At my age, as I decrease my workload and capacity, I realize that I will not be able to do it all. Over the years, I wrote in my notebook some thoughts and idea for research that I cannot and will not accomplish with the small research group that I’m part of.

I therefor decided to share these ideas with everyone who is interested in pediatric endocrine research.

You are free to use the ideas and to test them in your own clinics and laboratories. You don’t have to inform me when you pick anything from this list, as long as you are serious and honest about your research intentions. Feel free to discuss them with me if you so wish at but this is not required. You may wish to acknowledge this webpage.

From time to time, I will add a new thought for the community to freely utilize them.

1. The infancy childhood transition (ICT) has a major role in programming the adult height. The earlier the ICT the taller a child will be. We have shown that the IT is not genetically set (using a twins’ study). So, how is the ICT programmed for? What are the signals? We had the feeling that it is mostly set by the adiposity - at what age? And may be by growth velocity during a period before the ICT – what period?

2. Some years ago, we started a study that never finished showing that when children go to a kindergarten, during the normal age range for ICT (6-12m) they have a delayed ICT and end up shorter when they get to be 2 y o. I assumed that the reason being that during acute febrile illness or gastroenteritis, which the children undergo so often when they start kindergarten, ICT will be postponed. – is it true? -is it related the inflammatory process? Also at age 9 months the child develops strong attachment to his mother (?father) and separation at this age is traumatic for many children. -Check trauma at kindergarten separation, -its effect on growth? Its effect on attachment at age 15 mo. What about second-generation kindergarten goers?

3. Our life is stressful, and hence cortisol is constantly stimulated. Is it related to the obesity epidemic?

4. Our metabolism and cortisol levels evolved to accommodate the lifestyle of our ancestors, who walked and ran 20 km/d. Is our cortisol secretion and level appropriate for our sedentary lifestyle?


5. During the life history stage of juvenility (middle childhood) from age 6-7 (adrenarche) to the onset of puberty (takeoff velocity), growth decelerates despite an increase in adrenal androgens and BMI increase (adiposity rebound) despite androgens being secreted. In this trafe-off of height against BMI, Which is the preceding/leading event? BMI increase (leptin secreted) or the height deceleration. What is the endocrine mechanism? GH is probably decreasing and IGF1 too.

6. What happen to the 3 major pleiotropic hormones that are associated with decelerating longitudinal growth and increasing BMI: GH (def), thyroid hormones (def) cortisol (increase).

7. 11beta hydroxysteroid dehydrogenase type 1. Measure bioactivity in the blood or microdialysis in vivo, in adipose tissue, experimental animal, human, biopsy. Give cortisone and measure generation of cortisol.

8 Also, as a clinical test: suppress endogenous cortisol with DEX, give cortisone ( IP IV or oral) and measure cortisol. In minutes it will measure 11HSD-type1. In hours type 1+2.


9. ACTH stimulates DHEAS and DHEAS is suppressed by glucocorticoids. For patients under long term GC, do they need DHEA supplementation?

10. WE use hydrocortisone single dose pharmacodynamics for dose selection. PD is variable. According to what variables: early life events? stress? BMI? Nutrition? Age?

11. Fractures involving the distal radius of the forearm are common. ...Distal radial fractures are seen predominantly in children and adolescents. Add the distal radius to the routine DXA test.

12. Cortisol response to 1 mcg ACT test is a measure to individual ACTH sensitivity. Since this is such a common test, summarize previous tests and search for physiological correlation: BMI SDS, age. Pubertal stage, female cycle, PCO, insulin resistance.

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