The Daily Mail claims a study has found a ‘Vampire treatment that rejuvenates ageing hearts’.
But before you go to grab your cloak and false pointy teeth, the research it reports on was actually in mice.
The study looked at possible ways to treat age-related cardiac hypertrophy – when the muscles of the heart become thickened, leading to a corresponding decrease in functioning ability.
Researchers joined the blood circulation of pairs of young and old mice. And one month later they looked at the resulting effects on the animal’s heart muscle.
They found that old mice who shared blood with young mice had reduced levels of cardiac hypertrophy compared to similar mice not treated with ‘young blood’.
The researchers suggest that this could be due to a chemical called growth differentiation factor 11 (GDF-11), which is high in the blood of young mice, and could help repair tissue damage.
An obvious limitation of the study is that results in mice do not always apply to humans. In humans, heart failure is where the heart cannot pump enough blood to meet the body’s needs, and this can have many different causes.
Thickening of the heart muscle is just one type of heart failure, which can be caused by high blood pressure, but can also be an inherited condition.
It is difficult to know to what extent the same growth factor could be responsible for heart muscle thickening in people with this type of heart failure. Also, its relevance – if any – to other types of heart failure (for example due to muscle damage following heart attack, due to an abnormal heart rhythm, or due to heart valve disease) is even less clear.
The findings are of scientific interest but are not going to miraculously reverse the entire disease process of heart failure in humans.
Where did the story come from?
The study was carried out by researchers from the Harvard Stem Institute and other research institutes in the US, and was funded by the American Heart Association, Glenn Foundation and National Institute of Health.
The study was published in the peer-reviewed scientific journal: Cell.
The Mail over-interprets the findings from this animal research. It is also unclear where the sub-headline ‘could be ready for use in clinical trials within 4 years’ has come from.
What kind of research was this?
The researchers say that loss of normal heart function leading to heart failure is one of the most debilitating diseases of ageing.
In particular, they discuss the type of heart failure that is often caused by high blood pressure, where the heart muscle becomes thickened and stiff (cardiac hypertrophy) so the heart chambers cannot dilate so well and fill with blood. This is known as ‘diastolic’ heart failure, as it relates to a problem when the heart is trying to refill with blood (diastolic), rather than contract (systolic).
The researchers suggest that animal studies have previously shown that chemicals circulating in the body of a young animal have been shown to restore function to the skeletal muscle of an old animal.
This process was done by what is called ‘parabiosis’ where two animals are surgically joined and so share their blood circulation.
The current animal study aimed to use a parabiosis model to try and reverse the thickening of heart muscle.
What did the research involve?
For their experiments the researchers used old mice (aged about two years) and young mice (aged two months). They used parabiosis to surgically join the blood circulation of pairs of old and young mice.
After they had been joined for one month, the researchers analysed samples from the heart muscle of the mouse pairs.
For comparison they also looked at the effect of shared blood circulation between young-young and old-old mice pairs.
They also compared with a ‘sham’ parabiosis where they surgically joined the tissue of pairs of young and old mice (at the knee joint), but without sharing their circulation.
To look into what could be the cause of any observed effects upon heart muscle, they also intensively monitored the blood pressure of mice while they were joined, and looking at levels of different chemicals in the blood of young and old mice.
What were the basic results?
The researchers found that the effect of surgically combining the circulation of the young and old mice pairs was clearly visible. The hearts of old mice that had their circulation joined to a young mouse looked much smaller and were less heavy than those of old mice who had been joined to old mice.
When they looked at the heart muscle cells under the microscope they found that the cells of old mice joined to young mice had a significantly smaller cross-sectional area than those of old mice joined to old mice, or those in the ‘sham’ parabiosis condition where their circulation hadn’t been joined to the young mice.
The effect of parabiosis on heart muscle cells was similar in both male and female old mice.
Meanwhile, the heart muscle cells of the young mice were no different in any of their three combinations (young-young, young-old or sham parabiosis).
They also carried out a number of experiments into what could be having the observed effects.
They ruled out that the smaller heart muscle cells of the old mice could have been caused by a reduction in their blood pressure. This was because all of the joined mice actually showed increases in their blood pressure compared to before they were joined.
They also considered the possibility that the changes could be due to behavioural change from the physical constraint of being joined to another mouse, rather than any effect of the shared blood.
However, if this was the case then it would be expected the heart muscles of old mice in the sham parabiosis would also have decreased in size, and they had not.
Overall, the researchers considered the effects could be due to some chemical in the shared circulation. Separately analysing the blood from young and old mice they found that several components of their blood are different. In particular, levels of a molecule called growth differentiation factor 11 (GDF-11) are found to be lower in the blood of older mice.
When they went on to treat the heart muscle cells from rats with GDF-11 in the laboratory, they found that GDF-11 prevents the thickening of the heart cells. In a further experiment involving older female mice, the hearts of a group injected with GDF-11 were significantly lighter and the cells were significantly smaller than those of a group injected with a placebo.
How did the researchers interpret the results?
The researchers’ animal experiments suggest that the thickening of heart muscle can be influenced at least in part by certain chemicals circulating in the blood. They suggest that GDF-11 could reverse thickening of heart muscle, and so conclude that ‘at least one component of age-related diastolic heart failure is hormonal in nature and reversible’.
This study finds that sharing the circulation of young and old mice appears to reverse the age-related thickening of heart muscle cells in the older animal, and it seems this could be due to a certain growth factor in the blood of the young animal. The findings will be of scientific interest, and further our understanding of the processes of heart ageing in animals.
However, the findings have very limited direct relevance to humans, and do not suggest a new treatment for heart failure.
It is also certainly unknown at this point whether increasing levels of this factor in the blood of people with this type of heart failure would somehow reverse the entire disease process. Its relevance to other types of heart failure not associated with thickened heart muscle is even less clear.
Even if further research were to demonstrate that this growth factor could have a potential role in heart failure treatments in humans; joining the circulation of young people with those with heart failure in the manner used in this study is clearly not a possibility.
If the chemical were to be extracted from donor blood, or synthetically produced, there would still be many safety issues to considered, even if the treatment were found to have an effect.
Overall the research does not suggest a new treatment for heart failure in humans, though it may represent the first step towards a possible treatment at some point at the future.
However, due to the uncertainties discussed above it is impossible to estimate the likelihood of this prediction becoming fact.