Putting on a Happy Plate: How to eat your way through Seasonal Affective Disorder

veggies smile

Over time technology has made dramatic strides in the way food is processed and prepared. Being able to store foods for weeks at a time without it ever going bad has now become the norm. There is greater emphasis on having foods that compliment a person/family’s busy lifestyle. This has resulted in the increasing popularity of prepackaged foods. However, in the factory production of these meals, nutrients are stripped away and loaded with filler calories to make the foods energy dense but nutrient poor.

By combining these types of foods with a predominantly sedentary lifestyle has resulted in a dramatic increase in cardiovascular disease (CVD), such as heart attacks and stroke.

Chronic diseases such as CVD, diabetes, obesity, cancers and respiratory disease account for 59% of the 57 million deaths annual and 46% of the global burden of disease. Risk factors for the diseases, including high blood pressure, high cholesterol, obesity, physical in activity, and lack of fresh fruits and vegetables, are all related to diet and physical inactivity (WHO, 2003). It is apparent that nutrition and physical health is a key factor in determining a person/family’s well-being. These alterations in the food consumption and diet have influenced not just chronic physical conditions, but also mental and emotional well being. There’s a strong link between what a person eats and how they feel. Poor eating habits can aggravate mental illness and prevent overall good mental and emotional health (Somer, 1999). The brain is one of the most metabolically active organs in the body. It requires essential nutrients, vitamins, minerals, and essential fatty acids as cofactors for its maintenance. Without adequate intake of all these nutrients, the brain cannot function optimally (Horrobin, 2002).

Tryptophan:

A fundamental theory in understanding any form of depression (including Seasonal Affective Disorder) is the monoamine hypothesis. It is based on the presumption that essential amino acid supplementation will increase brain neurotransmitter levels and improve brain functioning. The essential amino acid tryptophan is obtained from diet and converted to 5-hydroxytryptophan (5-HTP), which is converted to serotonin, a neurotransmitter required for mood and psychological health, and thus used to treat forms depression. It has also been useful in treating fibromyalgia, binge eating, chronic headaches, obesity, and insomnia (Shannon 2001).

Figure 1: Tryptophan metabolism

tryptophan metabolism

SAMe:
Other nutritional supplements, such as S-adenosyl-methionine (SAMe), have been used to treat types of depression, dementia, and other neurological disorders. SAMe is an essential amino acid found in high-protein foods like meat and fish.” (Shannon 2001).It has the ability to limit the accumulation of homocysteine (see Figure 2), which can lead to increased arterial plaque formation; blood clotting; and elevated risk of heart disease, stroke, female reproductive cancers, colon cancer, Alzheimer’s disease, fibromyalgia, and various types depression. SAMe is required in methylation, where a methyl group is transferred from one molecule to another. SAMe donates methyl groups in 35 different reactions to DNA, proteins, lipids, and hormones. It is believed that depression may be related to a weakening methylation (Shannon, 2001).

B12 and Folic acid:

Other critical methyl donor groups, besides SAMe, include vitamin B12 (cyanocobalamin and folate [folic acid]). Often patients with major depressive disorder are also low in plasma and red cell folate levels, which causes them to respond less well to antidepressants (Shannon 2001) (See Figure 2).

Figure 2: Methylation Cycle

methylation cycle

Omega-3 and Omega-6:
Fatty acids can be subdivided into saturated, monounsaturated, and polyunsaturated. There are two main types of polyunsaturated fatty acids, omega-6 and omega-3. Arachidonic(AA) and docosahexaenoic (DHA) are the most abundant fatty acids in the brain. AA, dihomogamma-linolenic acid, and eicosapentaenoic acid (EPA) are also important cell-signaling and enzyme-regulating molecules. The parent precursors to these acids, linolenic (omega-6) and a-linolenic (omega-3), are known as “essential” fatty acids because they cannot be created by humans. The omega-3 fatty acids are primarily obtained from marine and vegetable sources and the omega-6 fatty acids from animal and plant sources (Peet 2002).

In the past, humans consumed a low-fat diet containing a large amount of omega-3 fatty acids and much less omega-6. Currently, the fatty acid consumption is generally reversed, whereby a disproportionately high amount of omega-6 fatty acids is consumed. This imbalance is associated with a greater increase in some major mental illnesses (Somer 1999).

How to put on a ‘Happy Plate’:

In order to help with seasonal affective disorder, try using as many of these foods in your everyday diet. Be sure to balance carbohydrates with healthy fiber, protein and fats. Consult a health professional, like a Nutritionist or Naturopathic Doctor on specific meal plans to aid in combating SAD.

Nutrient Sources
Tryptophan TurkeyChickenPumpkin seedsDairyLegumes
Magnesium Green leafy vegetablesAlmondsCashewPeanuts 
B-vitamins (including Folic Acid) Whole grainsBeansPapayaOrangeCantaloupe

Eggs

 

Omega-3 Flax seedsWalnutsSardinesSalmon
Omega-6 SafflowerSunflowerPumpkinWheatgrass

Reference:
Horrobin DF. Food, micronutrients, and psychiatry. Int Psychogeriatr. 2002;14(4):331-334.
Somer, E. Food and Mood. New York: Henry Holt and Company; 1999.
Shannon S. Handbook of Complementary and Alternative Therapies in Mental Health. San Diego, CA: Academic Press; 2001.
Peet M. Essential fatty acids: theoretical aspects and treatment implications for schizophrenia and depression. Advances in Psychiatric Treatment. 2002;8:223-229.
World Health Organization. The global strategy on diet, physical activity, and health [Web page]. 2003. http://www.who.int/dietphysicalactivity/media/en/gsfs_general.pdf. Accessed Dec. 17, 2008.

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