Children's Health Defense By
The Defender’s Weekly Science Digest delivers a roundup of the latest research on children’s health, including studies on vaccines, drugs, chemicals, pesticides and lead exposure.
Epstein-Barr causes MS but requires help
Gene–environment interactions: Epstein–Barr virus infection and risk of pediatric-onset multiple sclerosis; Multiple Sclerosis Journal, Feb. 9, 2024.
Epstein-Barr virus (EBV) infection is a leading cause of adult and pediatric multiple sclerosis (MS), but the mechanism is unclear.
Researchers affiliated with the Network of Pediatric Multiple Sclerosis Centers sought to explain how a viral infection nearly every human gets affects only 0.3% of the population in that manner.
Investigators examined data from 473 pediatric MS cases and 702 controls from the Environmental and Genetic Risk Factors for Pediatric MS study. Although their study failed to answer the question of causation it uncovered new additive relationships between prior EBV infection, type of anti-EBV response and two genetic risk factors associated with susceptibility to MS.
First, individuals with MS were more than 50% more likely (94.6% vs. 60.7%) to have antibodies to the virus’ capsid antigen, which is normally a sign of a new or active infection.
Second, previously infected subjects whose immune cells carry one specific gene family, DRB1*15, were 10 times as likely to develop MS as individuals with prior infection or the DRB1*15 gene alone. Having multiple DRB1 genes multiplied the effect.
One form of DRB1*15, DRB1*15:01, has a strong association with MS and may be considered a “genetic predisposition” for the disease. For example, DRB1*15:01 was found in all MS-affected members of one Italian family and 4 of 5 unaffected family members.
Finally, prior infection plus one specific mutation in the CD86 gene, which regulates antibody production, results in a 30% increased risk for pediatric MS.
So while genes play a role, EBV infection appears to be a necessary precondition for developing MS.
Inflammation during pregnancy may predict child’s depression
Sex-Specific Pathways From Prenatal Maternal Inflammation to Adolescent Depressive Symptoms; JAMA Psychiatry, Feb. 7, 2024.
A long-term observational study found a positive association between prenatal maternal inflammation (PNMI) and depressive symptoms in adolescent offspring years later.
Investigators evaluated frozen blood samples, collected from 674 pregnant women between June 1959 and September 1966, for four cytokine markers of PNMI associated with psychiatric symptoms: interleukin-6 (IL-6), IL-8, IL-1RA and soluble tumor necrosis factor receptor-II (sTNF-RII).
Then, between 1977 and 1979 (corresponding to children ages 15-17), mothers completed a 100-item questionnaire on their children’s behavior during childhood. The children completed self-evaluation surveys. Of 675 offspring remaining in the study, 350 were male.
Of particular interest were “internalizing” and “externalizing” symptoms — psychiatric shorthand for maladaptive behaviors involving self (withdrawal, anxiety, depression) or interactions with one’s social environment (aggression, impulsivity, hyperactivity), respectively.
Researchers expected inflammatory markers to have greater predictive power for boys than girls. They found instead that both sexes were affected but in different ways.
They found that elevated IL-6 during the first trimester was associated with childhood externalizing symptoms in males, while IL-6 levels during the second trimester predicted internalizing symptoms in females.
Investigators also found an association between second-trimester IL-1RA levels and internalizing symptoms, but only in females…
READ FULL ARTICLE HERE… (childrenshealthdefense.org)
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