Glucose, Uniqueness, and Rally-Car Mind: An Evidence-Based Answer to Three Personal Questions

Disclaimer: This article presents aggregated research findings. It is not a medical paper, cannot substitute for a physician, and should not be used as diagnostic evidence. The reasoning and conclusions in this article involved AI-assisted generation, have not undergone peer review or independent verification, and may contain errors.

TL;DR

Your "more-glucose-need" experience is best framed as a pattern, not a disease: there is robust evidence (a) of substantial inter-individual variation in cerebral glucose metabolism in healthy adults, (b) that acute drops in blood glucose reliably worsen mood, energy, and irritability in non-diabetic people, and (c) that ADHD, BPD, and bipolar disorder each show abnormal regional brain glucose metabolism — but no validated diagnostic category called "high-glucose-need brain." It is a real trait-level signal sitting on top of (and amplified by) interoceptive sensitivity and possibly diagnosed neurodivergence.
The feeling that "no one else has this" is partly a documented cognitive bias (personal fable, spotlight effect, illusion of transparency) and partly real: people with ADHD/BPD do show measurable differences in interoception, emotional reactivity, and sensory processing sensitivity. So you are simultaneously over-estimating your uniqueness AND genuinely processing internal signals differently than most people.
"Rally-car brain" is almost certainly a stress-diathesis combination, not pure innate nor pure stress: temperament research (Kagan) shows high-reactive infants exist from 4 months of age; ADHD research shows chronic cortical hypoarousal compensated by mental hyperactivity; chronic-stress research shows allostatic load and epigenetic changes to the HPA axis and locus coeruleus permanently upregulate arousal. Retrospective recall of "always being this way" is documented to be unreliable — adults' recall of childhood ADHD symptoms is driven by current symptom severity rather than the actual childhood phenotype — so your sense of lifelong persistence should be held with appropriate humility, even though the underlying trait is almost certainly present.

Key Findings

Question 1 (glucose and mood):

Healthy young adults show coefficients of variation of 11.1–15.2% in regional brain glucose metabolism on PET — meaning normal brains differ from each other by roughly 10–15% in resting fuel burn (Wang et al., 1994, PMID 8071692).
Greater temporal variability in cerebral glucose use, not the baseline level, predicts better cognitive performance (Deery et al., 2025, PNAS, doi:10.1073/pnas.2510850123).
Experimentally induced hypoglycemia in non-diabetic and diabetic adults produces measurable increases in anger and negative mood, with hostility-trait moderation (Hermanns et al., 1997, PMID 9006228).
Adults with childhood-onset ADHD show ~8.1% globally reduced cerebral glucose metabolism vs. controls, largest in premotor and superior prefrontal cortex (Zametkin et al., 1990, NEJM 323:1361–1366).
BPD shows prefrontal/cingulate/striatal hypometabolism (De La Fuente et al., 1997, Psychiatry Res); BPD and Bipolar-II both show hypometabolism in insula, brainstem, and frontal white matter (Bøen et al., 2019, Acta Psychiatr Scand 139:256).
Bipolar disorder shows dysregulated cerebral glucose metabolism plus high peripheral metabolic comorbidity; Calkin et al. (2015, Br J Psychiatry 206:52–57) found ~54% of bipolar patients have type 2 diabetes or insulin resistance, and IR was associated with roughly eight-fold higher odds of lithium resistance.
"Metabolic overdrive" hypothesis (Kuperberg et al., 2024, Mol Psychiatry): hyperglycolysis/glutaminolysis in bipolar mania.

