Depression, clinically termed major depressive disorder, is a complex and multifactorial mood disorder characterised by persistent low mood, anhedonia (loss of interest or pleasure), and a range of cognitive, emotional and somatic disturbances (1). It extends beyond transient sadness, representing a pathological state that significantly impairs daily functioning, quality of life and interpersonal relationships.

Core diagnostic features include feelings of hopelessness, low self-worth, fatigue, impaired concentration, sleep disturbances and changes in appetite (2). From a biomedical perspective, depression is increasingly understood as a systemic condition involving neurochemical, endocrine, inflammatory and psychosocial dysregulation rather than a purely ‘chemical imbalance’ (1,3). 

Under the umbrella of unipolar depressive disorders, there is major depressive disorder, which is depression without a manic or hypomanic phase; dysthymic disorder, which consists of a pattern of chronic, ongoing mild depressive symptoms that are less severe than major depression; and seasonal affective disorder (SAD), which is depression or depressive symptoms related to seasonal changes (4,5). 

Depression is a leading contributor to global disease burden. Current estimates suggest a global prevalence of approximately 5% (6). It is recognised as one of the leading causes of years lived with disability worldwide and is associated with increased mortality, including suicide risk (7). In 2022, the proportion of adults in the UK experiencing moderate to severe depressive symptoms had increased to 16%, up from 10% prior to the pandemic.

Women report higher rates than men (19% compared to 14%), with young people aged 16–29 most affected (28%). The burden is unevenly distributed, with markedly higher prevalence among individuals with disability (35% versus 7% in non-disabled adults), those unable to work due to long-term illness (59%), and unpaid carers providing more than 35 hours of care per week (37%), emphasising clear disparities across different population groups (8).

Up to 40% of patients do not respond adequately to conventional antidepressant therapies, highlighting the need for broader therapeutic strategies (9). The socioeconomic burden is substantial, encompassing healthcare costs, reduced productivity, and long-term disability (7).

The monoamine hypothesis remains a key framework in understanding depression. Monoamine neurotransmitters like serotonin, noradrenaline and dopamine are central to mood regulation, motivation, cognition and stress response (1,3). Reduced serotonergic activity is associated with low mood, anxiety, and sleep disturbance, while noradrenergic dysfunction contributes to fatigue, impaired concentration and altered stress resilience. Dopamine dysregulation, particularly within reward pathways contributes to anhedonia, reduced motivation and diminished goal-directed behaviour (1,3). 

Monoamine imbalance arises through multiple interacting mechanisms. These include impaired synthesis due to nutrient deficiencies or chronic stress, increased reuptake or degradation via transporter proteins and the enzyme monoamine oxidase (MAO) and altered receptor sensitivity. Inflammation further disrupts monoamine pathways by diverting tryptophan metabolism away from serotonin production, while chronic activation of the hypothalamic–pituitary–adrenal (HPA) axis and elevated cortisol can impair neurotransmitter function (1,3).

Neuroendocrine dysfunction also plays a role, as HPA axis hyperactivation with elevated cortisol levels and impaired stress adaptation contributes to hippocampal atrophy and mood dysregulation (1,3). Reduced levels of brain-derived neurotrophic factor (BDNF) are associated with impaired formation of new neurons and synaptic plasticity. There is emerging evidence showing that both pharmacological and herbal treatments can enhance BDNF expression (1).

Inflammation and gut microbiota are also implicated in the pathophysiology of depression (10). Low-grade systemic inflammation, characterised by elevated cytokines like IL-6 or TNF-α, is increasingly implicated in depression. This inflammatory state influences neurotransmitter metabolism and neural function. Alterations in gut microbiota composition can affect mood through immune, neural, and metabolic pathways, affecting neurotransmitter production and contributing to inflammation (10,11).

Depression arises from an interplay of biological, psychological and social factors.

