In Health

It is well known that mental health illnesses and conditions within Australia are on the rise, particularly amongst our most vulnerable; the homeless, low income earners, ethnic minorities, the aged and those suffering from multiple chronic conditions (1).

One of the most obvious, yet under-recognised factors in the development of major trends in mental health is the role of nutrition. The body of evidence linking diet and mental health is growing at a rapid pace. Poor nutrition can impair our daily health and wellbeing and reduce our ability to lead an enjoyable and active life. In the short-term, poor nutrition can contribute to stress, tiredness and our capacity to work (1,2).  Over time, it can contribute to the risk of developing some illnesses and other health problems such as:

  • Being overweight or obese
  • Tooth decay
  • High blood pressure
  • High cholesterol
  • Heart disease and stroke
  • Type-2 diabetes
  • Osteoporosis
  • Some cancers
  • Depression
  • Disordered eating

Mental illness is traditionally managed with medication and psychological intervention; however there is emerging evidence to support the contributing role of diet in the development, management and prevention of specific mental health problems such as depression, epilepsy, attention deficit hyperactivity disorder and Alzheimer’s disease (2,3,4,5,6).

A number of cross-country and population-based studies have linked the intake of certain nutrients with the reported prevalence of different types of depression. For example, correlations between low intakes of fish by country and high levels of depression among its citizens – and the reverse – have been shown for many types of depression (3,7). Complex carbohydrates as well as certain food components such as folic acid, omega-3 fatty acids, selenium and tryptophan are thought to decrease the symptoms of depression (7,8).

Those with low intakes of folate, or folic acid, have been found to be significantly more likely to be diagnosed with depression than those with higher intakes. Similar conclusions have been drawn from studies looking at the association of depression with low levels of zinc and vitamins B1, B2 and C (3,9). In other studies, standard treatments have been supplemented with these micronutrients resulting in greater relief of symptoms in people with depression and bi-polar affective disorder, in some cases by as much as 50% (3).

Manipulation of the macronutrient composition to reflect a reduced carbohydrate intake, particularly from refined sugars and high-GI foods, in adults and children with refractory epilepsy has been demonstrated to reduce the frequency of seizures and side effects by up to 90% (6). The idea behind a restricted carbohydrate diet is to mimic some of the effects of starvation, in which the body first uses up its glucose and glycogen stores before burning stored body fat; the body then produces ketones, which have an anticonvulsant effect. Ketone bodies also reduce alanine efflux, alter the charge of water and electrolyte imbalance within the body (10,11). In addition, recent research demonstrates ketone bodies playing a role in altering the functioning of nerve cell lipid membranes or neurotransmitter production (11).
Similarly, emerging research in the area of behavioural problems and diet has shown chronic deficiencies of certain minerals such as zinc, iron, magnesium and iodine and insufficient dietary intake of long-chain polyunsaturated fatty acids may have a significant impact on the development and deepening of the symptoms of ADHD in children (5). The authors of several studies also demonstrated the positive impact of the elimination food products containing synthetic food additives, like artificial food dyes and preservatives on the behaviour of children with ADHD (5,12).

The incidence of Alzheimer’s disease, a form of dementia, has similarly experienced significant growth amongst our aging population. Currently in Australia about 80 per cent of people with dementia have Alzheimer’s disease, either in pure form or combined with another kind of degeneration such as cerebro-vascular disease. Although Alzheimer’s disease can appear to run in families, it is only strictly inherited in a small number of cases (4). For most people, genes are only one part of the risk equation; your chances of developing the disease are also affected by other factors. It is a widely held theory that diet, physical and mental activity, environment, and cardiovascular disease may also play a role in Alzheimer’s. With regards to nutrition, people who eat a diet rich in antioxidants and those who adhere to a largely ‘Mediterranean diet’ have been shown to have a lower risk of developing Alzheimer’s disease. A Mediterranean diet is one that favours the consumption of moderate amounts of mono-unsaturated fatty acids (from fish and seafood, olive oil, nuts and seeds), complex carbohydrates (such as wholegrain breads and cereals), plenty of fresh fruit and vegetables and a limited intake of red meat and alcohol (4,13).

Whilst a healthy diet has long been thought to be the foundation of good health and well-being, the causative link between diet and mental health has, until recently, remained under-represented. There is now a growing body of research from across the world to support its link in the development, management and prevention of a wide range of mental health problems. The benefits of nutrition therapy for individuals with established conditions or those considered to be ‘at risk’ are substantial, and a referral to an Accredited Practicing Dietitian should be considered alongside traditional modalities.

Jarrah is based at our Cleveland office, to arrange an appointment please call (07) 3488 0483

References:
[1] Jacka FN, Kremer PJ, Berk M, de Silva-Sanigorsk AM,  Moodie M, Leslie ER, Pasco JA, Swinburn BA: A Prospective study of diet quality and mental health in adolescents; PLoS One September 2011, 6:9:e24805.

[2] Jacka FN, Cherbuin N, Anstey KJ, Butterworth P: Dietary Patterns and Depressive Symptoms over Time: Examining the relationships with socioeconomic position, health behaviours and cardiovascular risk; PLoS One January 2014, 9:1:e87657.

[3] Sanchez-Villegas and Martínez-González: Diet, a new target to prevent depression? BMC Medicine 2013 11:3.

[4] Opie RS, Ralston RA, Walker KZ: Adherence to a mediterranean-style diet can slow the rate of cognitive decline and decrease the risk of dementia: a systematic review; Nutrition & Dietetics September 2013, 70:3:206-218.

[5] Konikowska K, Regulska-Ilow B,Rózańska D: The influence of components of diet on the symptoms of adhd in children; Roczniki Państwowego Zakładu Higieny 2012, 63:2:127-34.

[6] Levy RG, Cooper PN, Giri P: Ketogenic diet and other dietary treatments for epilepsy; Cochrane Database of Systematic Reviews 2012, 3: CD001903. DOI: 10.1002/14651858.CD001903.pub2.

[7] Sánchez-Villegas A, Verberne L, De Irala J, Ruíz-Canela M, Toledo E, Serra-Majem L, Martínez-González MA: Dietary fat intake and the risk of depression: the SUN Project. PLoS One 2011, 6:e16268.

[8] Miura H, Ozaki N, Sawada M, Isobe K, Ohta T, Nagatsu T: A link between stress and depression: shifts in the balance between the kynurenine and serotonin pathways of tryptophan metabolism and the etiology and pathophysiology of depression. Stress 2008, 11:198-209.

[9] Jacka FN, Pasco JA, Mykletun A, Williams LJ, Hodge AM, et al: Association between western and traditional diets and depression and anxiety in women: Am J Psychiatry; 2010, 167: 305–311.

[10] Hsieh DT, Pfeifer HH, Thiele EA: Dietary management of epilepsy; AM FAM PHYSICIAN 2012 Dec 1; 86 (11): 1000-4.

[11] Korsholm K: Effects of a ketogenic diet on brain metabolism in epilepsy; Clin Nucl Med 2013 Jan, 38:1:38-9.

[12] Lomangino, Kevin: Benefit for elimination diet in adhd? CLIN NUTR INSIGHT 2011, 37:4: 8-9, 11.

[13] Aliev G, Ashraf G,  Kaminsky YG, Sheikh IA, Sudakov SK, Yakhno NN, Benberin VV, Bachurin SO: Implication of the nutritional and nonnutritional factors in the context of preservation of cognitive cerformance in patients with dementia/depression and alzheimer disease; AM J ALZHEIMERS DIS OTHER DEMENTIAS 2013 Nov,; 28:7:660-70.

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