How Nutrition Can Help Avoid a Mood Disorder

Good nutrition is key to prevent all sorts of health issues, however it plays a critical role in preventing many mood disorders including depression. It certainly did not surprise me when I would receive an endless amount of E:mails from my listeners on radio sharing their experience of depression going away in a short time after being on 1,000 mg. of Omega 3′s daily. Nutrition is key. When you eat highly processed foods, sugar or drink too much caffeine, your body as well as your brain gets ‘aggravated’ leading to mood disorders or depression. Read on for my list of foods that help you prevent this from happening in the first place.

1. Omega 3′s (fish oil) – is a great place to start so make sure you look for a good quality Omega 3 fish oil supplement that says enteric coated on the label. This will make it easier to digest and you will not burp up a fishy taste. Of course, include fish in your diet at least twice a week.

2. Fill your plate 1/2 full of vegetables at lunch and dinner. Build your meal around vegetables as much as possible. Not only will they help you stay full but you will be filling up on antioxidants which prevent free radicals (toxins, chemicals and pollutants) from attacking your healthy cells in your brain as well as throughout your body. The brigher and richer the color, the better.

3. Limit your fruit intake to 2 servings per day. Fruit is a natural form of sugar and is full of antioxidants too but people tend to eat too much of it which can create a craving for more sugary foods and beverages. If you eat an apple, dip it in some almond butter or peanut butter which will slow down the absorptiong of sugar in the blood.

4. Eat a handful of nuts for a delicious snack which are full of good fats and will help reduce inflammation throughout the body as well as your brain. Everything gets inflamed as we get older which can lead to mood disorders in the brain from this inflammation so eating nuts will help keep that in check.

5. Enjoy avocado everyday – this is one of the best ways to get some good fats for the brain. Add it to salads or enjoy guacamole with grilled chicken breasts or fish.

6. Eat Greek yogurt which will put some good bacteria into your gut building your immune system and your mood.

7. Mini-meals every 3-4 hours is a great way to stabilize blood sugar levels and your mood.

8. Do not skip breakfast. This is a great time to begin your day with some of the foods listed above, fruit, Greek yogurt, peanut butter, etc. Add them to a blender for a quick meal on the go.

9. Have you tried the ancient, super nutrient-dense food, the Chia seed? It is a great way to get lots of fiber, antioxidants, vitamins and minerals in just a small amount. I add it to my blender in the morning for a jumpstart on my day.

10. Notice how you feel after a meal – this will speak volumes as to whether or not your body and brain are responding well to the meal you just ate. Keep a journal for a few days and you may begin to see a pattern making it easier to make small changes.

The Neurobiological Basis For Mood Disorders

Chemical neurotransmission in the brain is responsible for regulating all physiological processes, including our ability to sense and respond to our environment, maintain consciousness, express emotions and display fluctuations in mood. If neural pathways are damaged or disrupted, then many of these functions cannot be performed effectively resulting in illness and/or disability.

To understand and appreciate the way in which medication may assist in the treatment of mood disorders it is therefore necessary to understand the basics of chemical neurotransmission. Just as the depressive cycle is represented by an interactive model, so too is the process of chemical neurotransmission.

Chemical processes in the brain ultimately regulate the expression of genes contained in neurons. These processes are mediated by the movement of neurotransmitter molecules from one neuron to the next across a juncture referred to as the ‘synaptic cleft’. When neurotransmitter molecules reach the receiving neuron they cause a cascade of chemical reactions that ultimately result in genes located deep within the nucleus of the second neuron being either ‘switched on’ or ‘switched off’. Gene expression can affect the working of the entire neuron and its ability to communicate and interact with other neurons in the brain. Gene expression is the fundamental end point of neurotransmission.

In models of chemical neurotransmission, axons in a presynaptic neuron store neurotransmitters in vesicles located at their extremities. When stimulated by an electrical ‘impulse’, these vesicles discharge their contents (i.e. neurotransmitters) into the extra-cellular space between neurons. Neurotransmitters can act as agonists or antagonists (they can excite or inhibit physiological processes within neurons).

Once discharged into the extra-cellular space (or synaptic cleft), neurotransmitters bombard receptors on the post-synaptic neuron and thus initiate a complex series of chemical reactions within the receiving neuron. Neurotransmitter ‘receptor-binding’, among other things, results in the opening or closing of ‘ion channels’ on the surface of the post-synaptic neuron. Ion channels control the passage of charged molecules to and from the neuron, which, in turn, initiate a number of other chemical processes within the cell. Ions that are admitted into the neuron include potassium, calcium and possibly lithium.

