Dear readers of ADxS.org, please forgive the disruption.

ADxS.org needs about $12450 in 2022. In 2022 we received donations from third parties of $USD 11523 until 10/31. Unfortunately, 99.7% of our readers do not donate. If everyone who reads this request makes a small contribution, our fundraising campaign for 2022 would be over after a few days. This donation request is displayed 4,000 times a week, but only 19 people donate. If you find ADxS.org useful, please take a minute and support ADxS.org with your donation. Thank you!

Since 01.06.2021 ADxS.org is supported by the non-profit ADxS e.V..

$11532 of $12450 - as of 2022-11-14
92%
Header Image
Abstract of ADxS.org

Abstract of ADxS.org

This text is an abridged version of the ADxS.org project and links to the respective subpages, which present the topics in detail and with over 5000 directly linked sources1.

This short version of ADxS.org is deliberately formulated in a “popular scientific” way in order to make it easier for those affected to get started with the topic of ADHD, and is shaped by our view of ADHD. The more in-depth articles, on the other hand, emphasize a scientific presentation. There, our own view is explicitly marked as such.

Contrary to professional convention, we use the term ADHD as a generic term for all subtypes in order to enable non-specialists to distinguish the subtype ADHD-HI (predominantly hyperactive) at any time. We refer to the other subtypes as ADHD-I (predominantly inattentive) and ADHD-C (equally hyperactive and inattentive). We assume that professionals can translate this at any time and ask them for their indulgence that ADxS.org sometimes makes such compromises to keep the texts more understandable for non-specialists.

This executive summary is divided into several sections that roughly correspond to the chapters of the compendium and whose contents are described in 1 to 2 sentences in the following outline.

1. What is ADHD?
There are very different answers to this, depending on what “is” means:

  • Disorder or expression of personality traits?
  • Causes
    • How does ADHD develop?
  • Correlates
    • What is (often) associated with ADHD?
  • Symptoms
    • How does ADHD manifest itself?
  • Symptom Mediation
    • What triggers the individual symptoms?
  • Follow
    • What does ADHD do to those affected?

We summarize these and a few other points in the brief.

2. Consequences of ADHD
ADHD has massive consequences that often remain lifelong. The presentation of the increased mortality, the increased risks for further mental disorders or the further consequential risks show a realistic picture of how serious ADHD is.

3. Symptoms of ADHD
Here we describe how ADHD appears externally and what approximately 35 other symptoms there are beyond the diagnostic symptoms listed by DSM and ICD.
For the diagnosis especially of borderline cases according to DSM or ICD as well as for any meaningful treatment, knowledge of all ADHD symptoms is essential.

4. Symptom Mediation
ADHD could, in our view, also be described as chronic overactivity or overreactivity of the stress regulatory systems, which is more likely to mediate the symptoms. This section describes why ADHD is nevertheless different from chronic (and even more so than acute) stress in non-affected individuals.

5. How does ADHD develop?
What genetic, epigenetic, and environmental circumstances can trigger AD(HHD)?
ADHD is a symptom cluster that can be caused by various factors. ADHD is predominantly caused genetically, although a distinction must be made between inherited gene variants, which can be tens of thousands of years old, and epigenetic causes, which are caused by a person’s life experiences and can be passed on over a few generations. A lack of dopamine in the period between conception and about 3 years of age, caused genetically or otherwise (e.g., by early childhood encephalitis or early childhood stress), can cause a brain developmental disorder or delay, which in turn can cause or mediate AD(H)DS symptoms….

6. Neurological mechanisms of action
Which neurophysiological and neurobiological processes mediate which ADHD symptoms?

7. The subtypes ADHD-HI / ADHD-I
We describe the differences between ADHD-HI (with hyperactivity) and ADHD-I (without hyperactivity). SCT is likely to be a disorder in its own right rather than an ADHD subtype.

8. Diagnosis of ADHD
How is ADHD diagnosed?
From which similar disorders is ADHD to be distinguished (differential diagnosis)?
What other disorders often occur together (comorbid) with ADHD?

9. Treatment of ADHD
How can ADHD be treated? We describe medication, psychotherapy, stress prevention, stress reduction, diet, neurofeedback and other methods.
How effective are these treatments (what is their effect size)?
What can be done to prevent ADHD?

10. Things to know about ADHD
What else can help you understand ADHD.

11. Tests and surveys
We offer several free online screening tests that can indicate whether a medical professional diagnosis might be appropriate:

  • ADHD symptom test (self-assessment)
  • ADHD Foreign Assessment Test
  • ADHD reaction test
  • SCT Test (Sluggish Cognitive Tempo)
  • High sensitivity test
  • Differential diagnostic test anxiety
  • Differential Diagnostic Test Depression
  • ADHD Medication Effectiveness Test
  • Besides we collect Contact details of doctors and therapists with experience in ADHD
    • Address collection is only available for the German-speaking area so far

The tests are still in German language. English language versions are being prepared.

Tests and surveys

12. ADHD FORUM
ADxS.org currently offers the most comprehensive German-language active forum on the topic of ADHD:
ADHD forum at adhs-forum.ADxS.org
Most of the contributions are also readable for visitors. Membership is free of charge.
For English-speaking readers, Reddit’s ADHD forum is recommended.

13. Does ADHD even exist? How do I find out what is true?
The discussion about ADHD sometimes has religious overtones.
We show how to find out for yourself which representations are trustworthy.

1. What is ADHD?

The question “Is ADHD a disorder or a manifestation of personality traits?” can be answered quite simply and succinctly, “Yes!”

ADHD - like most other mental disorders - is dimensional.2 Whereas pregnancy or a broken bone are categorical (they either exist or they do not), ADHD (like, for example, depression, anxiety, or narcissism) can only be diagnosed as a disorder by the degree and focus of the symptoms. In milder cases, ADHD represents only one personality dimension.

Almost everyone has a few ADHD symptoms frequently. Only the set of frequently occurring symptoms distinguishes between personality traits that are not a disorder and ADHD as a distressing disorder. While this makes diagnosis laborious (ADHD is indistinguishable when observed briefly (as a “photo”), it becomes recognizable only when observed over a longer period of time (as a “movie”)), it remains far clear enough to neatly distinguish ADHD from mere chronic stress. Whereas unaffected adults have 1 to 2 of 18 symptoms (according to Barkley) or 9 of 35 symptoms (in our online symptom test, version 2) frequently, ADHD sufferers have on average 12 of these 18 symptoms (according to Barkley) or 26 of the 35 symptoms (in our online symptom test, version 2) frequently. Which of the symptoms a particular sufferer has is unpredictable. They are often, but by far not always, the DSM / ICD symptoms, which represent only the symptoms (diagnostic symptoms) that are optimally distinguishable (from other disorders) and by no means represent all symptoms that may stem from ADHD itself (treatment-relevant symptoms).

The dimensional character of ADHD can be described as a continuum:

  • Not present at all, no symptom occurs frequently (this should affect rather few people)
  • Isolated symptoms frequently, without any subjective impairment (this affects most people)
  • Some symptoms common, recognizable in individual life situations (many people)
  • Noticeable symptoms, which sometimes become stressful in several life situations (but usually do not yet represent a disorder)
  • Clear symptoms that have a stressful effect in a number of life situations (this can already have the character of a disorder)
  • Severe symptoms that are disruptive in many life situations (usually this has disorder quality)
  • Very severe symptoms that make life very difficult in most life situations (almost always a disorder)

At what level the personality traits become a disorder must be decided on the basis of the individual subjective distress. Subjective distress is the decisive characteristic for speaking of a mental disorder. This is the case for almost all mental disorders, with the exception perhaps of rare xenophobic disorders and psychopathy.

About 5 to 10% of people have ADHD symptoms so severe that they suffer significantly. ADxS.org deals with ADHD as a disorder and uses the term ADHD to describe a disorder in the sense of a severity of occurrence within the continuum that is associated with subjective suffering for the individual affected. People who do not suffer from their symptoms from this continuum can nevertheless learn a lot about the correlations and backgrounds of their personality traits at ADxS.org.

According to a representative survey, 90% of Germans are familiar with the term ADHD. Of these, 20% believed ADHD was not an existing clinical disorder and 66% were against drug treatment with stimulants.3 The ADxS.org project is dedicated to reducing the rate of this misconception.

