What If We’re Missing Something About ADHD and Autism? The Biology That Begins Before Birth

I was diagnosed with ADHD at 33 years old, but I had been living with the differences in how my brain functions for as long as I can remember. Growing up, I struggled with attention, organization, and completing tasks that seemed relatively straightforward to other people. Yet I could become completely absorbed in subjects that interested me, sometimes spending hours investigating something without noticing how much time had passed. That contradiction followed me through school and into adulthood. I could understand complicated concepts, recognize patterns, and connect information across different subjects, but directing that same mental energy toward ordinary responsibilities could feel extraordinarily difficult. Interruptions were particularly frustrating, competing sounds could become overwhelming, and my ability to concentrate seemed to depend heavily on what I was doing and the environment around me. For a long time, I didn’t fully understand these differences. I knew what I was capable of intellectually, but that didn’t always translate into consistent executive functioning. When I finally received my ADHD diagnosis, it explained part of my experience, but it also opened an entirely different set of questions that eventually led me much deeper into neurodevelopmental biology.

One of the most interesting aspects of my experience came when I began trying ADHD medications. I was prescribed Adderall, and even at a very small dose, I experienced severe insomnia that lasted approximately two days. I subsequently tried several stimulant and nonstimulant treatments, but anxiety, agitation, and sleep disturbances repeatedly complicated the process. I knew that these medications could be extraordinarily effective for many people, so I became interested in why my response was different. Was my nervous system particularly sensitive to norepinephrine? Was dopamine being metabolized differently? Did stress physiology influence the way my prefrontal cortex responded to increased catecholamine signaling? Or were there developmental differences in the networks controlling attention and arousal that made the same medication produce a different outcome? I couldn’t answer these questions simply by looking at my symptoms, and I certainly couldn’t establish the underlying mechanism from my medication response alone. But those experiences motivated me to begin investigating my own genetics, neurotransmitter signaling, and the developmental processes that shape the nervous system long before someone receives a diagnosis.

Initially, I was particularly interested in COMT because my genetic results indicated the Val/Val genotype. COMT encodes catechol-O-methyltransferase, an enzyme involved in the metabolism of catecholamines, including dopamine. The common Val158Met polymorphism influences COMT enzymatic activity, and this becomes interesting when examining the prefrontal cortex, where dopamine regulation differs from that in the striatum. Dopamine transporters are relatively sparse in certain prefrontal regions, making norepinephrine transporters and enzymatic clearance important components of local catecholamine regulation. But having COMT Val/Val does not mean I have low dopamine throughout my brain, nor does it explain my ADHD or prove why I respond poorly to stimulants. This distinction became increasingly important as I examined more genetic information. I was also interested in my reported FKBP5 variation because FKBP5 encodes FKBP51, a protein involved in glucocorticoid receptor regulation and the cellular stress response. I began exploring the relationship between cortisol feedback, hypothalamic-pituitary-adrenal signaling, and the ability of the prefrontal cortex to maintain stable executive functioning under stress. My MTHFR and SOD2 findings raised additional questions about folate-dependent one-carbon metabolism and mitochondrial antioxidant regulation, although common variants in these genes cannot establish methylation dysfunction, oxidative injury, or a neurodevelopmental disorder. What I was beginning to understand was that biological relevance and genetic predictive power are very different things. A gene can participate in an important molecular pathway without a common variant in that gene providing a meaningful explanation for an individual’s diagnosis.

As I continued investigating, I moved beyond COMT and started examining dopamine receptors, dopamine and norepinephrine transporters, dopamine β-hydroxylase, intracellular cyclic AMP signaling, and the molecular mechanisms controlling synaptic activity. Dopamine doesn’t simply appear in a synapse and produce attention. Its synthesis begins with tyrosine, which is converted through tyrosine hydroxylase and subsequent enzymatic steps into dopamine. Dopamine can then be converted into norepinephrine by dopamine β-hydroxylase, encoded by DBH. These neurotransmitters are packaged into vesicles, released in response to electrical activity, recognized by specific receptors, removed through transporters, and metabolized through several enzymatic pathways. SLC6A3 encodes the dopamine transporter, while SLC6A2 encodes the norepinephrine transporter. Genes such as DRD2, DRD3, DRD4, DRD5, ADRA2A, and others influence different aspects of receptor signaling, reward regulation, or neuronal responsiveness. The relationships become even more complicated when we consider that the same neurotransmitter can produce different effects depending on the receptor, cellular compartment, and neural circuit involved.

