In a previous article
we discussed whether young blood might have regenerative effects. When researchers first saw positive effects in old mice when their circulatory systems were merged with a younger mouse, they looked deeper and found that a particular protein, GDF 11, declined with age. When they increased this protein, mice showed improved cardiovascular health – reversing some of the thickening of the arteries that comes with age. The community immediately jumped at the news, but a later study called the results into question, suggesting that GDF 11 levels actually increase in humans with age and inhibit muscle recovery.
So how can both groups be saying opposite things?
Well the second study displayed that the original team had been using a test which doesn’t distinguish between GDF 11 and another almost identical protein called myostatin. Myostatin is a well known muscle growth inhibitor, so it seemed odd that GDF 11 was having the opposite effect. This made researchers sceptical.
When they injected GDF 11 after damaging a mouse’s skeletal muscle, they also found it inhibited proper healing. The picture was now looking less rosy. In the first group, GDF 11 did thin aged heart tissue and enable better activity, but it apparently also inhibited recovery in other areas. The situation was quickly becoming another warning of not to get carried away after just one positive study. Importantly both studies used different methodology and researchers also wondered if too much or too little were both equally bad, so the case is far from settled.
Was GDF 11 responsible for health improvements in mice?
While GDF 11 may be another case of oversimplification and the benefits of young blood likely lie with multiple factors, new research at UCSF does reinforce that it has some positive effect, at least in cardiovascular health. A team analysed 1,899 people and found that those individuals with highest levels of both GDF 11 and myostatin were least at risk of dying from cardiovascular disease. The top 25% were also less than half as likely to die from any related causes.
“Individuals with heart disease who have relatively high concentrations of these proteins have much lower odds of dying and much lower odds of experiencing devastating outcomes that we associate with aging, including heart attacks, strokes and heart failure. We also found that combined levels of GDF11 and myostatin in humans decline with advancing age, but that the rate of this decline varies among individuals.”
Many processes in the body are a careful balancing act, like growing and losing muscle. GDF 11 or myostatin may prevent hypertrophy in the heart, but potentially have side effects like inhibiting muscle regeneration; at this point we simply don’t know enough. Are declining GDF 11 levels just a response to other changes, or are they a cause in themselves? Other questions remain as well, like are there multiple forms of GDF 11? Is myostatin getting confused with GDF 11? Could targeted GDF 11 treatment be beneficial, but only in specific organs? We shouldn’t forget that prior research was conducted on mice, so can these findings be applied to humans?
We need more research to uncover exactly what’s happening, but watch this space.
Read more at UCSF News