ADHD, Insulin Resistance….the fight to be seen (and treated) goes on…

What if we should all be offered a cheap, safe treatment costing pennies a day to stabilise our physiology, help brain fog and extend our lifespan….

You already know you don’t deserve treatment…..the doctor will shame you now….

Research increasingly shows that adults with ADHD experience not only executive dysfunction and emotional volatility, but also sugar cravings, post-prandial sleepiness, energy crashes, central adiposity, brain fog, and a pervasive sense of physiological instability that often worsens with age. These features are routinely framed as lifestyle failure. Increasingly, they look like insulin resistance (IR).

Large registry and meta-analytic studies consistently demonstrate roughly a twofold increased risk of type 2 diabetes (T2DM) in adults with ADHD, persisting after adjustment for medication exposure. Yet even in these papers the tired narrative remains. You can read, in the same breath, that ADHD is linked to T2DM via shared dopamine–glucose biology, and then that the association is ““is largely mediated by unhealthy lifestyle choices, including poor dietary habits (high consumption of processed foods and sugar-sweetened beverages) and low levels of physical activity, which are consequences of deficient self-regulation”. While we’re at it, we can also get in a cheap swipe at ADHD medication: “psychostimulants may potentially have hyperglycaemic effects” (err they actually don’t).

Goddamn those greedy ADHD-ers: biologically vulnerable and morally defective, apparently. Really, greedy and lazy AND having increased metabolic risk — what are the odds of that? Methinks these researchers are wanting to have their cake and eat it. Perhaps they have ADHD as well?

Look, I know we don’t want to let lack of evidence get in the way of lazy biases, but this is clinically inconsistent and intellectually embarrassing. And funny how that poor control goes away for ADHD-ers just like it does for anyone else with these symptoms, when given metformin.

Just imagine the outcry if research attributed increased metabolic risk to greed/laziness in other whole groups such as people of Asian or African ethnicity — and then used that framing to justify delayed treatment. Noooo, it’s biology for them For ADHD it’s “deficient self-regulation.” I’m calling diagnostic overshadowing, discrimination and medical bias (again). What a disgrace.

The Hunter Phenotype

From an evolutionary perspective, ADHD neurobiology may reflect traits that were adaptive in environments of unpredictability and intermittent food availability: novelty-seeking, rapid threat detection, flexible reward-driven behaviour — useful in foraging ecologies. A tendency toward relative insulin resistance and energy storage during abundance may have buffered against scarcity. In a world of continuous food abundance and extended lifespan, that buffering becomes maladaptive.

Stop calling us greedy

Neuroendocrine mechanisms — not insults — plausibly bridge ADHD and metabolic vulnerability. ADHD populations frequently show heightened sympathetic drive and stress-reactive HPA activity, which promote hepatic glucose output, visceral adiposity, and reduced peripheral insulin sensitivity. In modern conditions, that translates into glycaemic volatility and fatty-liver biology — not moral weakness. If we accept that reactive hypoglycaemia (the “crash”) and hyperinsulinaemia (the “fat-storage lock”) are biological drivers of hunger and exhaustion, then those symptoms are metabolic, not “behavioural,” regardless of whether the patient has ADHD or not.

It is clinically inconsistent to treat the metabolic symptoms of one high-risk group (e.g., patients of Asian heritage or with a family history of T2DM) as “metabolic” or “hormonal” while treating the same symptoms in ADHD patients as “behavioural.” This creates a discriminatory barrier to care. When a clinician tells an ADHD patient to “use more willpower” or “manage their executive function” instead of offering a metabolic stabiliser like metformin, they are effectively denying medical treatment for a biological dysfunction based on a psychiatric diagnosis.

Even worse for ADHD women…what are the odds?

The metabolic signal is present in both sexes, but in women it is often amplified by PCOS-spectrum physiology and then amplified again with perimenopausal shift from the late 30s onward, which further degrades insulin sensitivity and alters fat distribution. What are the odds eh?