• Genetic predisposition: Family and twin studies show moderate heritability, with multiple genes contributing to vulnerability (12). 
• Chronic stress and trauma: Early life adversity, ongoing psychosocial stress, and trauma are major contributors, often mediated through HPA axis dysregulation (13).
• Lifestyle factors: Poor diet, physical inactivity, sleep disruption, and substance misuse can all increase the risk of developing depression (14,15). 
• Medical conditions: Chronic illnesses (e.g., cardiovascular disease, diabetes), hormonal imbalances (e.g., thyroid dysfunction), and chronic pain are strongly associated with depression (16, 17).
• Nutritional deficiencies: Deficiencies in key nutrients such as omega-3 fatty acids, B vitamins, iron, and magnesium can impair neurotransmitter synthesis and brain function (18,19,20).
• Psychosocial factors: Isolation, lack of purpose, socioeconomic hardship and adverse life events play a significant role (21).

Major depressive disorder is diagnosed according to the criteria stipulated in DSM-5. One criterion requires the presence of five of the below symptoms almost every day for more than two weeks, and at least one must be either depressed mood or loss of interest/pleasure.

Emotional symptoms (22):

• Persistent sadness or low mood 
• Loss of pleasure or interest in activities (anhedonia)
• Feelings of hopelessness, worthlessness or excessive guilt
• Irritability or emotional numbness 

Cognitive symptoms (22):

• Poor concentration and memory or indecisiveness 
• Negative thinking patterns 
• Recurrent thoughts of death or suicidal ideation

Physical symptoms (22):

• Fatigue and low energy 
• Sleep disturbances (insomnia or hypersomnia) 
• Appetite and weight changes 
• Psychomotor agitation

Other behavioural symptoms can also include:

• Withdrawal from social activities 
• Reduced motivation 
• Decreased productivity

If the above feels relevant to you, for further guidance, please seek the care of a qualified medical professional via your GP,  NHS 111, or mental support charities such as Mind and Samaritans. 

Herbal approaches to depression often centre on restoring balance to the nervous, endocrine, and immune systems (5). Rather than acting through a single pathway, medicinal plants have multiple virtues and modes of action, including modulation of neurotransmitters, support for the HPA axis and reduction of inflammation. Emerging research suggests that certain herbs may help increase serotonin availability BDNF, while reducing cortisol levels, stress reactivity and pro-inflammatory cytokines (23).

Evidence suggests that herbal medicines can improve depressive symptoms, either alone (particularly in mild-to-moderate cases) or as adjuncts to conventional treatment, often with fewer side effects.

Herbs that can support people with depression include: 

• Nervine tonics, also called nervous system trophorestoratives.  These herbs help to nourish and restore long-term nervous system function. Examples include St John’s wort (Hypericum perforatum), skullcap (Scutellaria lateriflora), damiana (Turnera diffusa), and schisandra (Schisandra chinensis). They are traditionally used to support mood, improve resilience to stress and promote emotional balance (5).
• Anxiolytics, for individuals experiencing anxiety alongside depression. Anxiolytic nervines such as valerian (Valeriana officinalis) and passionflower (Passiflora incarnata) can help reduce nervous tension and improve sleep quality, both of which are commonly disrupted in depressive states (5,24). 
• Adaptogens play a particularly important role where chronic stress and HPA axis dysregulation are present. In depression, cortisol levels can be elevated and fail to switch off appropriately due to impaired negative feedback mechanisms. Adaptogens such as ashwagandha (Withania somnifera) and schisandra help regulate this stress response, supporting resilience and reducing fatigue (5, 24).

St John’s wort (Hypericum perforatum)

St John’s wort is one of the most extensively studied herbal antidepressants and has demonstrated efficacy comparable to standard antidepressants in mild-to-moderate depression, with favourable tolerability (25). Its mechanisms include inhibition of serotonin, dopamine, and noradrenaline reuptake, along with modulation of GABA receptors (26). This contributes to its anxiolytic and mood enhancing effects.

St John’s wort strongly induces liver enzymes (especially CYP3A4) and P-glycoprotein, which can reduce the effectiveness of some medications like oral contraceptives, HIV antiretrovirals, ciclosporin and chemotherapy agents (27, 28). The concomitant use with antidepressant medication that inhibits serotonin (e.g. sertraline, citalopram) needs to be monitored by a qualified herbalist due to the risk of serotonin syndrome (29). 

