Spinach vs. Easter Grass

The Tennessee Pre-K Debate: Spinach Vs. Easter Grass
September 29, 2015

“It’s like saying spinach is really good for you,” Farran says, “but we can’t afford spinach. But here, I’ve got this Easter grass. Maybe that will be just as good.”

That’s right, Easter grass — that shiny, plastic stuff you layer into an Easter basket.

Psychological Distress Across the Life Course and Cardiometabolic Risk

Psychological Distress Across the Life Course and Cardiometabolic Risk
Findings From the 1958 British Birth Cohort Study
Ashley Winning, ScD, MPH, et al.
J Am Coll Cardiol. 2015;66(14):1577-1586.

Background  Research suggests cardiovascular and metabolic diseases are influenced by psychological distress in adulthood; however, this research is often limited to adult populations and/or a snapshot measure of distress. Given emerging recognition that cardiometabolic diseases have childhood origins, an important question is whether psychological distress earlier in life influences disease development.

Objectives  This study sought to assess whether life course patterns of psychological distress assessed from childhood through adulthood predict biomarkers of cardiometabolic risk in adulthood and whether effects of sustained distress differ from more limited exposure.

Methods  The sample (n = 6,714) consists of members of the 1958 British Birth Cohort Study who completed repeated measures of psychological distress and a biomedical survey at age 45 years. Psychological distress profiles over the life course (no distress, childhood only, adulthood only, or persistent distress) were identified from 6 assessments between ages 7 and 42 years. Cardiometabolic risk was assessed by combining information on 9 biomarkers of immune, cardiovascular, and metabolic system function. Covariate adjusted linear regression models were used to assess associations between distress profiles and cardiometabolic risk.

Results  Compared with those with no distress, cardiometabolic risk was higher among people with psychological distress in childhood only (β = 0.11, SE = 0.03, p = 0.0002), in adulthood only (β = 0.09, SE = 0.03, p = 0.007), and persistent across the life course (β = 0.26, SE = 0.04, p < 0.0001).

Conclusions  Psychological distress at any point in the life course is associated with higher cardiometabolic risk. This is the first study to suggest that even if distress appears to remit by adulthood, heightened risk of cardiometabolic disease remains. Findings suggest early emotional development may be a target for primordial prevention and for promoting lifelong cardiovascular health.

journalistic version

There is no safe level of lead exposure

High Lead Levels In Michigan Kids After City Switches Water Source
September 29, 2015

… He’d been tested before the city switched its water source. At that time, he had a level of 2 micrograms of lead per deciliter of blood. After the switch, his level was 6.5.

The Centers for Disease Control and Prevention says a level of 5 is considered “much higher” than that found in most children. It also says there is no safe level of lead exposure — and the effects, like lower IQ, are irreversible.

… researchers from Virginia Tech found that Flint River water is highly corrosive. That means when it comes into contact with lead from service lines, household pipes or solder, it eats away at the lead and sends it right to people’s faucets.
[In 1986 lead pipes were banned.]

City officials and state regulators say they’re now putting together a corrosion control plan to reduce lead exposure.

Doctor Who Discovered Children Had Elevated Lead Levels Talks About What’s Changed
September 17, 2017

Dr. Hanna-Attisha

we’re surrounding our kids with science, with evidence-based interventions that we know promote development and can mitigate the impact of lead.

universal preschool.
Every kid in Flint gets a book mailed to them every month from the ages of 0 to 5.

early literacy and early intervention. And we have universal preschool


Perceived intensity for sweeteners decreases 2–5% per year

A Common Genetic Influence on Human Intensity Ratings of Sugars and High-Potency Sweeteners
Twin Research and Human Genetics / Volume 18 / Issue 04 / August 2015, pp 361-367
Liang-Dar Hwanga, et al

The perception of sweetness varies among individuals but the sources of this variation are not fully understood. Here, in a sample of 1,901 adolescent and young adults (53.8% female; 243 MZ and 452 DZ twin pairs, 511 unpaired individuals; mean age 16.2 ± 2.8, range 12–26 years), we studied the variation in the perception of sweetness intensity of two monosaccharides and two high-potency sweeteners: glucose, fructose, neohesperidine dihydrochalcone (NHDC), and aspartame. Perceived intensity for all sweeteners decreased with age (2–5% per year) and increased with the history of otitis media (6–9%). Males rated aspartame slightly stronger than females (7%). We found similar heritabilities for sugars (glucose: h2 = 0.31, fructose: h2 = 0.34) and high-potency sweeteners (NHDC: h2 = 0.31, aspartame: h2 = 0.30); all were in the modest range. Multivariate modeling showed that a common genetic factor accounted for >75% of the genetic variance in the four sweeteners, suggesting that individual differences in perceived sweet intensity, which are partly due to genetic factors, may be attributed to a single set of genes. This study provided evidence of the shared genetic pathways between the perception of sugars and high-potency sweeteners.

cited by:

We don’t accept talk like that here

House Calls To The Homeless: A Doctor Treats Boston’s Most Isolated Patients
September 29, 2015

I remember one night I was struggling. Some man had come in – this is early on – some man had come in and said he was going to kill himself. And I was in the shelter clinic. And I – that’s an alarm for all of us in medicine, … Barbara came in, and she looked at the man and she said, so what’s going on?
He said well, I’m going to kill myself. And she said well, we don’t accept talk like that here in the clinic. If you want to talk like that, please go outside in the alley and talk to whoever you want about it, but we don’t talk like that.
And I was horrified that you don’t do that. And then as I learned later, Barbara had known this man for years, knew exactly where he was coming from. She knew how to handle him. And in fact, all he was looking for was some reassurance and that people knew him, and that was the way out.
And I started to realize there’s many, many ways to take care of homeless people, and the best ones are based on who knows that person best and who knows how to handle them best.

