Dieet met veel suiker verhoogt risico op pancreaskanker

Knack

Suikerrijke voeding veroorzaakt de ontwikkeling van alvleesklierkanker en verhoogt de kans op een dodelijke afloop. Tot die bevinding zijn onderzoekers van het Vlaams Instituut voor Biotechnologie (VIB) en de KU Leuven gekomen.

Een suikerrijk dieet verhoogt niet alleen de kans op het ontwikkelen van pancreaskanker. Het stimuleert ook de agressieve groei van tumoren. Tot die conclusie komen onderzoekers van VIB-KU Leuven en collega's van het Babraham Institute van de Britse universiteit Cambridge.

De resultaten zijn gepubliceerd in het tijdschrift Cell Reports.

Alvleesklierkanker is een zeldzame maar dodelijke vorm van kanker door late detectie en een slecht begrip van risicofactoren. Bekende risicofactoren zijn obesitas, voeding en diabetes type 2, maar door de lage incidentie en de onderlinge samenhang is hun individuele bijdrage moeilijk in te schatten.

De onderzoekers voltooiden een uitgebreid project met experimenteel werk bij muizen en menselijke gegevens. Bij de dieren werd de progressie van pancreaskanker beïnvloed door voedingssuiker, met een snellere tumorgroei en verhoogde dodelijkheid.

Het effect bij mensen blijkt hetzelfde. Bij 500 deelnemers aan de studie onderzochten de onderzoekers de interactie tussen genen en voeding en ontdekten dat hoge niveaus van voedingssuiker het risico op alvleesklierkanker verhoogden. 'We hebben jarenlang gekeken naar verschillende voedings- en genetische veranderingen en niets komt in de buurt van de nadelige gevolgen van een dieet met veel suiker', zegt James Dooley, senior wetenschapper bij het Babraham Institute.

Plantaardige voeding met een equivalent van een avocado per dag vermindert het risico op pancreaskanker met tien procent.

Dietary sugar drives pancreatic cancer

Research using mice and human data shows how diet affects disease risk

Eating a diet high in sugar increases the likelihood of developing pancreatic cancer in some individuals and also drives the aggressive growth of tumours, a study by researchers from the Babraham Institute, Cambridge, UK, and VIB-KU Leuven, Belgium, has found.

The researchers completed a comprehensive project using experimental work in mice and human data, including from pancreatic cancer patients, to understand the influence of different dietary components on the development and progression of pancreatic cancer. The research is published today in the journal Cell Reports.

Pancreatic cancer is a rare but fatal form of cancer, due to late detection and a poor understanding of the risk factors. Known risk factors include obesity, diet and type 2 diabetes, however the low incidence rate and interconnection of these factors mean that it is difficult to tease apart their individual contribution.

The researchers first studied the effects of obesity, diet and diabetes on pancreatic cancer development, growth and lethality in mice. In parallel they analysed the effect of diet using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) study, which followed over half a million Europeans for 20 years.

The researchers found that obesity, diet and diabetes had profound and differing impacts on cancer incidence and growth. Using mice, the results indicated that obesity, dietary animal fats and dietary sugar were independent drivers of different facets of pancreatic cancer progression. In particular the results shed light on how pancreatic cancer might be affected by dietary sugar, with more rapid tumour growth and escalated lethality.

The effect of dietary sugars on pancreatic cancer development was preserved between mice and humans. In 500 study participants with pancreatic cancer, the researchers explored the interaction between genes and diet and found that high levels of dietary sugar increased pancreatic cancer risk in individuals with a certain genetic variation (found in 6% of the population).

Dr James DooleyDr James Dooley, senior staff scientist in the Immunology programme at the Babraham Institute, said: "Our study raises concern about the remarkable toxicity of sugar in our diet. We spent years looking at different dietary and genetic changes, and nothing has anywhere near the detrimental impact of a high sugar diet. Our findings suggest that it drives pancreatic cancer onset and makes it a more aggressive and lethal tumour."

Analysis of the human-derived data from the large EPIC study suggested that dietary plant fats reduced the risk of pancreatic cancer, estimating a 10% decrease in risk when eating the equivalent of an avocado a day.

Professor Adrian Liston, senior group leader at the Babraham Institute, said: "This study shows the power of combining animal research with the study of patients. We were able to use epidemiology and large patient-based resources to find a link in humans, and then go back to an animal model to formally test the direction of causality. Finding the same gene-diet link in both mice and humans makes us confident that diet is modifying disease risk, and gives us the tools to test preventative and therapeutic interventions."

Proliferating pancreatic cancer cells in mice fed high sugar dietsWhile the impact of nutrition on cancer development continues to be explored and debated, this study provides a vital foundation for further studies and important indications to explore. Armed with this knowledge, clinicians could be supported to identify individuals at increased risk for screening and individuals with a high-risk genetic background could take pro-active dietary changes to reduce their risk of pancreatic cancer.

Ali Stunt FRSA, Founder and Chief Executive of Pancreatic Cancer Action, concurs: "Here at Pancreatic Cancer Action, we strongly advocate for high quality research into this neglected cancer. Dr Liston and his team have made a major contribution into understanding how diet and genetics changes the risk for pancreatic cancer. Healthy lifestyle choices, such as avoiding sugar-sweetened beverages and choosing a diet rich in vegetables, can reduce your risk of pancreatic cancer, and may be especially important in families with a history of the disease."

Read the original article here.

Journal club: smell drives obesity

A fascinating study has just come out in Cell Metabolism. Two groups looked at the role of the sense of smell in altering metabolism.

In one set of experiments, mice were depleted of their sense of smell and then put on a high-fat diet. Unlike their smelling-competent peers, the smelling-defective mice did not put on as much weight. In fact, if mice were first made obese, removing the sense of smell resulted in weight loss. This was not due to altered food consumption, which was equal in both mouse strains. 

In a second set of experiments, a strain of mice were generated which were "super-sniffers", with an enhanced ability to smell. When these mice were put on a high fat diet, they gained weight at a faster level then their wildtype siblings, the reverse effect of knocking out the sense of smell. Again, this was not due to any change in the amount of food eaten - the conclusion is that smelling fatty foods acts in an independent circuit to eating fatty foods, and reprogrammes the adipocytes into a high storage setting.

These studies should be the end of the silly "physics model" of obesity, which postulates that humans are essentially perfect machines where weight is driven only by calories in (diet) and calories out (exercise). This model has been proven over and over again to be incorrect in essentially every aspect. Adipose tissue is not an inert storage for extra calories, it is an active tissue that can be programmed and reprogrammed to increase or decrease. This adipocyte program is altered by genetics, epigenetics, microbiomics, immunology and the environment, as well as the diet and exercise postulated in the physics model. Unfortunately I doubt very much that this study, or future studies, will throw off the allure of the "physics model" to replace it with a biological model - victim blaming is too well entrenched in both the public and medical spheres.

Read the paper here: Riera et al, "The sense of smell impacts metabolic health and obesity", Cell Metabolism 2017. 26(1) p198.