Saffron (Crocus sativus)

Saffron has been traditionally used as a nervine and mood enhancer, often prescribed for low mood, melancholy and emotional distress. It has shown efficacy for mild to moderate depression comparable to antidepressant drugs like fluoxetine and imipramine in several clinical trials, with a better side effect profile (30,31,32). Its active constituents crocin and safranal appear to modulate serotonin pathways and exert antioxidant and anti-inflammatory effects (32).

Lemon balm (Melissa officinalis)

Lemon balm is a calming herb traditionally used to ease nervous tension, restlessness and low mood, with a long history of use for both emotional and digestive complaints linked to stress (33). It has shown to be beneficial in alleviating symptoms of  mild to moderate anxiety and depression, especially irritability, agitation, poor sleep and difficulty concentrating. Clinical research suggests that lemon balm can help improve mood, reduce anxiety and stress, and support sleep quality and aspects of cognitive performance, such as memory and attention (34,35,36).

These effects are thought to arise through multiple mechanisms, including inhibition of GABA transaminase by rosmarinic acid (leading to increased GABA activity in the brain), modulation of cholinergic and serotonergic neurotransmission, and antioxidant and anti‑inflammatory actions — helping to calm the nervous system while supporting mood and cognition (37,38).

Tulsi (Ocimum tenuiflorum)

Tulsi is an adaptogenic Ayurvedic herb, which has been increasingly recognised for its ability to improve resilience to physical, chemical, metabolic and psychological stress (39). It has shown particular efficacy in cases of stress‑related anxiety and low mood, especially where symptoms also include mental fatigue, poor sleep and difficulty coping with daily demands. Clinical research suggests that tulsi can help reduce perceived stress and anxiety, improve mood and general wellbeing, and support cognitive function and sleep quality (40,41,42).

These effects are thought to arise through multiple mechanisms, including regulation of the HPA axis and cortisol response (via inhibition of cortisol release and antagonism at the CRF1 receptor), modulation of neurotransmitters and potent antioxidant and anti‑inflammatory activity — buffering the impact of chronic stress on both mental and physical health (43,44).

Lavender (Lavandula angustifolia)

Lavender has mild antidepressant and anxiolytic effects, making it useful for depression with anxiety or sleep disturbances (45). Its action likely involves modulation of GABA and serotonin pathways, as well as reduction of stress hormones (46). Clinical evidence supports the use of oral standardised lavender oil capsules (80 mg/day) or powdered flowers (500mg twice a day) for modest improvements in mood and anxiety (45).

Aromatherapy with lavender oil provides short-term relaxation and better sleep, though its direct effect on depression is less well understood (45,46). Lavender is generally well-tolerated, with few side effects (47).

Research supports mind-body therapies such as mindfulness-based cognitive therapy (MBCT) and mindfulness-based stress reduction, as they have shown significant reductions in depressive symptoms and reduced relapse risk when added to usual care, with MBCT demonstrating effectiveness comparable to traditional psychotherapy in some trials (48). Physical activity, especially regular aerobic exercise, has moderate evidence for improving mood and can serve as an effective adjunct to conventional treatment, with large reviews indicating benefits in mild to moderate symptoms (49).

A major Cochrane review of randomised controlled trials found that omega-3 supplementation had a small to modest reduction in depressive symptoms compared with placebo (50). Formulations with higher EPA content may show more benefit than those dominated by DHA. Omega 3s are not reliably effective as a standalone treatment, but they can be considered as a possible adjunct to other therapies.

Other approaches like acupuncture, music therapy, and yoga show promising but generally lower-quality evidence but can be helpful as complementary treatments (50). Nutrition, sleep hygiene, stress management, social support and structured psychological therapies are all important strategies to improve depressive symptoms (51).

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Insomnia is a common and complex sleep disorder characterised by persistent difficulty with sleep initiation, sleep maintenance, or early-morning awakening, despite adequate opportunity and appropriate circumstances for sleep (1). The diagnosis of insomnia requires the presence of associated daytime impairment, such as fatigue, reduced concentration, mood disturbances, or reduced occupational and social functioning (1).

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the International Classification of Sleep Disorders (ICSD-3), recognise insomnia as a disorder of both night-time sleep and daytime functioning, rather than a purely nighttime problem (2,3). Insomnia can be acute or chronic, with chronic insomnia defined as symptoms occurring at least three nights per week for a minimum of three months (3).

