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The science of ageing and how to promote longevity

Imagine a world in which everyone has the option of another year, and another, and another, with the health, vitality and vigour to enjoy it each and every day.

 

Tens of millions die from medical conditions caused by aging each and every year, and a staggering amount of money is spent on trying to defy ageing and promote longevity.

As it stands right now, the risk of suffering age-related conditions in later life can be significantly reduced for most people through diet and exercise, with serious scientific efforts presently underway to understand and intervene in the aging process; not only to prevent frailty and disease, but also to repair and reverse the root causes of aging.

Aging can be characterised as a three-stage process:

  • In the first stage, metabolic processes essential to life produce toxins (an unavoidable side effect of handling reactive chemicals)
  • Secondly, a small amount of the damage caused by these toxins cannot be removed by the body’s endogenous repair systems, and consequently accumulates over time.
  • In the third stage, the accumulation of damage drives age-related pathology, either directly (by interfering with normal metabolism) or indirectly, often where a normally benevolent repair process causes collateral damage due to maladaptive overstimulation.

In future decades researchers will assemble new biotechnologies that can defeat aging, restore the old to health and vigor, and prevent the young from ever suffering the ravages of age.

Some of these future therapies are already understood and envisioned in some detail, but remain in comparatively early stages of research. Others are just now starting to make the leap into clinical development.

Luckily there are a few things you can do right now to improve your longevity and curb anti-ageing and you may be surprised at how easy, low-cost, and downright pleasant it is to lead a healthier and thereby longer life…

Three things you can do right now:

  1. Stop damaging your health
  2. Adopt a better diet and lifestyle
  3. Support progress in rejuvenation research that may benefit you one day 

Stop damaging your health

At its most basic level, aging is nothing more than an accumulation of damage and breakages in the molecular machinery of your cells, a build up of metabolic waste products that your body cannot break down, leading to failing biological systems that are increasingly unable to cope.

Are you damaging yourself more rapidly than you realise? Do you smoke? Do recreational drugs occupy a central position in your life? Do you eat nothing but junk food or are overweight? Do you exercise little or not at all?  These things can hurt you far more than any presently available strategy for healthy living can help.

Adopt a better diet and lifestyle

The body is a complex, resilient machine. Unlike your cars, however, you can’t replace it when it breaks down. Fortunately, it’s neither difficult nor expensive to use diet and lifestyle to raise the odds of living a longer and healthier life.

 

Here are ways to how:

Adopt a calorie restriction diet – Calorie restriction is currently the only proven way of extending healthy life in mammals. While the present scientific consensus is that it will not extend life in humans to anywhere near the same degree as in mice, calorie restriction has been shown in human studies to provide a range of other beneficial effects on health, such as a greatly lowered risk of suffering all common age-related medical conditions – and it is highly praised by practitioners.

 

Eat foods that have themselves eaten well and which lower inflammation and strengthen immunity Reduce the intake of toxins (foods and substances) that cause inflammation. Choose high ORAC value foods, Give your body its essential nutrients needed for complete and optimised cell function, Build a strong immune system to withstand viruses and bacteria, Treat deficiencies, Fortress your body against any future diseases or ailments, Get rid of old and stuck toxins in the body, Try to eliminate all harmful environmental exposure, and get rid of all stress in your life.

 


Exercise as recommended by your physician or fitness coach The benefits of maintaining a modest regular level of exercise for most people are well known and well proven by many scientific studies. As is also true of calorie restriction, these benefits include a greatly reduced risk of suffering almost all of the common age-related diseases. S
trength and maintenance of muscle mass, are two critical components of longevity. Read this article by Ben Greenfield on a good fitness strategy to promote longevity.


Supplement – Take a modest amount of supplements appropriate to your age and health – There is a wealth of supplement information available, but much of it is worthless, propagated by irresponsible sellers. This is perhaps the hardest topic to research, and in the end you will have to make a number of decisions yourself based on incomplete or contradictory scientific evidence.

 

Support progress in rejuvenation research

Even the best of present day practices will make only a comparatively small difference to your expected future life span, thats why your support in further medical research aimed at extending the healthy human lifespan, is just as important as taking care of your health today.

The aging process causes great suffering for hundreds of millions worldwide each and every day, and without adequate scientific breakthroughs you will be one of them. Aging will one day be cured, just like any other medical condition, but with your help science can ensure that this day arrives soon enough to matter.

A revolution in biotechnology is presently underway, and the medicine of the near future holds great promise but the young field of rejuvenation research remains for the most part poorly funded, and most of the public neither understands nor appreciates the possibilities offered by this research.

 

Further reading…

 

What Is the Damage of Aging?

 

Fortunately, it seems that all aging-related damage known to accumulate in the human body can be classified into just seven clearly defined categories. For each category, the SENS foundation incorporates a mechanism for repairing the damage, using either existing biotechnology or readily foreseeable extensions thereof.



Cell Loss
The most straightforward damage category is the loss (death without replacement) of cells, either as a result of chronic injury or acute trauma, mediated by apoptosis, by autophagic cell death, and/or by necrosis. Such losses lead to tissue atrophy, compromising the function of the organs involved; examples include Parkinson’s disease, sarcopenia, autoimmune diabetes, and presbycusis. Therapy involves the introduction of stem or progenitor cells (and/or stimulation of the proliferation of endogenous progenitors), either systemically with the assistance of appropriate targeting mechanisms, or locally via a tissue-engineered construct.

