As part of the programme (click here to download the schedule at a glance), we are pleased to offer an additional day (Sunday, May 27) prior to the start of the formal Congress dedicated to Satellite Symposia sponsored by industry partners on topics of significant interest to our members and delegates.

For this meeting we are delighted to have two Symposia on very different topics.  Both are extremely  interesting and informative. Registration for the Satellite Symposia involves a small ($50.00 USD) additional fee but one registration permits attendance at both Symposia.


SATELLITE 1 (9:00 AM - Noon):
An Update on the Role of EPA and DHA for Brain Health

Sponsored by GOED
An update on the role/functions of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in human brain health will be explored. The presentations will explore the current state of the science and identify research gaps in the following areas: mental illness, Attention Deficit (Hyperactivity) Disorder, cognitive function and brain injury.

Captain Joseph Hibbeln, M.D.
EPA/DHA and Mental Illness

Kuan-Pin Su, M.D., Ph.D. 
EPA/DHA in Depression and ADHD

Karen Yurko-Mauro, Ph.D.
EPA/DHA and Cognitive Function/Decline

Adina Michael-Titus, D.Sc.
EPA/DHA and Brain Injury

An update on the role/functions of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in human brain health will be explored. The presentations will explore the current state of the science and identify research gaps in the following areas: mental illness, Attention Deficit (Hyperactivity) Disorder, cognitive function and brain injury.

Introduction: Harry Rice GOED

1)    CAPT Joseph R. Hibbeln, M.D. Acting Chief, Section on Nutritional Neurosciences LMBB, NIAAA, NIH
EPA/DHA and Mental Illness

2)    Kuan-Pin Su, M.D., Ph.D., China Medical University, Taiwan   
EPA/DHA in Depression and ADHD

~ Coffee Break ~

3)    Karen Yurko-Mauro, Ph.D., DSM Nutritional Products
EPA/DHA and Cognitive Function/Decline

4)    Adina Michael-Titus, D.Sc, University of London, UK
EPA/DHA and Brain Injury

Panel Discussion


SATELLITE 2 (2:00 PM - 5:30 PM):
Arachidonic and docosahexaenoic acids in infant development
Sponsored by DSM
The biological functions of arachidonic acid (ARA) and docosahexaenoic acid (DHA) in mammalian development, both human and animal, will be highlighted in this symposium.  An international panel of thought leaders in this area will be assembled for these presentations.

Co-chairs:  Norman Salem, Jr. and Susan E. Carlson

Format: 25 min lecture plus 10 min Q&A


Nicolas Bazan -  Developmental Implications of the Newly Discovered Elovanoids for Vision and Cognition

Toru Moriguchi  -  ARA and DHA Functions in Delta-6 Desaturase Knockout Mice: Teasing Apart Their Separate Functions Using Artificial Rearing

Kathleen Gustafson  -  Early Life Supplementation without LCPUFA Results in Long Term Differences in Brain Function

Eric Lien -  Addition of ARA and DHA to Infant Formula: Clinical Results and Future Directions

Berthold Koletzko  -  Interaction of Infant Diet and FADS Gene Polymorphisms on Cognition and Allergy: Implications for Policy

Panel Discussion: 30 min (All)

Speaker Abstracts Below: 

