He gets to the Reece committee around 15:00 but the first part is worth a listen too.
If you’re not familiar with the “Hispanic Paradox”, see the wikipedia page here: http://en.wikipedia.org/wiki/Hispanic_paradox
(read at least the first 2 paragraphs). The basic idea is that overall health statistics are normally positively correlated with wealth and income, but this correlation breaks down with hispanic immigrants to the USA. Note that the anomaly also applies to european immigrants to the USA.
Urban poor aging faster at cellular level – study
New blood tests show that poor populations in urban areas of the United States are actually aging faster at the cellular level than others, thanks to chronic stress connected to income and identity, according to a new study by scientists.
Conducted on a small group of black, white and Mexican adults in three Detroit neighborhoods, the tests were an attempt by scientists to learn what contributed to early aging-related diseases and excessive mortality rates in the urban poor. …
The Stanford study marks the first collaboration between science and social research that measures telomeres – the caps on chromosomes that protect them from deteriorating…..
They found poor whites had the shortest [telomeres] compared to nonpoor whites, and that poor and lower middle class blacks had equivalent [telomeres]. But poor Mexicans had longer telomeres than Mexicans with higher incomes. …
… Our small sample size precluded disaggregating
the Mexican population by nativity for statistical
analyses, but we note that Mexicans in the nonpoor
group were disproportionately U.S. born, while
those in the poor group were disproportionately foreign born. …
Race-Ethnicity, Poverty, Urban Stressors, and Telomere Length in a Detroit Community-based Sample; Journal of Health and Social Behavior April 30, 2015
Childhood Trauma Associated with Short Telomere Length
Post-traumatic stress disorder (PTSD) is associated with increased risk for age-related diseases and early mortality. An accelerated rate of biological aging could contribute to this increased risk. To investigate, we assessed leukocyte telomere length (LTL), an emerging marker of biological age, in men and women with and without PTSD. We also examined childhood trauma, a risk factor for both PTSD and short LTL, as a potential contributor to short LTL in PTSD.
Participants included 43 adults with chronic PTSD (n=18 with multiple categories of childhood trauma) and 47 controls (none with multiple categories of childhood trauma) (M age = 30.55, SD = 7.44). Exclusion criteria included physical illness, medication use, obesity, alcohol or substance abuse, and pregnancy. Structured clinical interviews were conducted to assess PTSD and other psychiatric disorders and childhood trauma exposure. LTL was measured with quantitative polymerase chain reaction.
As predicted, participants with PTSD had shorter age-adjusted LTL than controls. Exposure to childhood trauma was also associated with short LTL. In fact, childhood trauma appeared to account for the PTSD group difference in LTL; only participants with PTSD and exposure to multiple categories of childhood trauma had significantly shorter LTL than controls.
Childhood trauma is associated with short LTL in individuals with PTSD. Chronic exposure to the psychobiological sequelae of childhood trauma could increase risk for PTSD and short LTL. Thus, the lasting psychological impact of exposure to trauma in childhood may be accompanied by equally enduring changes at the molecular level.