This became particularly interesting when I began examining the relationship between norepinephrine, α2A-adrenergic receptors, cyclic AMP, and HCN channels in the prefrontal cortex. Working memory depends partly on recurrent neuronal networks that maintain information even after the original stimulus disappears. Under appropriate conditions, norepinephrine signaling through postsynaptic α2A receptors can reduce cyclic AMP activity, influencing HCN channels and strengthening the functional connectivity needed to sustain these representations. Dopamine acting through D1 receptors also participates in regulating the balance between relevant and irrelevant signals. Too little catecholamine signaling can impair executive functioning, but excessive signaling, particularly during stress, can also destabilize these networks. This inverted-U relationship changed how I understood my own attention. It suggested that cognitive performance isn’t simply determined by whether dopamine is high or low. The stability of a neuronal network depends on the amount, timing, location, and downstream effects of neurotransmitter signaling. That may help explain why someone with ADHD can demonstrate extraordinary concentration during highly stimulating activities yet struggle with tasks requiring sustained effort toward a distant reward. The ability to pay attention may be present, while the regulation and allocation of that attention remain difficult.

But the deeper I went into ADHD genetics, the more interested I became in genes that had relatively little to do with dopamine production. I began looking into SNAP25, BDNF, CACNA1C, GRIN2A, GRIN2B, ADGRL3, MAP1A, ANK2, and the broader molecular pathways involved in neuronal organization. SNAP25 participates in the SNARE machinery responsible for synaptic vesicle fusion, meaning it contributes to the process through which neurons release neurotransmitters. CACNA1C encodes a voltage-gated calcium-channel subunit involved in neuronal excitability and intracellular signaling. BDNF participates in neuronal growth, survival, and activity-dependent synaptic plasticity. GRIN2A and GRIN2B encode subunits of NMDA receptors, which are important for glutamate-dependent plasticity and the conversion of neuronal activity into lasting changes in synaptic strength. ADGRL3 is involved in synaptic organization and neuronal adhesion, while MAP1A and ANK2 connect us to microtubule biology, neuronal scaffolding, and axonal architecture. These genes do not all have equivalent genetic associations with ADHD, and identifying their biological functions is not the same as demonstrating that I carry pathogenic variants in them. What interested me was the convergence of their functions. They suggested that understanding ADHD requires looking at how neuronal networks are assembled, how precisely they communicate, and how they adapt over time.

That realization led me toward developmental genetics and the biology of the fetal brain. During pregnancy, billions of neurons and supporting cells emerge through carefully regulated developmental programs. Neural progenitor cells proliferate and differentiate, neurons migrate toward their destinations, axons extend through developing tissue, and early synaptic connections begin forming. Molecular guidance systems help growing axons determine which directions to follow and which targets to approach. One gene I became particularly interested in was DCC, which encodes a receptor involved in netrin-dependent axon guidance. DCC has also appeared in large-scale ADHD genetics, making it particularly relevant to the relationship between inherited susceptibility and neural development. Netrin signaling helps guide growing axons through the developing nervous system, and this brings us into a very different area of biology from neurotransmitter metabolism. A neural circuit depends not only on whether its neurons can synthesize dopamine or respond to glutamate but also on whether the appropriate connections were established during development. Genes associated with ROBO and SLIT signaling participate in other aspects of axonal navigation, while RELN contributes to neuronal positioning and cortical organization. PAX6, EOMES, and TBR1 participate in developmental programs influencing neuronal identity and cortical formation. These pathways help demonstrate how early the architecture of the nervous system begins taking shape.

