Makoto Koto is head of the Division of Anti-Ageing and Longevity Science at the University of Yokohama. His fascinating argument on how and why we age can be summarised as follows.
- Evolution has programmed us to be healthy long enough to reproduce and pass on our genes.
- To do that humans have evolved a sophisticated immune system that neutralises the frequent viral and bacterial (pathogen) attacks during the years before we have finished reproducing – ie have lived long enough to bring up children.
- An effective immune response unfortunately also triggers the release of pro-inflammatory proteins.
- So, each time the immune system overcomes a pathogen, it can leave a legacy of low level inflammation. This sub-clinical (unnoticeable) inflammation builds up over the decades and is strongly linked to the development of heart disease, arthritis, diabetes, cognitive decline and some cancers.
- In other words the mechanism that keeps us healthy until we have passed on our genes – (up to about age 50) – is the same mechanism that triggers disease in our later years.
Makoto Kota’s conclusions are echoed by other researchers:
“Inflammation may be considered a core process of human ageing … and the major degenerative diseases of later life, atherosclerosis, Alzheimer’s disease and cancer” Caleb E. Finch, Dept of Biological Sciences, USC College, University of Southern California
Woody Allen once quipped: “Nobody wants to get older – but look at the alternative!” But it’s not getting older that’s the problem – it is what sometimes comes with it. Luigi Ferrucci, chief of the Baltimore Longitudinal Study of Aging says: “If you talk to many older people, what they are really desperate about is that they are going to be sick, dependent and have to rely on others.”
But getting older doesn’t have to be like that – if you act when you are younger. There are people who are slow agers – who defy the ageing process. Do they have a secret? These and other scientists now think so.
According to a Discover magazine article by Kathleen McGowan—entitled “Can We Cure Aging?”—scientists in recent years “have overturned much of the conventional wisdom about getting old.” They now realize that aging “is actually something our own bodies create, a side effect of the essential inflammatory system”
“This (immune) inflammatory system is initially designed to protect us against infectious diseases . . . but as we fight off invaders, some residual inflammation usually remains, called chronic, sub-clinical inflammation”. ‘Chronic’ merely means continuous and ‘sub-clinical’ means undetected. The problem is that this chronic inflammation is not normally noticeable as it occurs at the cell level. But according to the Discover article it, “inflicts collateral damage on ourselves, breaking down our own tissues.”
In other words we age.
It logically follows that if we can reduce this residual inflammation, we should slow our aging and simultaneously reduce the risk of degenerative diseases like diabetes, dementia and heart disease. As Kathleen McGowan writes, tackling inflammation “would almost surely allow us to live better, increasing the odds that we could all spend our older age feeling healthy, vibrant and vital.”
Not something to worry about yet? The problem is that degenerative diseases – like heart disease, stroke and dementia do not occur overnight. They are the end result of success in warding off pathogen attacks in our earlier years and the consequent gradual increase in inflammation and tissue breakdown. These diseases typically develop over twenty years or more. So if you want to be healthy at 70, you need to take action at 50.
What to do is the subject of the free report called Inflamm-ageing. Get it here now.
Makoto Goto: Inflammation and regeneration: Vol.29 No.4 SEPTEMBER 2009 249 www.jsir.gr.jp/past_journal/2904/0249-0257.pdf
Inflammaging and anti-inflammaging: a systemic perspective on aging and longevity emerged from studies in humans. Franceschi C, Capri M, Monti D, Giunta S, Olivieri F, Sevini F, Panourgia MP, Invidia L, Celani L, Scurti M, Cevenini E, Castellani GC, Salvioli S. Department of Experimental Pathology, University of Bologna, via S. Giacomo 12, 40126 Bologna, Italy. email@example.com http://www.ncbi.nlm.nih.gov/pubmed/17116321