Insomnia is highly prevalent worldwide and represents one of the most frequently reported health complaints in primary care. Epidemiological studies suggest that up to 30–40% of adults experience transient or intermittent insomnia symptoms, and approximately 6–10% meet diagnostic criteria for chronic insomnia disorder (4,5).

Prevalence increases with age (6). It frequently coexists with cardiovascular disease, metabolic disorders, dysbiosis, chronic pain syndromes, anxiety, depression and complex trauma (7,8,9). It is associated with an increased cardiovascular risk, cognitive deficits, and reduced quality of life (10).

There is increasing evidence associating insomnia with hypertension, coronary heart disease and heart failure, as well as cardiovascular mortality (11). Patients with insomnia are 45% at a higher risk of developing cardiovascular disease (11). There is also an increased risk of stroke, with people with insomnia having a 54% higher risk of stroke within four years (12). 

Insomnia is best understood through a hyperarousal model, in which people present with a heightened physiological, cognitive, and emotional activation across the 24-hour cycle. Neurobiologically, normal sleep depends on a delicate balance between wake-promoting systems mediated by neurotransmitters, such as noradrenaline, dopamine, histamine, and orexin, and sleep-promoting systems involving gamma-aminobutyric acid (GABA), adenosine, and melatonin (13).

In individuals with insomnia, this balance is disrupted. Studies demonstrate increased metabolic activity in wake-promoting brain regions during both sleep and wakefulness, elevated nocturnal cortisol secretion, and heightened sympathetic nervous system activity (14).

These findings suggest that the brain of a person with insomnia remains in a state of persistent alertness, even during periods where they should be asleep. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis further contributes to difficulty initiating and maintaining sleep, particularly in stress-related insomnia (14). 

Circadian rhythm disturbances can also play a role, especially in individuals with delayed sleep-wake phase disorder or irregular sleep schedules (15). Additionally, insomnia often shows subjective-objective discrepancy, as patients often perceive less sleep than measured objectively (16).

Insomnia is often multifactorial, and research suggests that while insomnia may begin in response to a specific trigger (e.g.. acute or prolonged stress or illness), it often becomes self-sustaining through learned behaviours and ongoing hyperarousal, highlighting the importance of a multifactorial treatment approach (1).

Insomnia is commonly driven by hyperarousal of the central nervous system, meaning the brain remains in a heightened state of alertness when it should be transitioning into sleep (1).

• Psychological factors such as stress, anxiety, depression and trauma are strongly associated with both acute and chronic insomnia, with cognitive models showing that worry about sleep itself can perpetuate the condition (17,18).
• Behavioural contributors are also well established and include irregular sleep schedules like shiftwork, excessive screen exposure before bedtime, caffeine or alcohol intake, and conditioned arousal (where the bed becomes associated with wakefulness rather than sleep) (19,20,21). 
• Environmental factors like excessive light or noise in the bedroom, feeling too hot or too cold and who someone sleeps with are all precipitating and perpetuating factors (22).
• Physiological factors play a role too, particularly dysregulation of circadian rhythms, alterations in neurotransmitters involved in sleep–wake regulation (such as GABA, serotonin, and orexin), and increased activity of HPA axis, which elevates cortisol levels at night (1,19).

There is emerging evidence linking gut microbiota with sleep regulation and circadian rhythms. Certain gut bacteria ferment dietary fibres to produce short-chain fatty acids (SCFAs), notably butyrate, acetate, and propionate (23). These metabolites play a role in modulating immune and neural signalling and also influence the activity of sleep-related neural circuits (e.g., orexin neurons in the hypothalamus) (24).

They are found to be lower in individuals with insomnia. Higher microbial richness/diversity correlates with better objectively measured sleep efficiency and longer total sleep time (25). Reduced diversity and specific taxa shifts appear in insomnia and sleep disorder cohorts versus controls. 

Insomnia frequently co-occurs with medications that stimulate the nervous system, as well as medical conditions such as chronic pain, gastrointestinal disorders, dysbiosis or cardiovascular disease (26).

