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How Do We Age?

Two things no-one can avoid: Death and Taxes

Most of us have heard and joked about this little gem, but take away the black humour, and take on the services of a good accountant, we are left with thoughts of aging and what it will mean for each of us.

We know we have a finite time.

We know that our years will vary and that the latter ones are likely to be less vigorous than earlier years.

We know that “average life spans” change over time and that they appear to be lengthening.

We know that some behaviors are likely to shorten our lives (smoking, excessive drinking, drugs) and some “may” lengthen it (avoidance of the above) and overall adopting a healthy lifestyle.

We know that disease can occur but not always, and that our genetic predisposition is an important factor.

Much has been written on the subject so this will be a broad-brush overview designed not so much to explain in detail how we age, but to trigger an interest in what factors are in our control that can be of benefit to us during our aging process.

My first problem was the spelling of aging … both aging and ageing are correct but I have chosen the former for no reason; I just want to be consistent.

Why do we age? is different to How Do We Age? The former can only be theorised and there likely is just one answer and it may be along spiritual lines but it is the How Do We Age? that concerns most of us as we may like to think we can have a positive input in our “lot”. There are several theories, supported by research, and it is agreed that a number of them may simultaneously exist.

Cross-linking … glycation hypothesis of aging

Put simply, our proteins, DNA and other structural molecules develop inappropriate attachments or cross-links to one another. These unnecessary links or bonds decrease the mobility or elasticity of proteins and other molecules. Proteins that are damaged or are no longer needed are normally broken down by enzymes called proteases. However, the presence of cross-linkages inhibits the activity of proteases. These damaged and unneeded proteins, therefore, stick around and can cause problems.

Eg: Cross-linking of the skin protein collagen, for example, has proven at least 
partly responsible for wrinkling and other age-related dermal changes.

Eg: Cross-linking of proteins in the lens of the eye is also believed to play a role in age-related cataract formation.

Eg: Researchers speculate that cross-linking of proteins in the walls of arteries or the filtering systems of the kidney account for at least some of the atherosclerosis (hardening of the arteries) and age-related decline in kidney function observed in older adults.

The Evolutionary Senescene Theory of Aging

This is a widely accepted theory which proposes that aging is the biological deterioration of the functions characteristic of complex lifeforms and this includes the plant, animal and human kingdoms.

The Neuroendocrine Hypothesis of Aging

This theory purports that as time passes, our neuroendocrine system becomes less functional. The neuroendocrine system refers to the complex connections between the brain and nervous system and our endocrine glands, which produce hormones. Initially it was thought that growth hormones may prolong life but a recent study of humans who genetically lack an ability to use growth hormone found that these people were protected against cancer and the development of adult-onset diabetes. So once again, aging may certainly be tied to this system but conclusive answers have not yet been discovered.

The Oxidative Damage / Free Radical Hypothesis of Aging

Oxidative free radicals are one of the toxic byproducts of normal cell metabolism. Natural substances within our cells called antioxidants absorb and neutralize these dangerous free radicals. But those that escape this cleaning process can damage DNA, proteins, and mitochondria. This damage, called oxidative damage, accumulates over time.

Mitochondria within our cells transfer energy into useful forms. Mitochondria is vital to us; 90% of the cell’s free radicals are produced in the mitochondria so unless they are quickly neutralised by anti-oxidants, mitrochondrial damage occurs; the mitochondria become inefficient and unable to generate sufficient energy to meet cellular demands. And free radicals are introduced into our system in our diet, amongst other things, hence the big alert regarding the importance of anti-oxidants.

The Rate of Living Theory of Aging

The rate of living theory of aging 
is perhaps the oldest explanation of aging. Ancient philosophers believed that we possess a finite amount of some “vital­ substance.” When that substance is consumed, we die. 20th century scientists “tweaked” this theory to “energy consumption limits longevity” and modern day scientists have concluded (at this time) that oxidative damage is a mechanism that contributes to the aging process.