The newly-discovered elovanoids (ELVs) are engaged in retina and brain development.
Nicolas G. Bazan, MD, PhD.  Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, 70112, USA
Membrane phospholipids of the nervous system are enriched in omega-3 fatty acids, with docosahexaenoic acid(DHA) being the most abundant. DHA serves as a precursor of docosanoids.  Additionally, the elongase ELOVL4 (ELOngation of Very Long chain fatty acids-4) converts DHA or EPA to very long chain (≥C28) PUFAs (VLC-PUFAs) in brain, retina, testes and skin, that in turn became acyl chains at sn-1 of phosphatidylcholines (and in sphingolipids). Mutant retina ELOVL4 causes juvenile macular degeneration in autosomal dominant Stargardt’s disease. ELOVL4 is also selectively expressed in brain neurons and mutations leads to impaired neural development, neuronal dysfunction, hyper-excitability, and seizures.  The conversion of VLC-PUFAs to bioactive derivatives has recently been discovered. We characterized and uncovered a novel class of mediators, termed elovanoids (ELV), derived from VLC-PUFAs via previously unknown pathways (Jun,B. et al Sci. Rep. 2017; Bhattacharjee,S. et al. Sci. Adv.2017). Unlike known lipid mediators that are derived from 20-22 C length fatty acid precursors (including prostaglandins and docosanoids) the ELVs are made from 32:6 n-3 or 34:6 n-3. We have thus revealed a novel neuroprotective/ neurorestorative signaling that is set in motion upon homeostatic disruptions.
Retinal pigment epithelial cells (RPE) retrieve DHA during photoreceptor (PR) outer segment renewal by shedding and phagocytosis of PR tips and return the fatty acid to the cell inner segment for new PR membrane biogenesis. ELVs precursors are synthesized by photoreceptor specific ELVL4 (in the mature retina), and in turn, are acylated in sn-1 of a phosphatidylcholine (PC) for the biogenesis of PR outer segment discs, where the PC tightly interacts with rhodopsin. After shedding and phagocytosis by the RPE cells, the PC, upon impending disruptors of homeostasis, can release free VLC-PUFA,n-3 that are then converted into ELVs. Autocrine/paracrine signaling by ELVs sustain integrity of RPE and of PRC.
We have now found that during early postnatal retina development, prior to the onset of PR outer segment renewal, the retina displays the ELV synthesis pathway.  Retinas and RPEs from 6-day old mice from both wild type and AdipoR1 KO mice were studied. The AdipoR1 is necessary for DHA retina uptake and its genetic ablation lead to retinal degeneration (Rice et al. Nature Commun. 2015). We detected the formation of VLC-PUFAs (FA32:6 and FA34:6) as well as the synthesis of 27-mono hydroxy-32:6 and 29-mono hydroxy-34:6, which are the stable derivatives of  the hydro peroxide precursors of  ELVs before PR outer segments are formed. Thus, the fact that VLC-PUFAs - ELVs pathway is present in the retina at this stage is a clue that ELVs play a role in retina and brain development. These observations are supported by the fact that ELOVL4 is expressed in retinal cells other than PR early in development. We suggest that ELVs play an additional role during CNS development as compared with their functions later in life when their synthesis is driven by the sensing of needed pro-homeostatic signaling. (Support by NIH EY005121, GM103340, and EENT Foundation)

ARA and DHA Functions in Delta-6 Desaturase Knockout Mice: Teasing Apart Their Separate Functions Using Artificial Rearing
Toru Moriguchi, Akiko Harauma
School of Life and Environmental Science, Azabu University, Tokyo, Japan
Our group has previously presented results which examined effects of arachidonic acid (ARA) and docosahexaenoic acid (DHA) on physical growth and brain function.  We have employed the unique model of D6D KO mice which are unable to elaborate EFAs together with an artificial rearing system and artificial milk so that each fatty acid level can be prescribed. In this way, for the first time, animals extremely deficient in ARA but with adequate LA can be studied; also, animals with severe deficiencies of DHA but with ALA and/or EPA can be studied for specific functional losses.  In this manner, we have been able to demonstrate essential and unique functions for both ARA and DHA in mouse development. Our studies demonstrate that ARA is absolutely necessary for both body and brain formation and growth, and DHA is indispensable for the development of brain function after growth.  When tissue levels of ARA were extremely low, body and brain weight declined.  When tissue levels of DHA were extremely low, cognition as measured for example by the Morris Water Maze was poor. Motor coordination was also lost when both ARA and DHA were not supplied.  All functions were restored in the D6D KO mice when adequate levels of ARA and DHA were provided along with tissue and brain levels of these fatty acids.  Safety concerns were also raised when ARA was not added to a DHA-containing formula as the lowest levels of tissue and brain ARA were observed in this case and many mouse pups exhibited hemorrhagic stool in the small intestine; this was prevented by the addition of ARA to the pup formula.  Present studies seek to determine the level of ARA required to maintain optimal development, growth and brain function at a constant level of DHA.  

