Hyperneuroplasticity in Action: DecodeME as Case Study
- Dr. Patty Gently
- 5 days ago
- 8 min read
By Dr. Patty Gently on August 28, 2025
Bright Insight Support Network founder and president Dr. Patricia Gently supports gifted and twice-exceptional adults in their own autopsychotherapy through identity exploration, structured reflection, and alignment with inner values. A writer, educator, and 2e adult, Dr. Patty centers depth, integrity, and complexity in all aspects of her work.
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Hyperneuroplasticity in Action: DecodeME as Case Study
For decades, people living with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) have been told their condition was “psychological” or “all in the head.” The DecodeME study, published this month (August 2025), has changed that conversation irrevocably. With over 15,000 DNA samples from ME/CFS patients and nearly 260,000 controls, DecodeME is the largest genetic investigation of the illness to date. And its findings are clear: ME/CFS has a biological foundation, marked by eight genetic signals tied to immune response, nervous system function, and chronic pain pathways.
This is not only an important step for those living with ME/CFS, either. This is also a profound confirmation that our bodies and brains are not neatly divided systems but deeply inter-engaged. The DecodeME results are precise, scientific, and molecular. Yet they resonate deeply with the broader conceptual frame I’ve been calling hyperneuroplasticity (HNP).
HNP is not a disease category, nor is it a diagnosis. It is a systemic umbrella for understanding heightened responsivity across the brain and body. Where standard neuroplasticity describes the brain’s ability to adapt and rewire, hyperneuroplasticity describes an exceptional degree of adaptability and a permeability that extends into immune processes, stress responses, and sensory systems. This openness can be a gift (creativity, rapid pattern recognition, intensity of empathy) or a vulnerability (fatigue syndromes, dysautonomia, post-infectious collapse).
DecodeME roots this reality in DNA. It identifies the specific genomic signals where immune over-activation and nervous system dysregulation may intersect to produce ME/CFS. HNP provides the conceptual context in which systemic coupling is not unique to one illness. Rather, it is part of a larger spectrum of human variation in which heightened openness can cut both ways (a reality at the heart of the neurodiversity paradigm).
The significance of this information and conceptualization is twofold. First, patients with ME/CFS now have indisputable evidence that their condition is not imagined, not secondary, not psychosomatic, but instead it is written into the genome. Second, for those of us exploring systemic theories like HNP, DecodeME offers a biological foothold, support suggesting that what we’ve seen anecdotally and experientially (immune sensitivity and neuro-responsivity walking hand in hand) has genetic grounding.
What DecodeME Found
The DecodeME study compared the DNA of 15,579 people with ME/CFS to that of 259,909 controls of European descent. The team identified eight distinct genomic regions in the human genome where people with ME/CFS were more likely to carry certain variants than people without the illness. These regions carry different implications. Three of these regions are linked to infection response, resonating with patient experiences of ME/CFS beginning after a viral illness. One region is linked to chronic pain, reinforcing the neurological dimension of the condition. Others cluster in the nervous system, pointing toward dysregulation in how the brain and body communicate. Importantly, none are connected to depression or anxiety, decisively separating ME/CFS from outdated psychological explanations.
Because DNA does not change when someone becomes ill, these findings reflect predispositions, not consequences. In other words, people with ME/CFS are biologically tuned in ways that make them more vulnerable to this condition, especially following infection or stress. DecodeME is groundbreaking because it shines a narrowly focused light on eight precise areas of the genome, providing targets for future research and potential treatment development. It brings ME/CFS in line with other complex conditions, where genetics opens a path toward understanding mechanisms rather than blaming patients.
Where Hyperneuroplasticity Comes In
DecodeME is molecular. Hyperneuroplasticity is conceptual. Yet they converge on the same scientifically grounded terrain. Where the study identifies specific gene regions involved in immune and neural function, HNP frames the whole-system profile: heightened responsiveness across domains, from the immune system to the brain’s adaptive wiring.