The Replicative Senescence Hypothesis of Aging

This theory was put forward 50 years ago by Drs Leonard Hayflick and Paul Moorhead when it was discovered that many human cells have a limited capacity to reproduce themselves by dividing. It was seen that human cells can undergo 40-60 cell divisions, then can divide no more. They have reached the “Hayflick Limit”. What determines this Limit is the length of the cell’s telomeres (the protective caps at the ends of chromosomes). On each division, a chromosome loses a small bit of its telomeres until after 40-60 divisions, the telomeres are too short and the cells can divide no more.

But this theory is not without problems as some cells either do not replicate or do not replicate as often as others; an enzyme called telomerase exist in mice which routinely lengthens telomeres and when this enzyme is genetically engineered (in mice) to accelerate or slow, then their aging speeds up or slows down. Humans rarely have this enzyme in non-cancerous cells. So whilst this theory has some validity, it is not the full story.

But the following indicates that it may indeed play a part:
Certain skin cells produce collagen during their younger, reproductive years. When they reach senescence (old age) and can no longer divide, they produce collagenase, an enzyme that breaks down collagen. Some researchers suggest that this process may be responsible for the thinning and wrinkling of skin as we age.
(This is where you may like to look at what Sea Buckthorn Complete Vitality can do in terms of tissue regeneration)

As an aside, you may remember 1996 when Dolly the sheep was cloned from the mammary cells of a 6 year old ewe? At 3 years of age, Dolly’s biological age was calculated as 9 years of age. Long story short, Dolly gave birth to lambs but her health deteriorated rapidly until she was euthanized in 2003 at less than 7 years of age suffering from multiple age-related problems. It was concluded that the 6 year old ewe’s telomeres had naturally shortened over that time so Dolly was old before her time.

At Uni we were given a nutshell explanation of the above which most of us can understand quite readily … when you photocopy something, it is clear but if you continue to photocopy the photocopy (as opposed to the original) the result is a copy that becomes increasingly less clear. At some point one reaches a limit whereby any more copying is illegible.

So …. can we do anything to help ourselves?

Yes – apparently so:

  • caloric restriction: in a nutshell, not over-eating with increased effects the earlier on in life this is initiated. This is about reducing calories whilst maintaining adequate content of essential nutrients. Whilst this has been studied with animals, the same prolonged lifespan appears to occur with humans as shown by
    • the Okinawans (the people of Okinawa, an island SW of Japan’s main landmass, known for their longevity. They eat a plant-based diet that is high in nutrients but low in calories. Also, they live by spiritual values, have a strong social network, enjoy regular healthy levels of sun exposure and stay physically active. They also let bygones be bygones (an attitude) and enjoy simple pleasures and work at being likable so as to attract young people into their lives.)
    • the (short-lived – it was sabotaged) Biosphere 2 Project and
    • several short-term studies in humans (cannot give references here but credibility would more likely lie in long term cross-generational studies. The very nature of this theory wouldn’t seriously be supported by anything short term; what do you think?)
  • Resveratrol (found naturally in peanuts, pistachios, grapes, red and white wine, blueberries, cranberries, and even cocoa and dark chocolate
  • Vit E and possibly Vit C
  • Foods with a high oxygen radical absorbance capacity (ORAC) may be more protective than other antioxidant preparations
  • Methionine restriction which may be achieved using a predominately vegan diet so foods to avoid are chicken and fish; then milk, red meat and eggs. Foods that are low in methionine are fruits, nuts, vegetables, grains and beans. Pinto beans and lentils are the high protein foods that are also low methionine.

All this is very interesting, I think, and the dietary changes we can make are very much under our control but I shall leave it here and let you digest this information so you can further your own research. Good luck … live long and healthy!

We are not healthcare or medical professionals and the information contained here is not to be taken as medical advice. It is recommended that you consult you healthcare professional prior to taking any supplements and always read the label, use only as directed, and if symptoms persist, see your healthcare professional.