, as a Type 1 diabetic myself, that when I occasionally drop calories from fat below 20% while maintaining total calories, my insulin-to-carb ratio dramatically decreases and I must reduce my basal insulin to avoid hypoglycemia at night and between meals.

Jane McLelland excellently presents the case for starving cancer cells (tumor and stem cells) of their preferred and backup energy substrates after determining the unique metabolic phenotype of the specific type of cancer. While most cancer types ferment glucose as a primary fuel source, they can also rely on glutamine, fatty acids, and ketones, and their stem cells will shift to these fuels if access to glucose is restricted. Additionally, cancer cells have a high requirement of cholesterol for the synthesis of new membranes. McLelland discusses nutrition, exercise, supplements, and off-label drugs to starve cancer cells of these resources.

The ketogenic diet is growing in popularity in the treatment of cancer. Certainly, in many cases it has proven helpful. However, a classical high-fat ketogenic diet that is both low in protein and carbohydrate can raise blood sugar, fatty acids, and cholesterol along with the ketones. Although protein is restricted, there is a tendency toward increased muscle catabolism that will raise glutamine levels. I believe these are the reasons Thomas Seyfried finds more success with a calorie-restricted ketogenic diet plus a glutaminase blocker. Caloric restriction reverses the tendency for a ketogenic diet to raise glucose, fatty acids, and cholesterol but further exacerbates the muscle catabolic effects, increasing the need for the glutaminase blocker. But, should cancer patients with advanced stages, who are already susceptible to cachexia, be placed on calorie-restricted diets?

Gerson gave frequent and generous nourishment in order to replete micronutrients. While supplying ample calories, a Gerson-style diet reduces all of the circulating energy substrates. Glucose is reduced due to increased insulin sensitivity in the absence of fatty acids. Glutamine is reduced from the lack of protein intake and the protein-sparing effects of the dietary carbohydrate. Fatty acids are reduced due to the lack of fat intake and the reduction of adrenaline’s lipolytic effect. Ketones are not produced due to the supply of glucose to the liver. Cholesterol is reduced from the low fat intake. While all the energy substrates are lowered on this diet, the body does not starve. Instead, there is an ample supply of glucose that is cleared quickly from the blood due to the high insulin sensitivity. The cancer cells, however, have a restricted access to all the nutrients that they would otherwise use either for energy, as building materials, or as substrates for the de novo synthesis of cholesterol and their desired fuel source (e.g. gluconeogenesis and lipogenesis). Together, these effects make cancer less able to replicate and more vulnerable to apoptosis, immune killing, and the effects of cancer killing therapies.

Resources

Gerson, M. A Cancer Therapy; Results of Fifty Cases. Whittier Books, 1958.

McLelland, J. How To Starve Cancer... And Then Kill It With Ferroptosis. Agenor Publishing, 2021.

Mukherjee, P.; Augur, Z. M.; Li, M.; Hill, C.; Greenwood, B.; Domin, M. A.; Kondakci, G.; Narain, N. R.; Kiebish, M. A.; Bronson, R. T.; Arismendi-Morillo, G.; Chinopoulos, C.; Seyfried, T. N. Therapeutic Benefit of Combining Calorie-Restricted Ketogenic Diet and Glutamine Targeting in Late-Stage Experimental Glioblastoma. Commun Biol. 2019, 2 (1), 1–14.

Bravo-San Pedro J.M., Sica V., Kroemer G. Pseudodiabetes-not a contraindication for metabolic interventions. Cell Death Dis. 2019, 10 (10), 765.