Investigations of brain neurophysiology, functional connectivity and behavior in humans and primates suggest a role for LCPUFA in neurodevelopment linked to visual, attention and inhibitory mechanisms. We have followed cohorts from two randomized clinical trials (RCT). In the first trial, newborn infants were randomized to 1 of 4 infant formulas containing either no LCPUFA (control) or 3 different levels of DHA and the same level of ARA for the first year of life. The intervention in the second RCT was limited to the prenatal period where pregnant women were randomized to capsules containing either 600 mg of DHA or placebo oil during the 2nd and 3rd trimesters.
At age 5.5 years, children from both cohorts performed a task (Go, No-Go) while we recorded brain responses; event-related potentials (ERPs). This task is designed specifically to measure differences in brain function between the frequent response (press the button) and an infrequent response where children must inhibit their response (i.e., not press the button). Various components of the ERP are linked to evaluation of the visual stimulus (P2), response inhibition and conflict monitoring (N2, P3). At age 9, children from the formula supplementation cohort underwent multi-modal brain imaging consisting of structural and functional MRI, resting state MRI, a behavioral Go, No-Go task and spectroscopy.
Results of the ERP in both cohorts show that children who received LCPUFA supplementation had greater focal activation in regions responsible for visual processing and response inhibition when compared to placebo groups. Further, the results indicate that the timing and duration of supplementation may play an important role in these outcomes. In the formula supplemented cohort, functional MRI identified overall greater activation during inhibition tasks and resting state MRI showed greater functional connectivity between dorsal and ventral attention networks. During the behavioral Go, No Go task at age 9, children who were randomized to the supplemented groups the first year of life, had faster reaction times, were less impulsive and made fewer rule-learning mistakes.
Our results from these two independent RCT cohorts demonstrate a developmental programming effect of early life LCPUFA supplementation. Differences in brain function linked to attention and inhibition can be detected years after the experimental interventions ended. These results underscore the importance of LCPUFAs in neurodevelopment, long-term brain function and behavior.

Addition of ARA and DHA to infant formula: clinical results and future research directions
Eric L. Lien
University of Illinois, Department of Food Science and Human Nutrition, Urbana, Illinois, USA
Infants accrete substantial amounts of long chain polyunsaturated fatty acids (lcPUFAs) during the first year of life.  DHA is the predominant lcPUFA of the retina while both DHA and ARA are present in substantial amounts in the brain.  Although breast milk contains DHA and ARA, traditional infant formulas contain only their C18 precursors.  The synthesis of lcPUFAs from C18 precursors is limited, and therefore the addition of preformed DHA and ARA to formula is of substantial interest. 
Initial clinical assessment centered on visual and cognitive development.  Results demonstrated improvements in visual function, achieving the goal of formula-fed infants more closely matching the developmental milestones of breast-fed infants.  Some, but not all, cognitive development studies demonstrated that infants fed lcPUFA-fortified formula had responses closer to breast-fed infants than infants fed unsupplemented formulas.  Cognitive development is an exceptionally complex process and negative results may be due to the test utilized, age at assessment, duration of feeding and the levels of formula DHA and ARA.  The accretion of lcPUFAs also occurs in tissues outside of the CNS.  In addition to CNS endpoints, clinical trials have demonstrated improvements in immune function, respiratory tract illness and allergy development in infants receiving lcPUFA-supplemented formulas. 
A limited number of clinical trials have evaluated formula supplemented with DHA alone, but numerous lines of evidence demonstrate that ARA must be added to formula in addition to DHA.  Recent evaluation of FADS1 and FADS2 polymorphisms demonstrate that some mothers and infants may be at higher risk of impaired lcPUFA status than the general population, highlighting an important area of future research.  Infants with low lcPUFA status (due to either inadequate intake or limited ability to synthesize lcPUFAs) may benefit substantially from dietary lcPUFA supplementation.

(Abstract – Berthold Koletzko coming soon)