What Causes ADHD?: Understanding What Goes Wrong and Why by Joel T. Nigg Phd

Author:Joel T. Nigg Phd
Language: eng
Format: mobi
ISBN: 9781606233528
Publisher: The Guilford Press
Published: 2006-05-08T21:00:00+00:00

Question

Answer

Does faulty parenting cause ADHD?

No, but is related to aggression.

How common is ADHD with fetal

Probably 2–4% of cases.

alcohol problems?

Could prenatal smoking be a cause of

Possibly yes; evidence is still

ADHD?

accumulating.

Is lead poisoning a cause of ADHD?

Yes; findings on the magnitude of low-

level effects are still emerging.

How many cases are caused by lead?

Perhaps 2–4% by today’s standards,

but potentially as many as 12–15% if

lower-level lead exposures prove to be

important in ADHD.

Can we relax now about lead and

No. Children remain at substantial

mercury?

risk.

Why would ADHD be increasing? a

One reason might be the increased

survival of children with LBW.

Is LBW associated with ADHD?

Yes; a two- to fourfold risk increase

occurs with LBW.

a It is actually unclear whether ADHD incidence is increasing.

The key suggestion is to take a careful history to rule out significant

traumatic events; this should include asking the child about thoughts

that distract him of her, and interviewing multiple informants.

Finally, several questions that clinicians are often asked to address

have been answered in this chapter. The most significant or frequently

asked of these are summarized in Table 10.6.

CONCLUSIONS AND FUTURE DIRECTIONS

What we can conclude, cautiously, at this point is that several known

prenatal exposures (most importantly heavy alcohol use and possibly

cigarette use), perinatal problems (most notably LBW), and postnatal

exposures (most notably high- and low-level lead exposures) may each

increase to a small extent a child’s chances of developing ADHD, and

probably do so via causal action on the developing brain. A conserva-

tive to generous range of estimates would be that elimination of all of

these causes would reduce ADHD incidence by 10–15% (see Table

10.7). The estimates would go much higher if it is determined that low-

| Uncommon Experiential Risk Factors |

263

level lead exposure leads to increased risk of ADHD by even a small

margin, either via direct effects or via genotype–environment interac-

tions. Whether the target range is 10–15% or whether it ultimately

goes higher, this is a target well worth pursuing in view of the prevent-

able nature of these experiential agents. Encouragingly, with the excep-

tion of nonspecific LBW, alcohol, cigarette, and lead exposures are in

decline (at least in the United States) because of public health efforts to

address these issues. These efforts are to be encouraged, and it is to be

hoped that other toxicants will be targeted for more aggressive scrutiny

and for elimination from children’s environments.

Note that some of these cases would represent genotype–

environment correlations, in which the early brain injury is mediating

a genetic effect (e.g., maternal ADHD → smoking → fetal neural in-

jury → child ADHD → smoking). All the same, some of these effects

are doubtless being picked up by the nonshared environment term in

twin studies, the value of which ranges around 25–30%. Although

some effects in this table may prove high estimates (e.g., the smoking

effect apart from LBW and genetic effects may be smaller), others may

well prove low estimates (e.g., low-level lead effects appear increasingly

likely in ADHD, yet are excluded entirely from the table). In all, these

effects appear well positioned to help us begin to understand the

nonshared environment effects in the etiology of ADHD.

We also know that extreme psychological trauma early in life can

cause an ADHD syndrome.

Download

Copyright Disclaimer:
This site does not store any files on its server. We only index and link to content provided by other sites. Please contact the content providers to delete copyright contents if any and email us, we'll remove relevant links or contents immediately.