We are going to live beyond 100

Life expectancy vs health span

60% of the population spend the last 32 years with 1 or more chronic disease.

77 - 94%

of the adverse effects of biological ageing are related to lifestyle and epigenetic markers.

These variables are modifiable, yet we continue as if we do not understand what is happening.

And this is how we will perish.

Choices make chances

Humanity is getting sicker as the generations continue. As a race, we are not improving our genetic code.

The bioaccumulation of inflammation and toxins is becoming ever more apparent. Epigenetic weakness is at the core of our beings.

We are damaging our DNA and making each generation less tolerant, adaptable, and susceptible to illness and disease.

How do we know this is true? Just take a look at the autism rates in the USA. 1 in 40 children are now expected to be diagnosed with autism.
This goes to show how we are not improving our health or modelling healthy behaviour for our children, grandchildren and great grandchildren.

The 10 hallmarks of aging

The scientifically proven root causes of why you age.

01 / 10

Genomic instability

Throughout life, various endogenous or exogenous agents cause a range of negative DNA alterations.

And although our body has multiple repair mechanisms to overcome this, as we age, these defects are not corrected.

Loss of DNA repair genes leads to genomic instability and compounds to form excess DNA damage, which ultimately favours the ageing process.
02 / 10

Telomere attrition

Telomere shortening is the gradual loss of the protective caps of our chromosomes and is one of the ageing processes.

Telomere attrition limits the number of times our cells can divide, slowly leading to dwindling populations of cells in vital organs.

Eventually, the telomerase enzyme that adds telomeric repeat sequences gets silenced, and the telomeres are too short for cells to divide.
Shortened telomeres are associated with senescent ageing cells.
03 / 10

Epigenetic regulation

Epigenomic changes during ageing profoundly affect cellular function and stress resistance.

Alterations in DNA methylation patterns, post-translational modification of histones and chromatin remodelling lead to loss of cellular function.

Lack of epigenetic relevant enzymes mediates alterations in longevity regulators, reduced life span, and exacerbated ageing-related pathology.
Whereas the gain of their function extends longevity.
04 / 10

Loss of proteostasis

The loss of proteostasis is the failure of the protein-building machinery of the cell and the accumulation of misfolded proteins.

The folding, chaperoning, and maintenance of protein function collapses with age from slowed translation and cumulative oxidative damage.
Irreparably damaged proteins accumulate with age, increasingly distracting the chaperones from folding the healthy proteins the cell needs.

The tipping point to death occurs when replenishing good proteins no longer keeps up with losses from damage and aggregation.
05 / 10

Deregulated nutrient sensing

The four pathways of nutrient-sensing regulate metabolism and influence ageing.

The four associated key protein groups are IGF-1, mTOR, sirtuins, and AMPK.
We call these proteins “nutrient-sensing” because nutrient levels influence their activity.

Deregulated nutrient sensing is an antagonistic hallmark of cellular ageing.
The main overarching nutrient-sensing dysfunction that emerges during human ageing is insulin resistance.
06 / 10

Mitochondrial dysfunction

Mitochondrial dysfunction is one of the root causes of ageing.

The accumulation of somatic mtDNA mutations that occurs with ageing leads to a loss of mitochondrial function.

The resultant decline in energy capacity, increase in oxidative damage and ultimately increase in apoptosis lead to cellular loss, which results in organ failure.
07 / 10

Stem cell exhaustion

Stem cells are the building blocks of life, and possess the special ability to evolve into any other cell type, and can divide infinitely.

With age, stem cells become dysfunctional or die off.

Since stem cells are responsible for producing new copies of our cells when needed, having fewer or dysfunctional stem cells leads to our tissues being less replenished and maintained.
08 / 10

Cellular senescence

Senescent cells are cells that have become damaged but resist undergoing autophagy, otherwise known as programmed cell death.

These "zombie" cells resist dying, stay alive and secrete substances that damage the surrounding, still healthy cells.

During ageing, more and more senescent cells arise in our tissues.

Senescent cells undermine the proper functioning of tissues, especially when they accumulate above a certain threshold, secreting pro-inflammatory substances, damaging the tissues, and accelerating ageing.
09/ 10

ALTERED INTERCELLULAR COMMUNICATION

As we age, due to an increasingly toxic environment and inflammaging (ageing caused by inflammation), the communication between our cells becomes less efficient.

This process hinders cells, including stem cells, from functioning properly.

During the ageing process, our cells begin to bathe in extracellular substances full of inflammatory proteins, hormones, peptides and metabolites that accelerate ageing.

At the same time, we see a decline in substances that protect our cells and maintain cellular homeostasis.
10/ 10

Compromised autophagy

Autophagy is the process by which the cells of the body consume their components via programmed cell death.

Autophagy is a preservation mechanism that removes dysfunctional senescent cells and facilitates the recycling of cellular components.

Autophagy plays a significant role in regulating dna repair, and nutrient metabolism.
Impaired autophagy is implicated in ageing and the causation of various diseases. Additionally, autophagy has been directly linked to neurodegeneration.

51% of the population dies due to age-related diseases.

JESSICA ALANA

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