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The ADHD Explosion Part 1: Causes, Models, Rising Prevalence, and Policy Implications Stephen P. Hinshaw University of California, Berkeley Help Group.

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Presentation on theme: "The ADHD Explosion Part 1: Causes, Models, Rising Prevalence, and Policy Implications Stephen P. Hinshaw University of California, Berkeley Help Group."— Presentation transcript:

1 The ADHD Explosion Part 1: Causes, Models, Rising Prevalence, and Policy Implications Stephen P. Hinshaw University of California, Berkeley Help Group Summit 10/17/14


3 ADHD: Key Themes  Newsworthy  Cause of ADHD is SpongeBob Square Pants  Cause of ADHD is starting kindergarten at age 4  Stimulants lead to heart attacks  New York Times 2012/2013 opinion pieces:  Sroufe, Kureishi, Friedman, Brooks: Back to the past  Too much of the news and opinion is mythical (see subtitle of book)

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5 Facts  ADHD is a neurodevelopmental disorder with high genetic liability  ADHD incurs huge costs to those with high levels of symptoms  All too few people with ADHD have excellent life outcomes—if it’s a gift, in the words of Ned Hallowell, it’s hard to unwrap

6 Myths  Medications are poisons, destroying developing brains  Meds help in 80% of cases  May actually be neuroprotective for youth with ADHD  Medication alone is a sufficient treatment  Need family/school intervention for skill building  SEE PART 2 TOMORROW!  ADHD can be assessed and diagnosed in a 10’ office visit  Yet this, far too often, is the national standard  Results in both overdiagnosis and underdiagnosis

7 Impairment  Academic (school failure)/Vocational  $100 billion/year (youth) indirect costs (justice, sp. ed, SUD)  $200 billion annually (adults) indirect costs (job problems)  Social/peer (most peer-rejected condition)  Family (reciprocal chains of bidirectional influences)  Accidental injury (across the age span)  Impairment often independent of comorbidity…AND key comorbidities don’t respond optimally to ADHD tx  E.g., LD, delinquency, depression

8 DSM-5 vs. RDoC  DSM-5 changes:  Neurodevelopmental disorder  Types (Inattentive, HI, Combined) now ‘presentations’  Adult examples of most symptoms  Age of onset of impairing symptoms: < 12 years, not < 7  **Each successive edition of DSM has loosened criteria somewhat, which is one reason for “ADHD explosion”  Research Domains Criteria  Dimensional, multiple levels (genes to culture)  Search for underlying mechanisms

9 ADHD Cross Culturally  Appears in nearly all cultures (that feature compulsory education)  Polanczyk et al. (2007), AJP:  Diagnostic prevalence strikingly similar across world regions: 5%  Disparities linked to dx practices (ICD vs. DSM; informants; etc  Hinshaw et al. (2011)  Within-country variation high in many nations  However, treatments and systems of care vary radically across regions and cultures  MANY NATIONS ‘CATCHING UP’ WITH U.S. MEDICATION TRENDS  But some not: politics, history, penetration of Big Pharma

10 Nature of ADHD: Models  “Cognitive” models: Attention deficit, EF  “Inhibitory” models: Barkley (1997)  “Motivation” models: Reward undersensitivity  E.g., Volkow et al. (2009): large medication-naïve adult sample, PET scans of transporters and receptors

11 (Attention) (Motivation) (Attention) (Motivation)

12 (Attention) (Motivation) Transporter PET Image

13 Combination Models  Sonuga-Barke et al. (2010):  Top-down executive control  Bottom-up delay aversion  Time management  ADHD clearly implicates multiple brain regions and paths for different facets of symptomatology

14 Neural profiles  Structural/anatomical:  Overall lowered cerebral volume; caudate, cerebellum…  Key research: Shaw et al. (2006, 2007, 2009, 2012)  Delayed patterns of cortical thickening/thinning in ADHD vs. comparison samples, longitudinally  Roughly 3 year delay for ADHD groups: Immaturity come to life  Immaturity persists; thickness correlated with symptoms  Functional: Frontal-striatal paths  Until recently: must ‘scan’ during active cognitive performance  Default mode: reliable differences when S’s not ‘doing anything’; more ‘intrusions’ into task performance in ADHD

15 ADHD: Causes  Heritability and Genes:  H 2 of ADHD near.8  **What is heritability?  ‘genetic liability,’ but not inevitability  Too often, assumption is that ADHD is ‘fixed’ and largely immutable  PKU example  Height example  IQ example

16 Which genes?  Seemed a simple question years ago: Genes related to dopamine systems and pathways in brain  But any single gene variant explains only a tiny fraction of “ADHD-ness”  ‘Dark matter’ of genetics: missing heritability!  Recent discoveries: genes conferring risk for ADHD are SAME as those conferring risk for schizophrenia, mood disorders, and autism  MUST BE that early influences are epigenetic

17 Other Risk Factors  Low birthweight  Predicts ADHD, LD, Tourette’s, CP, retardation  Teratogenic effects  FAE: Many are nearly identical to ADHD symptoms  Smoking/nicotine: genetic mediation, too  Early parenting: No consistent evidence as causal  Middle-class; few prospective studies from early years  Insecure attachment?  Does NOT predict later ADHD, independent of comorbid aggression

