Sugar, blood glucose and cancer

A diet that causes high blood glucose levels is associated with weight gain and with chronic conditions including type 2 diabetes. Studies have also examined the relationship between blood glucose, sugary drinks and cancer risk. This page sets out what that research shows, and what Dr Coy’s own work investigates.

Research shows that 1 in 2 people will get cancer at some point during their lifetime. We don’t always know why some people develop cancer and others don’t, but common contributing factors are thought to include:

  • Inherited genetic defects
  • DNA damaging radiation
  • Smoking
  • Viral, fungal or bacterial infection
  • Diet and lifestyle

What the research says about blood glucose and cancer risk

A number of large studies have examined the association between blood glucose levels and cancer. Analyses of prospective cohorts, including the Metabolic Syndrome and Cancer Project, have reported a correlation between raised blood glucose and cancer incidence, and a 2019 study of more than 100,000 participants at the Sorbonne reported an association between sugary drink consumption and cancer risk. That association applied to sugared soft drinks and to undiluted fruit juice.

These are observational findings, which show association rather than cause. Dr Coy’s argument is that the mechanism explaining them is biochemical. Cells cannot divide, and cannot repair damaged DNA, without the sugar ribose. Ribose is made from other sugars by the enzyme transketolase, and his work identifies TKTL1 as a control point of that conversion. His philosophy, built on this research, is that the statistical link between blood glucose and cancer risk is not a coincidence of lifestyle. It reflects a direct dependency of cell division on sugar supply.

What Dr Coy’s research investigates

If cell division depends on sugar supply, Dr Coy’s conclusion is that the sugars we eat are not interchangeable. His position is that the question is not how much sugar but which sugar, because different sugars take different routes through the body and place different demands on the cell.
He divides them along two lines. Trehalose and isomaltulose release glucose slowly and produce a lower rise in blood glucose than table sugar. Galactose and tagatose are metabolised along different routes altogether, and it is these two his laboratory work has focused on. He notes that both occur naturally in breast milk, which he takes as an indication that the body is equipped to use them.
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Galactose

Galactose can be converted into glucose in the human body through the Leloir pathway, but this conversion costs the cell energy. Dr Coy’s argument is that the energy a cell must invest to convert galactose is as much as it would release by fermenting the resulting glucose to lactic acid, so the net energy yield from fermenting galactose is zero.
In his model, this forces a cell to fall back on its mitochondria and release energy through combustion with oxygen instead. He describes galactose as behaving, biochemically, as though the person were following a ketogenic diet, even though galactose is a sugar.
This effect has been observed in laboratory conditions. When cancer cells grown in culture have glucose replaced with galactose, their metabolism and behaviour change. In humans, a 2011 study in obese lactating and non-lactating women found that galactose was associated with greater mobilisation of fat than glucose. Other studies have reported galactose affecting the number and structure of mitochondria.

Tagatose

Tagatose has similar sweetness to table sugar with substantially fewer calories, because only a small part of it is absorbed and metabolised in the small intestine. Much of the remainder reaches the colon, where it is fermented by gut bacteria including bifidobacteria, which produce the short-chain fatty acid butyrate. Butyrate is a fuel source for the cells lining the intestine.
Dr Coy’s interest in tagatose combines this fermentation behaviour with its effect on blood glucose. Tagatose produces a lower blood glucose rise than sugar, and can also lower the rise produced by sugars eaten alongside it.

The Warburg effect and the discovery of TKTL1

Cells release energy from glucose in two ways. One uses oxygen and the mitochondria. The other, fermentation, converts glucose to lactic acid without oxygen. Textbooks describe fermentation in humans as what happens when oxygen runs short, as it does in working muscle.

In 1924 Otto Warburg described a second form of lactic acid production, one that oxygen does not switch off. He found it in carcinomas, and also in healthy tissues including the retina, the testes and the thymus. He named it aerobic glycolysis, and it became known as the Warburg effect. Warburg concluded that cancer was caused by damaged mitochondria. Dr Coy’s position is that this conclusion was wrong, and that Warburg’s own findings in healthy tissue contradict it.

