Entropy always wins.
Each multicellular organism, using energy from the sun, is able to develop and maintain its identity for only so long. Then deterioration prevails over synthesis, and the organism ages. Aging can be defined as the time-related deterioration of the physiological functions necessary for survival and fertility. The characteristics of aging—as distinguished from diseases of aging (such as cancer and heart disease)—affect all the individuals of a species.
Recent studies have indicated that there are genetic components to senescence, and that the genetically determined life span characteristic of a species can be modulated by altering genes or diet.
The maximum life span is a characteristic of the species. It is the maximum number of years a member of that species has been known to survive. The maximum human life span is estimated to be 121 years.
The life spans of tortoises and lake trout are both unknown, but are estimated to be more than 150 years. The maximum life span of a domestic dog is about 20 years, and that of a laboratory mouse is 4.5 years.
However, a person cannot expect to live 121 years, and most mice in the wild do not live to celebrate their first birthday. The life expectancy, the amount of time a member of a species can expect to live, is not characteristic of species, but of populations. It is usually defined as the age at which half the population still survives. A baby born in England in the 1780s could expect to live to be 35 years old. In Massachusetts during that same time, the life expectancy was 28 years. This was the normal range of human life expectancy for most of the human race in most times. Even today, the life expectancy in some areas of the world (Cambodia, Togo, Afghanistan, and several other countries) is less than 40 years. In the United States, a child born in 1986 can expect to live 71 years if male and 78 years if female.
So, now we understand what aging is, and what this means in respect of life expectancy (and now that we’re all suitably depressed, as a result), let’s look more closely at the actual causes of aging.
Oxidative damage
One major theory sees our metabolism as the cause of our aging. According to this theory, aging is a by-product of normal metabolism; no mutations are required. About 2–3% of the oxygen atoms taken up by the mitochondria are reduced insufficiently to reactive oxygen species (ROS). These ROS include the superoxide ion, the hydroxyl radical, and hydrogen peroxide. ROS can oxidize and damage cell membranes, proteins, and nucleic acids. Evidence for this theory includes the observation that Drosophila (or fruit flies) that overexpress enzymes that destroy ROS (catalase, which degrades peroxide, and superoxide dismutase) live 30–40% longer than do controls
General wear-and-tear and genetic instability
“Wear-and-tear” theories of aging are among the oldest hypotheses proposed to account for the general scenescent phenotype. As one gets older, small traumas to the body build up. Point mutations increase in number, and the efficiencies of the enzymes encoded by our genes decrease. Moreover, if a mutation occured in a part of the protein synthetic apparatus, the cell would make a large percentage of faulty proteins.
If mutations arose in the DNA-synthesizing enzymes, the rate of mutations would be expected to increase markedly, and the scientists Murray and Holliday (1981) have documented such faulty DNA polymerases in senescent cells. Likewise, DNA repair may be important in preventing senescence, and species whose members’ cells have more efficient DNA repair enzymes live longer. Moreover, genetic defects in DNA repair enzymes can produce premature aging syndromes in humans (Yu et al. 1996; Sun et al. 1998).
Another theory of the causes of aging is that of telomere length, and what this means for cell division.
Telomeres are repeated DNA sequences at the ends of chromosomes. They are not replicated by DNA polymerase, and they will shorten at each cell division unless maintained by telomerase. Telomerase adds the telomere onto the chromosome at each cell division. Most mammalian somatic tissues lack telomerase, so it has been proposed (Salk 1982; Harley et al. 1990) that telomere shortening could be a “clock” that eventually prohibits the cells from dividing any more. When human fibroblasts are cultured, they can divide only a certain number of times, and their telomeres shorten. If these cells are made to express telomerase, they can continue dividing (Bodnar et al. 1998; Vaziri and Benchimol 1998).
However, there is no correlation between telomere length and the life span of an animal (humans have much shorter telomeres than mice), nor is there a correlation between human telomere length and a person’s age (Cristofalo et al. 1998). Telomerase-deficient mice do not show profound aging defects, which we would expect if telomerase were the major factor in determining the rate of aging. It has been suggested that telomere-dependent inhibition of cell division might serve primarily as a defense against cancer rather than as a kind of “aging clock.”