Cell Death-Resistance
Conversely, the accumulation of excessive numbers of cells refractory to normal homeostatic apoptosis can also be harmful. The most obvious example in the context of Western societies is obesity, but there are more subtle manifestations; the imbalance between anergic and naïve T-lymphocytes that characterizes immunosenescence being a prime example. Treatment is in this case conceptually straightforward; identify biomarkers that selectively target the undesirable cells, and deliver cytotoxic drugs or viruses to ensure their destruction.

Cell Overproliferation
This deals with damage to the genomic DNA, in the form of mutation (changes to the base-pair sequence) and epimutation (changes to the moieties that decorate the DNA molecule and influence its transcription). Fortunately, this is one area in which evolution has done most of the hard work for you. Since the emergence of vertebrates (at least), the most serious problem originating from mutation has been cancer, which has the capacity to kill an organism if one single cell acquires enough mutational load, whereas any other mutation can in general become lethal only if it afflicts a substantial proportion of the cells in a given tissue. The proofreading mechanisms evolved to prevent cancer are, as a result, more than sufficient to keep non-cancerous mutations under control. Thus, this strictly molecular category of damage is in fact best treated as a cellular one.

 

Telomerase

The telomere is a special functional complex at the end of linear eukaryotic chromosomes, consisting of tandem repeat DNA sequences and associated proteins. It is essential for maintaining the integrity and stability of linear eukaryotic genomes. Telomere length regulation and maintenance contribute to normal human cellular aging and human diseases. The synthesis of telomeres is mainly achieved by the cellular reverse transcriptase telomerase, an RNA-dependent DNA polymerase that adds telomeric DNA to telomeres. Expression of telomerase is usually required for cell immortalization and long-term tumor growth. In humans, telomerase activity is tightly regulated during development and oncogenesis. The modulation of telomerase activity may therefore have important implications in antiaging and anticancer therapy.


Intracellular Junk
While cells are generally very efficient in detecting (particularly via the unfolded protein response) and recycling damaged or surplus biomolecules, there are some exceptions; substances which are genuinely refractory to degradation or excretion. The resulting accumulation of “junk” compromises the cell’s metabolism, at best impairing its normal function, and at worst leading to cell death. The accumulation of lipoproteins in atherosclerotic plaques and the phototoxicity of A2E that drives dry macular degeneration are two of the best-studied examples of this mechanism, which may be treated by augmenting the native degradation machinery by introducing novel enzymes capable of tackling the most recalcitrant targets. Such enzymes typically need to be introduced into the lysosome, cells’ “garbage disposal machinery of last resort.”

Extracellular Junk
Not all waste products accumulate within the cell; the infamous amyloid plaques of Alzheimer’s disease, as well as the amyloids associated with type II diabetes and systemic amyloidosis, accumulate in the extracellular space. Fortunately, the body already possesses an excellent mechanism for removing undesirable substrates from this compartment; the phagocytic cells of the immune system, and thus the elimination of this junk is essentially a problem of developing an effective and safe vaccine. (In a few cases, it may be necessary to apply the principles of the previous category, lysosomal enhancement, to ensure that the immune cells are able to fully degrade the substances they consume.)

Tissue Stiffening
Protein comprises the bulk of the extracellular matrix; in many cases the proteins involved are laid down in early life and then recycled very slowly, if at all, in adulthood. The function of the tissues supported by such proteins, such as the elasticity of the artery wall, is dependent on their maintaining the correct molecular structure. As the years pass that structure becomes progressively compromised, primarily due to crosslinking induced by reactive molecular species, especially a network of reactions initiated by circulating sugars and collectively termed “glycation.” In the arteries, this stiffening leads to increasing blood pressure and all its downstream consequences. Fortuitously, such crosslinks are chemically distinct from any that are enzymatically derived, and the therapeutic strategy is thus to develop drugs or enzymes capable of cleaving these crosslinks to restore the original biophysical function.

Mitochondrial Defects
Mitochondrial DNA (mtDNA) is uniquely vulnerable, being in close proximity to an intense source of reactive species (the respiratory chain) while lacking many of the sophisticated repair mechanisms available to nuclear DNA. There is a well-established accumulation of damage to mtDNA associated with aging, linked, as one would expect where such a vital cellular component is involved, to a very broad range of degenerative conditions. However, of the thousand or so protein components of a mature mitochondrion, only thirteen are actually encoded in the mtDNA, the remaining genes having moved over evolutionary time to the nuclear DNA, from where their products are efficiently translocated back to the mitochondrion. The solution in this case is thus not to repair damage to the remaining genes, but rather to introduce translocation-ready variants of them into the nuclear genome, a technique termed allotopic expression, obviating the issue of maintaining the mtDNA itself.

The above seven-category formulation is descriptive, not prescriptive. However, the fact that no new categories of damage have been discovered since 1982, despite the dramatic progress in bioanalytical techniques since that time, suggests that any other categories accumulate too slowly to have any bearing on health within the contemporary human lifespan.

 

Source + more info: Strategies for Engineered Negligible Senescence (SENS) coordinated by the SENS Research Foundation and other scientific groups.


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