2. Consequences of ADHD

ADHD has massive consequences that often persist throughout life. Among other things, mortality and the likelihood of depression and anxiety disorder are increased, and educational attainment, income, and quality of life are reduced.

ADHD is by no means “merely” stress (even if severe chronic stress and ADHD convey their almost identical symptoms in a neurobiologically quite similar way), but for those affected accordingly severely, it is a disorder to be taken seriously and a heavy burden for those affected, which massively impairs the quality of life if left untreated. ADHD that is not treated or not treated appropriately has massive effects on the entire lifetime,45 e.g.:

  • 1.77-fold risk of substance dependence (addiction)6
  • Premature mortality, depending on the study between 1.27-fold (boys and men),7 2.85-fold (girls and women)7 1.4-fold (children and adolescents) and more than 4.6-fold (in adults),8 especially from accidents.9101112131415
    ADHD medication reduces the frequency of accidents in affected boys and girls, as children as well as adolescents.16 by 2/3.17
    With the number of additional comorbidities, the likelihood of premature death increases up to 25-fold.818
    4.25-fold risk of premature mortality with first ADHD diagnosis in adulthood.7
    In contrast, no increased mortality was found for ADHD medication use (stimulants or atomoxetine).19
  • 2 times the risk of falling victim to murder20
  • More than 2 times medical costs21
  • 2.35 times22 to 8.61 times risk of smoking6
  • 2.4-fold risk of suicide in ADHD overall, especially in women23 to 4.1-fold risk of suicide (correspondingly higher in untreated ADHD)2425
  • 1.2 to 3.3-fold risk of anxiety disorders. Lifetime prevalence 10-15% total population,26 12-50% in ADHD.25
  • 3.6-fold risk of eating disorders in girls27
  • 2.5-fold28 to 4-fold risk of depression in girls
  • 3 to 5 times the risk of separations and divorces25
  • 7 times the risk of ending up in prison due to crime

For details, see Consequences of ADHD.

3. The symptoms of ADHD

As a non-affected person, you can understand what ADHD feels like if you imagine your desk in the middle of a busy pedestrian zone instead of in a normal office, right next to the streetcar tracks, and try to feel how much more strenuous your day would be and how much more stressed you would be when you got home. Or one compares it with the life circumstances under which some non-affected people temporarily suffer comparable symptoms, such as a contentious divorce, an insolvency or learning that one has cancer29 - only that here the whole life consists of this condition.
Affected persons usually cannot recognize for themselves whether they have ADHD on the basis of this description. This is because each person perceives his or her ongoing life circumstances and reactions as the normal measure of things. By themselves, only categorical deviations are recognizable (when something is not acceptable under any circumstances), but not dimensional deviations (according to the measure), because the standard of comparison is missing for this. The standards, the “normal zero” of a person, are regularly based on one’s own life-long experiences - and one’s own life has always been like that. ADHD sufferers do not know themselves differently and therefore identify themselves with their symptoms as “normal”.
After all, ADHD has one indisputable advantage over all other mental disorders: it is the most treatable mental health problem of all.

As with all mental disorders, a distinction must be made between the smaller number of diagnostically relevant symptoms and the totality of treatment-relevant symptoms.
ADHD can cause many more symptoms than the much-cited DSM or ICD criteria.
DSM and ICD are diagnostic manuals. They aim to identify disorders. Therefore, DSM and ICD list only the diagnostically relevant symptoms, i.e., those that have a particularly high discriminatory power to other disorders. Those symptoms, on the other hand, which also frequently (co-)occur in other disorders are not listed in DSM and ICD. Even the renowned American psychiatrist Allen James Frances, chairman editor of the DSM-IV, criticizes that diagnoses are far too often based on the DSM or ICD criteria alone.

DSM 5 lists 8 symptoms of ADHD:

  1. Inattention (distractibility and concentration problems, but not task switching problems)
  2. Forgetfulness
  3. Disorganization
  4. Hyperactivity
  5. Impulsivity
  6. Impatience
  7. Inner drivenness
  8. Excessive talking

DSM and ICD - statistical tools, not diagnostic scales

DSM IV (until May 2013) and ICD 10 were still exclusively focused on children’s symptoms and therefore, by their very nature, did not take into account that ADHD symptoms in adults (⇒ ADHD in adults) Change seriously: motor hyperactivity largely disappears, whereas inner restlessness and being driven become more visible, and emotional problems increase (Emotional dysregulation - mood swings in ADHD). Attention problems may also decrease or even disappear altogether (although less frequently than hyperactivity).

The misunderstanding that the DSM or ICD symptoms would be the only original (directly caused by ADHD) symptoms is common even among physicians and therapists. However, knowledge of the totality of all possible symptoms is essential for treatment and therapy. The consequences can be fatal, for example, if physicians confuse ADHD-typical dysphoria during inactivity with depression and therefore make unsuitable medication attempts with antidepressants, or if therapists do not consider procrastination, mood swings, or sickliness (Rejection Sensitivity: Offensiveness / Sensitivity to Rejection and Criticism as a Specific ADHD Symptom) Do not consider them as an original consequence of an existing ADHD, but torture the affected persons with nonsensical attempts to treat them as consequences of negative life experiences or lack of discipline - which can deepen the life experience of being insufficient in the affected persons. Such malpractice is unfortunately not uncommon.

At Symptoms of ADHD We have collected all symptoms that can result originally from ADHD and substantiated them with source references from the ADHD literature (as ADHD symptoms):

At ADHD symptoms are stress symptoms We have collected references where the stress literature names these as stress symptoms. At Stress benefits - the survival-enhancing purpose of stress we describe for each symptom the stress benefit, that is, the purpose that the particular symptom has or used to have in combating stressors.

Many professional books confirm ADHD sufferers (besides their specific symptoms) specific positive character traits. Interestingly, these positive characteristics seem to be largely congruent with the typical character traits of gifted people mentioned in the literature on giftedness. This does not mean, however, that all ADHD patients are highly gifted (a clear under-giftedness is even a known risk factor for ADHD).
Giftedness and ADHD.

4. How ADHD mediates its symptoms

In our view, ADHD mediates many of its symptoms via dysfunctional control of stress regulatory systems, primarily the HPA axis (stress axis).
Almost all ADHD symptoms are identical to symptoms of severe chronic stress. In both constellations, they are triggered by a deficiency of certain neurotransmitters (mainly dopamine and norepinephrine) in specific brain areas (mainly dlPFC and striatum).
ADHD symptoms are stress symptoms

But even though both phenomena cause similar symptoms in a similar neurobiological way, ADHD is nevertheless something different than “just” chronic stress: Stress goes with the stressor, ADHD stays. This is because the almost identical neurotransmitter deficiency has different causes in ADHD than in stress.
ADHD as a chronicized stress regulation disorder

Almost everyone develops stress symptoms in really stressful life situations, for example, the loss of a close person or an economic existential crisis: concentration, attention, memory, etc. can then be massively impaired. For example, healthy children can develop full-blown ADHD symptoms when they arrive at a new school and are bullied there. While in non-affected persons the stress symptoms disappear again with the stress load, ADHD sufferers (in our opinion) from symptoms that correspond to severe stress symptoms without there being an appropriate reason (stressor) for this in the life circumstances. In ADHD, the HPA axis (the stress axis) seems to be chronically permanently activated for other reasons (ADHD-HI) or to ramp up too fast, while at the same time shutting down cleanly (ADHD-I).
Thus, a distinction must be made between the causes of ADHD (which are clearly different from the stressors that cause chronic severe stress) and the effect of ADHD (which is little different from that of chronic severe stress).

Stress is a very ancient and fundamentally vital function. Our stress responses today are still the same as they were tens of thousands of years ago, from a time when we were not yet sedentary and still had to gather and hunt our own food, from a time far before sheltering homes, stocked supermarket shelves, office jobs in big cities, and all-encompassing media exposure. As much better as our current living comforts are, our stress systems, which have changed little since the dawn of hominids a few million years ago, have not been able to adapt optimally to today’s living conditions in the few thousand years we have been sedentary and the few hundred years of our modern lives. In the past, their reactions, the stress symptoms, were a very healthy protective reaction of the body and mind to ensure survival in life-threatening emergency situations. All stress symptoms are fundamentally useful for this purpose - at least they were in relation to the typical stressors of the last millennia to millions of years.
Stress utility-the survival purpose of stress symptoms
Stress symptoms are (or were during a long time of human developmental history) therefore very healthy reactions - if the emergency situation to which the affected person reacts with them actually exists.
However, the core of ADHD, as we understand it, is that stress exists without an adequate stressor: The stress systems are profoundly disturbed without the need for a stressor.
ADHD as a chronicized stress regulation disorder

More on the neurophysiological mediation of individual ADHD symptoms below under 6.