Question 2 (uniqueness):

The "personal fable" — belief that one's experiences are uniquely incomprehensible — is a well-described construct (Elkind, 1967, Child Development 38:1025).
Gilovich, Medvec & Savitsky (2000, J Pers Soc Psychol 78:211) demonstrated the spotlight effect; Gilovich, Savitsky & Medvec (1998, J Pers Soc Psychol 75:332) demonstrated the illusion of transparency — both show systematic overestimation of how much others notice and detect.
Kutscheidt et al. (2019, ADHD Atten Defic Hyperact Disord 11:395) found ADHD adults had significantly lower heartbeat-tracking accuracy (mean 0.55 vs. 0.71, p=0.025); Wiersema & Godefroid (2018, PLOS ONE 13:e0205221) found no significant difference, and the 2025 Bruton et al. systematic review (Psychophysiology) concluded 3 of 5 case-control studies show reduced interoception in ADHD.
Müller et al. (2015, JAMA Psychiatry 72:1077) found reduced heartbeat-evoked potentials in acute BPD that correlated with emotional dysregulation and childhood maltreatment; Flasbeck et al. (2020) found the opposite direction with frontal electrodes, indicating altered (not uniformly reduced) interoceptive cortical processing.
Sensory-processing sensitivity (Aron & Aron, 1997, J Pers Soc Psychol 73:345–368) is a validated trait construct estimated to occur in 20–35% of the population (Aron & Aron, 1997; Pluess et al., 2018) — meaningfully higher than the 15–20% lower bound often cited from the original 1997 paper.
Emotional granularity / alexithymia varies meaningfully across individuals; higher granularity predicts less maladaptive coping (Kashdan, Barrett & McKnight, 2015, Curr Dir Psychol Sci).

Question 3 ("rally-car brain"):

ADHD reflects unstable cortical arousal; hyperactivity and sensation-seeking are interpreted as auto-regulatory attempts to stabilize brain arousal (Hegerl & Hensch, 2014, ADHD Atten Defic Hyperact Disord 6:141).
Kagan's research shows ~20% of 4-month-old infants are "high-reactive," with persistent amygdala hyper-reactivity into adulthood (Schwartz et al., 2003, Science 300:1952; Schwartz et al., 2012, Mol Psychiatry 17:1042).
Chronic stress amplifies locus coeruleus reactivity to subsequent stressors and is coupled with the emergence of pathological anxiety-like behaviors in rodents (Morris, McCall, Charney & Murrough, 2020, Brain and Neuroscience Advances 4:2398212820930321).
Early life adversity produces persistent epigenetic changes to glucocorticoid receptor (NR3C1) and FKBP5 genes, durably altering HPA axis function (McGowan et al., 2009, Nat Neurosci 12:342; Klengel et al., 2013, Nat Neurosci).
Adult retrospective recall of childhood ADHD symptoms is driven by current symptom severity and does not correlate with parents' contemporaneous childhood ratings — a recall bias that questions retrospective reports even in clinical samples (Miller et al., 2010, J Atten Disord; Breda et al., 2020, J Psychopathol Behav Assess).

Details

Question 1: "Why does my brain seem to need more glucose, and if it doesn't get enough, emotional problems arise — is this a disease or a pattern?"

Is there real inter-individual variation in brain glucose use? Yes, robustly. Wang et al. (1994, PMID 8071692) measured PET-FDG cerebral metabolic rates in healthy young men and found regional coefficients of variation of 11.1–15.2% on absolute measures (4–10% on relative measures) — meaning normal brains differ from each other by roughly 10–15% in resting glucose burn. Deery et al. (2025, PNAS, doi:10.1073/pnas.2510850123) extended this by showing that glucodynamic variability (within-person temporal variation in glucose use) maps to functional network architecture and predicts cognitive performance; lower glucodynamic variability in aging is associated with reduced metabolic-network efficiency and worse cognition. Brain fuel use is not a fixed setpoint; it is a continuously varying, individual trait.

Does hypoglycemia really cause mood disturbance? Yes, under controlled conditions. In a stepwise hyperinsulinemic-hypoglycemic clamp study, Hermanns et al. (Patient Educ Couns 1997, PMID 9006228) showed that as glucose was stepped down from 4.0 to 2.0 mmol/L in IDDM patients, Profile of Mood States anger scores rose significantly (p<0.05) and overall mood worsened progressively at each glucose step, with hostility (SCL-90) trait moderating the anger response (P<0.05 at 2.5 mmol/L). The pattern shows large inter-individual variability — some people experience hypoglycemia as a profound stressor; others tolerate it.

