What is Ageing?
Ageing, the exact mechanism is unknown, however Genetic influences are thought to be paramount.
This is the theory of programmed ageing. It says that when we are born our cells are already programmed to die at a certain age:
- Bigger animal species tend to live longer than smaller ones, and this is not related to their metabolic rates
- Longevity tends to show familial patterns in humans suggesting that there may be a longevity gene
- The gene for a disease characterized by early ageing (Werner syndrome) has been discovered
- There is clearly a genetic component to ageing
Environment does play a role
Adverse environmental factors may occasionally accelerate ageing but mostly they increase vulnerability to the diseases of old age, including those that are potentially fatal. The basis of preventative medicine is to remove negative environmental influences such as a high fat diet, or else increase beneficial ones, such as exercise. There is some evidence that dietary restriction without malnutrition can slow down ageing.
The ageing body
The longest we can currently hope to live to is about 120 years Deterioration in body function, and death, is ultimately inevitable. Only one woman, Madame Jeanne Calment, from Arles in France, had reliable proof that she had lived longer. She was born on February 21, 1875 and died August 4, 1997 at the age of 122. She took up fencing at 85, still rode a bicycle at 100, and released a rap CD at 121. She claimed she was "never bored." By the end she was blind, nearly deaf and in a wheelchair, but still mentally alert and spirited.
The goal of most research on ageing is to improve the quality of our later years. Already, we are living longer than ever before but we urgently need to find ways to slow or prevent conditions like Alzheimer's disease, osteoporosis and arthritis, that make life a misery for so many older people.
The ageing cell DNA mutations are more likely the older a cell is, simply because every time a cell divides (its way of reproducing) it is vulnerable to damage, and older cells will have undergone more divisions. Mutations have a number of effects:
- Some mutations result in altered cell and tissue function
- Most cells are programmed to reproduce a fixed number of times and then die by cell suicide (apoptosis). Apoptosis is triggered abnormally by some DNA mutations
- When apoptosis is inhibited (also by mutations), a cancer may develop
Another type of cell or tissue death called necrosis occurs when several cells are irreversibly damaged by an overwhelming external injury, such as oxygen starvation. Nerve, kidney and heart muscle cells do not divide and reproduce and so as they are lost through necrosis and wear and tear they are not replaced.
The ageing immune system
Slowing of cell division, which may occur through DNA mutations, reduces the response of the immune system, which depends on rapid defence cell reproduction and mobilization. Reduced immunity with age means that:
- Infections are more likely to take hold
- Dormant infections can be reactivated
Auto antibodies (directed at their host body), and therefore autoimmune problems such as rheumatoid arthritis, are more common in old age
As well as causing autoimmune problems, auto antibodies may be implicated in a number of age-related problems, including vascular disease.
Main Consequences of ageing
- Loss of neuronal function Ð Dementia, age related deafness, age related visual problems
- Poorer immune response
- Decreased elasticity and self repair of the skin, hence the development of wrinkles and sagging skin
The University of Sunderland carried out independent research into the effect of various wavelengths of infrared light upon human white blood cells. Published paper
The most significant finding of this independent research was the phenomenon of Cytoprotection conferred by treatment with 1072nm light which is thought to be associated with stimulation of iNOS. iNOS is currently thought to be associated with cellular repair and regeneration.
We age because our cells lose the desire to regenerate and repair themselves, which ultimately results in cell death and decline of the organ functions.
But what if… there was a technology that told the cells to repair themselves and that technology was something as simple as a specific wavelength of light Ð 1072nm.
Near infrared light penetrates human tissues relatively well, even penetrating the human skull, as much as 2-5% of incident infrared light penetrates the skull to reach the human cortex or higher brain.
Independent research at Sunderland University has demonstrated that low power 1072nm light improves the memory and intelligence of middle aged mice with memory impairment. Published paper
Ageing and the Skin
In addition to the natural programmed ageing process which determines that skin becomes less elastic and more easily damaged environmental UV light has been shown to cause significant photo ageing which accelerates the process. Research at Sunderland University showed that 1072nm light not only increased longevity of human cells but also protected the cells against the toxic effects of UV irradiation. Restorelite anti-ageing treatment was the spin off development from this research. Published paper
Ageing and the Brain
The brain below is a normal brain
Cerebral atrophy occurs when a substantial number of brain cells are lost due to many processes including the ageing process. We believe 1072nm light, if used daily can prevent this loss of brain cells and prevent and to a certain extent reverse the intellectual loss associated with ageing.
The brain below has cerebral atrophy
Comparing the normal and the atrophied brain it can been seen that are there gaps between the folds of the brain indicating substantial loss of neural tissue.
“Working memory (WM), the process by which information is coded into memory, actively maintained and subsequently retrieved, declines with age. To test the hypothesis that age-related changes in prefrontal cortex (PFC) may mediate this WM decline, we used functional MRI to investigate age differences in PFC activity during separate WM task components (encoding, maintenance, retrieval). We found greater PFC activity in younger than older adults only in dorsolateral PFC during memory retrieval. Fast younger subjects showed less dorsolateral PFC activation during retrieval than slow younger subjects, whereas older adults showed the opposite pattern. Thus age-related changes in dorsolateral PFC and not ventrolateral PFC account for WM decline with normal aging.”
Isolating the neural mechanisms of age-related changes in human working memory
Bart Rypma & Mark D'Esposito
Helen Wills Neuroscience Institute and Department of Psychology, University of California, Berkeley, 3210 Tolman Hall, Berkeley, California 94720-1650, USA
Ageing and hearing
A young adult has this type of audiogram below, which is a flat sensory line from the low to the high frequencies:
With advancing years there is loss of hearing initially in the higher frequencies, however this loss gradually is extended to the more useful lower frequencies:
Noise related or industrial deafness has the classic loss in the lower frequencies, which in old age be superimposed upon age related losses.
Young adult with noise related hearing loss:
Older person with age related hearing loss together with the classic noise induced hearing loss:
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