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The resilience of our threatened cells, a risk of poor health

The resilience of our threatened cells, a risk of poor health
The resilience of our threatened cells, a risk of poor health

Various mechanisms protect our cells from the various stresses they undergo, protecting us from diseases. However, various clues seem to indicate that these resistance capacities could be threatened.


All cells in living beings have compensation mechanisms that allow them to adapt to stress. The latter can be either inherent in the normal functioning of living organisms (by functioning, cells can produce deleterious substances for themselves), or induced by exposure to environmental factors (acute stress resulting from traumas or infections, chronic stress due to pollution, extreme temperatures, deleterious social relations, etc.).

This cellular compensation, guaranteeing tissue resilience, constitutes the assurance of our ability to protect us from diseases. Aging results in an erosion of the compensation and resilience capacities of our cells.

However, our environment, when it is degraded by industrial practices, reaches the integrity of this mechanism in the same way as aging, which can weaken us before the hour. This reduction is a danger of life in poor health. Seizing the problem involves awareness of the mechanism which is at the root of this reduction.

What is resilience?

The concept of resilience covers the capacities to overcome the alterations caused by disturbing elements in various situations.

A well -known form of resilience concerns recovery after particularly aggressive stress, such as psychological resilience highlighted by the neuropsychiatrist Boris Cyrulnik. Coming from physics, the concept of resilience is now going through many disciplines, from economics to psychology, including ecology or computer science. We are talking today about the resilience of logistics systems (water, energy, transport) or health systems.

But resilience does not concern that “after-crisis”, it is also the ability to overcome stress that affects a system or an individual in a discreet, even silent manner, before the occurrence of the worst.

Living stress and resilience

The living is constantly confronted with cell stress. The response to cell stress (especially during development and reproduction) is a guarantor of adaptation and expansion of a given population.

Low stress can stimulate cell longevity. However, excessive stress, for example under the effect of environmental factors, can erode cellular resilience capacities. However, the erosion of these capacities is at the center of fabric aging. It is an “whole body” risk because the organs communicate with each other. For example, the intestinal microbiota communicates with the brain and its alteration can be harmful to the brain. It is an “whole life” risk because the success of the response to cell stress deals with the critical phases of existence such as reproduction (birth rate), pregnancy (fetus health) or the development of the child.

Thinking about the resilience of the body from the angle of recovery, once the worst occurred is to underestimate the damage that industrial practices and air-water-food pollution are incurred on our health. It is to lock up more and more individuals in the perspective of poor health whose deadline is uncertain, but which will occur too early and too strong.

On the other hand, to think of the resilience of the body as a mechanism always at work is to be able to fight against what prevents our tissues from being resilient is to be able to improve precaution and prevention.

Cellular resilience mechanisms

These mechanisms are not only those who protect us against infections (such as immunity, for example).

These are also the mechanisms of cellular integrity, for example DNA repair – whose alteration has a risk of anarchic division of cells and cancer, elimination of proteins with manufacturing defects or damaged by natural oxidation of tissues -, or it can be the production of energy necessary for the functioning of cells, for example in mitochondria.

These mechanisms are crucial in cells that do not renew themselves, or little, such as neurons of the brain and the central nervous system. Their failure will undoubtedly go hand in hand with the transition of light to severe stages of diseases. For example, the progression of Huntington’s disease is marked by the transition of a phase of “functional compensation” to a phase of “decompensation”, with cellular resilience mechanisms which no longer manage to compensate for neural damage, a model that would also be worth for Alzheimer’s disease.

But that’s not all: cellular resilience mechanisms are at the center of tissue aging.

In the past thirty years, at least twelve characteristics of aging have been identified, some of which directly deal with cellular resilience mechanisms, such as reducing the function of mitochondria or autophagia (elimination of intracellular waste), alteration of DNA and protein integrity, and the increase in cellular senescence, in a model where aging is mainly due to an accumulation genetic mutations, accompanied by epigenetic erosion.

There is therefore a solid bundle of presumptions to think that these mechanisms are opposed to the effects of aging and the occurrence of chronic diseases.

Cell resilience jeopardized

The weakening before the time of cell compensation is opposed to the benefits that one expects to see from the adoption of a “good” lifestyle aimed at reducing the burden of morbidity by acting on so -called “modifiable” risk factors, such as food, sedentary lifestyle, addictions, places of life, hygiene to work, or even social isolation.

As such, any disruption of cellular resilience mechanisms by pollutants, directly (for example by altering DNA repair, autophagy), or indirectly (for example by promoting mutations in DNA is a risk of life in poor health more or less short maturity.

In view of the extent and severity of the problem (such as, for example, in the case of PFAS in Europe and the United States), it is also a risk of systemic “lack of gain” for society.

In such a context, avoiding industrial practices to always error our cellular resilience capacities is a responsibility that obliges all the actors concerned, and this responsibility is proportional to the power of the actors. But how to take this major risk into account?

Measure resilience

Currently, individual resilience is estimated against the occurrence or progression of a disease from the weight, more or less important depending on people, of the factors of susceptibility. These are not organic strict sensebut often behavioral (smoking, alcoholism), cyclical (proximity to a factory, loneliness) or socio -professional (income, mobility). However, the absence of a factor of susceptibility does not necessarily mean that one is resilient.

Incorporating cellular resilience factors in addition to susceptibility factors when it comes to assessing the risk of life in poor health could provide more robust prediction models. But it is necessary to have reliable markers of cellular resistance, which is not easy.

The most precise markers are often organic markers (biomarkers). Ideally, they are simple to measure (for example in blood or urine). A resilience biomarker must account for the state of a compensation mechanism or the integrity of an essential element of cells.

There are relatively little to date, and the development of a new biomarker is expensive. It is based in particular on data collected on long time, thanks to large cohorts, such as inchianti, Constances or the UK Brains Bank Network.

Currently, DNA oxidation, an indirect marker of the integrity of this essential molecule, is one of the potential biomarkers under study. In this context, new tools are explored, for example epigenetic clocks, a pioneer of which is researcher Steve Horvath in the United States.

This tool detects certain chemical modifications of DNA (methylation, in other words the addition of a methyl group on certain parts of the DNA molecule) to measure an “epigenetic age”. This one, which testifies to the aging of the tissues, is in a way a “biological” age, and can differ from chronological age.

It is important to emphasize that this tool does not yet make it possible to measure the biological age of everyone: it is not validated for this, being still at the stage of research.

Change

The challenge, today, is to reduce chronic diseases in a global way, and to get out of occasional responses. However, the current model, focused on “proven diseases”, limits the scope of prevention and anticipation of societal costs. Indeed, hidden costs are undervalued, even ignored.

Putting reflections on prevention at the center of reflection of a fundamental health mechanism of life (our cellular capacities to protect us from diseases) could constitute a vector of transformation of public health policies.

The scientific data which justifies this mutation accumulate, including epidemiological data with high geographic granularity (these have notably been highlighted in recent years by various surveys carried out by certain investigative journalists).

This necessary transformation is however hampered in various ways (monopolies, industrial lobbying, bilateral agreements, disinformation, manipulation of studies, relegation in the background of health issues, budgetary priorities, or even under-dimensions of actors in vigilance, etc.). These obstacles limit our ability to adopt a health-responsible policy, even though the overcoming of cellular resilience capacities could be part of a “chain” risk model, chemical pollution accompanied by frozen health at a mediocre level, resulting in increased systemic costs.

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