The False Binary: Starvation or Obesity

In clinic, a pattern emerges rarely discussed publicly. Some high-conscientious ADHD adults maintain a “normal” BMI only through chronic starvation and sympathetic overdrive. The alternative is rapid weight gain with ordinary eating. Both are unstable states. Insulin resistance creates erratic fuel signalling; dopamine fragility amplifies reward-seeking under volatility; sleep loss worsens leptin–ghrelin imbalance. Appetite is neuroendocrine drive. To assume obesity equals greed ignores endocrine reality and collapses under clinical scrutiny. Many patients are exerting extraordinary effort simply to remain functional; others have oscillated for decades between restriction and rebound.

Insulin Resistance as a Physiological Driver

Insulin resistance is not a binary event that begins at HbA1c 6.5%. It is a progressive signalling failure. Peripheral tissues respond poorly to insulin; the pancreas compensates with hyperinsulinaemia; glucose clearance becomes unstable. When cellular uptake is inefficient, the brain experiences fluctuating fuel delivery as threat.

Sugar cravings are symptoms of biochemical urgency. Energy crashes reflect fuel-delivery mismatch: glucose may be present in the bloodstream but unavailable intracellularly; reactive dips follow post-prandial spikes and people feel lethargic after eating rather than satiated. “Brain fog” reflects unstable cerebral fuel flux: oscillation (spike, overshoot, crash) degrades cognitive clarity and executive reliability, compounding dopaminergic fragility. By the time HbA1c rises, the disturbance may be a decade old and the damage is often permanent.

Why don’t we treat it before that happens?

Great question. The greed narrative collapses in seconds under biological scrutiny. Metformin and GLP-1 drugs have already run the sociological experiment. When treatment quiets lifelong “food noise,” patients discover they have the same willpower as everyone else. Metformin stabilises hepatic glucose output and improves insulin sensitivity; patients often describe fewer crashes, reduced cravings, steadier weight and clearer cognition. These are metabolic stabilisers, not willpower dispensers. Shaming insulin resistance is as absurd as shaming hypothyroidism: a medieval category error, confusing signalling failure with moral failure.

But don’t worry, as ever medical research shows us how wrong we are, just greedy and lazy after all. But before you go too crazy with I told you so….

Research doesn’t pass the common sense test

Dr Google informs me that doctors don’t prescribe metformin because “, metformin “lost” to lifestyle (diet and exercise) in the landmark DPP study (58% vs 31% risk reduction) and of course “Doctors generally prefer the “most effective” intervention first, which is lifestyle modification, as it addresses the root cause of metabolic dysfunction without medication side effects” Excellent, don’t worry about me then doc we both know I’m just greedy and lazy…

Ahem common sense alert here. Given that cravings, crashes, fatigue and obesity are caused by metabolic difficulties, and those of us in the real world know that overweight people never do lose the weight for long, but often cycle between starvation and rapid weight regaining, it is obviously ridiculous to claim that lifestyle change works better than actual treatment.

A closer look at these metabolic studies shows us our common sense intuition — that the “lifestyle vs. metformin” study must be biased or incomplete — is 100% bang on right. Look closely at the longer term effects and we can see that (a) lifestyle effects fade with time and weight regain is common, and (b) biology fights back hard against diet-only weight loss via appetite upshift and metabolic adaptation.

Biology vs. “Willpower”

Guys a metabolically stable person doesn’t want to eat cake all day. When a person loses weight via diet alone, their body triggers metabolic adaptation: ghrelin (the hunger hormone) increases, and leptin (the fullness hormone) decreases. For every 1kg of weight lost, resting metabolism drops by about 20–30 calories, but appetite increases by approximately 100 calories. So if you lose 10kg, you are fighting a 1,000-calorie-per-day biological urge to eat, while your body is burning 300 fewer calories than before. This “gap” is why almost everyone eventually regains the weight — and often more — as the body over-compensates to ensure it survives the “next” famine. Some effective intervention…..