Reactive ("relative") hypoglycemia — symptoms appearing with rapid glucose decline even within normal range — was first described clinically by Harry Salzer (1966) and remains contested in mainstream endocrinology because many symptomatic patients have normal glucose tolerance tests. The continuous-glucose-monitoring literature on glucose volatility and mood is genuinely mixed: Muijs et al.'s 2021 systematic review (Endocrinology, Diabetes & Metabolism 4:e152) screened 2,316 studies, found 8 meeting criteria, and concluded that 4 found a positive association between higher postprandial glucose rate-of-increase and negative mood, while 4 found none — they concluded "there is no clear empirical support for a link between GV and mood in adults with type 1 and type 2 diabetes." So this is a real phenomenon experienced by many people that has not yet been clearly nailed down empirically.

ADHD, BPD, and bipolar disorder all show abnormal brain glucose metabolism, but in different patterns:

ADHD: Zametkin et al. (1990, NEJM 323:1361) PET study found 8.1% lower global glucose metabolism in 25 adults with childhood-onset ADHD vs. 50 controls (9.05 ± 1.20 vs. 9.85 ± 1.68 mg/min/100g; two-tailed p = 0.034), with the largest reductions in premotor and superior prefrontal cortex. Stimulant treatment did not normalize global metabolism (Matochik et al., 1994, Am J Psychiatry, PMID 8166305). Ernst et al. (1998, J Neuropsychiatry Clin Neurosci 10:168) found age-and-sex-dependent effects that complicate the original finding.
BPD: De La Fuente et al. (1997, Psychiatry Res, PMID 9368195) found hypometabolism in premotor/prefrontal cortex, anterior cingulate, thalamus, caudate, and lenticular nuclei. Bøen et al. (2019, Acta Psychiatr Scand, PMID 30552759) compared 22 BPD, 22 Bipolar-II, and 21 healthy controls without reciprocal comorbidity: both patient groups showed hypometabolism in insula, brainstem, and frontal white matter; BPD additionally in hypothalamus, midbrain, and striatum.
Bipolar disorder: Meta-analysis (Wu et al., 2021, Brain Behav 11:e02117) of 7 studies (126 BD, 160 controls) found increased metabolism in right precentral gyrus and decreased in left superior/middle temporal gyri and cerebellum. Kuperberg et al. (2024, Mol Psychiatry, doi:10.1038/s41380-024-02431-w) proposed the "metabolic overdrive" hypothesis: hyperglycolysis and glutaminolysis during mania. Calkin et al. (2015, Br J Psychiatry 206:52–57, doi:10.1192/bjp.bp.114.152850) found approximately 54% of bipolar disorder patients have type 2 diabetes or insulin resistance — roughly three times the general-population rate — and IR conferred roughly eight-fold higher odds of lithium resistance, supporting that bipolar disorder partly is a metabolic disorder.

Healthy-volunteer glucose-and-mood literature is more directly relevant to your subjective experience:

Donohoe & Benton (1999, Psychopharmacology 145:378) showed glucose drinks improve Porteus Maze performance, verbal fluency, and problem-solving in healthy young adults.
Owens et al. (1997, Physiol Behav 62:471) showed falling blood glucose during cognitive demand reduces subjective energy.
Benton's comprehensive review (2002, Neurosci Biobehav Rev 26:293) concluded that in non-diabetic adults, lower glucose during cognitively demanding tasks is associated with poorer mood, and rapidly falling glucose is consistently associated with irritability.
Young et al. (2019, Proc Roy Soc B 286:20190244, doi:10.1098/rspb.2019.0244) found interoceptive accuracy moderates the glucose-mood link: people with higher interoceptive accuracy experienced larger glucose-induced declines in hunger and anxiety — meaning some people genuinely feel glucose drops more.
The Gailliot & Baumeister "willpower depletion" model (2007, J Pers Soc Psychol 92:325; Personality and Social Psychology Review 11:303) proposed glucose mediates self-control, but this has been substantially challenged by Vadillo et al. (2016) meta-analysis and Job et al. (2013, PNAS) showing effects depend on lay theories about willpower. Cite with caveat.