5. How does ADHD develop?

Origin

There are several paths of origin that act in concert:

  • Genetic: ADHD can be caused by the interaction of a number of randomly formed genes (up to tens or hundreds of thousands of years old gene variants) without the need for environmental influences. These gene variants have arisen without any stress influence. If several such gene variants come together in such a way that they have a mutually reinforcing influence on the course of certain processes in the brain, these influences can add up in such a way that the healthy balance of the processes is disturbed. Depending on which processes are affected (e.g., which neurotransmitters are increased or decreased in which brain regions), different disorder patterns develop. In ADHD, several gene variants, all acting to reduce dopamine and norepinephrine action in the brain, can combine to reduce this action to such an extent that the typical ADHD symptoms develop. In order to be able to distinguish it, let’s call it “genetically inherited ADHD” here.
    These gene variants can mediate further causes already in the first years of life. For example, a dopamine deficit in the first years of life leads to a developmental disorder of the brain, because dopamine is important for brain development (a so-called neurotrophic factor). ADHD is often described as a brain development disorder.
    Genetic and epigenetic causes of ADHD - Introduction
    Brain developmental disorder and ADHD
  • Environment: ADHD can be caused by environmental factors (early childhood or chronic severe stress). Stress medicine already describes this as a pathway for depression.
    Early or chronic severe stress can have a neurotoxic effect and change the expression of genes, i.e. their activity (epigenetics). This can also cause the ADHD-typical changes in neurotransmitter levels and the like. While active stress increases dopamine and norepinephrine levels, chronic stress is associated with long-term decreased dopamine levels. Early childhood chronic stress can thus trigger the dopamine deficits that subsequently cause a brain development disorder. This ADHD cause is particularly amenable to prevention through caring, warm parenting behaviors.
    Furthermore, diseases can also stimulate the immune system to ADHD-typical behavioral changes. For example, encephalitis destroys the dopaminergic cells in the brain and can thus trigger a dopamine deficit that causes ADHD-typical symptoms. In principle, however, there is little evidence for immunological causes. It seems more likely that diseases contribute to ADHD by activating the stress systems that mediate most ADHD symptoms, just as psychological stress does. Immune system and behavior Let’s call it “acquired ADHD.”
    Environmental factors as a cause of ADHD
  • Epigenetic (Inherited Experience): ADHD acquired through severe or chronic stress can be passed on to one’s own descendants. In contrast to the “genetically inherited” ADHD of the first variant, here only the epigenetic changes in gene activity acquired through environmental influences are passed on. Toxins, severe early or chronic stress, or disease can alter gene expression. Animal experiments as well as studies in humans have demonstrated inheritance of such acquired gene expression over 2 to 4 generations. Let’s call it “epigenetically inherited ADHD.”
    Genetic and epigenetic causes of ADHD - Introduction

ADHD has a strong genetic component of about 76%. Some studies quote even higher values, The heritability (hereditability) of ADHD is thus greater than that of intelligence. Among ADHD cases with clinical intensity, up to 90 % are genetically caused.30 However, single genes are not causative, although certain gene variants are more frequently involved. Many hundreds of candidate genes are known. It would not be surprising if there were thousands. More than 200 of these we have Candidate genes in ADHD Named. Nevertheless, so far only 5% of genetic heritability can be attributed to specific gene variants. This is probably also due to the fact that genes (in most mental disorders) only represent a disposition and do not yet say that ADHD exists.

The most frequently mentioned gene candidates (more precisely: certain polymorphisms of these genes) for ADHD, DRD4-7R (which makes the D4 dopamine receptor less sensitive) and 5HTTPR short (which affects the serotonin balance), as well as some other ADHD gene candidates (such as COMT Val158Met, which significantly accelerates dopamine degradation in the PFC) are chance-risk genes. On the one hand, children with these gene dispositions react particularly vulnerable to stress or unfavorable parenting styles - here, even an insecure (i.e. unreliable or cold) attachment to one parent can have a lasting negative impact on development (risk). On the other hand, they respond better than average to support and favorable parenting styles (opportunity). Opportunity-risk genes are a kind of lever for environmental influences. We suspect that they may be a cause of the increased sensitivity often described in ADHD.
The (genetic and developmental) causes of ADHD: Opportunity-risk genes In the article How ADHD develops: genes or genes + environment

ADHD is thought to be characterized in particular by decreased levels of dopamine and norepinephrine in the brain areas dlPFC and striatum. While acute stress shows increased dopamine and norepinephrine levels in these brain areas, chronic stress, like ADHD, is typically associated with decreased dopamine and norepinephrine levels in these brain regions. Acute as well as chronic stress nevertheless show partly similar symptoms, since the symptom-triggering dysfunctions of the brain regions relevant here arise at any deviation from an average dopamine or norepinephrine level.

Dopamine is a neurotrophic factor, i.e. necessary for the neuroplasticity of the brain. Dopamine deficiency (which can be triggered by certain gene constellations or by chronic stress) causes a developmental disorder of the brain. ADHD is often described as a consequence of delayed brain development. We hypothesize that the brain developmental delay or brain developmental disorder often described in ADHD is a direct consequence of a genetically or environmentally induced early childhood dopamine deficiency. ⇒ Brain development disorder and ADHD

Dopamine is also closely related to the regulation of circadian rhythms. Dopamine and the sleep-promoting melatonin are antagonists. Around 75 % of ADHD sufferers have a retarded circadian rhythm (or would have it if they were allowed to. This explains the close connection between ADHD and sleep problems.
Sleep problems and ADHD are mutually reinforcing. Sleep problems with ADHD.

Stress has a special significance in ADHD.
Stress is a factor that can trigger the development of ADHD, and ADHD acquired in this way is hereditary as a disposition.
In addition, ADHD symptoms are mediated in large part by the stress systems.
This importance has hardly been considered by the ADHD literature so far. All the more important to us is a comprehensive presentation of the stress systems and their influences.
Stress

Early childhood stress experiences are particularly significant for ADHD because the stress systems in the brain are just forming in the first years of life. Early childhood stress causes permanent damage to the physiological stress systems (HPA axis, vegetative nervous system, PFC). The second particularly dangerous phase for ADHD is puberty. ADHD sufferers who experienced many severe stressors during puberty were much more likely to retain their ADHD into adulthood than children with few stressors during puberty.

Acute stress increases levels of the neurotransmitters dopamine,31 norepinephrine and serotonin31 as well as the hormones CRH, ACTH and cortisol, among others. Stress hormones such as CRH, ACTH, and cortisol have a helpful short-term effect, but they are neurotoxic in the long term. If threatening stress is too prolonged, various neurological maladaptations result. In chronic stress, dopamine and norepinephrine are decreased. If stress-induced altered neurotransmitter or hormone levels repeatedly occur acutely or permanently in an (early) infantile phase in which the brain systems working with these neurotransmitters or hormones are just growing, the altered levels cause the affected brain regions to develop dysfunctionally. These dysfunctions then usually persist throughout life. Brain regions that rely on these neurotransmitters or hormones are therefore particularly vulnerable to chronic stress in their growth phases.
If a corresponding genetic disposition is added to this, prolonged stress can cause massive psychological damage in children or lay the foundations for this.
ADHD as a chronicized stress regulation disorder
Stress damage - effects of early childhood and/or prolonged stress

The standard works of stress medicine now discuss which areas of the brain develop at which age and deduce from this at which childhood stress levels have occurred because the brain regions that are developing at that time are “maladjusted.” For example, severe maternal anxiety during pregnancy only increases the risk of ADHD in certain weeks of pregnancy.
In contrast, severe stress is less harmful outside the vulnerable years from conception to age 3 and puberty; it is even less dangerous outside the brain’s developmental period (i.e., from about age 25) because it causes less irreversible damage - although it is still toxic then.