In 1995, as a doctoral student at the German Cancer Research Centre in Heidelberg, Dr Coy discovered the gene transketolase-like-1 (TKTL1), publishing it in 1996. At the time most specialists classified it as a defective gene. He postulated instead that the TKTL1 protein could pair with normal transketolase and carry out reactions that ordinary transketolase cannot. Working with the University of Barcelona, he reported in 2016 that TKTL1 can perform a reaction resembling the phosphoketolase found in some bacteria, producing acetyl-CoA from sugar without losing a carbon atom as carbon dioxide, and producing lactic acid alongside it.

In his view, this is the biochemical basis of the effect Warburg observed, and it is not itself a disease mechanism. TKTL1 is a normal mammalian pathway. In 2022 Wieland Huttner at the Max Planck Institute and Nobel laureate Svante Pääbo reported that acetyl-CoA production by TKTL1 underlies the greater formation of neurons in the frontal neocortex of modern humans compared with Neanderthals. The same pathway that Dr Coy associates with tumour behaviour is, on his reading, one of the things that built the modern human brain.

Dr Coy set this out in detail in a two-part article published in 2025. For the fuller version of the science, see our TKTL1 page.

Nutrition and the effectiveness of cancer therapies: what Dr Coy has published

In 2025 Dr Coy published a two-part article in the journal OM & Nutrition setting out the biochemical reasoning behind his interest in diet during cancer treatment. The following describes what he argues in that publication. It is a summary of a scientific position, not guidance, and anyone undergoing cancer treatment should discuss diet only with their treating oncologist.

Why ribose matters

All living organisms use the sugar ribose to build DNA and RNA. New cells cannot be formed, and damaged DNA cannot be repaired, without it. Ribose is produced from other sugars by the enzyme transketolase.

Dr Coy points out that mammals evolved no backup. Unlike many other systems in the body, there is no second enzyme able to make ribose if transketolase fails. Transketolase also depends on vitamin B1, thiamine, as a cofactor. That double dependency is, in his argument, both a vulnerability and an opportunity.

Why fat cannot become sugar

The human body cannot make sugar from fatty acids. This is a fixed biochemical constraint rather than a matter of debate. Only the glycerol part of a fat molecule can be converted, which Dr Coy quantifies: in a typical fat of three sixteen-carbon fatty acids attached to glycerol, three carbon atoms out of forty-eight, around 6 per cent, can become sugar.

It follows that a diet in which fat replaces carbohydrate reduces the raw material available for making ribose. This is what a ketogenic diet does, and it is the basis of his reasoning about diet during treatment.

 

The proposed effect during treatment

Radiotherapy and many chemotherapies work by damaging DNA. Cells survive that damage by repairing it, and repair requires ribose. Dr Coy’s proposition, which he first set out in 2006 and in his 2009 book, is that reducing ribose availability during treatment narrows a cancer cell’s capacity to repair the damage those treatments cause.

He also points to a second mechanism. Lactic acid is now understood to do more than end a metabolic pathway. It attaches chemically to proteins, a process called lactylation, and in doing so switches genes on. A 2024 study in Cell reported that DNA damage from the chemotherapy cisplatin triggers lactylation of the MRE11 protein, which activates a repair process called homologous recombination. Other work has reported lactic acid contributing to suppression of the immune response around a tumour, and to resistance to immune checkpoint inhibitors.

Because lactic acid, like sugar, cannot be formed from fatty acids, Dr Coy argues that a diet high in fat reduces its production. A 2013 study in patients with head and neck cancer used microdialysis probes to measure lactate directly within tumours, and reported a decline following a ketogenic diet.

What has been tested clinically

Clinical evidence in this area is early. A randomised controlled trial published in 2019 examined an MCT-based ketogenic diet alongside treatment for breast cancer and reported a survival difference in favour of the diet group. Dr Coy describes this trial as testing the recommendations he had set out a decade earlier. The trial was small, and findings of this kind need replication in larger studies before firm conclusions can be drawn.