Disease or pattern? The literature does not support framing this as a discrete disease. Cerebral glucose metabolism varies continuously; psychiatric populations differ but in ways that look more like risk factors and trait markers than causes. The most defensible framing: you have a metabolic trait — likely shaped by genetics, possibly amplified by ADHD-type frontal hypometabolism, and made phenomenologically vivid by elevated interoception — sitting on the continuous variation in how brains use fuel. It is a pattern with biological substrate, not a disease in the DSM sense.

Question 2: "Why do I feel this experience is unique to me — others don't seem to have this problem?"

The feeling of uniqueness has both a documented bias component and a real-signal component.

Bias side. Elkind's "personal fable" (1967, Child Development 38:1025) describes the belief that one's inner experiences are uniquely incomprehensible. Originally framed as adolescent, the construct persists in adulthood under emotional stress. Gilovich, Medvec & Savitsky (2000, J Pers Soc Psychol 78:211) experimentally demonstrated the spotlight effect: in their T-shirt studies, participants estimated about 50% of observers would notice an embarrassing shirt; actual observer recall was about 25%. Gilovich, Savitsky & Medvec (1998, J Pers Soc Psychol 75:332) demonstrated the illusion of transparency: participants in social-evaluative settings systematically overestimate how much others can detect their internal states. The reciprocal corollary — pluralistic ignorance of inner states — explains why we assume others don't share our experience: we don't see it in them because they too are concealing or assuming uniqueness.

Real-signal side. Some neurodivergent populations process internal signals differently:

Interoception in ADHD: Kutscheidt et al. (2019, ADHD Atten Defic Hyperact Disord 11:395, doi:10.1007/s12402-019-00299-3) found 14 ADHD adults had significantly lower Schandry heartbeat-tracking accuracy than 16 controls (0.55 ± 0.15 vs. 0.71 ± 0.17, p=0.025), while subjective interoceptive awareness did not differ. Wiersema & Godefroid (2018, PLOS ONE 13:e0205221) found no significant difference. Bruton et al.'s 2025 systematic review (Psychophysiology) of 17 articles concluded that 3 of 5 case-control studies showed reduced interoception in ADHD, and in general-population samples, higher ADHD symptoms correlated with lower interoceptive accuracy and awareness. The direction: interoceptive accuracy may be reduced while interoceptive sensibility (subjective awareness) is intact or elevated — meaning ADHD adults may feel internal signals strongly but interpret them less accurately.
Interoception in BPD: Müller et al. (2015, JAMA Psychiatry 72:1077, doi:10.1001/jamapsychiatry.2015.1252) found reduced heartbeat-evoked cortical potentials in acute BPD, inversely correlated with emotional dysregulation and childhood maltreatment; remitted BPD did not differ from controls. Schmitz et al. (2020, J Affect Disord) replicated. Flasbeck et al. (2020, Borderline Personal Disord Emot Dysregul 7:24) found higher frontal HEP amplitudes — opposite direction. Hart et al. (2013, J Pers Disord) found behaviorally intact heartbeat detection. The consensus: interoceptive processing is altered in BPD, not simply "more" or "less."
Sensory-Processing Sensitivity / HSP: Aron & Aron (1997, J Pers Soc Psychol 73:345–368) introduced and validated SPS through 7 studies. The 27-item Highly Sensitive Person Scale shows adequate reliability and discriminant validity from introversion and neuroticism. Aron & Aron originally estimated 15–20% of the population; subsequent work raises this estimate to 20–35% (Pluess et al., 2018; a 2025 Frontiers in Psychology Spanish general-population study cites "around 20–35%"). Smolewska, McCabe & Woody (2006, Pers Individ Differ 40:1269) found SPS is multidimensional (Aesthetic Sensitivity, Low Sensory Threshold, Ease of Excitation), not unidimensional as originally claimed. SPS is moderately associated with the behavioral inhibition system, anxiety, and depression; it is not a clinical disorder. Aron explicitly argues HSP is distinct from autism, ADHD, and sensory-processing disorder, though they may co-occur.
Emotional granularity: Barrett et al. (2001) and Kashdan, Barrett & McKnight (2015, Curr Dir Psychol Sci) show people genuinely differ in how finely they represent emotional states. High granularity predicts better emotion regulation and less reliance on maladaptive coping (binge drinking, self-injury, aggression); low granularity (alexithymia) is the inverse.