The etiology of “genes or gene disposition plus an early stress experience activating it” is not peculiar to ADHD but is the genesis of many mental disorders. Gene disposition and early childhood stress as cause of other mental disorders

This makes it clear why a parenting license would make sense. Not as an admission requirement for having children, but as a minimum knowledge transfer about the defenseless being entrusted to its parents. It probably won’t help all children. But that is not the point. Seat belts do not protect life in every accident. On the other hand, every single child whose soul could be saved from injury by them would be worth it.
ADHD - Prevention and screening - What parents can do and⇒ Secure attachment beats genetic disposition in ADHD

Rats as ADHD models

There are several rat breeds that represent ADHD-HI, ADHD-I, and non-affected individuals as animal models.
The Spontaneous(ly) hypertensive rat (SHR) is a genetically distinct strain representing ADHD-HI (with hyperactivity), whereas Wistar-Kyoto rats (WKY) usually represent non-affected individuals as a counterpart model.
That these animals express their disorders solely because of genetic makeup and without the influence of early childhood stress is a strong argument that certain genes alone represent a distinct pathway for the development of mental disorders such as ADHD and that the developmental pathways genes alone and genes + environment coexist.
Interestingly, the findings about SHR do not weaken the theory that ADHD symptoms are mediated by HPA axis dysfunction, but rather strengthen it-because SHR, by virtue of their genetic predisposition alone, already exhibit a dysfunctional HPA axis, the kind of dysfunction that would otherwise only result from early childhood stress.
SHR were originally bred as a model for hypertension. Only later were they found to be a model for ADHD-HI at the same time. If the animals are treated with dexamethasone (a corticosteroid), the hypertension that would otherwise occur in all animals at the age of 15 months does not occur - and the ADHD symptoms also disappear.
Research topic: ADHD in animal models Unfortunately, this is not a universal solution for the treatment of ADHD but would be for only those affected individuals whose ADHD is mediated by quite the same mechanisms as exist in (genetically distinct) SHR. The causes of ADHD, on the other hand, are more diverse.
However, for certain subgroups of ADHD-HI, dexamethasone shock treatment could potentially be helpful. ⇒ Dexamethasone for ADHD. Meanwhile, this method, which we have theorized, has not yet been researched or tested.

6. Neurophysiological mechanisms of action in ADHD

Every thought, every feeling, every action has a neurophysiological correlate. This means: everything we do is represented by specific processes in the brain. This correlation is reciprocal. The brain, depending on its neurophysiological state, influences what we think, do and feel, while everything we think, do and feel in turn influences neurophysiological changes in our brain. Likewise, the brain influences the body and the body influences the brain. Again, there are cycles of perception and consequences that influence each other.
Neurophysiological correlates are thus merely a momentary reflection of the brain state that occurs simultaneously with a particular state or behavior and do not imply that there is unilateral causality (that is, that brain states are always only the cause and behavior is always only the consequence). Neurological aspects

How exactly ADHD symptoms are based on neurophysiological mechanisms is exceedingly complex and far from fully understood. Therefore, only some mechanisms can be explained. Most explanatory models of ADHD are derived from the neurophysiological principles of action.

In ADHD, it is primarily the balance of the neurotransmitters dopamine and norepinephrine in the brain that is disturbed. GABA, glutamate, serotonin, and acetylcholine play additional (secondary) roles. Neurotransmitters in ADHD Various causes can be considered for a reduction in dopamine levels or dopamine action in different brain areas, including:

  • Too many or too active dopamine transporters (DAT), which reabsorb dopamine from the synaptic cleft into the presynapse before it can act at the postsynapse, (especially in the striatum, where dopamine degradation is primarily by DAT and little by COMT)
  • Too much of the dopamine-degrading enzyme COMT (especially in the PFC, where dopamine is degraded from the synaptic cleft less by DAT than by metabolization by the enzyme COMT)
  • Reduced sensitivity of postsynaptic D4 dopamine receptors (mainly in the PFC; the D4 receptor is rare in the striatum)
  • Fewer postsynaptic D2 and D3 dopamine receptors32
  • Etc..

For the importance of PFC and striatum in ADHD, see subtypes below.

Each of these causes is controlled by other genes. Depending on the variant of the gene and on the epigenetic modification, genes are differently active. The more gene variants that contribute in their own way to reduced dopamine levels coincide in a person, the lower the dopamine level in total and the more severe the dopamine deficiency symptoms in the affected person. Stimulants such as methylphenidate or amphetamine drugs fill this dopamine deficit a. very slowly for - depending on the preparation - 3 to 13 hours to the b. normal level. Drugs, on the other hand, a. very quickly lead to an b. excessive level of dopamine. While a rapid rise to an excessive level can trigger a feeling of intoxication, the slow compensation of the deficit by drugs merely remedies the dopamine deficiency symptoms.
Methylphenidate (MPH) for ADHDAmphetamine medication in ADHD
Other medications cause the dopamine deficit to be corrected via detours.

Examples of neurophysiological influences and correlations in ADHD

The number of dopamine transporters is halved in adults (50 years) compared to children (15 years). Therefore, adults require (sometimes significantly) lower doses of dopaminergic drugs than children.
ADHD in adults

Inhibition and impulse control problems have their own neurological correlates.
Neurophysiological correlates of inhibition problems and impulsivity in ADHD

Motivation problems result from a deviant evaluation of expected rewards. Rewards are only interesting for ADHD patients (and just as interesting as for non-affected persons) if they are available immediately. The more distant an expected reward is in the future, the less interest ADHD sufferers have in it compared to non-affected people. Important things, on the other hand, must happen immediately (impatience).
Neurophysiological correlates of drive and motivation problems in ADHD

These symptoms make a lot of sense from the point of view of stress as a coping system for life-threatening situations: first survive (impatience for this). Collecting nuts for the winter can wait that long (devaluation of distant rewards).
Stress benefits-the survival purpose of stress

Aggression and social disorders often occur comorbidly, especially in ADHD-HI sufferers, but are not an original symptom of ADHD.
Neurophysiological correlates of aggression in ADHD

ADHD sufferers (especially in ADHD-HI and likewise procrastination sufferers) often have a deep-seated aversion to relaxation and mindfulness.
Where does aversion to mindfulness come from in ADHD and procrastination? This aversion is also a healthy stress benefit: Anyone facing an acute danger should not relax until that danger is removed. Stress benefits - the survival-enhancing purpose of stress As with all ADHD symptoms, it is not the symptom itself that is the problem, but rather that the person in stress mode is subject to other guiding principles.

Many ADHD patients suffer from an inability to enjoy. As with attention, it is not the ability to enjoy per se that is disturbed, but the self-direction ability to allow and experience enjoyment in a self-determined way. This is a serious problem, because the ability to enjoy is closely linked to the ability to recover. Those who cannot enjoy sufficiently usually also have the problem of not being able to recover sufficiently. This is reflected, for example, in the frequent aversion to mindfulness exercises, meditation, yoga or other relaxation techniques. This leads to a vicious circle that aggravates the symptoms more and more.
Neurophysiological correlates of delay aversion, pleasure inability, and recovery inability in ADHD
However, inability to enjoy is also a stress benefit, in that it drives one not to be distracted from fighting the stressor until it is defeated.

7. The difference between ADHD-HI and ADHD-I - the subtypes

In ADHD, the subtypes ADHD-HI (predominant hyperactivity), ADHD-I (predominant inattention), and ADHD-C (attention problems and hyperactivity) are distinguished.
SCT (sluggish cognitive tempo) does not seem to be an ADHD subtype, but an independent disorder. This is consistent with the fact that high SCT scores by our ADxS-SCT online test were found equally in ADHD-HI and ADHD-I sufferers.
The pure ADHD-HI type is predominantly found in children up to 15 years of age. This is likely due to the fact that inattention symptoms are very difficult to diagnose at ages less than 6 years and can only be reliably diagnosed at ages greater than 15 years. ADHD-C is therefore often likely to be the later developmental form of the ADHD-HI subtype. However, there is still - even in adults - a proportion of about 10% of ADHD sufferers with the pure ADHD-HI subtype with minor attention problems.

