19 March 2020

As we get older, we are at risk of developing many diseases such as type II diabetes, alzheimer’s disease, chronic kidney disease, strokes and heart failure.

At a recent OBN meeting, the topic of “what makes us age, and can we stop it?” was discussed. Pharmaceutical companies focus efforts on targeting specific disease areas rather than the underlying pathology of ageing. However, extending life expectancy is not the answer if in the last decade of our lives, we are plagued by one or more of these “age related diseases”.  We need to increase “healthy life” expectancy. 

Senescent cells have irreversible cell cycle arrest and their numbers increase with increasing age. If senescent cells are implanted into young mice, the animals age quicker than normal. In addition, senescent cells fail to correctly recycle intracellular proteins. This “cellular housekeeping” removes the misfolded proteins via destruction in the lysosome and is known as autophagy. Fasting and exercise induce autophagy.

So, what has broccoli got to do with this?
Broccoli contains a compound called spermidine and diets rich in spermidine have been associated with increased lifespan. External supplementation with spermidine extends lifespan and health span across species, including in yeast, nematodes, flies and mice. Spermidine stimulates cytoprotective autophagy and this is how it is thought to increase lifespan.

So, what is the future for those of us who hate cruciferous vegetables?
Fortunately for me and many small children, wheat germ is an alternative. If you believe this theory, maybe the real way forward is brown bread broccoli sandwiches!

In future, health care providers, pharmaceutical companies, regulatory agencies and payers will need to consider a paradigm shift where age-related changes, rather than specific diseases, are targeted.

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