Hugs prompt the body to produce ample amounts of the hormone oxytocin, which is released in response to physical touch and repairs muscle.
The hormone is presently used to induce labour in pregnant women but it could be put to new use in slowing down sarcopenia – or muscle wasting – in the elderly, a new study claims.
Oxytocin is associated with maternal nurturing, social attachments, childbirth and sex is essential for healthy muscle maintenance and repair.
Research has found that unlike other treatments for muscle wasting, the hormone does not cause cancer and when injected, it could help old people recover from muscle injuries faster.
‘Unfortunately, most of the molecules discovered so far to boost tissue regeneration are also associated with cancer, limiting their potential as treatments for humans,’ said Irina Conboy, associate professor of bioengineering at the University of California, Berkeley.
‘Our quest is to find a molecule that not only rejuvenates old muscle and other tissue, but that can do so sustainably long-term without increasing the risk of cancer.’
The study, which was published in the journal Nature Communications, found that oxytocin, which is secreted into the blood by the brain’s pituitary gland, is a good candidate as it reaches every organ and is not known to be associated with tumours or to interfere with the immune system.
Levels of oxytocin are high in children, but it is not known when levels of the hormone start to decline in later life and how much is needed to maintain healthy tissues.
Previous research found that administering oxytocin helped prevent the development of osteoporosis in mice.
The new research also involved mice and found that blood levels of oxytocin declined with age and there were fewer receptors for oxytocin in muscle stem cells in older mice.
To determine its role in muscle repair, the hormone was injected under the skin of old mice for nine days.
The scientists found that the muscles of the mice that had received oxytocin injections healed far better than those of a control group of mice without oxytocin.
Researcher Dr Christian Elabd said: ‘The action of oxytocin was fast. The repair of muscle in the old mice was at about 80 per cent of what we saw in the young mice.’
However, the muscles of young mice given the extra boost of oxytocin did not regenerate especially quickly, leading researchers to believe it ‘boosts aged tissue stem cells without making muscle stem cells divide uncontrollably.’
The researchers also found that blocking the effects of oxytocin in young mice rapidly compromised their ability to repair muscle, which resembled old tissue after an injury.
They also studied mice whose gene for oxytocin was disabled and those left unaltered. At a young age, there was no significant difference between the two groups in muscle mass or repair efficiency after an injury.
It wasn’t until the mice with the disabled oxytocin gene reached adulthood that signs of premature ageing began to appear.
Professor Conboy said: ‘When disabling other types of genes associated with tissue repair, defects appear right away either during embryonic development, or early in life.
‘To our knowledge, the oxytocin gene is the only one whose impact is seen later in life, suggesting that its role is closely linked to the ageing process.’
Further research is planned to examine oxytocin’s role in extending a healthy life in animals and in conserving its beneficial anti-ageing effects in humans.
A growing number of scientists believe that ageing is the underlying cause of a number of chronic diseases, including Parkinson’s and Type 2 diabetes.
‘If you target processes associated with ageing, you may be tackling those diseases at the same time,’ Professor Conboy said.