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Brain Biology, Food and Mood: Identifying neurobiological correlates of depression in adolescents.

Background information

An increasing proportion of children and youth are being treated for depression, anxiety, eating disorders and obesity.  With depression being the strongest single risk factor for attempted or completed suicide and substance abuse, strategies to reduce the experience of depression among young people is essential.

The cause of depressed mood in adolescents is multifactorial, involving both early social development and responses to life experiences (such as trauma and loss), and the child's own neurobiology. Psychosocial causes of depression have been widely studied. However researchers are now beginning to uncover strong relationships between a person's neurobiology (i.e. their brain biochemistry) and a person's risk of experiencing depressive symptoms.

The brain contains a high level of fat. These fats play an importantly role in helping brain cells communicate.  A deficiency of essential fats such as omega-3 has been shown to alter the structure and function of membranes and produce measurable brain changes. A decrease in omega-3 content has been associated with depression, autism, dyslexia and the decline in mental function in older adults. Recently a link between omega-3- and depression in adolescents was reported.1 Since omega-3 fatty acids are obtained only from the diet, it may be highly detrimental to the mental health of Australian adolescents if this dietary intake is not being met. There is evidence that the current omega-3 intake in Australian diets is very low.2-3 

While a diet low in omega-3 essential fatty acids may contribute to a breakdown of cellular communication, there are other complex systems within the brain that influence and control mood. Abnormal activation of these systems may also promote conditions of depressed mood, enhancing the likelihood of developing depression.

The hypothalamic-pituitary-adrenal (HPA) axis is a major neuroendocrine system that modulates how the body responds to external physical and psychological stressors. Recent evidence has suggested that over-activation of the HPA axis is a key factor in the development of depression.4-5  A possible dietary contributor to increased HPA activity is high caffeine intake. It has been shown that caffeine can activate the HPA axis, thus increasing circulating stress hormones.6-7 Because of its unrestricted use in society, it is worthwhile investigating the current caffeine intake of adolescents as a possible contributor to the experience of stress, anxiety and low mood.

A family history of mental health disorders is also a strong predictor of a person's susceptibility to such an illness. Two important proteins linked to depression and anxiety are the serotonin transporter (5-HTTLPR) short-chain polymorphism and the rs16147 genotype for Neuropeptide Y (NPY).

The short allele of the 5-HTTPR gene has been found to reduce the functional role of serotonin uptake,8 a key site of antidepressant drug action. Neuropeptide Y plays a part in the stress response and overall functioning of the HPA axis. Brain response studies have shown that low expression levels of NPY predict decreased coping ability in stressful situations.

Study Aims

  • To idenetify the current prevalence of depression among adolescents in an Australian context.
  • To idenetify the possible links between the experience of depressed mood &/or anxiety and any one or combination of the following neurobiological factors; cellular omega-3:6 ratios, genetic polymorphisms in the serotonin transporter and NPY genes, salivary cortisol levels and caffeine intake.


  1. Mamalakis G, Kiriakakis M, et al. Depression and serum adiponectin and adipose omega-3 and omega-6 fatty acids in adolescents. Pharmacol Biochem Behav. 2006;85(2):474-9.2.
  2. Meyer BJ, Mann NJ, et al. Dietary intakes and food sources of omega-6 and omega-3 polyunsaturated fatty acids. Lipids. 2003;38(4): 391-8.
  3. Howe PRC, Meyer BJ, Record S, Baghurst K.  Nutrition. 2006;22(1):47-53
  4. Wichers MC, Myin-Germeys I, et al. Susceptibility to depression expressed as alterations in cortisol day curve: a cross-twin, cross-trait study. Psychosom Med. 2008;70(3): 314-8.
  5. Carroll BJ, Cassidy F, et al. Pathophysiology of hypercortisolism in depression. Acta Psychiatr Scand. 2007;Suppl(433): 90-103.
  6. Lin AS, Uhde TW, et al. Effects of intravenous caffeine administered to healthy males during sleep. Depress Anxiety. 1997;5(1): 21-8.
  7. Patz MD, Day HE, et al. Modulation of the hypothalamo-pituitary-adrenocortical axis by caffeine. Psychoneuroendocrinology. 2006;31(4): 493-500.
  8. Greenberg BD, Tolliver TJ, et al. Genetic variation in the serotonin transporter promoter region affects serotonin uptake in human blood platelets. Am J Med Genet. 1999;88(1): 83-7.

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