Even the very people who discovered the existence of telomerase – nobel prize winners Elizabeth H Blackburn, Carol W Greider and Jack W Szostak – advise of the serious side-effects of having too much telomerase in your system (the fact that this can lead to serious cancers), and also acknowledge the lack of scientific correlation between human lifespan and telomere length – beyond the extreme scenario where telomeres have depleted completely and therefore prevent continued cell division.
So, if telomeres aren’t the answer to – or even the measurement of – the years we have remaining on this Earth, what can we do to improve our longevity?
Here’s the 5 most effective ways to slow aging
- Receive sufficient vitamin E and C
This relates back to the first cause of aging that we explored, regarding Reactive Oxygen Species (or ROS for short).
Vitamin E and Vitamin C both have strong antioxidant properties and are both therefore capable of scavenging ROS and reducing the oxidation of cellular molecules, thus alleviating OS (Gilgun-Sherki et al., 2001). Antioxidants obtained from the diet are essential in supplying endogenous antioxidants for the neutralization of OS.
Piecing these two pieces of information together – the fact that ROS contributes to aging (and also, the occurrence of disease), and the fact that Vitamins C and E suppress ROS – points firmly to the indication that Vitamin C and Vitamin E intake (either through diet or supplementation), could have a positive effect on longevity.
- Caloric Restriction
A recent 2022 study by neuroscientists at the Peter O’Donnell Jr Brain Institute examined the effects of both caloric-restriction and time-restricted eating on mice, and found that:
- Mice that ate as much and whenever they wanted lived nearly 800 days median life span – an average period for their species
- Restricting calories but making food available around the clock extended their lives only 10% to 875 days despite restricting calories by 30-40%.
- Restricting this reduced-calorie diet to the inactive period of the circadian cycle boosted lifespan by nearly 20% to an average of 959 days
This is just one of many studies conducted around the correlation between longevity and both time-restricted and calorie-restricted eating. With most evidence pointing to the most beneficial effects being seen when exercising both time and caloric restriction simultaneously.
- Exercise
Harvard Medical School published a paper in 2014 expressing the many proven benefits of exercising vs aging. They summarised this evidence clearly in a table that showed the typical effects of aging on heart and circulation, blood, lungs, bones, muscles, metabolism, and much more, and then succinctly mirrored the effect of aging on each aspect of health, with the effect of exercise.
It was found that out of 23 negative health effects of regular aging, exercise had the reverse effect on 19 of these same aspects of health – indicating much of the aging process can be slowed or at least controlled somewhat, through regular physical activity.
And in terms of the physical activity studied by Harvard Medical School, they looked at both cardiovascular and resistance training – so a balance of these two approaches is likely to produce the best results in terms of combatting the aging process.
- Antioxidants
We spoke earlier about Vitamin C and Vitamin E, and their effect on slowing the aging process by suppressing ROS. However, are these the MOST impactful antioxidants when it comes to reducing the impact of ROS?
A 2019 study titled Protective Effect of Glutathione against Oxidative Stress-induced Cytotoxicity in RAW 264.7 Macrophages through Activating the Nuclear Factor Erythroid 2-Related Factor-2/Heme Oxygenase-1 Pathway, found that H2O2-induced cytotoxicity and ROS generation were significantly reversed by glutathione.
Therefore, supplementing with glutathione or glutathione precursors may well – amongst numerous other health benefits such as protection against various diseases – help to slow the aging process insofar as minimising the impact of ROS on the body.
- Genetics
Definitely the least-actionable way to slow or reverse the aging process – but important to acknowledge nonetheless, is the effect that genetics can have on your lifespan.
It is estimated that about 25 percent of the variation in human life span is determined by genetics, but which genes, and how they contribute to longevity, are not well understood unfortunately.
However, genes determine our predisposition to life-threatening conditions, so if you are able to analyse your family history of health, it will help you to identify areas in which you can take pro-active action to offset or minimise any potential predispositions – whether that be through supplementation, dietary, or lifestyle changes.
Genome sequencing can also help you dig deeper into your genetic make-up and understand potential health risks that may stem from your DNA.
We’re all getting older, and unfortunately we don’t yet know how to stop the aging process (and maybe we never will) – but there are definite, science-backed ways of at least slowing the process to deliver maximum longevity. I hope this post helped you to identify these methods, and implement them into your own lifestyle and routines.