The synthesis: You are probably right that others around you don't experience exactly what you experience, AND you are also subject to the well-documented egocentric biases that exaggerate this. The neurodivergent reality is layered on top of normal uniqueness illusion. The corrective insight: 20–35% of the population qualifies as highly sensitive on the SPS construct alone; ~5% of adults have ADHD; ~1.4% have BPD; many more sit at sub-threshold levels. The feeling of isolation is itself statistically shared.

Question 3: "Why does my brain run at 'rally car' speed without my choosing to? Is it chronic survival pressure, innate, and could my memory be biased?"

This is best answered by the stress-diathesis model: the evidence supports BOTH innate predisposition AND environmental amplification.

The innate-temperament evidence is strong. Kagan et al. (1987, 1988; Kagan & Snidman, 1991, Psychol Sci) demonstrated that ~20% of 4-month-old infants are "high-reactive" — vigorous motor activity, crying, and physiological arousal to mild novel stimuli — and this predicts behavioral inhibition in childhood and amygdala hyper-reactivity into adulthood (Schwartz et al., 2003, Science 300:1952; Schwartz et al., 2012, Mol Psychiatry 17:1042). High-reactivity is biologically rooted in a low amygdala arousal threshold (Kagan, 1994), with persistent right-frontal alpha asymmetry, elevated heart rate, and lower vagal tone. Some children genuinely arrive in the world wired for higher baseline arousal.

The ADHD-as-compensatory-hyperactivity hypothesis is well-supported. The vigilance regulation model (Hegerl & Hensch, 2014, ADHD Atten Defic Hyperact Disord 6:141) proposes ADHD reflects unstable cortical arousal; hyperactivity and sensation-seeking are auto-regulatory attempts to maintain it. This is consistent with Zametkin's PET finding of reduced prefrontal glucose metabolism — the PFC is under-firing, so the system seeks stimulation. Bellato et al. (2020, Front Psychol 11:1991) supports locus coeruleus-norepinephrine dysfunction in ADHD. Stimulants raise PFC tonic firing, paradoxically calming compensatory mental hyperactivity. If you have ADHD, "rally-car brain" may be your PFC compensating for low intrinsic arousal — not pure choice and not pure pathology but a homeostatic response to a hypoaroused substrate.

The allostatic-load and epigenetic evidence is strong. Morris, McCall, Charney & Murrough (2020, Brain and Neuroscience Advances 4:2398212820930321, doi:10.1177/2398212820930321) state explicitly: "Chronic stress leads to amplification of locus coeruleus reactivity to subsequent stressors, which is coupled with the emergence of pathological anxiety-like behaviors in rodents." Borodovitsyna et al. (2018, Neuroscience) showed acute stress persistently alters LC function and anxiety-like behavior. McGowan et al. (2009, Nat Neurosci 12:342) showed childhood abuse is associated with hypermethylation of the glucocorticoid receptor gene (NR3C1) in human postmortem brain, durably altering HPA axis feedback. Murgatroyd & Spengler (2011, Stress 14:581) demonstrated in mice that early life stress epigenetically marks the arginine vasopressin (AVP) gene, sustaining elevated HPA activity into adulthood through MeCP2 phosphorylation. Klengel et al. (2013, Nat Neurosci) showed FKBP5 epigenetic changes after childhood adversity confer lifelong HPA dysregulation. Chronic survival pressure can permanently raise the set-point of your arousal system through specific, documented molecular mechanisms.