Subclinical delusional thinking

Subclinical delusional thinking predicts lateral temporal cortex responses during social reflection
Soc Cogn Affect Neurosci (2014)   9  (3):  273-282.
Benjamin K. Brent

Neuroimaging studies have demonstrated associations between delusions in psychotic disorders and abnormalities of brain areas involved in social cognition, including medial prefrontal cortex (MPFC), posterior cingulate cortex, and lateral temporal cortex (LTC).
General population studies have linked subclinical delusional thinking to impaired social cognition, raising the question of whether a specific pattern of brain activity during social perception is associated with delusional beliefs.

Here, we tested the hypothesis that subclinical delusional thinking is associated with changes in neural function, while subjects made judgments about themselves or others [‘social reflection’ (SR)]. Neural responses during SR and non-social tasks, as well as resting-state activity, were measured using functional magnetic resonance imaging in 22 healthy subjects. Delusional thinking was measured using the Peters et al. Delusions Inventory.

Delusional thinking was negatively correlated with responses of the left LTC during SR (r = −0.61, P = 0.02, Bonferroni corrected), and connectivity between the left LTC and left ventral MPFC, and was positively correlated with connectivity between the left LTC and the right middle frontal and inferior temporal cortices. Thus, delusional thinking in the general population may be associated with reduced activity and aberrant functional connectivity of cortical areas involved in SR.

Key words:
lateral temporal cortex
default mode network

Ketamine-induced psychosis

Individual Differences in Psychotic Effects of Ketamine Are Predicted by Brain Function Measured under Placebo
The Journal of Neuroscience, 18 June 2008,  28(25): 6295-6303
Garry D. Honey, et al.

The symptoms of major psychotic illness are diverse and vary widely across individuals.
Furthermore, the prepsychotic phase is indistinct, providing little indication of the precise pattern of symptoms that may subsequently emerge.
Likewise, although in some individuals who have affected family members the occurrence of disease may be predicted, the specific symptom profile may not.
An important question, therefore, is whether predictive physiological markers of symptom expression can be identified.
We conducted a placebo-controlled, within-subjects study in healthy individuals to investigate whether individual variability in baseline physiology, as assessed using functional magnetic resonance imaging, predicted psychosis elicited by the psychotomimetic drug ketamine and whether physiological change under drug reproduced those reported in patients.
Here we show that brain responses to cognitive task demands under placebo predict the expression of psychotic phenomena after drug administration.
Frontothalamic responses to a working memory task were associated with the tendency of subjects to experience negative symptoms under ketamine.
Bilateral frontal responses to an attention task were also predictive of negative symptoms.
Frontotemporal activations during language processing tasks were predictive of thought disorder and auditory illusory experiences.
A subpsychotic dose of ketamine administered during a second scanning session resulted in increased basal ganglia and thalamic activation during the working memory task, paralleling previous reports in patients with schizophrenia.
These results demonstrate precise and predictive brain markers for individual profiles of vulnerability to drug-induced psychosis.

We used a drug model of psychosis to relate presymptomatic physiology to symptom outcome.
Ketamine induces transient psychotic symptoms in healthy volunteers (Krystal et al., 1994) …


Ketamine-Induced Loss of Phenotype of Fast-Spiking Interneurons Is Mediated by NADPH-Oxidase
Science 7 December 2007: Vol. 318  no. 5856  pp. 1645-1647
M. Margarita Behrens

Abuse of the dissociative anesthetic ketamine can lead to a syndrome indistinguishable from schizophrenia.
In animals, repetitive exposure to this N-methyl-d-aspartate–receptor antagonist induces the dysfunction of a subset of cortical fast-spiking inhibitory interneurons, with loss of expression of parvalbumin and the γ-aminobutyric acid–producing enzyme GAD67.
We show here that exposure of mice to ketamine induced a persistent increase in brain superoxide due to activation in neurons of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.
Decreasing superoxide production prevented the effects of ketamine on inhibitory interneurons in the prefrontal cortex. These results suggest that NADPH oxidase may represent a novel target for the treatment of ketamine-induced psychosis.


Ketamine-Induced Exacerbation of Psychotic Symptoms and Cognitive Impairment in Neuroleptic-Free Schizophrenics
Neuropsychopharmacology (1997) 17 141–150.
Anil K Malhotra MD, et al.

The N-methyl-d-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia.
We administered subanesthetic doses of the NMDA receptor antagonist ketamine in a double-blind, placebo–controlled design to 13 neuroleptic-free schizophrenic patients to investigate if schizophrenics will experience an exacerbation of psychotic symptoms and cognitive impairments with ketamine.
We also examined whether schizophrenics experienced quantitative or qualitative differences in ketamine response in comparison to normal controls.
Schizophrenics experienced a brief ketamine-induced exacerbation of positive and negative symptoms with further decrements in recall and recognition memory. They also displayed greater ketamine-induced impairments in free recall than normals. Qualitative differences included auditory hallucinations and paranoia in patients but not in normals.
These data indicate that ketamine is associated with exacerbation of core psychotic and cognitive symptoms in schizophrenia.
Moreover, ketamine may differentially affect cognition in schizophrenics in comparison to normal controls.

Keywords: Ketamine; NMDA; Schizophrenia; Cognition; Psychosis