Menopause is also strongly associated with insomnia, largely due to fluctuating and declining oestrogen and progesterone levels, which disrupt thermoregulation, circadian rhythms, and neurotransmitters involved in sleep regulation like GABA and serotonin. Vasomotor symptoms such as night sweats and hot flushes frequently cause nocturnal awakenings, and menopause-related anxiety and low mood also contribute to hyperarousal and difficulty maintaining sleep (27).

Night-time symptoms of insomnia (1,28)

• Difficulty falling asleep
• Frequent nocturnal awakenings
• Difficulty returning to sleep after awakening
• Early morning awakening with insufficient total sleep time
• Subjective non-restorative or poor-quality sleep

Daytime symptoms of insomnia (1,28)

• Persistent fatigue or low energy
• Impaired concentration, attention and memory
• Irritability, mood instability or emotional distress
• Reduced motivation and decreased work or academic performance
• Increased risk of accidents and errors

These symptoms often lead to significant distress and reduced quality of life, reinforcing maladaptive sleep behaviors and perpetuating the disorder.

Some of the key herbal strategies include (29):

• Nervine and sedative herbs that modulate central nervous system activity
• Adaptogens that support stress resilience and HPA axis balance
• Digestive and hepatic support particularly when sleep disturbance is linked to metabolic factors, gastrointestinal discomfort and potential dysbiosis

It is important to highlight the relevance of synergy in herbal medicine. A randomised controlled trial investigating the efficacy and safety of a polyherbal formulation containing valerian (Valeriana officinalis), passionflower (Passiflora incarnata), and hops (Humulus lupulus), found it to be as effective as the conventional sleep medication zolpidem in the treatment of primary insomnia (30).

Participants taking the herbal formula experienced significant improvements in total sleep time and sleep latency, along with a reduction in the number of nightly awakenings. Insomnia Severity Index scores also improved markedly, suggesting that this polyherbal approach offers a well-tolerated and effective alternative to pharmaceutical hypnotics like zolpidem for managing insomnia.

For hyperarousal insomnia and heightened sympathetic nervous system states, the focus should be on GABAergic modulation, HPA-axis regulation and anxiolytics. Herbs that can work through GABA modulation include valerian, hops, passionflower, skullcap (Scutellaria lateriflora) and lemon balm (Melissa officinalis) (31,32). 

For fatigue-dominant insomnia when there is chronic stress, it is important to not just include sedative herbs but also adaptogens (33). The main emphasis should be on providing circadian support, taking restorative tonics, anti-inflammatory herbs and mitochondrial-supportive herbs. Melatonin can be helpful, starting with 2 mg slow release and increasing gradually depending on response (34).

Herbs that are suitable for this type of insomnia are ashwagandha (Withania somnifera) as it reduces cortisol, improves sleep quality and upregulated GABA neurotransmitters (33). Tulsi (Ocimum tenuiflorum), can help with circadian and stress modulation and is not a sedating herb (35). Schisandra (Schisandra chinensis) is an adaptogenic plant that improves stress and is also a GABA and serotonin modulator (33).

Valerian (Valeriana officinalis)

Valerian root has been used in European herbal medicine for centuries as a remedy for nervous tension and insomnia (35). Preclinical studies suggest that valerian may enhance GABAergic neurotransmission by inhibiting GABA breakdown and reuptake (36). Clinical trials have produced mixed results with no improvement when taking a single dose. A meta-analysis showed improvement in sleep latency and improved sleep quality (37). Valerian appears to be most effective when taken consistently over several weeks rather than as an acute sedative.

Chamomile (Matricaria chamomilla)

Chamomile is traditionally used as a mild sedative and anxiolytic, particularly for insomnia associated with nervousness or digestive discomfort (35). Its flavonoid constituents, including apigenin, bind to benzodiazepine receptors in the brain, providing a plausible mechanism for its calming effects (38). Clinical evidence shows it improves onset of sleep and the number of awakenings after sleep (39). Chamomile is a safe herb suitable for children (35).

Hops (Humulus lupulus)

Hops have a long tradition in European medicine for restlessness and sleep difficulties. Constituents such as humulone and lupulone exhibit sedative properties and can influence GABA_A receptor activity. Hops are often combined with valerian in herbal formulations, with some evidence suggesting synergistic effects on sleep quality (40,41). 