The memory-bias concern is legitimate. Miller et al. (2010, J Atten Disord, PMID 19794136) followed N=94 children with childhood ADHD to ages 16–22 and found retrospective recall of childhood symptoms was substantially unstable; current symptom severity drove recall accuracy — when current symptoms are endorsed, participants are more likely to "remember" clinically significant childhood symptoms. Breda et al. (2020, J Psychopathol Behav Assess, doi:10.1007/s10862-020-09852-1) confirmed in 55 adults with childhood ADHD assessed longitudinally: adults' retrospective self-ratings did not correlate with parents' contemporaneous childhood ratings, and current adult symptom severity drove recall — they explicitly call this "a recall bias … question[ing] the validity of retrospective reports, even in clinical samples." Sibley et al. (2017, Am J Psychiatry) similarly argue that adult-onset versus persisting childhood ADHD distinction is murky in retrospective work. Your sense of "I've always been this way" is partly real (high-reactive temperament does persist) and partly reconstructive: people with current symptoms naturally see their childhood through the lens of current symptoms.

The stress-diathesis synthesis. The most evidence-supported answer: you arrived with a high-reactive or ADHD-vulnerable nervous system (innate vulnerability); environmental pressure (chronic stress, attachment instability, or whatever your history holds) upregulated that system through epigenetic and allostatic mechanisms (environmental amplification); and your current arousal level is the sum of these. Neither pure innateness nor pure stress accounts for the data. This is Caspi & Moffitt's gene-environment interaction framework (2006, Nat Rev Neurosci) applied to arousal regulation.

Recommendations

Short-term, this week:

Run a 7-day glucose-mood log. Use a continuous glucose monitor (Dexcom Stelo or Abbott Lingo, both available over-the-counter in the US since 2024) and rate mood/irritability on a 0–10 scale every 2 hours. This converts subjective experience into testable data. Threshold for action: if mood crashes correlate with glucose excursions >40 mg/dL within 60 minutes, you have personalized evidence of glucose-mediated mood lability worth treating.
Eat protein + fat + fiber at breakfast within 60 minutes of waking and avoid simple carbs solo. This pre-empts the 3-hour postprandial crash that drives reactive symptoms. If "rally-car brain" calms within two weeks, the metabolic substrate hypothesis is supported. If not, the issue is primarily arousal-regulation rather than fuel.

Medium-term, next 1–3 months: 3. Get a formal evaluation for adult ADHD if you have not already. If ADHD is present, stimulant medication addresses the cortical hypoarousal driving compensatory mental hyperactivity at the substrate level. Threshold to change recommendation: if ADHD evaluation is negative, redirect toward (4). 4. If trauma/chronic stress is in your history, pursue trauma-informed therapy — modalities with the strongest evidence for HPA axis normalization: Trauma-focused CBT, EMDR, or somatic experiencing. Preliminary evidence (Pacella et al., 2013) suggests these can normalize HPA reactivity. 5. Test interoceptive training. Mindfulness-based interventions and specifically interoception-targeted protocols (Khalsa & Lapidus, 2016) improve interoceptive accuracy. If your problem profile is high interoceptive sensibility plus low interoceptive accuracy (the ADHD profile suggested by Kutscheidt et al. and the 2025 Bruton review), this is the targeted intervention.

Long-term: 6. Adopt the "trait, not disease" frame in self-narrative. The evidence supports treating this as a pattern to work with — sleep, glucose stability, exercise (which raises PFC tonic arousal and reduces compensatory mental restlessness), trauma processing — rather than a fixed disease state. Threshold to revise: if symptoms remain disabling despite 6 months of these interventions, escalate to psychiatric evaluation for medication.