My investigation also brought me to FOXP1, FOXP2, MEF2C, and genes involved in chromatin regulation. FOXP1 and FOXP2 encode transcription factors that participate in networks of gene regulation relevant to neural development, with rare pathogenic variants associated with particular neurodevelopmental and speech-language phenotypes. MEF2C contributes to developmental transcription and synaptic regulation. In autism genetics, genes such as CHD8, ARID1B, DYRK1A, SCN2A, SYNGAP1, SHANK3, and NRXN1 illustrate how different molecular processes can converge on neurodevelopmental outcomes. Some influence chromatin accessibility and gene expression, others regulate neuronal excitability, and others participate in synaptic signaling or adhesion. Rare pathogenic variants in certain genes can have substantial effects, while common genetic variation usually contributes much smaller changes in statistical susceptibility. The distinction matters because it would be misleading to treat every developmental gene as an ADHD or autism gene, or to assume that the presence of an ordinary polymorphism means a person’s neural circuitry developed incorrectly. Nevertheless, these pathways reveal how much of neurodevelopmental biology involves the construction and regulation of neurons rather than simply the concentration of neurotransmitters after those neurons have matured.

This is where my attention began shifting toward the prenatal environment. The developing fetal nervous system depends on carefully coordinated cellular metabolism, nutrient transport, endocrine signaling, and placental physiology. Iron availability supports mitochondrial enzymes and contributes to oligodendrocyte biology, while thyroid hormones influence neuronal differentiation, migration, and myelin development. Folate-dependent pathways support nucleotide synthesis and one-carbon metabolism, and choline contributes to phospholipid synthesis and methyl-group metabolism. Essential fatty acids influence neuronal membrane structure, while adequate oxygen and glucose availability support the energetic demands of rapidly developing tissues. These are ordinary requirements of healthy development, not evidence that ADHD or autism results from one missing nutrient. But they demonstrate that inherited developmental programs operate within a physiological environment. I became interested in whether differences in inherited susceptibility might interact with changes in maternal metabolism, inflammation, placental signaling, or environmental exposures during particular periods of fetal development. At the same time, I think this subject requires considerable caution. Observational associations involving pregnancy stress, infection, maternal immune activity, or other exposures do not prove that a particular event caused a child’s ADHD or autism. Shared genetics and numerous confounding factors complicate these relationships, and it would be scientifically unjustified to blame a mother for her child’s neurodevelopmental differences based on speculative interpretations of pregnancy history.

Epigenetics introduced another dimension because the development of a nervous system requires precise regulation of when genes are expressed and how strongly they respond to signals. DNA methylation, histone modifications, chromatin remodeling, and transcription-factor activity help regulate cellular differentiation and maturation. A neuron and an oligodendrocyte may contain essentially the same genetic sequence, but they express very different combinations of genes because their developmental programs are different. I became interested in how these regulatory processes interact with stress physiology, particularly in relation to FKBP5 and glucocorticoid receptor signaling. Certain FKBP5 variants have been investigated for their interactions with early adversity and stress-responsive epigenetic regulation. However, an epigenetic change detected in blood or saliva does not necessarily reflect the same process inside developing cortical neurons, and a genetic variant does not prove that a particular methylation change occurred. I see this area as an important example of why developmental biology cannot be reduced to genetics alone, but neither can it be used to explain someone’s ADHD through an unverified story about prenatal stress or childhood trauma.

One of the developmental processes that interested me most was synaptic pruning. Early neural development involves the formation of extensive connections, followed by prolonged periods during which those connections are strengthened, weakened, stabilized, or removed. Synaptic pruning is part of how the brain refines its circuitry, allowing experience and developmental signaling to shape the efficiency and organization of neuronal networks. Microglia participate in certain aspects of synaptic remodeling, including processes involving complement proteins such as C1q and C3. These pathways can help identify synaptic elements for removal under particular conditions, although synaptic pruning also depends on neuronal activity and numerous other regulatory signals. I began wondering whether variations in the timing of cortical maturation and synaptic remodeling could contribute to differences in attention, sensory processing, and executive functioning. Some neuroimaging findings in ADHD indicate differences in the developmental timing of cortical maturation, while autism research has identified heterogeneous differences in synaptic development and connectivity. But cortical thickness is not a direct measurement of synapse number, and those observations do not demonstrate that everyone with ADHD experienced excessive pruning or that every autistic person experienced insufficient pruning. The value of this biology is that it shows how neural circuits are continuously refined during development, not that we can diagnose abnormal pruning through a stool test, a genetic polymorphism, or a routine brain scan.

