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Winter Blues: Seasonal Affective Disorder (SAD)

Winter Blues: Seasonal Affective Disorder (SAD)

Seasonal Affective Disorder (SAD)

Depression can occur at any time of year. However, for many, winter represents the most vulnerable time. Changes in sunlight, temperature, changes in the brain and body’s internal chemistry, and the stress of the Holidays can all play a role. In some ways, Winter Depression is built into our biology – just think of bears that hibernate during the winter. Indeed, symptoms of winter depression can mimic hibernation, with lack of energy, sleepiness with difficulty getting out of bed, and an increased appetite with carb-cravings. Difficulty with concentration and focus can also be a symptom. Because of the physical symptoms, some describe seasonal affective disorder (SAD) as “vegging out.”

Some individuals only experience depression during the winter while others may experience it any time of year but more so during the winter.

Some specific findings associated with winter depression include:

1) Lower available levels of the brain chemical messenger serotonin. There is evidence that serotonin remains less available to stimulate neurons for people with SAD. This is because after serotonin is released from a neuron, thereby making it available to attach to and activate docking stations (known as receptors) on surrounding neurons, it is sucked back in by the releasing neuron too quickly in people with Seasonal Affective Disorder (SAD).

2) People with SAD may make too much melatonin, a hormone that promotes sleepiness. Excess melatonin levels can cause daytime fatigue. This can also throw off a person’s day-night cycle (circadian rhythm).

3) Insufficient Vitamin D levels may play a role in SAD. Vitamin D may be involved in the action of serotonin.

4) Activity of a structure deep in the brain called the hypothalamus may be uniquely sensitive to sunlight in people with SAD. The Hypothalamus controls sleep and appetite, and also may play a role in mood.

Treatment for Seasonal Affective Disorder (SAD):

First, it is important to rule out other possible causes, such as low thyroid or anemia as examples. I have had a number of patients where these were uncovered as causes of fatigue.

Very effective treatment for SAD is available. Bright Light therapy, Cognitive-Behavioral Therapy (CBT), and antidepressants are the most evidence-based. These and others that are often helpful are listed below.

Bright Light therapy

There are lots of different styles and price points of bright light lamps or boxes. Specific levels of luminosity (often 10,000 lux is recommended) and timing of bright light are important components. The timing of bright light may depend on the type of depression. For pure SAD or winter worsening of depression, the morning is usually best. Morning bright light resets circadian rhythm, activates the hypothalamus, and suppresses melatonin secretion. Melatonin release is regulated by light. Melatonin is always primed to be released in the brain but held back or suppressed by bright light. This is why melatonin is released at night (and also why you shouldn’t bring your phone or laptop into bed at night!).
(Note that although using bright light later in the day can make SAD worse by messing up circadian rhythm, there are always exceptions. I occasionally find that bright light later in the day whether exclusively or in addition to morning light paradoxically is more beneficial. Also, mid-day bright light is better for Bipolar depression).

Antidepressants

Many antidepressants are used for winter depression but one is specifically FDA approved for it. However, your doctor needs to make sure this is the right antidepressant for you (for example, it’s not as good for some symptoms of depression or anxiety).

Cognitive-Behavioral therapy (CBT)

This can help change unhelpful behaviors and negative thinking, help change perspectives on the winter, and teach stress-reduction techniques.

Exercise. For those who are not inclined towards exercise, thinking of this recommendation simply as “getting the blood flowing” can be helpful, as even 10 minutes of physical activity a day can be beneficial. Outdoor activities can be especially helpful.

Vitamin D. Consult your doctor for Vitamin D dosing for SAD.

This article was originally published on Dr. Neal Ranen, Baltimore Psychiatric Services

How to Break Out of Default Mode

How to Break Out of Default Mode

What Depression Looks Like in the Brain:  Stuck in Default Mode (and How to Break Out of It)

Even though depression is usually referred to as a chemical imbalance, it is actually an imbalance in networks of interconnecting regions of the brain. Specifically, sophisticated new brain imaging studies reveal that depression shows up in the brain as being stuck in “Default Mode.”  This is a looping network deep in the middle portion of the brain that, in depression, is more active than the other major networks.  The Default Mode (DMN) has strong connections to the emotional, anxiety, and fear centers of the brain, and parts of the brain that reflect thoughts about self, the past and the future.  It is also involved in thinking about the intentions behind others’ behavior.  So, a disproportionately active DMN results in a hyper-connection to the depression, anxiety, and fear centers of the brain, causes people to be sensitized about how they’re feeling, and whether other people are acting with bad intentions towards them or thinking that they’ve disappointed others.

Also, when the DMN is disproportionately active, the other important networks can’t function normally.  One of these other networks is called the Executive Network. The Executive Network is also sometimes termed the “Task Positive” Network because it is activated when we need to effectively interact with the outside world to get things done or look at things rationally.  It is more on the outer, more advanced part of the brain, rather than buried deep like the DMN, and involves important areas of the Frontal Lobes (by the way, the EN is impaired in ADHD, but that’s for another blog!). In contrast, the DMN is often referred to as the “Task Negative” network because it involves an internally-oriented focus.  This overactive Default Mode Network causes you to literally and figuratively “be in your own head.”

Importantly, with depression, not only is the DMN overactive, it also cannot be deactivated when the brain is trying to activate the Executive Network. Deactivating the DMN is essential to allow the Executive Network to work effectively and not be straining against or clashing with the DMN, again because the EN is Task Positive and the DMN is Task Negative. This is why, in addition to depressed mood, lack of enjoyment, and pessimism, people with depression also have trouble concentrating and getting things done – it is because of an overactive DMN that cannot be deactivated.

