By Marc Dellière, Medical Consultant & Trainer – Specialist in Stress, Prevention & Integrative Health
You know what you need to do. Your brain does too. Yet a notification, a passing thought, or a worry can suddenly shift the priority.
What if some attention difficulties were less about a lack of attention than about difficulty assigning the right priority to the right signal at the right time?
Attention is not a single function. It relies on a dynamic balance between detection, selection, maintenance, and inhibition.
In ADHD, some of these mechanisms are impaired. Stress, fatigue, and lack of sleep can also weaken them or amplify their manifestations.
Dopamine and norepinephrine maintain the signal
Dopamine and norepinephrine play a major role in prefrontal networks involved in attention, working memory, and executive functions.
But their action is not linear.
Catecholamine levels that are too low or too high can impair prefrontal functioning.
The brain therefore performs best within an optimal zone of activation.
In simplified terms, catecholamines help stabilize the relevant signal, while inhibitory mechanisms, including GABAergic transmission, help constrain competing activity.
GABA helps filter competing signals
GABA is the main inhibitory neurotransmitter in the central nervous system.
Its role is not simply to “calm” the brain. Inhibition helps limit competing neural activity and therefore contributes to more precise information processing.
A magnetic resonance spectroscopy study in children with ADHD reported reduced GABA concentrations in the sensorimotor cortex, while other studies have pointed to alterations in cortical inhibition.
These findings do not imply a generalized “GABA deficiency”, but they support growing interest in the balance between excitation and inhibition in ADHD.
Catecholamines maintain the signal; GABA contains the noise.
What about serotonin?
Its role in ADHD is less established than that of dopamine and norepinephrine. However, recent reviews support an involvement of serotonergic pathways and their interactions with catecholaminergic systems, particularly in impulsivity, emotional regulation, and related behavioral dimensions.
When stress disrupts priorities
Acute stress can temporarily increase vigilance.
But when activation becomes excessive or prolonged, prefrontal circuits become less efficient, while signals related to threat, uncertainty, or internal concerns gain priority.
The brain detects more.
It filters less effectively.
The problem is therefore not always a lack of attention.
It may be paying attention to too many things at once.
What can help?
In diagnosed ADHD, management remains medical and condition-specific.
However, several complementary levers can help preserve attentional resources: physical activity, sleep, task structuring, reducing distractions, and stress management.
Supporting attention does not necessarily mean increasing arousal. Sometimes, reducing competing physiological and cognitive load may be equally important.
Sometimes, improving the signal also means reducing the noise.
Where does Lactium® fit?
Lactium® is a milk protein hydrolysate containing the bioactive peptide α-casozepine, developed in the field of stress management.
Research on α-casozepine and αs1-casein hydrolysates has notably explored their interactions with GABAergic neurotransmission and their effects in stressful situations.
Lactium® is not a treatment for ADD/ADHD.
If stress increases the noise competing with the relevant signal, reducing this overload could help preserve attentional availability.
For cognitive nutrition, this perspective suggests moving beyond an exclusively stimulatory approach.
Supporting performance may not always mean increasing the signal.
It may also mean reducing the noise that prevents it from emerging.
Because an attentive brain is not one that processes everything.
It is one that knows what matters now.
Learn more about Lactium® for stress management!
Scientific sources :
Arnsten AFT. Catecholamine influences on dorsolateral prefrontal cortical networks. Biol Psychiatry. 2011;69(12):e89–e99.
Arnsten AFT. Stress signalling pathways that impair prefrontal cortex structure and function. Nat Rev Neurosci. 2009;10:410–422.
Edden RAE et al. Reduced GABA concentration in attention-deficit/hyperactivity disorder. Arch Gen Psychiatry. 2012;69:750–753.
Faraone SV et al. Role of serotonin in the neurobiology of attention-deficit/hyperactivity disorder: a systematic literature review. Expert Opin Ther Targets. 2025;29:637–654.
Miclo L et al. Characterization of alpha-casozepine, a tryptic peptide from bovine alpha(s1)-casein with benzodiazepine-like activity. FASEB J. 2001;15:1780–1782.
Messaoudi M et al. Effects of a tryptic hydrolysate from bovine milk alphaS1-casein on hemodynamic responses in healthy human volunteers facing successive mental and physical stress situations. Eur J Nutr. 2005;44:128–132.