DecodeME’s findings show that the immune and nervous systems are jointly implicated, and HNP interprets this as part of a larger systemic permeability where infection, stress, and neural plasticity co-activate. This immune–neural coupling illustrates how biological and experiential realities are inseparable. The research also reveals genetic predispositions. HNP broadens this by showing how those predispositions can express divergently: in some people as illness such as ME/CFS, POTS, or MCAS, and in others as adaptive intensity, inclusive of creativity, giftedness, or rapid learning. And context gets to matter deeply here, right? The same openness that fuels brilliance, pattern-finding, and sensitivity can also fuel collapse, brain fog, or chronic dysfunction. DecodeME maps one end of the spectrum, while HNP frames the whole continuum.
In this way, DecodeME does more than validate ME/CFS patients. It validates the broader reality that our biology can be both adaptive and fragile when tuned toward intensity. Hyperneuroplasticity is the name I give to that systemic tuning, one that links molecular findings to lived experience across conditions.
DecodeME In Relation to Hyperneuroplastic Experiences
The DecodeME study gives us genetic confirmation for what patients have described for decades, while being gaslit or ignored by the medical community. Indeed, though, a body that is unusually permeable may also be unusually reactive and open to infection, stress, and overload. In my work with hyperneuroplasticity (HNP), I’ve offered that this heightened responsivity is not unique to ME/CFS, but a broad systemic profile that shows up across seemingly different conditions.
Histamine, MCAS, and Immune Permeability
In previous articles, we explored how histamine regulation more broadly reflects a system primed for heightened responsivity. In some individuals, this manifests as mast cell activation syndrome (MCAS), where histamine release occurs in unpredictable cascades that overwhelm rather than protect. In others, histamine sensitivity shows up as exaggerated allergic reactions, gut disruption, or neurological symptoms. DecodeME’s immune-linked genetic signals resonate with this entire spectrum, where the same over-responsivity at the heart of histamine dysregulation is now mapped in DNA for ME/CFS. Both highlight immune systems tuned toward vigilance, where under stress, they might tip into dysfunction.
Connective Tissue and EDS
In Ehlers-Danlos Syndrome (EDS), connective tissue bends, stretches, and breaks down more easily. It is another form of biological openness. DecodeME shows that in ME/CFS, nervous and immune systems likewise stretch past stability, unable to reset after infection or exertion. Both reveal how structural fragility and systemic sensitivity mirror one another: one in tissue, the other in signaling pathways.
Trauma, CPTSD, and Functional Disorders
Those with complex PTSD (CPTSD) often describe hypervigilance, exhaustion, and body-wide dysregulation. Functional neurological disorder (FND) overlays this terrain, where stress and neural plasticity combine into misfiring systems. DecodeME’s nervous-system loci affirm that this coupling is not “imagined” but rather biologically apparent. The overlap with HNP becomes clear when we see again that plasticity under stress can become maladaptive, encoding trauma in the body as much as in the mind.
Autism, ADHD, and Giftedness
On another branch of HNP, heightened responsivity shows up not as collapse, but as intensity of learning, pattern-finding, and sensitivity. In gifted neurodivergence, autism, and ADHD, we see the same tuning related to an openness to sensory input, rapid adaptation, or divergent processing that, under other pressures, can manifest as overwhelm or emerge as brilliance, intensity, and creativity. These are not separate species of human functioning but different expressions of the same systemic tuning.
Leaky Brain, Blood-Brain Barrier, and Systemic Permeability
When we explored leaky brain and blood-brain barrier fragility, we touched on more of the same theme of boundaries between systems being more permeable in some individuals. DecodeME adds scientific weight to this idea. If genetic predispositions already tune immune and neural systems toward reactivity, then permeability at the barrier level is not a stretch (pun alert… SNS). It is part of the same biological openness.