“Symptom vs. Driver” Flaw

Our doctors harrumphing about lifestyle are treating obesity as the cause of insulin resistance. However in reality it is a feedback loop. If you have high circulating insulin levels, your body is biologically locked in “storage mode.” Trying to lose weight without lowering that insulin (via metformin or similar) is like trying to empty a bathtub while the tap is still running at full blast.

So I think we should all be able to agree that the “either/or” choice seen in studies should not dictate treatment. Using metformin to achieve glycaemic stability provides the biological foundation needed for lifestyle changes to actually stick. Obviously….

So what are we waiting for???

UK practice remains largely glucose-threshold driven. HbA1c is the gatekeeper: metformin arrives once pre-diabetes/diabetes is biochemically established (or in selected PCOS cases). That is biologically late. HbA1c is a lagging indicator. It reflects the outcome of metabolic strain, not the strain itself. A patient can maintain “normal” glucose while requiring pathological levels of insulin to do so. Chronic hyperinsulinaemia is not benign. It drives fat storage, inflammatory signalling, and the very crashes that make “lifestyle advice” so patronising and biologically illiterate.

Waiting for HbA1c to rise is like waiting for your house to collapse before fixing cracks. It is arguably negligent and certainly tragic in symptomatic patients from high risk populations.

Treat the patient not the blood test

In most areas of medicine, we treat suffering. In metabolic health, we often treat numbers. Post-prandial somnolence, reactive hypoglycaemia patterns, cravings and crash-cycles are not “willpower issues”; they are clinical symptoms of glycaemic instability — biological data. A monitored trial of a safe, low-cost medication in a symptomatic, high-risk patient is not reckless; it is proportionate. If crashes resolve and cognitive steadiness improves, that is clinically meaningful data; if not, the medication can be stopped. We already treat PCOS and perimenopause on symptoms, not blood tests. We treat asthma by response. We treat depression by trial of therapy. The ethical barrier should not be higher for metabolic stabilisation than for any other endocrine correction.

How should we assess risk of metabolic harm?

Risk for Type 2 Diabetes (T2DM) should be assessed cumulatively — genetics, medical history, physiological symptoms, and established risk categories. Relative risk is additive. Someone who sits in multiple high-risk groups (for example ADHD plus PCOS, or ADHD plus obesity and family history) carries compounded metabolic burden long before HbA1c crosses a diagnostic threshold.

Clinical markers already recognised as high risk include pre-diabetes (5–10× risk, 5–10% annual progression), obesity (7–12× risk), severe obesity (up to 40–80× risk depending on age and distribution), and metabolic syndrome (~5× risk).
Several medical conditions reflect chronic hyperinsulinaemia even when glucose appears “normal”: ADHD (~2–3× T2DM risk), PCOS (3–4× risk), gestational diabetes (7–10× lifetime risk), and NAFLD (2–3× risk).
Genetic and demographic factors further lower the threshold for failure: one affected parent (2–3× risk), both parents (5–6×), certain ethnic backgrounds (2–4× risk at lower BMI), and increasing age.
Lifestyle stressors such as sedentary behaviour and smoking add incremental risk — but they operate on top of underlying biology, not in isolation.

When a patient presents with metabolic symptoms — crashes, cravings, post-prandial somnolence, central adiposity — and belongs to several of these categories, progression risk is not theoretical. It is statistically substantial. In that context, early metformin is not indulgence; it is risk reduction.

What is the fuss about metformin?

Metformin is one of the most extensively studied, safest, and least expensive drugs in modern medicine. Its reputation rests not on hype, but on outcome data.