What would change these recommendations:

A diagnosis of bipolar disorder shifts priorities sharply — mood stabilizer becomes primary, and unsupervised stimulants become contraindicated.
Finding of insulin resistance (HOMA-IR > 2.5) shifts metabolic interventions to primary.
A pattern of glucose crashes WITHOUT mood crashes during your 7-day log would suggest the glucose-mood link is correlational, not causal in your case.

Caveats

The Zametkin (1990) NEJM finding of 8.1% lower glucose metabolism in adult ADHD has not consistently replicated. Ernst et al. (1998, J Neuropsychiatry Clin Neurosci) found complex age-and-sex interactions; subsequent studies have given mixed results. Treat as suggestive, not definitive.
The Gailliot & Baumeister glucose-willpower model is contested. Vadillo et al. (2016) meta-analysis and Job et al. (2013, PNAS) suggest the effect may be weak or moderated by beliefs. The general "low glucose → worse mood" finding in healthy adults (Benton 2002) is more robust than the specific willpower mechanism.
Reactive hypoglycemia as a clinical entity remains contested in mainstream endocrinology. Many symptomatic patients have normal glucose tolerance tests. Muijs et al.'s 2021 systematic review concluded there is "no clear empirical support" for a link between glucose variability and mood in diabetic adults across the 8 qualifying studies (4 positive, 4 null). The Salzer (1966) clinical descriptions remain useful but the diagnostic category lacks consensus.
Sensory-Processing Sensitivity / HSP is a popular construct with psychometric controversies. Aron's original unidimensional model is not well supported; the construct appears multidimensional (Smolewska et al., 2006). The population estimate has widened from 15–20% to 20–35% as larger samples have been studied. It is not a clinical diagnosis.
The interoceptive-deficit-in-ADHD literature is small (k≈18 studies in the 2025 Bruton systematic review) and inconsistent. Kutscheidt positive, Wiersema null. Don't over-anchor on a single positive study.
Retrospective recall bias is real but does not invalidate trait persistence. Longitudinal cohort studies (Caspi et al., 1996; Moffitt et al., 2015) confirm high-reactive temperament does persist; what is unreliable is your memory of how you were, not necessarily the trait itself.
Brain glucose metabolism abnormalities in psychiatric populations are not specific. Prefrontal hypometabolism shows up across ADHD, BPD, MDD, and other conditions — it is a transdiagnostic signal, not pathognomonic of any single disorder.
Cross-sectional PET studies cannot determine whether metabolic abnormalities are cause, consequence, or correlate of symptoms. Treat all "X disorder has Y metabolism" findings as associational, not causal.
No primary study has directly tested whether ADHD/BPD adults have differential subjective sensitivity to glucose drops vs. controls. Your inference that this is part of your neurodivergence is biologically plausible (documented interoceptive differences plus the Young et al. 2019 finding that interoceptive accuracy moderates the glucose-mood link in healthy adults) but is not directly empirically established. This is a real gap in the literature.
Epigenetic findings on HPA axis programming from early stress are well-replicated in animals but more variable in human studies (Turecki & Meaney, 2016, Biol Psychiatry — discusses methylation signatures but heterogeneity is large). The principle that early stress programs adult stress reactivity is well supported; specific mechanistic claims for individuals should be held loosely.
The "rally-car brain" subjective phenomenology you describe is not itself a research construct. It maps reasonably onto mental restlessness/hyperactive mind in ADHD literature, ruminative DMN hyperconnectivity in depression/anxiety literature, and elevated locus coeruleus tone in chronic stress literature — but these are three distinct mechanisms that may all be partially operating. Disentangling which is dominant in your case requires the personalized data collection recommended above. Disclaimer: This article presents aggregated research findings. It is not a medical paper, cannot substitute for a physician, and should not be used as diagnostic evidence. The reasoning and conclusions in this article involved AI-assisted generation, have not undergone peer review or independent verification, and may contain errors.