Lemon balm (Melissa officinalis)

Lemon balm is a calming nervine with anxiolytic and mood-supportive properties. Traditionally used for insomnia linked to anxiety or digestive upset, lemon balm has been shown to inhibit GABA transaminase, therefore increasing GABA availability (32,35). Clinical studies suggest benefits for sleep quality, particularly when used in combination with other sedative herbs (41,42). 

Passionflower (Passiflora incarnata)

Passionflower has a history of use in both Western and traditional American herbal medicine for nervous insomnia (35). Research supports its anxiolytic and mild sedative effects, possibly mediated through modulation of GABA activity. Trials have used both a water extract (infusion) and ethanolic extract (tincture) (44).

Ashwagandha (Withania somnifera)

Ashwagandha powder or tincture is increasingly being used to help with insomnia. It can be useful particularly through its adaptogenic effects on the stress response. Clinical studies suggest it can reduce hyperactivation of the HPA axis and lower cortisol levels, supporting relaxation and improved sleep onset and quality, particularly in stress-related insomnia. Evidence also indicates that ashwagandha can modulate GABAergic signalling and reduce anxiety, both of which are key contributors to difficulty initiating and maintaining sleep (45,46). 

Herbal medicine is most effective when integrated into a holistic framework that addresses behavioral, psychological and environmental factors. Key strategies include maintaining regular sleep–wake schedules, optimising sleep environments and reducing physiological arousal before bedtime.

Cognitive-behavioral therapy for insomnia (CBT-I) remains the gold standard non-pharmacological treatment and may be complemented by mindfulness practices, gentle movement, and stress-management techniques (47). Regular physical activity and exposure to natural daylight can further support circadian regulation and sleep quality (48).

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What is ADHD?

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental condition, meaning that rather than being a disorder as its name suggests, it is a complex neurotype involving a range of behavioural traits (1).

It can affect individuals differently, impacting their lives practically, behaviourally and psychologically. Symptoms usually appear in childhood, before 12 years of age, and up to 85% of patients experience symptoms into adulthood (2,3). 

ADHD can present in various ways, detailed in “signs and symptoms”.

Prevalence, diagnosis and treatment

Today, worldwide ADHD prevalence in children is 5% and 3–4% in adults (4).

While brain imaging scans and other neurophysical markers are associated with ADHD, it is diagnosed clinically through a case history of the patient, using the DSM 5 criteria:

The patient displays characteristics of one of three ADHD subtypes:

• Predominantly inattentive
• Predominantly impulsive or hyperactive
• Combination type
  

Other criteria include:

• The onset of symptoms is (usually) before age 12
• Symptoms present in multiple settings: school, work, home
• Symptoms cause significant impairment in social, occupational or academic function
• The disorder is not explained by any other behavioural disorder.
  

Primary treatment is pharmaceutical, with first-line options being central nervous system (CNS) stimulants: Methylphenidate (MPH), lisdexamfetamine or dexamphetamine, non-stimulant atomoxetine (a serotonin-norepinephrine reuptake inhibitor or SNRI), guanfacine, a selective α2A adrenergic receptor agonist or modafinil, a non-amphetamine narcolepsy treatment (5–9).

Non-pharmacological treatment options are limited, with patients having variable access to funding for coaching or online therapy services (10,11). Despite this lack of support, especially in resource-poor settings, the World Health Organization recommends that children and adolescents receive “psychosocial interventions” alongside first-line treatments (12). Equally, NICE recommends that people with ADHD “have a comprehensive, holistic…treatment plan that addresses psychological, behavioural and occupational or educational needs” (13).

Characteristics

ADHD is characterised by symptoms like inattention, hyperactivity and impulsivity (the most commonly associated — and researched — traits, but by no means all) and may impact multiple aspects of a person’s life (14–16). Not all symptoms will always occur in all individuals with ADHD (2,3). ADHD often co-occurs with mental health conditions including anxiety, depression or behavioural disorders (14–16). For example, 75% of adults with ADHD experience some degree of co-occurring mental health condition (2,3).