18 Risk Factors: Equifinality  Carlson et al. (1995):  In low-income sample, early maternal insensitivity predictive of ADHD symptoms to a greater extent than early temperament  Need genetically informative design  Institutional deprivation (Kreppner et al., 2001)  English and Romanian Adoptive Study Team: Inattention/overactivity associated with length of severe institutional deprivation in first 4 years  Specific effect: Conduct problems and internalizing symptoms not similarly associated with deprivation  Yet, different “feel” from typical ADHD presentation  AND, EF deficits may be distinct from ‘typical’ ADHD presentation  Hence, equifinality apparent


20 Role of Parenting  Maintaining cause, if not primary cause  Parents tend to fight fire with fire  Coercive discipline (too lax, too harsh)  Cycles of dysregulated emotion  Given heritability of ADHD, parents likely to have ADHD symptoms themselves  Parent management: PART 2, TOMORROW!

21 Important New Findings Harold et al. (2013a, 2013b)  Adoption study in UK  Controls for biological relatedness  Even in adoptive families, kids’ levels of ADHD elicit overcontrolling parenting from parents  AND, levels of harshness predict further ADHD symptoms, over time  It’s not all in the genes!

22 Ultimate cause?  The “real” cause of ADHD has to be compulsory education (same as for LD)  Certainly, ‘attention’ or ‘impulse control’ genes have been around for the history of our species, but extremes not salient until we made children sit and learn to read  If it’s true that achievement pressure “reveals” ADHD, is it also true that current high rates of pressure are fueling the recent explosion?

23 Developmental Paths  Infancy/temperament:  Activity level vs. effortful control  Preschool Manifestations (S. Campbell)  Careful evaluations of 3 and 4 year olds  See AAP Guidelines (2011)  Prospective predictions to mid-late childhood:  PPP =.5! Hence, multifinality apparent  That is, suggestions of (a) “he’ll grow out of it” and (b) “medicate today” are each fraught with error  Predictors of continuation:  (a) severity of early ADHD  (b) negativity of early parent/child interaction, controlling for severity of child’s ADHD

24 Parenting Influences on Positive Peer Status Hinshaw, Zupan, et al. (1997)  Aim: Predict peer acceptance from parenting  Ideas About Parenting (Heming et al., 1989)  3 factors = Authoritarian, Authoritative, Permissive  Authoritative Factor: 15 items  Warmth, Limits, Autonomy Encouragement--e.g.,  “ I encourage my child to be independent of me”  “I expect a great deal of my child”  “I have clear, definite ideas about childrearing”  “Raising a child is more pleasure than work”  “When I am angry with my child, I let him know”  “I reason with my child regarding misbehavior”


26 Results  Mothers of ADHD boys: lower on Authoritative  ES =.75  Yet variance in ADHD group equivalent to comparisons  Tested predictive power of parenting factors, observed overt and covert behavior, and internalizing score (CDI, observed withdrawal) via hierarchical regressions  Neither Authoritarian nor Permissive beliefs predicted peer nominations, but Authoritative beliefs did so (beta =.3), even with diagnostic group controlled

27 Explained Variance in Positive Nominations

28 Moderation and Implications  Prediction applies only to ADHD group (beta =.30); for comparisons, beta =.00.  Key theme: “firm yet affirming” parenting style

29 Sex Differences/Female Presentation More in Part 2, tomorrow  Another myth: ADHD effects only boys!  Our sample (BGALS):  Largest in existence of preadolescent girls with ADHD (140, with 88 matched comparison girls)  Baseline: marked impairments across symptoms, impairments, neuropsych measures  Impairments maintained at 5-year follow-up  11/11 domains, with widening gap in math  Sources: Hinshaw (2002); Hinshaw et al. (2006), Journal of Consulting and Clinical Psychology 

30 10-year follow-up  95% retention rate (vs. 92% at 5 year)  How? Facebook, relentless staff  Despite ‘losing’ ADHD status majority of time, impairments maintain in academics, comorbidities, social functioning.  Yet, self-harm findings: Different adolescent path for girls??  Suicide attempts: 22% ADHD-C 8% ADHD-I 6% comparisons  NSSI: 51% ADHD-C 29% ADHD-I 19% comparisons

31 BGALS Follow-up: Self-harm 10-year follow-up (M age = 20) Hinshaw et al. (2012), Journal of Consulting and Clinical Psychology

32 Conclusions  ADHD not a static “entity”  Different pathways lead to ADHD: Equifinality  Differential outcomes from early ADHD symptoms: Multifinality  What predicts, moderates, mediates differential outcomes?  Peer deficits and social skills; EF deficits; Motivation  Developmental, contextual factors crucial  Parenting styles, which may not be causal, are important determinants of outcome, even for a condition with h 2 =.7/.8  Systems, health-care, legislative, cultural, stigma-related factors related to underutilization and disparities in care

