Sugar doesn’t feed cancer

Revisiting the Warburg-Based “Sugar Feeds Cancer” Hypothesis: A Critical Appraisal of Epidemiological, Experimental and Mechanistic Evidence

https://tinyurl.com/3v2tysdt

Many clinical care professionals receive queries from cancer patients about whether they should modify their diet to reduce consumed sugar. This concern is based on a misunderstanding of some basic medical research known as the Warburg effect. Research from 1956 showed that cancer cells alter their metabolism to enable increased glucose uptake and increase energy production.

A misunderstanding of this effect has led to incorrect dietary advice to cancer patients suggesting sugar restriction may be beneficial. As a result, malnutrition, which is already a significant cause of morbidity for cancer patients, can be exacerbated. No hard evidence that low sugar diets alter survival exists. Some anecdotal reports suggest a slight correlation with risk. This study is an appraisal of all credible reports which link cancer risk and sugar restriction.

Data was collected for multiple different cancer types. No evidence of any increased cancer risk was found when high sugar consumers are compared to those whose diet fits within the WHO guidelines with sugar, being 10% or less of energy intake. Similarly, no evidence of any survival benefit was shown for cancer patients who restrict sugar intake. It is however important to recognise that obesity does increase cancer risk, possibly due to inflammation.

A complex Genetic profile

Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions

https://tinyurl.com/3znkudu5

The genetic profile of ovarian cancer is complex with more information being acquired all the time. Mutation of the P53 gene is found in almost all cases of High Grade Serous Ovarian Cancer, which is the commonest type.

Normally the P53 gene has a protective action which inhibits abnormal cell division, promotes DNA repair and may cause death of abnormal cancer cells. P53 mutation is common in many cancers and has been the subject of much research. It is unclear whether the mutation has a cancer promoting effect due to loss or gain of function.

This study performed on ovarian cancer cells under laboratory conditions looks at gain of function with increased activity of Erythrocyte Transformation Specific factors (ETS). The ETS promotes cancer spread by multiple means such as new vessel formation, immune suppression and cellular invasion.

Findings from the study show that multiple different ETS proteins have increased activity after binding with mutant P53 genes. With this understanding, the authors suggest that reversal of this TP53 mutation effect may be an important target for new treatments of ovarian cancer.

False assumptions about BMI

Body Mass Index and Chemotherapy Completion among Patients Newly Diagnosed with Ovarian Cancer

https://tinyurl.com/y9jdtek8

It has been common knowledge that obese ovarian cancer patients did not have the same therapeutic benefit from chemo, with lower blood levels of drug activity called relative drug intensity, RDI.

Often women during their course of chemo have variations of the dose, this may be due to adverse side effects prompting dose reduction. Obese women require higher doses of chemo because of their high body surface area. This sometimes meant that the adverse effects were more intense, as a result drug capping of chemo was introduced, especially of the drug Paclitaxel which is part of the commonest initial chemo drug course for oavrian cancer.

The result was that maximum RDI at 100% in the obese is rarely achieved, with consequently less likelihood of cure. As a result, this drug capping was discontinued in 2012. This study looked at RDI achieved in 622 patients from the Yale Tumour Registry who started Paclitaxel treatment during the period 2012-2022.

The results showed that about 1/3rd of the group stopped treatment early with nearly all patients having some interruption of their chemo. Most patients did not achieve an RDI of 100%. The obese patients showed no worse RDI compared to the non-obese and were no more likely to not complete the treatment course.