When the brain lives in a state of constant alert
For a long time, it was thought that the brain was relatively isolated from the inflammatory processes of the rest of the body. Today we know that the central nervous system is closely connected to the metabolic, immune, and nutritional state.
Neuroinflammation is a condition characterized by the persistent activation of brain immune cells and the production of inflammatory mediators within the central nervous system. When this response is mild but continuous over time, it is often referred to as low-grade chronic inflammation.
This biological state can be promoted by multiple factors:
hypercaloric and nutrient-poor diet
excess refined sugars
sedentary lifestyle
disruption of the sleep-wake rhythm
chronic stress
intestinal dysbiosis
accumulation of visceral adipose tissue
In recent years, it has emerged how neuroinflammation, cortisol regulation, and insulin metabolism are closely interconnected.
Neuroinflammation: what happens in the brain
The brain has a specialized immune system represented mainly by microglia.
Under physiological conditions, microglia protect nerve tissue, remove cellular debris, and support proper neuronal functioning.
However, when inflammatory stimuli become persistent, an increased production of molecules such as:
interleukin-1 beta (IL-1β)
interleukin-6 (IL-6)
tumor necrosis factor alpha (TNF-α)
These signals can alter neuronal functioning and influence processes involved in:
mood regulation
motivation
memory
concentration
perception of stress
From a clinical point of view, this can be associated with:
mental fatigue
irritability
reduced mental clarity
drop in concentration
poorer psychophysical recovery
Cortisol: from an adaptation hormone to a persistent alert signal
Cortisol is the main hormone produced by the hypothalamus-pituitary-adrenal axis.
Under normal conditions, it follows a circadian rhythm:
physiological peak in the morning
progressive reduction during the day
The problem is not cortisol itself, but the prolonged maintenance of high levels or a loss of normal biological oscillation.
The presence of low-grade chronic inflammation can contribute to altering the regulation mechanisms of the stress axis.
Over time, the following may appear:
initial hyperactivation with a greater stress response
sleep alterations
difficulty recovering
modifications of the neuroendocrine response
It is important to emphasize that the concept of “adrenal exhaustion” is not recognized as a medical diagnosis. However, there are documented alterations in the regulation of the stress axis under conditions of chronic stress and persistent inflammation.
Insulin resistance and the brain: a bidirectional relationship
Insulin does not act only on muscle and adipose tissue.
Insulin receptors are also present in the brain, where they participate in:
energy regulation
neuronal plasticity
cognitive functions
appetite control
Chronic inflammation and prolonged exposure to glucocorticoids can reduce insulin sensitivity.
When insulin resistance appears, mechanisms may develop that favor:
greater accumulation of visceral fat
further production of inflammatory mediators
alteration of energy regulation
worsening of metabolic function
Thus, a self-perpetuating cycle is created between inflammation, stress, and metabolism.
Leptin, energy, and the stress axis
Leptin is a hormone produced mainly by adipose tissue.
It does not simply represent a satiety signal but participates in communication between energy status, the brain, and neuroendocrine systems.
Some experimental data suggest that alterations in leptin sensitivity may also influence the regulation of the stress axis.
However, there is no evidence that a single dietary strategy alone is capable of “reactivating” the adrenal gland.
Restoring neuroendocrine balance requires a comprehensive approach that includes diet, physical activity, sleep, and stress management.
Omega-3 and the brain: the role of healthy fats
Contrary to the belief that all fats are unfavorable, the brain is one of the most lipid-rich organs.
Omega-3 fatty acids, particularly EPA and DHA, are fundamental structural components of neuronal membranes.
The main areas of interest studied include:
synaptic plasticity
membrane fluidity
neuroinflammatory regulation
cognitive function
emotional balance
Several clinical studies and meta-analyses have observed favorable effects of Omega-3s in some clinical contexts related to mood tone, psychological stress, and cognitive support, although results are not always uniform.
The main dietary sources include:
oily fish
salmon
sardines
flaxseeds
chia seeds
algae
Essential oils, relaxation, and stress response: what the literature says
Aromatherapy is a growing field in integrative medicine.
Lavender oil is one of the most studied essential oils.
The main active components include:
linalool
linalyl acetate
Clinical studies have observed that inhalation protocols can be associated with:
reduced subjective perception of stress
improved sleep quality
reduced state anxiety in some contexts
The proposed mechanisms include interactions with:
the GABAergic system
the serotonergic system
voltage-gated calcium channels
neurovegetative modulation
These effects do not replace clinical interventions but can be considered complementary wellness strategies.
How to break the vicious cycle
Current evidence suggests that the most effective strategies are:
anti-inflammatory Mediterranean diet
adequate Omega-3 intake
regular physical activity
sleep optimization
reduction of sedentary behavior
exposure to natural light
structured stress management
care for the intestinal microbiota
The goal is not to completely eliminate cortisol or inflammation, but to restore the body's ability to return to its physiological balance.
Bibliography
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Donelli D et al. Effects of lavender on anxiety: systematic review and meta-analysis. Phytomedicine. 2019.
Kang SY et al. Aromatherapy and cortisol response: controlled clinical study.
Lopresti AL. Neuroinflammation and mental health. Prog Neuropsychopharmacol Biol Psychiatry. 2017.
Kullmann S et al. Brain insulin resistance at the crossroads of metabolic and cognitive disorders. Mol Metab. 2016.