33 Assessment Full coverage requires a day-long workshop  Brief visit: false positives and false negatives  Must get informant ratings, for kids, teens, or adults  Brief/narrow vs. broader scales  Ideal to get info from past as well as present teacher  Must get full developmental history  Must appraise rule-out and comorbid conditions  LD, Anxiety, Depression, etc. require different interventions

34 Tidal Wave/ADHD Explosion National Survey of Children’s Health (Visser et al., 2013) Tidal Wave/ADHD Explosion National Survey of Children’s Health (Visser et al., 2013)  Parent-reported ADHD ‘ever diagnosed’  For all 4-17 year olds in U.S.:  2003: 7.8% 2007: 9.5% 2012: 11.0%  > 40% INCREASE IN 9 YEARS!  Low income rates now = middle class; Black = White  Hispanic lower (but fast growing)  Medication higher, too:  Just under 70% of those ‘currently diagnosed ‘now receive medication  From other sources: Largest medication increases: adolescents, adults

35 Earlier Explosions: 1990s  Policy shifts:  IDEA: ADHD as OHI  Medicaid: authorizes ADHD  SSI: ADHD (with other impairment) can qualify  Late 1990s: FDA changes regs on DTC ads  2000: Concerta (first effective long-acting form)  More and more LBW babies survive

36 Huge Regional Variation Now  Rise across entire nation, but major-league state-by-state variation, too  :  Arkansas now #1, Indiana #2, NC #3  NC had been #1 in 2007  Medication trends similar to 2007, but slightly higher overall

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39 What does not explain variation  Demographics  Hispanic population clearly higher in California, and traditionally the lowest rates of diagnosis  Eliminated a little of the CA-NC difference but not most  **Hispanic rates growing FAST, esp. in California  Rates of health-care providers  Explains other disorders, but not here  State “culture”  May explain regional differences within state -- but not state-by-state per se

40 ** Consequential accountability  1970s-80s: public school reforms “input focused”  Reduce class size, pay teachers more, etc.  Results not consistent; shift in 1990s to “output focused”  I.e., incentivize test score improvements per se  Consequential accountability—districts get ‘noted’ or even cut off from funds, unless test scores go up  30 states implement such laws <2000  Then, becomes law of the land for all states with No Child Left Behind (takes effect )

41 41 Consequential accountability laws prior to NCLB (but not psychotropic medication laws): In the South Sources: Investigators' Research, Dee & Jacob 2011, Dee & Jacob 2006, and Center for Education Policy

42 Findings From “triple difference” model  Between , in the 20 “NCLB states,” poorest children showed huge increases in ADHD Dx:  In these states, 59% increase in ADHD dx for kids within 200% of FPL  vs. only 8% in middle- or upper-class kids  Nothing like that in states with previous consequential accountability (all kids in those states went up 20% or so)  Nothing like that in private schools  This trend reverses by 2012, with Obama’s dismantling of NCLB

43 Consequential accountability introduced via NCLB was associated with higher ADHD diagnostic prevalence increases among low- income children aged 8-13 from , but there was no association from (unadjusted results) District of Columbia is included within the 21 No Child Left Behind consequential accountability states. NCLB: No Child Left Behind; FPL: Federal poverty level N=24,982 (2003), 22,467 (2007), 24,426 (2011) Sources: 2003, 2007, and 2011 National Survey of Children’s Health

44 “Unintended effect”  Accountability laws encourage ADHD diagnosis for at least two reasons:  #1: Diagnosis may lead to treatment, which may help boost achievement test scores  Scheffler et al. (2009), Zoega et al. (2012)  #2: In some states/districts, diagnosed youth are excluded from the district’s average test score!  Gaming the system, although NCLB eventually outlaws this  Why poorest kids? NCLB targets Title I schools

45 Psychotropic medication laws  In 2001, Connecticut passed a law ‘pushing back’ against rising ADHD medication use in students  By now, 14 states have passed such “psychotropic medication laws,” of one or more of 3 types:  Schools are prohibited from recommending meds  Schools cannot require meds as a condition of enrollment  Parental refusal to medicate the child cannot, in and of itself, be considered neglect  IN THESE STATES, NO RISE IN ADHD DIAGNOSES FROM , VS. > 50% RISE IN OTHER STATES

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47 Findings  In the 14 states with these laws, essentially no change in ADHD diagnostic prevalence between 2003 and 2011, versus a > 50% increase in other states!

48 Where have we been?  ADHD requires multi-level thinking  Genes matter  Families matter  Cultural values placed on performance matter  Educational policies matter  Pharma matters  ADHD is too important and too impairing to think about it reductionistically  When kids, learning, schools, productivity, and medicating young minds are in play, stakes are high

49 Diversion (Part 2 tomorrow)  Define: non-prescription use  Rates extremely high (why??)  How effective are stimulants as ‘neuroenhancers’ for general population?  Smith & Farah (2011), Psychological Bulletin  Ilieva et al. (2013), Neuropharmacology  Rates of abuse/addiction: Policy implications

50 Thanks…  NIMH and NIDA grants  Robert Wood Johnson Policy Investigator Award  Participants in many studies  The Help Group  You, the audience

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