Myelination became equally important to me because neuronal communication depends on timing as well as connectivity. Oligodendrocytes produce myelin, the lipid-rich insulating structure surrounding many axons in the central nervous system. Myelin influences conduction velocity and the reliability of communication between neural regions. Genes such as OLIG1, OLIG2, SOX10, MYRF, MBP, and PLP1 participate in different aspects of oligodendrocyte development and myelin biology. The maturation of white-matter pathways begins before birth and continues through childhood, adolescence, and adulthood. This prolonged developmental process is particularly interesting when thinking about networks involved in attention, working memory, language, sensory integration, and motor control. These functions depend on coordinated activity across multiple brain regions, and the timing of signals matters. If a distributed network is going to maintain information, inhibit irrelevant responses, and coordinate behavior, it needs more than adequate neurotransmitter concentrations. It needs appropriately organized connections and efficient communication between them. White-matter differences have been reported in some groups with ADHD and autism, but findings vary by developmental stage and imaging method. They do not justify concluding that a specific child has defective myelination without appropriate clinical evidence.

Another developmental relationship I find fascinating involves the changing function of GABA. GABA is usually described as the principal inhibitory neurotransmitter in the mature brain, but during early neuronal development, GABA-A receptor activation can produce depolarizing responses in some immature neurons. This depends partly on intracellular chloride regulation through transporters including NKCC1 and KCC2, encoded by SLC12A2 and SLC12A5. As neurons mature, changes in chloride transport influence the electrical effects of GABA signaling. This developmental transition is more complicated than a simple switch from excitation to inhibition, but it demonstrates that the functional effect of a neurotransmitter depends on the developmental state of the cell receiving it. Glutamate signaling also changes as neural circuits mature. NMDA receptors permit calcium-dependent signaling involved in synaptic plasticity, influencing intracellular pathways such as CaMKII and the regulation of receptor trafficking, gene transcription, and dendritic structure. These mechanisms are fundamental to how neuronal activity becomes learning and how repeated experiences alter the strength of connections. They also explain why I am interested in the relationship between developmental timing, neurotransmitter receptor expression, and the maturation of neural networks. The chemical messenger is only part of the system; the machinery receiving and interpreting that signal is equally important.

As I investigated these developmental processes, I began connecting them with another major area of my work: the intestinal microbiome, microbial metabolites, and their interactions with host physiology. Through BiomeLogic, I have examined complex pediatric cases involving autism, ADHD, gastrointestinal dysfunction, restrictive eating, immune abnormalities, and unusual metabolic findings. Some of these investigations involved years of laboratory records collected during different periods of the child’s life. What stood out to me was that the underlying neurodevelopmental diagnosis could remain relatively stable while gastrointestinal symptoms, immune findings, microbial metabolites, nutritional status, and behavioral difficulties changed considerably. This is a distinction I think deserves much more attention. A child with autism or ADHD can also experience abdominal pain, constipation, reflux, sleep-disordered breathing, iron deficiency, infection, medication adverse effects, or another medical condition that influences their comfort and functioning. When communication is limited, discomfort may be expressed through changes in sleep, agitation, withdrawal, or behavior rather than through a detailed verbal description. These problems should not automatically be attributed to the neurodevelopmental diagnosis, but neither should they be used to suggest that treating the gut will reverse autism or ADHD.