Hyperactivity and impulsivity on the one hand and inattention and executive functions (organizational problems) on the other hand are significantly controlled in different brain regions. Whereas hyperactivity and impulsivity are primarily regulated in the striatum, where dopamine degradation occurs primarily through dopamine transporters and hardly through COMT, attention and executive functions are primarily controlled in the PFC, where dopamine degradation occurs primarily through COMT and only slightly through DAT. Similarly, the D4 receptor, which is often impaired in ADHD, is found only in the PFC and not in the striatum. This might suggest that hyperactivity/impulsivity on the one hand and inattention/executive functions on the other hand are distinct disorders that do not occur at all in some people (non-affected) in some people only alone (ADHD-HI subtype, ADHD-I subtype) and in some people together (ADHD-C).
Neurological correlates of hyperactivity Neurophysiological correlates of inhibition problems and impulsivity in ADHD
Neurophysiological correlates of attention problems in ADHD

On the other hand, it should be noted that sufferers with hyperactivity/impulsivity have a different stress phenotype than sufferers without these symptoms. It would be quite conclusive to portray ADHD-HI as a uniform disorder that is outwardly differentiated only by the stress phenotype pathway. Affected individuals with hyperactivity/impulsivity show an externalizing form of how they express stress and also have primarily other, qualities that are also externalizing. Affected individuals without hyperactivity/impulsivity, on the other hand, show an internally realizing form of expressing stress and continue to show internalizing comorbidities more frequently.
3. Chapter of ADHD subtypes: the different types (ADHD-HI, ADHD-I, ADHD-C, and others).

Meanwhile, in SHR, a strain of rats with typical ADHD symptoms, a subgroup was found to show no hyperactivity instead of the ADHD-HI symptoms usually described, and thus to be more like the ADHD-I subtype. The ADHD-I subgroup showed (as expected only in the cortex) decreased norepinephrine levels, decreased serotonin levels, and fewer cannabinoid receptors.
Research topic: ADHD in animal models

Basal cortisol levels are identical in all subtypes. As in people with severe stress, basal (tonic) cortisol levels are decreased compared with nonaffected individuals. In contrast, subtypes differ in terms of cortisol response to acute stress. Whereas ADHD-HI and ADHD-C often respond to an acute stressor with a cortisol stress response that is too weak (= flattened or even reduced), the (phasic) cortisol stress response in ADHD-I is very often excessive. Cortisol in ADHD

Cortisol is not only a strong stress hormone, but - as the last stress hormone of the HPA axis chain - it also has the task of shutting down the HPA axis, which is not designed for continuous operation as an emergency system. To put it casually: Switching up to “130%” in an emergency is conducive to survival. In contrast, a high stress level is unhealthy as a permanent condition, and a high cortisol level is neurotoxic.
The HPA axis / stress regulation axis Also, the lack of hyperactivity in the ADHD-I subtype could possibly be explained by the fact that the often excessive (phasic) cortisol and norepinephrine responses to acute stress in ADHD-I can effectively inhibit the HPA axis (cortisol) and the PFC (norepinephrine) at the end of the stress response, so that a steady state of stress does not occur in ADHD-I, which accounts for the hyperactivity. Our hypothesis that ADHD-HI and ADHD-C sufferers lack the stress axis cutoff switch due to a tendency for a reduced phasic cortisol response, so that the HPA axis remains in a long-term steady state in ADHD-HI (unlike in ADHD-I), is supported by an evaluation of about 1700 records of the ADxS online symptom test, according to which inability to recover is much more pronounced in ADHD-HI than in ADHD-I and that almost universally all ADHD symptoms tend to be more severe in ADHD-HI and ADHD-C than in ADHD-I.
The ADHD-I subgroup of SHR was found to have decreased (tonic) levels of norepinephrine. (When considering whether a neurotransmitter level is high or low, a distinction must always be made between tonic (basal) levels and phasic stress response)

Comparable differences in cortisol stress responses exist in atypical and bipolar depression (flattened cortisol stress response) and melancholic and psychotic depression (exaggerated cortisol stress response), as well as (although less markedly) in several other mental disorders.
Cortisol in other disorders. The different cortisol stress response types have also been found in healthy individuals.
Different cortisol stress response types in healthy subjects In post Stress theories and stress phenotypes: a possible explanation of ADHD subtypes.

The different subtypes can also be described as different stress phenotypes of one and the same disorder. While ADHD-HI sufferers externalize their stress, ADHD-I sufferers compensate for their stress by escaping inward, by blocking it internally. The different cortisol responses to stress are phenotypic of externalizing stress responses (as in ADHD-HI/ADHD-C) on the one hand and internalizing stress responses (as in ADHD-I) on the other.

For a detailed discussion of the differences among the subtypes of ADHD, see The subtypes of ADHD: ADHD-HI, ADHD-I, SCT, and others.

8. The diagnosis of ADHD

We present the diagnostic procedures of ADHD and explain from which similar disorders ADHD has to be distinguished (differential diagnosis) and which disorders often occur together with ADHD (comorbidities).
Diagnostics

ADHD is not infrequently overdiagnosed as well as underdiagnosed:

  • Because severe acute stress (threatening self-esteem or existence) or severe chronic stress can trigger the same symptoms as ADHD in non-affected individuals.
    In our opinion, ADHD acts as a chronic disorder of the stress regulation systems, so that ADHD sufferers suffer from massive stress symptoms even when there is no acute cause, no adequate stressor.
    The diagnostic manuals (DSM, ICD) require for a diagnosis that the symptoms exist in several areas of life and for more than 6 months in order to exclude temporary stressors. This is easy to determine in adults, but much more difficult in children.
  • Because the ability to pay attention and concentrate is not fundamentally lacking in ADHD, but (as makes sense in stressful emergency situations) only the control of attention and concentration is subject to a different regime. ADHD sufferers suffer from the fact that their (especially extrinsic, but also intrinsic) motivability is reduced. They therefore need stronger incentives to be allowed to feel the same motivation as non-affected people. If something is personally exciting enough to arouse motivation, ADHD sufferers show up to equivalent attentional performance as non-affected people in tests as in real life. They may even be able to concentrate better and longer than non-affected individuals. This is what is known as hyperfocus. In fight or flight, focus on just that is highly helpful. Under stress probably not only the technical ability to pay attention changes, but also the object for which attention and concentration are worthwhile. The only thing that should be important is what is (personally) considered to be helpful for one’s own survival. Everything less important must wait.
    The fact that this attention control profile is activated in ADHD without an adequate stressor leads to misunderstandings such as “You can do it if you want to”. Correct: ADHD sufferers can if they are interested in something. But they cannot direct their interest - or at least not as well as non-affected people.
    As a result, they can’t control their wanting the way others can, even though they wish they could.
  • If attention were a car, then in ADHD attention basically works - the car can drive. The steering also works perfectly: attention can change focus as well as hold it. The problem is the driver who operates the steering: he often avoids a deer on the road that is not there (stress symptoms without adequate stressor). And then it just rumbles across the meadow.
    Attention thus follows a different regime in ADHD: a pattern that would be helpful in survival-threatening stress but is less helpful in “normal” life.
  • ADHD is, according to our understanding, hardly recognizable in a momentary observation. The dysfunction of the stress regulation systems only becomes visible in a long-term observation. Therefore, it requires considerable experience to be able to correctly detect ADHD in a selective medical diagnosis. In order to recognize ADHD, a film is needed, not a photo.

ADHD is primarily diagnosed using questionnaires (self-assessment and parent/teacher assessment). However, these alone are not sufficient for a solid diagnosis.
Interviews By experienced diagnosticians have the advantage that they can better assess and compare the degree of severity of a symptom.
Tests Are seemingly more objective in terms of assessing test results - but only in terms of test results.
ADHD - Diagnostic Methods.

Interviews, questionnaires and tests can also lead to falsified results if the subjects have a very high personal interest in the investigation and are motivated accordingly. With appropriately high (and personally interesting) rewards, which succeed in overcoming the ADHD-typical motivability deficit, the attentional performance of ADHD sufferers can no longer be distinguished from that of non-affected persons.
Smoking can also skew test results because nicotine, like methylphenidate, increases dopamine levels and is often used as a self-medication.
Diagnostic methods: problems with ADHD-HI testing-ADHD-HI symptoms do not consistently occur

Therefore, there is no one universal test that alone could provide a reliable objective diagnosis.
Apart from that, performance tests can always confirm only the momentary stress symptomatology, but not the duration of its existence and its origin.
Stress damage - effects of early childhood and/or prolonged stress

Objective measurement procedures, which use biomarkers To identify whether ADHD exists, do exist, but even these are not so clear that a definite diagnosis could be made on the basis of the biomarkers alone. Whether a dexamethasone/CRH/ACTH test can provide an indication of an underlying stress system disorder remains to be determined. It could potentially be helpful in identifying the subtype.
The fact that ADHD cannot be diagnosed on the basis of clear biomarkers is not a peculiarity. There is no mental disorder that can be clearly diagnosed by biomarker tests.

