One of the most significant findings about cancer was made by the German biochemist Otto Warburg. He was awarded the Nobel Prize in Medicine in 1931 for his discovery of the oxygen-transferring enzyme of cell respiration. Here is an extract from a lecture he presented in 1966 (1).

Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause. Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar. All normal body cells meet their energy needs by respiration of oxygen, whereas cancer cells meet their energy needs in great part by fermentation. All normal body cells are thus obligate aerobes, whereas all cancer cells are partial anaerobes. From the standpoint of the physics and chemistry of life this difference between normal and cancer cells is so great that one can scarcely picture a greater difference. Oxygen gas, the donor of energy in plants and animals is dethroned in the cancer cells and replaced by an energy yielding reaction of the lowest living forms, namely, a fermentation of glucose.”

Essentially what this means is that for cancer cells to survive and thrive they need plenty of readily available glucose. So a diet with a high content of refined carbohydrates, especially sugar, facilitates the development of cancers. By contrast, if the cancer cells are starved of glucose by limiting the consumption of carbohydrate-containing  foods, they will find it difficult to survive and consequently the cancer may regress. This knowledge provides the key to the development of strategies to prevent and even cure cancers.

In an immune cell study, 10 healthy people were assessed for fasting blood-glucose levels and the phagocytic index of neutrophils, which measures the ability of immune cells to destroy invaders such as cancer. Eating 100 grams of carbohydrates from glucose, sucrose, honey and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria. Starch did not have this effect (2). Cancerous cells are being formed continuously but normally the body destroys them. However if the abilty to control these cells is impaired, a cancer is likely to develop. Hence this is one way in which a reduction in sugar consumption would help in controlling cancer.

In a study in Korea data were analysed for 1,298,385 men and women. During the follow-up period of 10 years there were 54,385 deaths in the men of which 20,566 were attributed to cancer. The corresponding values for women were 20,362 and 5,907 (3). Table 1 shows quite clearly that the death rate from all causes increases steadily with the increase in the blood glucose. There is also an increase in the cancer death rate which was especially marked for cancers of the pancreas and liver, oesophagus and colon in both men and women. It was reported that the incidence of cancer was not influenced by Body Mass Index (BMI).

 

 

 

 

Table 1 Variation in death rate per 100,000

Cause of death                             Fasting blood   glucose levels, mg/dL
<90 90-109 110-125 126-139 >140
                                                          Men
All cause 677.3 697.7 847.2 1029.2 1371.6
All cancers 266.0 270.9 303.7 334.5 341.0
                                                        Women
All cause 371.7 374.5 453.5 525.1 803.4
All cancers 118.8 117.1 121.9 143.9 150.5

 

 

In the Vasterbotten Intervention Project conducted in northern Sweden data was collected from 31,304 men and 33,293 women. During the next 10 years there were 2,478 incident cases of cancer. It was found that high levels of blood glucose in both men and women were associated with an increased risk of pancreatic cancer, malignant melanoma and urinary tract cancers among those with high blood glucose levels. It is noteworthy that this study also found that these relationships were independent of BMI (4).

In the Me-Can study researchers identified 274,126 men and 275,818 women from existing health studies in Norway, Austria, and Sweden for whom data had been recorded on blood glucose level, height, and weight. For each participant a baseline measurement was defined, consisting of data from the first health examination, which had complete data (including a blood glucose measurement and whether the participant smoked). Mean age at baseline was 44.8 years and mean follow-up time was 10.4 years. Any cancer diagnosis was recorded, whether the participant survived to the end of the study, and causes of death for participants who died during the study. Excluding the first year of follow-up, 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer The researchers analyzed the data to determine whether a higher blood glucose level was associated with increased risk of certain cancers, in both men and women

A raised blood glucose level was significantly associated with an increased risk of incident and fatal cancer at all sites combined, and of several specific cancers. In women, a linear association between glucose and risk of overall incident and fatal cancer was observed, and levels within the upper normal range were also related to increases in risk. In men, the association between glucose and total incident cancer was somewhat weaker, and risk of fatal cancer was only significantly increased at levels approximately equivalent to impaired glucose levels. It was found that for both men and women those with the highest blood glucose levels had almost double the risk of fatal cancer when compared with those who had the lowest glucose levels (5).

A raised blood glucose level is also a risk factor for other diseases, especially cardiovascular disease so it is not surprising that for those in this category the all-cause mortality was 3 times that of subjects with low blood glucose.

The result of this study is totally in agreement with the Korean work reported above. These studies provide strong evidence that high blood glucose is a risk factor for cancer.

Type 2 diabetes (T2D) has consistently been related to an increased risk of cancer at various sites. The common factor is the raised blood glucose coupled with the increased production of insulin which in turn can cause insulin resistance in many different organs. There is a large body of evidence which demonstrates that reducing the consumption of carbohydrates, especially sugar, can be a successful treatment for T2D so the possibility arises that the same approach may also be effective with some cancers.

The specific question:

Is there a role for carbohydrate restriction in the treatment and prevention of cancer?”

 

has recently been addressed in a review by 2 research workers in Germany (6).

 

It was noted that as tumours develop they become increasingly dependent on a steady supply of glucose which means that they are vulnerable to glucose deprivation. In fact it has been shown that cancer cells die when starved of glucose. By contrast, the excess glucose which occurs in diabetics, causes changes in gene expression which promotes cell proliferation, migration and adhesion in the tumours in several organs including breast, colon, prostate and bladder. It has also been established that hyperglycaemia (raised blood glucose), is a predictor of poor survival in patients with various cancers and has been positively correlated with an increased risk for developing cancer at several sites including the pancreas, oesophagus, liver, colon, rectum, stomach and prostate.

The evidence that a raised level of blood glucose is linked to a range of chronic diseases continues to pile up. There is absolutely no doubt that if this is lowered it will be beneficial and one of the best (and easiest) ways to achieve this is to limit the consumption of sugar.

REFERENCES

  1. http://www.healingcancernaturally.com/warburgcancer-cause-prevention.html
  2. A Sanchez et al (1993) American Journal of Clinical Nutrition 26 (11) pp1180-1184
  3. S H Jee et al (2005) Journal of the American Medical Association 293 (2) pp 194-202
  4. P Stattin et al (2007) Diabetes Care 30 (3) pp 561-567
  5. T Stocks et al (2009) PLoS Med 6 (12) e1000201
  6. R J Klement and U Kammerer (2011) doi:10.1986/1743-7075-8-75