In some previous pediatric investigations, I examined urinary organic-acid profiles containing unusual patterns involving quinolinic acid, kynurenine metabolites, p-cresol-related compounds, pyroglutamate, and intermediates associated with mitochondrial metabolism. In certain longitudinal records, several abnormalities were more pronounced during periods of greater clinical difficulty and less pronounced in later testing. These were observations involving changing physiological states, not evidence that a particular metabolite caused autism or that correcting a biomarker produced improvement. The kynurenine pathway interested me because tryptophan is not exclusively used to synthesize serotonin. It also enters pathways involving kynurenine, kynurenic acid, quinolinic acid, and other downstream compounds. Inflammatory signaling can influence enzymes involved in tryptophan metabolism, including IDO1, while some kynurenine metabolites interact with glutamatergic and immune pathways. Quinolinic acid is relevant to NMDA-receptor biology, but a urinary measurement does not establish its concentration inside the brain or around individual neurons. I became interested in whether peripheral metabolic changes could reflect broader physiological pressures that were relevant to the child’s health, while remaining careful not to equate an abnormal urinary result with direct neurotoxicity or altered synaptic pruning.

P-cresol-related metabolism presented another interesting question. Certain intestinal microorganisms metabolize aromatic amino acids, including tyrosine, generating phenolic compounds such as p-cresol. After absorption, these metabolites undergo additional host processing, including sulfation, and are subsequently eliminated through pathways involving the kidneys. Elevated p-cresol sulfate therefore reflects more than the presence of one bacterial species. Its concentration can be influenced by dietary substrate availability, intestinal microbial activity, absorption, hepatic metabolism, renal function, and the laboratory method used. In children with severely restricted diets or gastrointestinal dysfunction, I am particularly interested in whether changes in digestion, intestinal transit, or fermentation are influencing the metabolic environment. But p-cresol sulfate is not an established diagnostic biomarker for ADHD or autism, and a high result does not prove that the compound is damaging the developing brain. The value of investigating it lies in understanding what biological questions it raises and whether those questions can be answered with additional clinical context.

The stool microbiome has provided similarly interesting observations. In some longitudinal pediatric records, microbial composition changed substantially across different periods, with certain organisms becoming more abundant while others were no longer detected. Stool secretory IgA also changed markedly in some records. Secretory IgA participates in the relationship between the intestinal immune system and resident microorganisms, influencing microbial adherence, immune exclusion, and aspects of mucosal homeostasis. However, a high stool secretory IgA measurement does not independently establish pathological immune activation, and a low value does not automatically diagnose immune deficiency. Differences between commercial stool testing methods can make longitudinal comparisons especially difficult. When I review these findings, I am interested in the broader ecological context: food diversity, intestinal transit, mucus-associated metabolism, bile acids, antibiotic exposure, inflammation, and microbial interactions. A microbiome is not simply a list of good and bad organisms. It is an ecological network operating within a living host.

This is particularly clear when examining microbial cross-feeding. Certain bifidobacteria ferment carbohydrates and produce acetate and lactate, while other organisms can use these products in pathways that generate butyrate. Faecalibacterium prausnitzii, for example, is associated with butyrate production and participates in metabolic relationships involving other members of the intestinal ecosystem. But the relative abundance of a bacterium does not establish how much of a metabolite is being produced, and the amount present in stool does not reveal how much is absorbed or metabolized by the intestinal epithelium. I have also investigated the relationship between microbial sulfur metabolism and epithelial energy production because hydrogen sulfide can act as a physiological signaling molecule at low concentrations but interfere with mitochondrial respiration at sufficiently high local exposure. These mechanisms are biologically interesting, particularly in relation to colonocyte metabolism and intestinal homeostasis, but ordinary stool testing cannot establish mitochondrial inhibition or abnormal brain metabolism from bacterial abundance alone.