An earlier study he co-authored, published in 2008, reported delayed growth of human gastric cancer cells in mice on a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides.

Dr Coy’s caution about long-term ketogenic eating

A point Dr Coy makes emphatically in the 2025 articles is that a strict ketogenic diet is not something he considers suitable as a permanent way of eating.

His reasoning follows from his own argument. If restricting carbohydrate restricts ribose formation, it restricts the body’s general capacity to repair DNA, not only a tumour’s. It also reduces the material available to form glutathione, which the body uses to neutralise free radicals, while increased mitochondrial activity produces more of them. He describes the result as faster ageing.

He illustrates this with population data. Traditional Inuit diets are very low in starch and sugar and are associated with low cancer rates, but also with markedly lower life expectancy than comparable populations. In the genetic condition Werner syndrome, where this metabolism fails entirely, life expectancy is lower still.

His conclusion is that the ketogenic approach is a phased tool used around treatment, not a lifestyle, and that natural sugars such as galactose and mannose, which can be converted to glucose when the body needs ribose, offer a way of moderating that trade-off. This is his hypothesis and it remains an area of active research.

Sugar increases cancer risk and promotes cell division of cancer cells

Two current studies from different disciplines show that beverages containing sugar increase the cancer risk and sugar promotes the cell division of cancer cells, i.e. the proliferation of unwanted cells. At the same time, new options are emerging for the prevention of sugar consumption associated diseases such as cancer, obesity, metabolic syndrome, diabetes, cardiovascular diseases and Alzheimer’s disease as well as to increase the cognitive and physical performance by sugar,” said cancer researcher and author Dr. Johannes Coy, Monheim am Rhein, September 2019…. continue reading

Sugar is an important source of energy for the body and at the same time an essential component of our genetic material, DNA. For a cell to be able to duplicate itself, it needs sugar building blocks to form new DNA. The production of these sugar building blocks requires enzymes that convert glucose to ribose-5-phosphate. A study by Chinese scientists published in June 2019 under the title “APC/C-CDH1 synchronizes ribose-5-phosphate levels and DNA synthesis to cell cycle progression” identified the enzyme transketolase-like-1 (TKTL1) as the decisive control point of this sugar conversion.

These results, published in Nature Communications, revise the previous account under which cell duplication is initiated first and the consumption of DNA sugar building blocks then triggers their production, the so-called pull effect. Instead, the building blocks are pre-produced in quantity and the duplication follows, a push effect. The sugar concentration in the cell is thereby identified as a decisive factor in cell doubling, and in the repair of the body that depends on it. The unwanted duplication of cells is what leads to tumour growth.

The results of another 2019 study, “Sugary drink consumption and risk of cancer: results from NutriNet-Santé prospective cohort“, point in the same direction. A research team from the Sorbonne in Paris, in a study involving more than 100,000 participants, found that consumption of beverages containing sugar was associated with cancer risk. The association applied not only to sugared soft drinks but also to undiluted fruit juices.

“The results of both studies show once again the risks of a sugar-containing diet. At the same time, they also open up new options for the prevention of sugar-related diseases such as cancer, obesity, metabolic syndrome, diabetes, cardiovascular diseases and Alzheimer’s disease,” said Dr. Johannes Coy, discoverer of the TKTL1 gene and the associated sugar metabolism. In addition to drug intervention, he also sees the possibility of influencing sugar metabolism, and thus cell duplication, through diet.

About Dr Coy

Johannes F. Coy is a biologist and worked for eleven years at the German Cancer Research Centre in Heidelberg, where he discovered the transketolase-like gene TKTL1. His research focuses on the diagnosis and therapy of cancer and neurodegenerative diseases. He is also an expert in biochemistry, metabolism, and nutrition. Find out more at dr-coy.info.

This page describes published research. It is not medical advice and nothing on it should be used to make decisions about the treatment of cancer or any other condition. If you have cancer, or think you may have, speak to your doctor. Diet during cancer treatment should only be changed in discussion with your treating oncologist.

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