In diabetes prevention, multiple large trials show consistent benefit. In the Diabetes Prevention Program (DPP), metformin reduced progression from pre-diabetes to type 2 diabetes by 31% over nearly three years. Long-term follow-up (DPPOS) demonstrated durable effect, with sustained risk reduction over 10–15 years and delayed diabetes onset. Similar benefit has been replicated internationally, including in the Indian Diabetes Prevention Programme. Meta-analyses of randomised trials show pooled risk reductions in the 30–40% range. This is not marginal.
In PCOS, metformin improves insulin sensitivity, reduces androgen excess, restores menstrual regularity, supports ovulation, improves lipid profiles and blood pressure, and reduces progression to diabetes. It is already accepted as a metabolic stabiliser in that context.
Mechanistically, metformin reduces hepatic glucose output, improves peripheral insulin sensitivity, and dampens glycaemic volatility. It lowers cumulative hyperinsulinaemia — the driver of NAFLD, vascular dysfunction, beta-cell strain, and systemic inflammation.

How might this translate to ADHD populations?

If insulin resistance contributes to post-prandial somnolence, reactive hypoglycaemia, cravings, central adiposity and cognitive fog, then stabilising insulin signalling should reduce those symptoms. Clinically, many patients report fewer crashes, reduced sugar urgency, steadier energy, and more sustainable weight regulation. Rather than acting as a weight-loss drug, metformin functions as a metabolic equaliser, making lifestyle change biologically achievable rather than psychologically punitive.

There is emerging evidence that metformin may also reduce depressive risk and neuroinflammatory burden, with potential downstream effects on cognition and executive function. At minimum, preventing progression to diabetes reduces microvascular complications and long-term cardiovascular risk — outcomes that matter profoundly in ADHD populations already carrying elevated metabolic burden.

In short: metformin reduces progression to diabetes, stabilises metabolic physiology, and carries a six-decade safety record. It is an all round brilliant drug for anyone with metabolic symptoms. The question is not whether it works, but why we reserve it for biochemical failure rather than physiological instability.

Why medicine is slow to change

Despite the logic of early metabolic stabilisation, most clinicians remain bound by glucose-threshold guidelines (NICE in the UK, ADA in the US) that prioritise HbA1c over physiology. Treatment is triggered by biochemical failure rather than by symptomatic strain. Hyperinsulinaemia with “normal” glucose is rarely measured and even more rarely treated. The result is a glucose-centric system that intervenes late.

Two forces sustain this model. First, residual moral bias: a lingering belief that medication is the “easy way out” and that patients should “earn” metabolic health through discipline. Second, risk asymmetry: doctors are generally blamed for harm from prescribing more than harm from refusing to prescribe, especially if a treatment is “off license” ie not in the guidelines. Medico-legally it is safer to ignore the slow-motion vascular and beta-cell damage of chronic hyperinsulinaemia.

There is also an equity problem. Private precision medicine and longevity clinics (and my ADHD clinic) are starting to do this. Patients able to self-fund specialist metabolic care increasingly receive symptom-led trials of metformin, while everyone else must wait for the permanent damage point when diagnostic thresholds are finally crossed.

A cheap, safe, extensively studied drug with genuine transformational power becomes gatekept by a late biomarker.

In the future it may become ethically difficult to justify not offering metformin to a symptomatic, high-risk patient. Yay

However the paradigm is starting to shift from “glucocentrism” to cellular energy and insulin signalling. As insulin assays and longitudinal data mature and shared neuro-metabolic architecture between dopamine and insulin becomes clearer, behavioural blame will collapse. Ignoring compensatory hyperinsulinaemia will become increasingly difficult for doctors to defend.

Cost-benefit logic supports this shift. It makes little sense to require expensive assays to justify a low-cost drug with a six-decade safety record when the alternative is years of cumulative metabolic strain. The gate should be proportionate to the risk.

In the future, offering metformin to a symptomatic high-risk patient will be standard preventative care, and ADHD-ers will no longer be blamed for their physiology, but will take their rightful place alongside those who should be offered it.

Research

Tagged ADHD, Adult ADHD, Diagnosis, Mental Health, Diagnosis, Psychiatry, Depression, Anxiety, therapy, discrimination, health, lifespan, longevity, shame, treatment, weight