Butyrate is another molecule that connects several of my research interests. It is produced through microbial fermentation, serves as an important energy substrate for colonocytes, and can influence gene regulation through mechanisms including histone deacetylase inhibition under appropriate experimental conditions. This creates a potential biochemical interface between intestinal microbial metabolism and epigenetic regulation. However, the concentration of butyrate inside the colon is not equivalent to the amount reaching the systemic circulation or the central nervous system. Much of the butyrate produced in the intestine is consumed locally, and its effects depend on transport, tissue exposure, metabolism, and concentration. I am interested in how microbial metabolites influence immune and epithelial physiology and whether particular pathways may affect developing neural systems under specific conditions. But it would be incorrect to claim that increasing butyrate can restore synaptic pruning, repair myelination, or reverse autism or ADHD. Those conclusions would require direct clinical evidence that we do not currently have.

The maternal microbiome raises another important developmental question. During pregnancy, the maternal intestinal ecosystem participates in the production and transformation of metabolites that can influence maternal metabolic and immune physiology. Some circulating metabolites may interact with placental transport systems and developmental signaling. The fetal nervous system is therefore developing within a larger physiological environment that includes maternal metabolism, endocrine regulation, immune activity, and nutrient availability. Yet this does not mean the fetal brain is directly colonized by maternal gut bacteria, and claims about a stable prenatal microbiome remain scientifically contested. The more meaningful question is whether particular maternal metabolic or inflammatory states influence developmental pathways under defined conditions, and how these effects interact with inherited susceptibility. Again, population-level associations and experimental mechanisms cannot simply be translated into a causal explanation for an individual child’s neurodevelopmental condition.

Working with pediatric cases has also reinforced how frequently conventional medical findings may matter more than highly specialized biomarkers. Iron deficiency can influence fatigue, sleep, and cognitive functioning. Thyroid dysfunction can affect growth, metabolism, and neurological development. Celiac disease, significant constipation, nutritional restriction, and sleep-disordered breathing can produce substantial symptoms that overlap with behavioral or attentional difficulties. A child with a limited diet may have nutritional vulnerabilities that deserve careful assessment, while another child may have persistent anemia that requires investigation even after iron indices improve. In these situations, a reticulocyte count, appropriate iron studies, thyroid evaluation, or clinical sleep assessment may be more informative than another expensive microbiome panel. I have become increasingly cautious about interpreting every unusual organic acid, bacterial species, or genetic variant as a target for intervention. Sometimes the most useful analysis identifies a conventional medical question that has not been adequately addressed.

My interest in neurodevelopment has also expanded into how ADHD presents in girls and women. Some girls experience predominantly internal difficulties with attention, organization, emotional regulation, or mental exhaustion rather than the overt hyperactivity that traditionally attracts attention in childhood. They may compensate for years, maintaining performance at the expense of considerable effort, and the diagnosis may not be recognized until adulthood. Hormonal transitions introduce another layer because estradiol and progesterone can influence neural signaling systems involved in cognition, sleep, and mood. Progesterone-derived neurosteroids, including allopregnanolone, interact with GABA-A receptors, while estrogen signaling can influence aspects of catecholamine and serotonin physiology. Some women report changes in ADHD symptom severity across the menstrual cycle, postpartum, or during perimenopause. These experiences do not mean that hormone levels explain ADHD, and the evidence for individualized hormonal treatment strategies remains incomplete. What interests me is how reproductive physiology may modify the functioning of an already-established neurodevelopmental phenotype.

This brings me back to an important part of my own experience. I have spent years trying to understand why my brain can function so differently depending on the task, environment, stress level, and sleep. My genetic findings raised questions about catecholamine regulation and stress responsiveness, but they did not provide one definitive explanation. Investigating developmental genes such as DCC, FOXP1, MEF2C, SNAP25, and the broader pathways associated with synaptic organization showed me how early neural architecture is established. Studying myelination and synaptic pruning helped me understand that these networks continue maturing for many years after birth. My interest in epigenetic regulation showed me how gene expression can change during development and in response to physiological conditions. And my work involving pediatric gastrointestinal and immune abnormalities reminded me that the functioning of a nervous system can change even when its underlying developmental characteristics remain relatively stable.