Research is being conducted on test procedures that should support diagnostics by measuring QEEG frequencies, determining the beta-theta ratio in the EEG or measuring evoked potentials. It would also be conceivable to measure changes in CRH, ACTH, cortisol, or alpha-amylase stress responses to acute stressors, although the problem here is that such stress tests are costly. Genetic tests do not yet exist. Although much knowledge is now known about the influence of gene variants and epigenetic changes on ADHD, this is still not researched far enough to be able to make a meaningful diagnosis.

ADHD cannot be reliably determined on the basis of a specific effect of medications. Some affected persons do not respond at all to one medication (nonresponders), to the other hardly at all, to the third moderately or only temporarily (especially tricyclic antidepressants), and only the fourth medication brings the desired success, which can then be clearly surpassed by the fifth and sixth medication. Even switching between different preparations with the same active ingredient can (especially with methylphenidate) mean the difference from ineffective or effective or from side-effect-rich to side-effect-free. The increased sensitivity that regularly exists in ADHD leads to very sensitive reactions to minimal differences, especially with regard to the timeline of active ingredient release.

Dosing issues: why too much of a neurotransmitter causes almost the same symptoms as too little

Non-affected individuals can also benefit from a low dose of stimulants. Optimal signal transmission in the brain requires optimal neurotransmitter levels. If neurotransmitter levels are too low, increasing them with medication can compensate for this and thus raise performance. A slight increase in dopamine and norepinephrine is associated with increased alertness, as in acute stress. Even a little more, however, can raise neurotransmitter levels too much and thus again cause the very symptoms that existed even when levels were too low. Non-affected and overdosed persons often describe the closing of the stimulus filter caused by a slight increase of the dopamine level by methylphenidate as a narrowing of perception, as “being cut off from the world”. This may have certain advantages in examination situations, but is rather unpleasant for the rest of life. We know of no reports of non-affected persons who have voluntarily taken stimulants for a longer period of time outside of examination (stress) situations.
ADHD medications have no intoxicating effect on either non-affected or affected persons. For sufferers, on the other hand, the reduction in the far too high stimulus level that accompanies the normalization of DA and NE levels is a blessing.
In principle, the use of prescription ADHD medication without a medical prescription is punishable in several respects and is risky to health without medical examination for contraindications and without medical supervision, which is why this is expressly warned against.

There are diagnostic guidelines that should be carefully followed.

Put simply, anyone who is prescribed stimulants after a twenty-minute initial consultation should change doctors. The perseverance required for a good diagnosis may clash with the symptom-typical impatience and volatility of ADHD sufferers. Even the fastest diagnosis is of no use if it is wrong. Such a speed of diagnosis is usually not an indication of a special experience with ADHD, but a serious indication of an insufficient experience with ADHD. Even if a flash diagnosis was happily correct, it is questionable whether the experience and patience required even for the demanding and lengthy adjustment of optimal medication and dosage is available.
Even a too fast starting or up-dosing (of stimulants) increases (even with an actually suitable drug) the risk of side effects and thus of a therapy failure considerably - which could unnecessarily permanently obstruct this therapeutic path for the future. Apart from this, there is a considerable proportion of ADHD sufferers who require dosages that are below the typified starting dosage (in the case of amphetamine drugs, even below the smallest drug doses sold, which is why a division of the smallest doses at the start should be considered here from a scientific point of view).

The fact that there are far too few doctors and therapists who have sufficiently in-depth experience with the complex subject of ADHD is a serious problem.

A careful diagnosis includes:
ADHD - Diagnostic Methods

  1. A clean differential diagnosis Differential diagnostics in ADHD
    • Exclusion of organic causes
      This is impossible without blood tests (for vitamin deficiency, thyroid hormones, etc.).
      In addition, several other differential diagnoses must be clarified.
    • Exclusion of mere stress symptoms due to acute stress-causing life circumstances (duration of the existence of the symptoms and occurrence in different areas of life)
    • Exclusion of other psychological causes that may better explain the symptoms
  2. Thorough recording and analysis of symptoms
    • Complete symptom query Symptoms of ADHD
      • DSM/ICD are important clues, but contain only those symptoms that are particularly well differentiated from other disorders and not the totality of all symptoms that can result from ADHD. The symptoms existing in the individual case therefore do not necessarily have to correspond to DSM/ICD and in almost all cases go far beyond it.
      • Self-awareness questionnaires
      • Interviews with affected person(s)
      • Third-party assessment questionnaires and interviews with parents/guardians
    • Test psychological performance diagnostics

Again, because of special importance: The symptom catalogs of DSM and ICD are not final, complete lists of all ADHD symptoms. DSM and ICD are diagnostic tools, statistical and billing instruments that contribute significantly to medical quality assurance. However, to use them as the sole standards for diagnosis would be malpractice. Diagnostic ADHD symptoms according to DSM, ICD, Wender-Utah etc.

Only the overall view of the results leads to a definite diagnosis.

In addition to differential diagnostics (the differentiation of whether the existing symptoms stem from ADHD or from another disorder), the recording of comorbidities is an important component of ADHD diagnostics.
At Differential diagnostics in ADHD Most possible differential diagnoses are listed, and at Comorbidity most comorbidities are listed in descending order of probability of occurrence.
Comorbidity means that in addition to the existing (here: ADHD) disorder, other disorders also exist. Mental disorders often occur together with other disorders (comorbid). Most mental disorders have the etiology in common that either certain gene constellations alone cause the disorder or that environmental influences (usually early and/or long-lasting and/or very intense stress experiences) manifest certain existing genetic dispositions (epigenetic) and thus lead to the disorder.
Gene disposition plus early childhood stress as a cause of other mental disorders
An interesting aspect of the comorbidity to ADHD are eating disorders. Overweight up to obesity (adiposity) and binge-eating (more rarely anorexia) occur more frequently than average together with ADHD-HI (with hyperactivity). In the case of comorbid ADHD, ADHD treatment can make an impressive contribution to weight loss in obesity.
ADHD, obesity and eating disorders. The same is true for depression. One third of all treatment-resistant depression results from unrecognized ADHD.

9. Treatment of ADHD

Our guide presents AD(HHD) treatment that makes sense from a scientific point of view.
We present many appropriate and less appropriate medications for ADHD as well as possible non-drug treatment pathways. Particularly important is the comparison of effect sizes of the different treatment options.
Treatment and therapy

There is no one-size-fits-all, one-size-fits-all treatment for ADHD. Each treatment must be tailored to the individual symptom expression and the personal circumstances and personality traits of the person affected. Therefore, an individual medical history and case-by-case assessment is always required.

From a scientific point of view, the procedure described below makes sense in most cases and thus forms a basic intellectual framework.
ADHD Treatment Guide

The first step Requires a definite diagnosis by questionnaire AND tests, family history with complete differential diagnosis and identification and differentiation of comorbidities.
Differential diagnostics in ADHD and ⇒ ADHD - comorbidity

The second step Is to take acute measures. As a rule, this is primarily an appropriate and carefully adjusted medication. The acute medication enables the patient to experience what a symptom-free life feels like, so that this can be anchored for several months as the target state, which is aimed for with the therapeutic measures in the third step. Usually, it is only when dopamine levels are normalized by stimulants that adequate learning and therapeutic ability is achieved. Dopamine is neurotrophic, i.e. necessary for the anchoring of learning experiences.

If children up to 6 years of age are affected, therapeutic measures for parents and caregivers are indicated as a second acute measure. In young children, parental work causes a reduction of stressors and protects against a deepening of the ADHD disorder at a still vulnerable age. Therapeutic interventions for children up to 6 years of age themselves, on the other hand, tend to be ineffective. ADHD - Prevention and precaution - What parents can do.

