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EDITORIAL
Year : 2012  |  Volume : 2  |  Issue : 3  |  Page : 165-166

Taking note of modifiable neurobiological risk factors in adolescent depression


Australasian Research Institute, Sydney Adventist Hospital, Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, Australia

Date of Web Publication8-Aug-2012

Correspondence Address:
Ross Grant
Australasian Research Institute, Sydney Adventist Hospital, Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney
Australia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.99467

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How to cite this article:
Grant R. Taking note of modifiable neurobiological risk factors in adolescent depression. Int J Nutr Pharmacol Neurol Dis 2012;2:165-6

How to cite this URL:
Grant R. Taking note of modifiable neurobiological risk factors in adolescent depression. Int J Nutr Pharmacol Neurol Dis [serial online] 2012 [cited 2019 Oct 16];2:165-6. Available from: http://www.ijnpnd.com/text.asp?2012/2/3/165/99467

Adolescent depression is a significant problem in many societies with some studies indicating that around one-third of young people in industrialized countries will experience an episode of major depressive disorder by the age of 19. Treatment options generally center on programs that identify and deal with the psychosocial contributors and/or attempt to pharmacologically stimulate neurotransmitter activity (in particular serotonin and dopamine), without reference to the underlying neurobiology. However, increased risk of depression, with or without contributing social triggers, has been linked to potentially modifiable biological factors. The major contributors include chronic inflammation, alteration of cell membrane fluidity, hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis (i.e. stress response), and reduced availability of the amino acid tryptophan. This article briefly discusses the relationship of each of these factors to depression within the context of modern lifestyle. It is suggested that by taking steps to eliminate these factors, the incidence of depression among the young may be reduced and the reliance on symptomatic pharmacological treatments may be significantly decreased.

Adolescent depression is a significant problem in many societies. While the incidence may vary geographically, studies suggest that around one-third of young people in industrialized countries will experience an episode of major depressive disorder by the age of 19. Treatment options generally center on programs that identify and deal with the psychosocial contributors and/or attempt to pharmacologically stimulate neurotransmitter activity (in particular serotonin and dopamine), without reference to the underlying neurobiology.

While psychosocial treatments and pharmacological inhibitors undoubtedly have a role to play in the treatment of this multifactorial disease, investigators are beginning to recognize that certain lifestyle habits, not directly linked to social misadventure, can alter the existing neurobiology, increasing a child's risk of experiencing a depressive illness. This may be particularly true in children with underlying genetic predispositions to either hyper-anxiety, due to reduced neuropeptide Y signaling in the brain's amygdala, or reduced reuptake of serotonin in limbic serotonergic pathways through dysfunctional transporters.

The brain, like other body organs, requires a high degree of communication and coordination between its many millions of cellular components to carry out its complex biological activities. A disruption in those subset of processes linked to the maintenance of mood will logically result in depressive symptoms. The experience of depression has been linked to alterations in a number of biological systems within the brain, including chronic inflammation, alteration of membrane integrity, hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis (i.e. stress response), and reduced availability of the amino acid tryptophan from which the key neurotransmitter serotonin is made.

Hyperactivation of the HPA axis, or stress response, is a common precursor to the development of depression. While the HPA axis can be psychosocially activated, it can also be stimulated pharmacologically. The experience of anxiety due to the overuse of caffeine is a well-described phenomenon. It may be relevant that in many countries, marketing of a wider range of caffeinated beverages, including energy drinks, to children has significantly increased over the past decade. It is yet to be established whether the predicted increase in caffeine intake by children is linked to psychological disturbances in adolescents, including depression. Urgent research is needed in this area.

Physiologically, depression has also been linked to reduced availability of the amino acid tryptophan from which serotonin is made. What is generally not appreciated is the link between tryptophan metabolism and inflammation. Tryptophan is the precursor to two major pathways in the brain: The short pathway results in serotonin and melatonin production, while the much more complex kynurenine pathway ultimately produces the essential pyridine nucleotide, nicotinamide adenine dinucleotide (NAD + ). Inflammation tends to increase tryptophan catabolism via the kynurenine pathway, thus reducing tryptophan availability for serotonin synthesis. Therefore, any condition that promotes chronic, acute, or subacute inflammatory activity, such as chronic illness or obesity, is likely to result in decreased serotonin synthesis, thus reducing serotoninergic signaling in the limbic system (i.e. emotion center) of the brain.

Cell signaling in the brain is dependent not only on the availability of neurotransmitters like serotonin but also on membrane fluidity. A more flexible membrane is thought to promote better receptor kinetics, and therefore improved signaling. Importantly, membrane fluidity is enhanced by omega-3 concentrations. During the last few years, epidemiological studies as well as clinical trials have convincingly linked reduction in omega-3 fatty acid levels, relative to omega-6, to depression in adults. Recent work by Murakami K. of the University of Tokyo and our own laboratory has observed the same association in adolescents. As omega-3s are obtained only from the diet, it may be highly detrimental to the mental health of adolescents if dietary intakes of these essential fatty acids are deficient.

Unfortunately, most modern societies are at risk of omega-3 deficiency. Food security for most developed nations requires the manufacture of edible products with long shelf lives, enabling long transit times. In order to achieve this, most manufacturers include omega-6 rich oils in their foods in preference to the much more oxidizable omega-3 oils. The trade-off is a shift in the omega-6 to omega-3 ratio in the food supply that greatly favors omega-6 (averaging around 8:1). However, for optimum health, the target ratio should be closer to parity (i.e. 1:1). As omega-3 fats play a role in membrane fluidity and anti-inflammatory modulation, this marked imbalance logically promotes conditions under which depressed mood may more easily develop.

Therefore, while psychosocial elements do play a role in the development of depression in young people, it is essential to also take into account modifiable lifestyle factors that may be contributing to the condition. Effective management options should include treatments that address possible neurobiological causes such as low omega-3 intake (particularly in the presence of high omega-6), chronic activation of the HPA axis, potentially through high caffeine intake and causes of chronic inflammatory activity. With reference to this final point, chronic subacute inflammation has been associated with diets that are high in calorie-dense nutrient-deficient foods. By taking steps to eliminate these factors, the incidence of depression among the young may be reduced and the reliance on symptomatic pharmacological treatments may be marginalized.




 

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