The Emerging Pattern
Before listing the conditions, it is worth noticing how the act of pattern-finding and meaning-making itself is part of what hyperneuroplastic systems do most naturally. This capacity is not incidental; it is the way individuals with heightened responsivity connect seemingly separate pieces of experience into a coherent whole. Just as DecodeME links immune, neural, and genetic findings, HNP highlights how our minds and bodies connect across domains. By drawing parallels, noticing resonance, and constructing meaning from fragments, hyperneuroplastic systems reveal a larger coherence. A pattern emerges that unites conditions often treated as separate:
Immune over-responsivity (ME/CFS, MCAS, histamine issues)
Structural fragility (EDS, connective tissue permeability)
Neuroplastic vulnerability (FND, CPTSD, trauma encoding)
Cognitive and sensory intensity (autism, ADHD, giftedness, tinnitus)
Barrier permeability (leaky brain, blood–brain barrier fragility)
DecodeME roots ME/CFS in genetics. HNP ties them all together under a single conceptual umbrella. They are not identical conditions. They are, however, parallel expressions of heightened systemic openness. Sometimes that openness yields illness, sometimes brilliance, and often both.
Moving Forward from Signals to Systems
DecodeME gives us eight genetic signals, which act as anchors of evidence that ME/CFS is a biological condition rooted in immune and nervous system pathways. This is a milestone. Yet genes are only the beginning. The bigger story is how those genes are expressed in lives, communities, and systems. This is where hyperneuroplasticity offers a lens. DecodeME provides the genetic signals, while HNP provides the systemic route towards understanding. Together they point to a truth we best not ignore: that some human systems are tuned toward greater permeability, adaptability, and reactivity (Dabrowski might call this developmental potential, ya’ll). That tuning can yield brilliance, creativity, and intensity, and it can also yield collapse, chronic illness, and suffering.
For Researchers and Clinicians
The DecodeME results reaffirm what patients have long reported: ME/CFS is not psychological or a matter of willpower. It is a biologically rooted condition. Knowing this, the call is to integrate the evidence into practice by treating patients with respect and care, while also widening medical frameworks to account for both molecular findings and systemic complexity. With findings that highlight specific genomic regions linked to immune and nervous system function, the call also involves studying and understanding these loci in their broader systemic interplay, examining how they connect with conditions such as connective tissue disorders, mast cell activation, trauma responses, and neurodivergent intensities. Research that traces these overlaps will help move beyond single-diagnosis silos toward a fuller understanding of shared mechanisms.
For Patients and Communities
DecodeME offers validation. Your illness is real, and it is written into biology and expressed scientifically. And HNP reframing adds another layer. You are part of a larger landscape of systemic openness, one that includes vulnerability and possibility. Naming that broader context can help reduce shame, bridge communities, and create solidarity across conditions too often seen as separate and too often written off by society and the medical community.
Solidarity becomes a powerful next step here. People living with ME/CFS share something fundamental with those navigating MCAS, EDS, autism, ADHD, trauma, and gifted intensity. All these fellow travelers exist with a body and brain tuned toward openness and responsivity. The details may differ (immune cascades, connective tissue fragility, sensory overwhelm, or relentless creativity), yet the underlying systemic tuning unites these experiences. Recognizing this kinship can create new forms of community, where groups that have long been siloed can stand together. Instead of competing for legitimacy or resources, each can recognize the shared terrain of hyperneuroplasticity, where intensity and fragility exist collectively. And this collective recognition matters not only for validation but also for advocacy. When disparate groups speak with one voice about systemic openness and its implications, the call for research, resources, and respect becomes harder to dismiss. In this way, DecodeME’s genetic signals can extend outward, supporting not just ME/CFS patients, but an entire network of people whose lives are shaped by heightened responsivity.
A Call to Reframe
The DecodeME study marks a turning point. It acts as a compass pointing us to a terrain where ME/CFS is genetic, biological, and systemic, rather than irrational or hyperbolic. Hyperneuroplasticity tells us that this terrain is shared with those navigating MCAS, EDS, autism, ADHD, trauma, giftedness, and beyond. To move forward with this understanding, we must also understand the precision of science and the breadth of conceptual reframing. DecodeME found the genome. HNP widens the lens to the human condition. Together, they invite us to stop fragmenting our understanding and start building it back into a coherent structure that honors both the suffering and the potential of lives lived at the edge of systemic openness.