In the third step, various therapeutic measures are taken with the aim of making medication dispensable. In the short term, stressors in the environment should be reduced and sleep problems aggressively addressed.
Sleep problems in ADHD. In the medium term, mindfulness-based therapies such as mindfulness-based behavior therapy (MBCT), mindfulness training (MBSR) are recommended. In the long term, neurofeedback, trauma therapies such as EMDR or DBT may be useful. In addition, environmental interventions, psychoeducation and group experiences occur.
Neurofeedback is particularly fascinating in this context because the treatment successes - although unfortunately only completely curative in rare exceptional cases - are permanent.
Neurofeedback as ADHD therapy

Medication in ADHD is a highly complex topic. In ADHD, dopaminergic, noradrenergic and other neurotransmitter systems are involved in mediating symptoms. Detailed information can be found in the individual articles on the respective medications.
When fine-tuning medication, it should be kept in mind that a healthy state is not the absence of all ADHD symptoms present, but that healthy individuals (and those optimally controlled with medication) have an average of 20 to 25% of possible symptoms occurring frequently (instead of the average of 75% of symptoms in affected individuals). Medication should therefore only reduce the number of frequently occurring symptoms to the level of non-affected persons and not completely eliminate all possible symptoms. Otherwise, an overdose is risked, which in extreme cases leads to a restriction instead of an improvement in the enjoyment of life.

Special attention should be paid to the treatment of sleep problems. Sleep problems (like all ADHD symptoms) can be symptoms of stress. Since sleep is one of the most important factors in reducing stress, sleep problems can lead to an ADHD vicious cycle. About 3/4 of all ADHD sufferers have a chronorhythm that is shifted backwards, so the circadian system is affected. Especially for children who have to get up (often much too) early due to school, an advance of the time of falling asleep (e.g. by unretarded melatonin) can be helpful.
In detail on this topic at Sleep problems with ADHD and A separate article is dedicated to the interesting topic ⇒ Binaural music as therapy for ADHD and sleep problems is dedicated to a separate article.

Food, food additives and ADHD

ADHD is not caused by food or food additives alone. However, food or food additive intolerances can act as stressors to increase the intensity of ADHD, or in sufferers who have ADHD so weak that it is not disruptive without additional stressors (keyword: dimensional disorder), shift it into the pathological range. This is not a pattern that applies to ADHD alone: eliminating food intolerances can also reduce or eliminate symptom intensity in other mental disorders.
For example, early or prolonged stress can impair the barrier function of the intestinal mucosa and thereby promote chronic intestinal inflammation - especially in people who externalize stress rather than bottling it up, as this stress phenotype is associated with a flattened cortisol stress response and therefore often increased inflammatory problems. Cortisol immunologically inhibits inflammation and instead promotes foreign body clearance (TH1/TH2 shift). Too little cortisol leads to inadequate inflammatory shutdown.
Further, (especially early or chronic) stress can alter the expression of genes responsible for providing certain enzymes in the digestive tract. Oxidative stress (which is promoted less by psychological stress than by suboptimal nutrition and toxins such as smoking) can also cause digestive problems and food intolerances.
More on this at Nutrition and diet in ADHD.

Prevention:
Based on the understanding that inherited stress experiences can cause an ADHD risk (disposition) and that especially warm and caring parental behavior can contribute to the fact that such a disposition does not develop into actual ADHD (manifestation), the presentation of ADHD prevention options for parents and caregivers is very important to us. These principles are likely to apply to other multigene mental disorders as well.
Prevention

10. Things to know about ADHD

At ADHD - Literature for Beginners, Affected Persons, Professionals and Specialists You will find some books on the topic that are worth reading.

After some consideration between the heartfelt reluctance to expose third parties and the advantage of showing many sufferers that ADHD is nothing to be ashamed of and that very successful careers are possible with it, references to prominent people with ADHD who have self-published their diagnosis and people in contemporary history who are believed to have ADHD can be found at ⇒ Prominent ADHD sufferers.

The typical terms on the topic are explained in the articles Glossary And Other and older names for ADHD. In all articles on the website, underlined technical terms are also explained by a mouseover text (a text that appears when the mouse is pointed at the word).

A few remarks on the question of how misleading some scientific investigations are, and how to recognize scientifically reliable(r) investigations, can be found at Investigations prove - often enough nothing at all.

11. Tests and surveys

In our testing section, we offer several free online screening tests:

Tests and surveys

These are unvalidated screenings that are not intended to make a medical diagnosis, but to give an idea of whether a medical diagnosis might be useful.
The tests are completely free of charge. It is necessary to create an account, which serves the sole purpose that several test results can be assigned to the same test person and that the results are permanently available for the test person.
Our data protection concept is extreme: We wish NOT to know which person is behind an account. Therefore, no personal data is requested, especially no mail address, no name information or other data. We also do not store any IP data or other information about test persons.
On the contrary, it is consequently not allowed to use name details or mail addresses in the account name or password to be chosen by the user.

12. ADHD forum, virtual support groups

ADxS.org offers a free forum on the topic of ADHD:
ADHD forum at adhs-forum.ADxS.org

Via the forum, it is also possible to participate in virtual self-help groups or to found one’s own virtual self-help group (if necessary, on specific topics for which there are not enough interested parties regionally for a face-to-face group).

13. Does ADHD even exist? How do I find out what is true?

There is sometimes a lively discussion on the Internet about whether ADHD exists at all. The discussion sometimes has religious overtones.

Interested parties who ask themselves or us whether the
ADHD drugs are poison or money-making” or “ADHD doesn’t even exist” camps
or the
ADHD is an existing and, with appropriate symptom severity, serious mental disorder” or “ADHD medications are an effective medicine with manageable side effects”-camp
is right, we are happy to recommend the following:

The first step is to look at the consequences of ADHD to get a sense of what the effects of ADHD are-often lifelong: Consequences of ADHD

In the second step, an analysis of the presentation style helps:

1. Search per stock 30 to 40 web pages
2. Print the web pages and sort them separately by stock in two folders
3. Do not read the content for the statements
4. Take different highlighters and mark each one:

  • Is argued factually (green) or emotionally (yellow)
  • Is differentiated (green) or flat-rate (yellow)
  • Are arguments also given that speak against one’s own opinion (green)
  • If relevant statements are made that are not supported by (idR multiple) verifiable sources (orange)
  • Do source citations reflect what they were cited for (green) or not (RED)
  • If sources that contradict the statement are suppressed = (RED)
  • Are there “them”, “the others”? Are dissenters or opponents grouped together? (DOUBLE RED)
  • Are negative motives imputed to the opponents / the others? (LARGE DOUBLE RED)

5. Play flip book and look at the colors.
6. Form your own opinion.

The whole thing works quite universally with pretty much all topics. The more controversial a topic is, the easier it is to separate the wheat from the chaff by measuring the degree of populism using the method described above.


  1. Dies ist ein Beispiellink: Dieser Artikel ist eine extrem verkürzte Zusammenfassung des ADxS.org-Kompendiums und enthält daher (fast) keine Quellenangaben. Die einzelnen Kapitel und Beiträge, die die jeweiligen Themen vertieft darstellen, enthalten insgesamt über 5.000 unterschiedliche Quellenangaben, die als direkte Links auf die jeweiligen Fundstellen verweisen. Die meisten Quellenangaben verweisen auf Primärliteratur.

  2. McLennan (2016): Understanding attention deficit hyperactivity disorder as a continuum. Can Fam Physician. 2016 Dec;62(12):979-982. PMID: 27965331; PMCID: PMC5154646.

