Thursday, March 29, 2012

The Seven Deadly Things

Jack Dikian
March 2012

We know that life expectancy has increased over the last 200 years. An average man born in 1800 had a life expectancy of 35 years. In 1900, he would have made to 47 and by 1950, average life expectancy was up to 68 years. Today it's up to about 78.

We also hear of people living well past the age of 100 and when they are asked to tell us their secret, they may tell us it’s the food they eat, the wine they drink, etc. Others list their no-no’s. For example one very elderly women in the US explained her 3 no-no’s as rules growing up. No smoking, no drinking, and no sex.

Although Ponce de Leon never found the legendary fountain of youth, today many are working towards stopping the clock or at least slow it down. And, I’m not talking about anti-age or anti-wrinkle creams freely advertised everywhere we care to look.

In the 1999 book The Mitochondrial Free Radical Theory of Aging by British biogerontologist, Aubrey de Grey1 the author coined the term Strategies for Engineered Negligible Senescence (SENS) which is basically a tissue-repair strategy intended to rejuvenate the human body and allow an indefinite lifespan. De Grey proposed 7 types of aging damage (see below) or “The Seven Deadly Things”.

As an aside, in 2005, the Methuselah Foundation and MIT Technology Review announced a $20,000 prize inviting any molecular biologist, with a record of publication in biogerontology, to prove that the alleged benefits of SENS were so wrong that it is unworthy of learned debate. No one has claimed the prize.

The Seven Deadly Things

1. Cancer-causing nuclear mutations/epimutations

These are changes to the nuclear DNA (nDNA), the molecule that contains our genetic information, or to proteins which bind to the nDNA. Certain mutations can lead to cancer, and, according to de Grey, non-cancerous mutations and epimutations do not contribute to aging within a normal lifespan, so cancer is the only endpoint of these types of damage that must be addressed.

2. Mitochondrial mutations

Mitochondria are components in our cells that are important for energy production. They contain their own genetic material, and mutations to their DNA can affect a cell’s ability to function properly. Indirectly, these mutations may accelerate many aspects of aging.

3. Intracellular aggregates

Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can’t be digested simply accumulate as junk inside our cells. Atherosclerosis, macular degeneration and all kinds of neurodegenerative diseases (such as Alzheimer's disease) are associated with this problem.

4. Extracellular aggregates

Harmful junk protein can also accumulate outside of our cells. The amyloid senile plaque seen in the brains of Alzheimer’s patients is one example.

5. Cell loss

Some of the cells in our bodies cannot be replaced, or can only be replaced very slowly - more slowly than they die. This decrease in cell number causes the heart to become weaker with age, and it also causes Parkinson's disease and impairs the immune system.

6. Cell senescence

This is a phenomenon where the cells are no longer able to divide, but also do not die and let others divide. They may also do other things that they’re not supposed to, like secreting proteins that could be harmful. Immune senescence and type 2 diabetes are caused by this

7. Extracellular crosslinks

Cells are held together by special linking proteins. When too many cross-links form between cells in a tissue, the tissue can lose its elasticity and cause problems includingarteriosclerosis and presbyopia.

1 In 1986, he co-founded Man-Made Minions Ltd to pursue the development of an automated formal program verifier.

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