Antioxidants may ‘feed’ some cancers, scientists discover

Antioxidants may ‘feed’ some cancers: Scientists discover that vitamin E thought to protect against the disease may HELP lung cancer spread

  • Antioxidants are thought to help contain cancer-fueling free radicals 
  • Vitamins C and E and beta-carotene are considered to have these protective properties
  • But New York University researchers found that vitamin E may actually help a common form of lung cancer spread  

Taking vitamin E – an antioxidant supplement once thought to have protective effects against cancer – may fuel the spread of the disease in some cancer patients, a new study suggests. 

The new research from New York University (NYU) found that vitamin E may block the self-destructive tendencies of certain lung cancers. 

Antioxidants may actually protect these tumors from destroying themselves, instead helping them to spread. 

They advise that lung cancer patients stay away from vitamin E, and that patients more broadly don’t assume that antioxidants are always the right thing to take to combat cancer. 

The antioxidant vitamin E is supposed to help clean up carcinogenic free radicals, but new research reveals how it can actually fuel the spread of a common lung cancer 

Oxygen molecules are constantly splitting in the body, releasing chemicals called free radicals. 

Free radicals are unstable and can roam around wreaking havoc on other cells. 

In peak condition, the body is able to keep the number and activity of free radicals in check, but when if the body is under too much ‘oxidative stress,’ these transient chemical waste products can damage cells, DNA and proteins. 

High oxidative stress is involved in aging and has been linked to increased risks of several diseases and chronic conditions, including cancer. 

Antioxidants, however, act as neutralizing agents. 

These compounds can be found in vitamin C, beta-carotene and vitamin E to name a few. 

Balanced diets that consist of plenty of fruits and vegetables, like broccoli, berries, spinach as well as nuts and green tea are rich in antioxidants. 

Once ingested, angioxidants bind to free radicals and keep them from needling other cells or DNA and encouraging mutations – including mutations that fuel cancer development. 

So, many studies have suggested that diets high in antioxidants or taking antioxidant supplements may reduce cancer risks. 

But we also know that the relationship between oxidative stress, free radicals and cancer is not quite that simple – and the new research, published the journal, Cell, paints a clearer picture of how antioxidants can actually fuel cancer, too. 

We know that we need free radicals, which play an important role in the way the we extract energy from the raw materials of air and food we consume, as well as aiding our immune system. 

They also appear to have a paradoxical effect on adenocarcinomas, which account for about 40 percent of lung cancers, according to the new study. 

What makes these cancers dangerous is their ability to spread to other parts of the body, or metastisize. This has already happened when about 22 percent of diagnoses are made. 

Through work on mouse models, the NYU team found that cancer cells produce their own self-destructive byproducts. 

They also found that a protein called BACH1 helps cancer to migrate and spread. 

Tumors that are positive for a particular gene mutation that boosts antioxidant production in the body can spread particularly aggressively. About 30 percent of non-small cell lung cancers have this mutation.  

These patients have shorter survival times, too.  

Sustained, high levels of antioxidants – triggered by the mutation – protect BACH 1 proteins from the cancer’s own self-destructive tendencies, and encourage the disease to spread, the researchers saw. 

So the very antioxidants a cancer patient might be taking to keep oxidative stress low, might actually be feeding their disease. 

The good news, according to the NYU researchers, is that a drug that may block this pathway to migration may already be on the market. 

‘Our results finally clarify the web of mechanisms surrounding the BACH 1 signal, and suggest that an already approved drug class may counter cancer spread in about 30 percent of lung adenocarcinoma patients,’ says senior study author Dr Michele Pagano, chair of the Department of Biochemistry and Molecular Pharmacology at NYU School of Medicine.

On the other hand, her co-author Dr Thales Papagiannakopoulos a professor of pathology at NYU said: ‘For lung cancer patients, taking vitamin E may cause the same increases in cancer’s ability to spread as the NRF2 and KEAP1 mutations that our team has linked to shorter survival.

‘We hope these findings help to dispel the myth that antioxidants like vitamin E help to prevent every type of cancer.’ 

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