  3. Speerforck, Hertel, Stolzenburg, Grabe, Carta, Angermeyer, Schomerus (2019): Attention Deficit Hyperactivity Disorder in Children and Adults: A Population Survey on Public Beliefs. J Atten Disord. 2019 Jul 4:1087054719855691. doi: 10.1177/1087054719855691. n = 1.008

  4. Steinhausen, Sobanski in Steinhausen, Rothenberger, Döpfner (2010): Handbuch AD(H)S, Kohlhammer, Seite 158 ff und 165 ff mit etlichen Nachweisen

  5. Leffa, Torres, Rohde (2018): A Review on the Role of Inflammation in Attention-Deficit/Hyperactivity Disorder. Neuroimmunomodulation. 2018;25(5-6):328-333. doi: 10.1159/000489635. mit etlichen Nachweisen

  6. Groenman, Oosterlaan, Rommelse, Franke, Roeyers, Oades, Sergeant, Buitelaar, Faraone (2013), Follow‐up of substance use in ADHD. Addiction, 108: 1503-1511. doi:10.1111/add.12188, n = 1017

  7. Dalsgaard, Østergaard, Leckman, Mortensen, Pedersen (2015): Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study, The Lancet, Volume 385, Issue 9983, 2015, Pages 2190-2196, ISSN 0140-6736, https://doi.org/10.1016/S0140-6736(14)61684-6. n = 1,92 Millionen

  8. Sun, Kuja-Halkola; Faraone, D’Onofrio, Dalsgaard, Chang, Larsson (2019): Association of Psychiatric Comorbidity With the Risk of Premature Death Among Children and Adults With Attention-Deficit/Hyperactivity Disorder. JAMA Psychiatry. Published online August 7, 2019. doi:10.1001/jamapsychiatry.2019.1944, n = 2675615

  9. Shem-Tov, Chodick, Weitzman, Koren (2019): The Association Between Attention-Deficit Hyperactivity Disorder, Injuries, and Methylphenidate. Glob Pediatr Health. 2019 May 5;6:2333794X19845920. doi: 10.1177/2333794X19845920

  10. DiScala, Lescohier, Barthel, Li (1998): Injuries to Children With Attention Deficit Hyperactivity Disorder. Pediatrics, December 1998, VOLUME 102 / ISSUE 6

  11. Grigorian, Nahmias, Dolich, Barrios, Schubl, Sheehan, Lekawa (2019): Increased risk of head injury in pediatric patients with attention deficit hyperactivity disorder. J Child Adolesc Psychiatr Nurs. 2019 Jul 21. doi: 10.1111/jcap.12246.

  12. Romo, Sweerts, Ordonneau, Blot, Gicquel (2019): Road accidents in young adults with ADHD: Which factors can explain the occurrence of injuries in drivers with ADHD and how to prevent it? Appl Neuropsychol Adult. 2019 Jul 16:1-6. doi: 10.1080/23279095.2019.1640697.

  13. Kittel-Schneider, Wolff, Queiser, Wessendorf, Meier, Verdenhalven, Brunkhorst-Kanaan, Grimm, McNeill, Grabow, Reimertz, Nau, Klos, Reif (2019): Prevalence of ADHD in Accident Victims: Results of the PRADA Study. J Clin Med. 2019 Oct 8;8(10). pii: E1643. doi: 10.3390/jcm8101643.

  14. Curry, Yerys, Metzger, Carey, Power (2019): Traffic Crashes, Violations, and Suspensions Among Young Drivers With ADHD. Pediatrics. 2019 Jun;143(6). pii: e20182305. doi: 10.1542/peds.2018-2305.

  15. Raman, Engelhard, Kollins (2019): Driving the Point Home: Novel Approaches to Mitigate Crash Risk for Patients With ADHD. Pediatrics. 2019 May 20. pii: e20190820. doi: 10.1542/peds.2019-0820.

  16. Ghirardi, Larsson, Chang, Chen, Quinn, Hur, Gibbons, D’Onofrio (2019): Attention-Deficit/Hyperactivity Disorder Medication and Unintentional Injuries in Children and Adolescents. J Am Acad Child Adolesc Psychiatry. 2019 Jul 11. pii: S0890-8567(19)30452-6. doi: 10.1016/j.jaac.2019.06.010. n = 1.968.146 AD(H)S-Betroffene

  17. Ghirardi, Chen, Chang, Kuja-Halkola, Skoglund, Quinn, D’Onofrio, Larsson (2019): Use of medication for attention-deficit/hyperactivity disorder and risk of unintentional injuries in children and adolescents with co-occurring neurodevelopmental disorders. J Child Psychol Psychiatry. 2019 Oct 18. doi: 10.1111/jcpp.13136. n = 9.421

  18. Roy, Garner, Epstein, Hoza, Nichols, Molina, Swanson, Arnold, Hechtman (2019): Effects of Childhood and Adult Persistent Attention-Deficit/Hyperactivity Disorder on Risk of Motor Vehicle Crashes: Results From the Multimodal Treatment Study of ADHD. J Am Acad Child Adolesc Psychiatry. 2019 Aug 22. pii: S0890-8567(19)31458-3. doi: 10.1016/j.jaac.2019.08.007.

  19. McCarthy, Cranswick, Potts, Taylor, Wong (2009): Mortality associated with attention-deficit hyperactivity disorder (ADHD) drug treatment: a retrospective cohort study of children, adolescents and young adults using the general practice research database. Drug Saf. 2009;32(11):1089-96. doi: 10.2165/11317630-000000000-00000.

  20. Chen, Chan, Wu, Lee, Lu, Liang, Dewey, Stewart, Lee (2019): Attention-Deficit/Hyperactivity Disorder and Mortality Risk in Taiwan. JAMA Netw Open. 2019 Aug 2;2(8):e198714. doi: 10.1001/jamanetworkopen.2019.8714.

  21. Leibson, Katusic, Barbaresi, Ransom, O’Brien (2001): Use and Costs of Medical Care for Children and Adolescents With and Without Attention-Deficit/Hyperactivity Disorder. JAMA. 2001;285(1):60-66. doi:10.1001/jama.285.1.60

  22. Charach, Yeung, Climans, Lillie (2011): Childhood Attention-Deficit/Hyperactivity Disorder and Future Substance Use Disorders: Comparative Meta-Analyses, Journal of the American Academy of Child & Adolescent Psychiatry, Volume 50, Issue 1, 2011, Pages 9-21, ISSN 0890-8567, https://doi.org/10.1016/j.jaac.2010.09.019

  23. Yeh, Westphal, Hu, Peterson, Williams, Prabhakar, Frank, Autio, Elsiss, Simon, Beck, Lynch, Rossom, Lu, Owen-Smith, Waitzfelder, Ahmedani (2019): Diagnosed Mental Health Conditions and Risk of Suicide Mortality. Psychiatr Serv. 2019 Sep 1;70(9):750-757. doi: 10.1176/appi.ps.201800346.

  24. Fitzgerald, Dalsgaard, Nordentoft, Erlangsen (2019): Suicidal behaviour among persons with attention-deficit hyperactivity disorder. Br J Psychiatry. 2019 Jun 7:1-6. doi: 10.1192/bjp.2019.128. n = 2,9 Millionen

  25. Häge (2018): Psychostimulanzien und medikamentöse Behandlung der ADHS; Curriculum Entwicklungspsychopharmakologie; Potsdam, den 13.09.2018

  26. ZI Mannheim (Download 2019): Flyer Angststörungen

  27. Biederman, Ball, Monuteaux, Surman, Johnson, Zeitlin (2007): Are Girls with ADHD at Risk for Eating Disorders? Results from a Controlled, Five-Year Prospective Study. Journal of Developmental & Behavioral Pediatrics: August 2007 – Volume 28 – Issue 4 – p 302-307. doi: 10.1097/DBP.0b013e3180327917

  28. Biederman, Ball, Monuteaux, Mick, Spencer, McCreary, Cote, Faraone (2008): New Insights Into the Comorbidity Between ADHD and Major Depression in Adolescent and Young Adult Females, Journal of the American Academy of Child & Adolescent Psychiatry, Volume 47, Issue 4, 2008, Pages 426-434, ISSN 0890-8567, https://doi.org/10.1097/CHI.0b013e31816429d3

  29. Miller, Ancoli-Israel, Bower, Capuron, Irwin (2008): Neuroendocrine-Immune Mechanisms of Behavioral Comorbidities in Patients With Cancer; J Clin Oncol. 2008 Feb 20; 26(6): 971–982. doi: 10.1200/JCO.2007.10.7805, PMCID: PMC2770012, NIHMSID: NIHMS147295

  30. Barkley (2018): Vortrag an der Universität Göteborg, ca. Minute 75

  31. Goldstein, Rasmusson, Bunney, Roth (1994): The NMDA glycine site antagonist (+)-HA-966 selectively regulates conditioned stress-induced metabolic activation of the mesoprefrontal cortical dopamine but not serotonin systems: a behavioral, neuroendocrine, and neurochemical study in the rat. Journal of Neuroscience 1 August 1994, 14 (8) 4937-4950; DOI: https://doi.org/10.1523/JNEUROSCI.14-08-04937.1994

  32. Volkow, Wang, Newcorn, Kollins, Wigal, Telang, Fowler, Goldstein, Klein, Logan, Wong, Swanson (2011): Motivation deficit in ADHD is associated with dysfunction of the dopamine reward pathway; Mol Psychiatry. 2011 Nov;16(11):1147-54. doi: 10.1038/mp.2010.97. Epub 2010 Sep 21.