It’s important to note that not all ADHD characteristics are inherently negative, though. Research shows that traits and characteristics such as the energy, creativity, hyperfocus, unconventional thinking styles, pursuit of new experiences, growth mindset and resilience that often accompany people with ADHD can have positive impacts on the lives of those living with the condition, although the effects may vary depending on the specific context in which it is experienced and on the individual (17). 

Co-occurence

There is increasing recognition of the co-occurence of other neurotypes and conditions alongside ADHD including autism spectrum disorder (ASD), Tourette’s, dyslexia, depression, dyspraxia and obsessive compulsive disorder (OCD) (1,18). Of the adults with ADHD, 75% experience a range of co-occurring mental health disorders (2,3). This intersection of multiple conditions has real implications for those living with ADHD.

A 2025 study published in the British Journal of Psychiatry (BJP) found that the life expectancy of ADHD males is 6.8 years shorter than those without, and that females’ is 8.6 years shorter. The co-occurring mental health conditions may be in part responsible for the shorter lifespan of those with ADHD, although ADHD doesn’t shorten life expectancy directly (19). 

A 2025 research study identified that people diagnosed with ADHD who have a menstrual cycle are three times more likely to have premenstrual dysphoric disorder (PMDD) and two 2021 studies found evidence suggesting generalised joint hypermobility and connective tissue pathology are associated with ADHD (20–23)

ADHD subtypes

These findings show that through associated conditions’ pathophysiology and within its own broad range of manifestations, ADHD can and does reach far beyond the ‘classic’ symptoms of inattention, hyperactivity and impulsiveness. Far more ADHD subtypes than the main recognised three (inattentive, hyperactive-impulsive, and combined types) may exist, and research is pointing ever more in this direction (24).

Gender

Women and girls with ADHD typically present differently from men and boys, which can be problematic since diagnostic criteria are designed around males, meaning females are often underdiagnosed and under supported (25). Symptom severity for hyperactive-impulsive symptoms is lower in females than males, and inattention can present more as disorganisation, overwhelm, lacking in effort or low motivation (rather than the ‘classic’ inattentive male symptoms such as trouble focusing or appearing not to listen). Common co-occurring conditions might be internalised in females, leading to fewer referrals, lower academic attainment outcomes, or misdiagnosis (25,26).

The complexity of ADHD’s neurological picture reflects its complex symptom presentation. 

Brain development

ADHD traits are a result of differences in early brain development that occur during pregnancy or in infancy, and can be genetic in origin or caused by physical or birth trauma, infection, immune disorders or nutritional status (1). 

The structure of an ADHD brain differs from neurotypical brains in several ways.

The frontal lobe, limbic system and basal ganglia are all impacted, leading to a range of challenges in planning, memory, decision-making, attention, impulsivity and focus (27).

Nervous system

Nervous system regulation and neurotransmitter signalling, involving dopaminergic, noradrenergic, glutamatergic and serotonergic pathways, is disrupted in ADHD, and oxidative stress and inflammation both occur — in the central nervous system (CNS) and systemically (throughout the body) and can exacerbate symptoms (16). 

Dopamine and norepinephrine

Primary neurotransmitters involved in ADHD are dopamine and norepinephrine, although glutamate and serotonin are also involved. Dopamine regulates our mood, memory, motivation and attention, and supports emotional regulation, but reduced dopamine transporter (DAT) expression in people with ADHD means lower levels of dopamine in cells, and therefore increased dysregulation of the functions it usually supports (28,29).

Dopamine is a precursor to norepinephrine, and dysregulated norepinephrine reuptake by cells is understood to contribute to executive dysfunction, inattention and impulsivity in ADHD (30).

Other neurotransmitters

Higher glutamate levels, serotonin and altered GABA levels are also associated with exacerbated symptoms (28,31–34).

ADHD can present with any combination of the following signs and symptoms, and may vary on a daily or even hourly basis, and not all symptoms occur in all people with ADHD (2,3).

