Food and diet

Too many antioxidants 'bad for your heart'

Despite popular belief, antioxidants could be doing more harm to health than good reported the Daily Mail . Antioxidants are thought to be beneficial as they neutralise free radical molecules and many disorders “are wholly or partly blamed on free radicals”, the newspaper explained on August 10 2007. Free radicals are highly reactive, unstable molecules that cause atoms in the cells of the body to lose an electron; this process, called oxidative stress, causes damage.

However, the Daily Mail said that scientists have found that too much antioxidant can also damage cells. Researchers found that “high levels of antioxidants could make atoms gain electrons, in a process called reductive stress – causing untold damage” the newspaper reported. Yet, it is too soon to conclude that antioxidants are bad for health

The newspaper stories are based on the reports of research carried out in mice. The study underlying these stories was well-conducted, although we must be cautious about extrapolating findings from animal studies directly to humans. The findings are interesting and should be the basis for further research into the characteristics of degenerative diseases in humans. Importantly the study is about antioxidants occurring naturally in cells and does not consider the effects of ingested antioxidants, for example, from fruit and vegetables.

Where did the story come from?

Namakkal Rajasekaran and colleagues from the University of Utah School of Medicine and other medical institutions in the US conducted this research and it was published in the peer-reviewed medical journal, Cell .

What kind of scientific study was this?

This study is a laboratory-based animal study carried out in mice. A genetic mutation that occurs in humans and is known to be linked to degenerative diseases, such as cardiomyopathy (weakness and damage of heart muscle), was inserted into the DNA of the mice. This mutation causes cells to produce a malformed protein and in this experiment, the mice were bred so that the mutation appeared in heart tissue. The mutation caused the heart tissue to overproduce this malformed protein and this led to a cardiomyopathy-like disease in the mice.

The mice were bred in different groups, one group of mice had a high level of malformed protein in the heart tissue and the other group had a lower amount of malformed protein. The researchers then compared the disease characteristics between the two groups of mice with the human gene inserted into their DNA with normal mice. 

What were the results of the study?

The following three findings are most relevant to this story:

  • Cardiac hypertrophy, progressive heart failure and premature death occurred in the mice who produced a large amount of malformed protein; there were some heart weaknesses in the group of mice who  produced a lower amount of malformed protein.
  • In the group of mice who produced a large amount of malformed protein, the protein caused the activation of a stress response in the cells. 
  • This stress response pathway was linked to an increase in the concentration of antioxidant enzymes in the cells. This excess production of antioxidant enzymes in the cell resulted in a process called “reductive stress”. This is when cells gain an electron and results from the over-correction of the effects of free radicals – this can also be harmful to cells.

What interpretations did the researchers draw from these results?

The researchers recognise that reductive stress is an important metabolic step in of this type of cardiomyopathy. They say that this reductive stress "might also represent a common mechanism" in the disease chain for several degenerative diseases.

What does the NHS Knowledge Service make of this study?

This research appears to have been well conducted and its findings should be a starting point for further research into the cellular effects of diseases such as cardiomyopathy. As the study was conducted in mice, we should be cautious about extending the findings directly to humans, where metabolism is quite different.

  • It is unclear how many mice were included in this study; this is important as smaller studies are inherently less reliable than larger ones.
  • Although the study used a human gene mutation (expressed in mice), it only explored the effects of one particular mutation on disease. Degenerative diseases, including cardiomyopathy, are likely to be complex diseases with a variety of different causes. The effects of other mutations on cell function, or the role of other medical factors in the development of disease have not been studied here.
  • Additionally, no assumptions can be made on the role of reductive stress in the disease processes of other conditions such as Alzheimer’s disease and Huntington’s disease, both of which are mentioned by the newspaper reports.
  • This study also did not investigate the effects of externally ingested antioxidants (for example from fruit and vegetables) on health outcomes.

With these limitations in mind, it is too soon to conclude that antioxidants are bad for health.

NHS Attribution