Cover Photo by Simon Migaj

Basically, different people or different cultures, age at different rates and some tend to age more gracefully than others simply because of their genes and their environment. But aging is also about time and time perception. Time perception is a construction of the brain. How fast we perceive time to be passing — or “mindtime” — can be manipulated or distorted, with our evaluations of time based on our state of being at the time of judgment (i.e. five minutes can be perceived as eternity or just seconds depending on how we feel). 

So, could how we age and how long we live depend on time perception?

But what is time?

Time is the indefinite continued progress of existence and events that occur in an apparently irreversible succession from the past, through the present, to the future. But, while most people think of time as a constant, physicist Albert Einstein showed that time is an illusion. Also according to theoretical physicist Carlo Rovellipassing time is an illusion and our naive perception of its flow doesn’t correspond to the physical reality.

Basically, more and more physicists believe that past, present and future coexist. They believe that every moment is co-creating every other moment both forward and backward in time”, meaning that the past influences the future and the future influences the past in an endless feedback loop.

But, if “passing time is an illusion”, “time perception is a construction of the brain”, and “every moment is co-creating every other moment both forward and backward in time”… can we say that our only way out of this loop is by influencing our “future” with thoughts of longevity (i.e. Can I live to be 150?), that would eventually “make” our “future” accept a mutation that will change our perception of time and therefore change our future and past…so we can live longer?!? 

In the end, it’s just a mind game. It is just our brain that defines a chronological order and accepts a life span of 70-85yrs as normal. And as Søren Kierkegaard beautifully stated: If you name me, you negate me. By giving me a name, a label, you negate all the other things I could possibly be”.

Moreover, the fact that our chronological and biological age can differ so much is probably the indication that the process of aging can be “manipulated” in relation to genes and environment or all together. And this “manipulation” creates a gap where lies our ability to change aging.

In fact, between stimulus (how long are you going to live?) and response (I am gong to live 150 yrs) there is a gap. In that gap is our power to choose our response (Viktor E. Frankl). In our response lies our growth and our freedom from the physical constraints of our physical reality.

Now that you know that mind games with time might affect your lifespan, let’s talk about some genes that affect longevity. 

We now know that changing single genes within certain pathways can extend lifespan dramatically in animal models. Many of these mutations that extend life span perturb endocrine signaling pathways and the best understood mutations are those of the insulin/IGF-1 pathway (daf-2, chico,Insulin/IGF-1 receptor mutations), which influence life span in worms, flies and mammals.

The insulin/IGF-1 pathway was first linked to life span in C. elegans (a nematode worm used as a model in aging research), when mutations in DAF-2a known regulatory gene encoding an insulin/IGF-1 receptor ortholog — were found to double the life span of the animal.

Insulin and IGF-1 are anabolic hormones that promote food storage and growth. Yet, reducing the activities of these hormones seems beneficial since it lengthens life span. Most likely low signaling levels shift cells from states of growth, which may not equip them for long-term survival, to states of maintenance, which do equip them for long-term survival, thereby delaying aging. Probably, the insulin/IGF-1 longevity regulatory module arose during evolution not to influence longevity per se but to allow animals to endure harsh environmental conditions.

In actual fact, many DAF-2/DAF-16 downstream longevity genes not only extend life span but also protect the animal from harsh environmental stress, such as heat, UV, and oxidative-damaging agents (The Plasticity of Aging: Insights from Long-Lived Mutants).

Moreover, the longevity gene INDY (for I’m not dead yet) has been discovered that helps determine the life-span of the fruit fly Drosophila. When the gene is mutated, it can double the life-span of Drosophila. It appears that the protein encoded by INDY transports and recycles metabolic byproducts. Defects in the gene may lead to production of a protein that renders metabolism less efficient so that Drosophila appears to dieting, even though its eating habits haven’t changed. Mutations in Indy thus appear to create a metabolic state that mimics caloric restriction (environment), which has been shown to extend life-span.

Furthermore, scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, California, and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan in C. elegant. This new research uses a double mutant, with both the insulin signaling (IIS) and mTOR pathways being genetically altered amplifying its lifespan by 500%. Despite this discovery it hasn’t been clear yet how these pathways interact.

But even though longer lifespans tend to run in families — which suggests that shared genetics, lifestyle, or both play an important role in determining longevity — twin studies, however, suggest genetics only account for approximately 20-30% of an individual’s chance of surviving to age 85.

To tell the truth, lifestyle choices, particularly diet, exercise and smoking habits, play an undisputed role in determining not only how long one will live, but also how well one ages. 

So, remember, regular exercise appears to boost cognitive health in old age while diet is also a protective factor, especially for diets delivering omega-3 fatty acids, polyphenols, vitamin D and the B vitamins. There’s also evidence that having a healthy social life in old age can protect against cognitive decline. 

And as stated by Dorothy Canfield Fisher — an educational reformer, social activist, and best-selling American author in the early decades of the twentieth century“Those who love deeply never grow old; they may die of old age, but they die young”.

Thanks for reading 

PS: if you want to monitor your aging journey just buy AgeCurve’s test and always remember that, “if you take care of things they last”.



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