So, the DMN causes negative emotions and thoughts and prevents clearheaded thinking and productivity.  In addition, recent evidence reveals connections between this network and the brainstem that controls things like sleep, appetite, sex drive and a sense of physical sluggishness.  So, we can see how a disproportionately active DMN can contribute to all three domains of clinical depression – 1) mood and self-attitude, 2) concentration and productivity, and 3) physical symptoms like lack of energy and changes in sleep and appetite.  One can see why depression causes everything to feel so effortful.

The most effective way to treat depression, and rebalance the brain networks, is through therapy and the targeted, judicious use of medication.  So, break out of Default Mode and start the path towards feeling better!

If you are battling with depression, contact Dr. Neal Ranen to set up an appointment today!

This article was originally posted on DrNealRanenBaltimorePsychiatrist.com

Newer Antidepressants: The “Reuptake-Plus” Antidepressants

Newer Antidepressants: The “Reuptake-Plus” Antidepressants

The “Reuptake-Plus” Antidepressants by Dr. Neal Ranen, M.D. Baltimore Psychiatrist

I previously reviewed antidepressants known as SSRI’s and SNRI’s that work as reuptake inhibitors (see June 27, 2010 blog). This mechanism of action allows serotonin and norepinephrine to remain available long after release, increasing the likelihood that they will occupy docking stations, or receptors, on surrounding neurons, and exert an effect.  There are a couple of newer antidepressants that work not only as reuptake inhibitors but also directly occupy receptors.  I reviewed one of these, vilazodone, or Viibryd, in a previous blog, and since then a newer “Reuptake-Plus” antidepressant has become available, called Trintellix.  This medication acts as a serotonin-reuptake inhibitor plus directly occupies serotonin receptors, either stimulating or inhibiting them, creating additional effects.  There are many types of serotonin receptors, and Trintellix has effects on 5 of them. As above, Trintellix activates some of these receptors but inhibits others. This may sound confusing, but the inhibitory effect can actually activate certain other chemical messenger pathways in the brain. To understand this, it is important to know a couple of pieces of information.  The first is that some chemical messengers in the brain (known as neurotransmitters) activate neurons (known as being excitatory) and some inhibit them (known as being inhibitory). They do this by having stimulating or inhibiting effects when they attach to receptors on surrounding neurons. Serotonin, for example, is an excitatory neurotransmitter.

The next layer of complexity is that serotonin neurons can connect to a second neuron that itself is either excitatory or inhibitory.  So, if serotonin attaches to a receptor on an excitatory neuron, more excitatory activity will be triggered, but if it attaches to a receptor on an inhibitory neuron then there will be more inhibition of brain pathways because it is activating the inhibition.

The next level of understanding is that there are a lot of intermediary neurons in the brain that function as connections between two other neurons.  There will be a first neuron that will connect to the intermediary neuron, known as an interneuron, which will, in turn, connect to the third neuron. These interneurons are usually inhibitory – they hold back activity in the third neuron. The first neuron is usually excitatory – the neurotransmitter it releases, like serotonin, will activate this inhibitory interneuron which results in suppressing the activity of the third neuron. So, serotonin receptors, although always excitatory, can either suppress activity if it is on an inhibitory interneuron or stimulate activity if it is on another neuron that itself is excitatory.  Now we can understand how Trintellix can increase activity in the brain even though it stimulates some and blocks other serotonin receptors: the receptors it stimulates are on neurons that are also activating, and the receptors it blocks are on neurons that are inhibitory.  In the latter case, this will prevent activation of the inhibitory neuron, thereby taking away the brake on activity in the next neuron. This may or may not be associated with certain advantages  (or disadvantages) depending on the type of symptoms of depression a person is experiencing.  For example, in addition to its overall antidepressant effect, this may result in an increase in cognitive processing speed and be less associated with weight gain, but in my experience not work as well if there is a high level of anxiety or irritability associated with the depression. So, a lot may depend on the person’s specific symptom pattern. This is why a careful psychiatric assessment is critical to determine what antidepressant might be right for any particular individual.

To learn more or to make an appointment with Dr. Neal Ranen, M.D. call 410-413-2145.

This article was originally posted on Dr. Neal Ranen

Antidepressants Work!

Despite publications and media attention to the contrary, those of us in clinical practice, as well as our patients, have no doubt that antidepressants work. Confusion may arise because of the nature of FDA Registration clinical trials and what they are designed to achieve, and the placebo effect. Now, a large-scale analysis, published in the rigorously peer-reviewed Archives of General Psychiatry, has strongly validated the experience of patients and clinicians — that antidepressants work. The researchers reviewed a large number of trials of two popular modern atidepressants, fluoxetine (Prozac) and venlafaxine (Effexor) which included 9,182 patients. Extremely robust and clinically relevant improvements were seen, including on measures of both response and remission. In addition, the benefit of antidepressants was seen regardless of the severity of depression, which ranged from mild to severe. Every patient is unique, and despite overall similarities in response rates in clinical trials of antidepressants, a thorough assessment of patient characteristics, including symptoms that might be co-existing with depression, like anxiety or lack of motivation, and the unique features of particular antidepressants, can determine the best option for each individual patient.

Best Regards, Dr. Ranen

Neal G. Ranen, M.D., Psychiatrist Baltimore County

https://drnealranenbaltimorepsychiatrist.com