I also find it important to recognize that the adult nervous system retains the capacity for adaptation. Synaptic plasticity continues throughout life, and repeated experience influences learning, behavior, reward processing, and the strength of neural connections. BDNF-related signaling, NMDA receptor activity, calcium-dependent pathways, and transcriptional regulators all contribute to aspects of this process. Repeated stimulation can produce longer-lasting adaptations in reward circuitry, including mechanisms involving transcription factors such as ΔFosB. I have also been interested in emerging approaches that influence glutamatergic signaling and plasticity, including research involving ketamine. But the existence of neuroplasticity does not establish that ADHD or autism can be cured by resetting the brain, nor does experimental synaptic remodeling demonstrate that early developmental differences can be reversed. What matters is that meaningful improvements in functioning, learning, communication, and quality of life can occur without requiring the underlying neurodevelopmental diagnosis to disappear.

When I reflect on everything I’ve investigated, I no longer think of ADHD as simply having too little dopamine. I think about prefrontal network stability, reward valuation, norepinephrine signaling, working-memory regulation, synaptic architecture, developmental timing, and the interaction between inherited susceptibility and experience. I think about the genes involved in axon guidance, neuronal migration, synaptic vesicle release, calcium signaling, myelination, and transcriptional regulation. I think about how the fetal nervous system develops, how its connections are refined through childhood, and how those networks continue adapting throughout adulthood. I also think about how gastrointestinal disorders, nutritional deficiencies, sleep problems, inflammation, and other medical conditions can influence a person’s functioning without being responsible for the original neurodevelopmental diagnosis.

This is the distinction I increasingly try to make in my work with children and adults. The developmental architecture of a nervous system is one part of the picture, while the person’s changing physiological state is another. They can interact, but they should not be confused. A child with autism may experience substantial improvements in sleep, gastrointestinal comfort, communication, or emotional regulation while remaining autistic. An adult with ADHD may learn to function more effectively through appropriate support, treatment, environmental changes, and experience while continuing to have ADHD. Those improvements are meaningful without needing to be described as cures or evidence that the original diagnosis was incorrect.

I believe that understanding ADHD and autism requires looking much deeper than any single neurotransmitter, gene, biomarker, or microbiome result. The brain develops through the coordinated activity of genetic programs, cellular metabolism, hormonal and immune signaling, neuronal migration, synaptic formation, pruning, myelination, and activity-dependent plasticity. These processes operate across different developmental periods, and the evidence connecting them to individual clinical outcomes varies considerably. Some relationships are well established, others remain plausible mechanisms, and many cannot yet be measured or interpreted reliably in an individual person.

For me, the most important question has become how to distinguish these different layers without forcing everything into one explanation. When investigating a complex case, I want to understand what was present from early development, what changed later, which findings may be secondary to another medical condition, which biomarkers are genuinely informative, and which proposed mechanisms remain uncertain. I want to know why one child experiences substantial gastrointestinal or immune difficulties while another with the same diagnosis does not. I want to understand why a person may experience dramatic changes in daily functioning despite having a relatively stable neurodevelopmental diagnosis. And I want to investigate the biology with enough precision to recognize when a connection is meaningful and when two findings may simply coexist.

I was diagnosed with ADHD at 33, but the developmental processes involved in building my nervous system began long before I was born. The diagnosis helped me understand part of my experience, while investigating the underlying biology showed me just how much more there is to understand. That investigation has influenced the way I approach complex neurodevelopmental, gastrointestinal, metabolic, and immune presentations through BiomeLogic. I don’t believe every biological difference is a defect that needs to be corrected, and I don’t believe every symptom can be traced to one hidden mechanism. I do believe that understanding the developmental history of the nervous system, the physiological environment in which it functions, and the medical factors that may affect it can provide a much more complete picture of the individual.

And perhaps that is the question we should be asking more often. Not simply which diagnosis describes the person, but how their particular nervous system developed, what influences its functioning today, and which aspects of that biology we can understand well enough to support them more effectively.

Mohammed Attallah
Founder | BiomeLogic
Mechanistic Health & Systems Biology Consultant

https://biomelogic.net