Practical (2,3,20,35–39)

• Difficulty managing daily tasks such as washing up, cooking, cleaning
• Difficulty focusing on work or tasks for sustained periods
• Hyperfocus for sustained periods, sometimes forgetting to eat and/or drink or use the bathroom
• Time ‘blindness’, e.g. difficulty being on time and keeping or making appointments

Psychological (2,3,20,35–39)

• Poor mental health or co-existing mental health conditions (anxiety, depression, stress)
• Sleep disturbances
• Poor memory and executive function
• Impaired learning
• Emotional dysregulation
• Low confidence
• Rejection sensitivity dysphoria (RSD)

Behavioural (2,3,20,35–39)

• A lack of inhibition
• Inattentiveness
• Interrupting
• Hyperactivity
• Substance dependency
• Novelty-motivated
• Ideas-driven
• Creativity

Physiological (2,3,20,35–39)

• Fluctuations in energy levels
• Headaches
• Gastrointestinal disturbances
• Cardiovascular health issues
• Fluctuations in weight and appetite
• Connective tissue disorders

A broad range of herbs have been reviewed for their effects on various aspects of ADHD including hyperactivity, impulsivity, attention, mood and other co-occurring symptoms.

Neurocomplexity is a key feature in ADHD, so it is important not to be reductive when considering herbal treatments — one herb is unlikely to treat most or all ADHD presentations, and research suggests this is the case (31,34,40,41).

Herbs work via a variety of different molecular pathways and could be used in combination or singly for ADHD subtypes and/or co-occurring conditions (31,42,43).

Here are some herbs for ADHD treatment based on randomised clinical trial (RCT) evidence:

Brahmi (Bacopa monnieri)

Bacosides found in brahmi are able to cross the blood brain barrier, and can modulate gamma-aminobutyric acid (GABA) and N-methyl-D-aspartate (NDMA) glutamate receptors, making this herb supportive for memory improvement and reducing inflammation (43).

Valerian (Valeriana officinalis)

Valerenic acid found in valerian causes increased dopamine production and a calming effect (43).

Passionflower (Passiflora incarnata)

Passionflower acts as a GABA receptor agonist and exerts a calming effect on the nervous system (44,45).

Saffron (Crocus sativus)

Saffron has been shown to increase tryptophan availability in the brain (44,45).

Ginseng (Panax ginseng)

Ginseng shows moderate improvements in attention and impulsivity, and strong improvements in cognitive function in ADHD patients (43).

Rosemary (Salvia rosmarinus)

Rosemary has high antioxidant levels which also stimulate nerve growth factor (NGF) and inhibits acetylcholinesterase activity, which work to improve memory, so could be a useful factor in ADHD treatment (31,46).

Turmeric (Curcuma longa)

A powerful anti-inflammatory herb, turmeric could play a role in reducing CNS and systemic inflammatory biomarkers in ADHD patients due to its high levels of anti-inflammatory compounds like curcumin (47–49). It is also a neurotrophorestorative, which is helpful in ADHD where neurological oxidation is implicated (50).

Diet

Inflammatory foods are linked with exacerbation of ADHD symptoms, as are altered nutrient levels, and whilst dietary research on ADHD is still emerging, it appears healthy eating is associated with fewer symptoms (51). Research shows gut microbiome disruption correlates with symptoms, so management of gut microbiota could also support symptom reduction (52).

Exercise

Evidence supports aerobic, strength-based and mind-body exercise for reducing neuroinflammation and brain health (53).

Supplements

Whilst there are limited studies on supplementation for ADHD, a range of vitamins and minerals aid short-term memory, slow cognitive decline in Alzheimer’s patients, with antioxidant supplementation showing most promising results (53). Since ADHD involves neuroinflammation, there is a case for further research into antioxidant supplementation for ADHD.

Behavioural therapies

There is limited access to behavioural therapy, but studies suggest combined cognitive and pharmaceutical treatment increases efficacy (54).

Practical support

Practical measures can be of enormous help in symptom management. Apps, reminders, daily self check-ins, body doubling for task management and digital planners are some technologies now at our disposal (55).

Many people (adults and children alike) with ADHD benefit from combination support alongside flexibility in work, home or school environments to allow them to flourish (56,57).

Individuals may benefit from formal diagnosis or not, and many people explore and find a mix of treatments that works for them and their unique neurotype as they work to understand their needs (58).

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