Within the synaptic cleft, neurotransmitter molecules that have not bound to receptors in the second neuron are re-absorbed by the pre-synaptic neuron through a ‘reuptake pump’ or destroyed by enzymes located in the synaptic cleft. Neurotransmitter molecules that are re-absorbed may also be destroyed by intracellular enzymes or re-packaged into vesicles for re-use. Neurotransmitters that have docked onto receptors are usually rapidly released so that they do not continue to stimulate the post-synaptic neuron. ‘Autoreceptors’ on the first neuron also respond to high concentrations of neurotransmitters in the synaptic cleft to inhibit their further release.

Neurotransmitter molecules (or ‘First Messengers’) that find their way to receptors on the post-synaptic neuron form a neurotransmitter-receptor complex which initiates a cascade of chemical reactions and involves other substances such as proteins (G proteins) and intracellular enzymes. These chemical processes result in the production of another type of molecule referred to as a ‘Second Messenger’.

In some chemical reactions, there can also be a third and fourth messenger. The second messenger together with a number of enzymes and other substances referred to as ‘transcription factors’ can also open and close ion channels. However, their primary function is to communicate with the DNA located in the nucleus to either ‘switch on’ or ‘switch off’ specific genes.

Neurotransmitters and Depressive Disorders

The key neurotransmitters thought to be implicated in the development and maintenance of depressive disorders are norepinephrine or noradrenalin (NA), dopamine (DA) and serotonin or 5-hydroxy-tryptophan (5-HT).

Specific neurotransmitter pathways are thought to underpin a number of normal behavioural patterns, and, when disrupted, a series of clinical symptoms may develop (see diagrams below, adapted from ‘Effects of Antidepressants’ by Leonard & Healy, 1999).

But there are several other neurotransmitter chemicals found in the brain as well which interact with each other. Neurotransmitters and other brain chemicals are responsible for a number of activities:

- Neurotransmitters can excite or inhibit nerve cells (e.g. GABA)
- Receptors can mediate a fast or slow responses (excitation or inhibition)
- Neuromodulators (e.g. CCK and DA) can enhance or reduce the
- Physiological response caused by a neurotransmitter.

Antidepressants in the Treatment of Depressive Disorders

It is important to realise that we really do not know exactly how antidepressant medications work in alleviating depressive mood. What we do know, however, is that they appear to interact with neurotransmitter pathways and enzymes located in the brain.

There are several theories about how the antidepressants work:

1) That they directly work on a general ‘affective’ pathway (i.e. anxiety and depression)
2) That they are selective for certain symptoms (panic, depression, obsessiveness, etc), which once controlled, can lift mood
3) That they act on decreasing overall levels of ‘nervousness’ for example through the serotonin system
4) That they help to normalise a number of neurotransmitter systems which then act to restore mood

In early studies of antidepressant response, virtually all antidepressants were found to have the same response rate of approximately 67%. That is, after 8 weeks of treatment, approximately 67% of a sample of depressed patients prescribed an antidepressant medication demonstrated a positive response. On the other hand, up to 33% tended to be non-responders to that medication. This figure tended to be reversed among placebo responders so that up to 33% demonstrated a positive response to a placebo and up to 67% were nonresponders. However, in randomised controlled trials conducted over the last few years the placebo response rate has increased (8% per decade), and is now akin to antidepressant drug response – presumably reflecting subjects’ likelihood of being spontaneous remitters. Most efficacy studies to date have not yet been able to accurately identify who will or will not respond to any given antidepressant.

If they are going to be effective, most antidepressants will affect some level of improvement within 5 to 7 days (especially for non-melancholic depression) and correct depressed mood within 2-3 weeks. For melancholic depression, the initial antidepressant response may be slightly longer. Nevertheless, it may take several weeks or months for social functioning to return to normal.

Antidepressant medications, which may be used alone or in combination with other medications, remain the most popular form of medical intervention to restore imbalances of these brain neurotransmitters. Evidence also exists to support the use of antidepressants in combination with psychological or other non-drug interventions. However, antidepressants are not without some drawbacks. Not everyone can tolerate antidepressants and disturbing and serious side-effects, including dizziness, agitation, seizures or liver disease, can occur. Some antidepressants may interact with other medications, cause allergic reactions or necessitate dietary restrictions. Nursing mothers are generally advised against antidepressants which may be excreted in breast milk. And finally, while the risk of suicide has been minimised by the introduction of ‘safer’ drugs, the problem of overdose, intentional or otherwise, remains a concern for treating physicians.