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The Relationship Between Mood Disorders and Metabolic Syndrome

The brain is the seat of the mind – this fundamental governing principle has driven the study of the biological causes of mental illness for the past century and beyond. For years, scientists have studied the inner workings of our brains in order to better understand mental illness, its causes, and potential treatments. Initial efforts in this area focused on the gross anatomy of the brain and the study of large brain regions. With the discovery of effective psychotropic medications, this gave way to investigation of neurotransmitters such as serotonin and dopamine, and their role in mental illness. In recent history, the focus of scientific investigation has shifted towards the study of brain networks, and the expression of the genes they contain.

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Ch-Ch-Ch-Ch Changes!  What Causes Depression and How Do Antidepressants Work, Part II

Five years ago, I reviewed some of the scientific literature on the neuroplasticity model of depression – a fascinating new way to think about mood disorders.  Departing from the earlier, monoamine-based ideas – too little serotonin or dopamine –  this model suggests that depressive states are associated with a reduction in the brain’s ability to change in response to experience.  In my earlier review of neuroplasticity, I described how our brains are not fixed organs but are instead constantly changing in response to novel information and new learning.  These changes involve strengthening or weakening of synaptic connections along with growth or shrinkage of neurons.  In health, there is a constant growth, sculpting and refinement of neural pathways. This plasticity becomes impaired in depression:  the brain becomes less malleable, there is reduced new learning and people become trapped in despair.  The neuroplasticity model is a radically different way of thinking about mood disorders.  What follows is an update on research on this area, which has focused on several major developments.  These include the following: 1) investigations of brain plasticity based on visual evoked potentials (VEPs); 2) the use of learning and memory tests to evaluate structural change in the CNS and; 3) emerging research on the impact of antidepressants on neuroplasticity.

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Neuroplasticity: What’s Sleep Got to Do with It?

We start with a powerhouse team of neuroscience researchers at the University of Wisconsin:  Giulio Tononi and Chiara Cirelli. These two have been wrestling to understand the basic function of mammalian sleep:  why do we do it? What critical functions does it serve?   In 2003, using a collection of EEG, fMRI and some behavioral memory data, they formulated a new theory on the role of sleep:  The Synaptic Homeostasis Theory, or SHY, for short [3].   This theory asserts four main points:

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Ketamine for Depression in 2018: What You Need to Know

What is ketamine?

Ketamine is a medication that was developed in the 1960s. It was approved as an anesthetic agent for use during medical and surgical procedures by the Food and Drug Administration (FDA) in 1970. Since that time, it has been used primarily as a medication to induce anesthesia (loss of consciousness), and has been used in the management of chronic pain conditions. It is generally given to patients through an IV, but can also be given in inhaled and oral forms. Ketamine is also a drug of abuse that is used illicitly in the United States, and can lead to addiction.

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‘My mood is better so why am I struggling so much?’: Cognitive Challenges in Bipolar Disorder

Patients with bipolar disorder often manifest cognitive disturbances during acute manic, depressive, and mixed states which include difficulties with attention, concentration, planning and memory.   It may come as a surprise, though, to learn that cognitive deficits can persist into euthymia – a state of relative mood stability.   Indeed, approximately 40 % of euthymic bipolar patients show evidence of cognitive impairment (1,2) involving attention, executive function (i.e. planning and organization, cognitive flexibility and set-shifting, and working memory), verbal memory, processing speed and visual memory (3,4).  Patients with bipolar I and bipolar II disorder appear to have a similar pattern of deficits (4).   The purpose of this brief review is to identify cognitive deficits that help distinguish bipolar disorder from other disorders of mood, memory, and executive functioning.   An improved understanding of these deficits will help clinicians tailor their treatment interventions to address the individual needs of patients.

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Mood and Affect: Definitions and Basic Concepts

If you’ve come to this website and are reading this article, the odds are good that you or someone that you know has been diagnosed with a mood disorder.  You might be seeking more information about emotional illnesses.   But before diving into any of the numerous areas of research presented at our site, what if we pause and ask a very basic but important question:  what are moods?  We use this term all the time, but do we truly understand what they consist of and why we experience them?  Even more fuzzy, what about the term, ‘affects’?  We specialize in the treatment of ‘affective illness’ here, but what is an affect and how is it different from a mood?  This brief review will summarize a generally accepted concept of emotions, describe their composition and functional purpose and present current research in this area.  To start, let’s begin by taking a look at how these terms are currently used in clinical practice.

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Understanding The Therapeutic Action of Lithium: The Brain as Complex Real Estate

lithium-membrain

The Lithium Membrain by Anne Naylor.  Lithium coursing through veins in the brain (blue) provides mood stability by acting as a membrane that prevents the effects of the various faces of the illness (circles) on the brain (neural networks).

(Copied with permission from: Anne Naylor and Malhi, G. S. “Lithium therapy in bipolar disorder: a balancing act?” The Lancet 2015 386(9992): 415-416.)

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Affective Temperaments Part II: Approach, Avoidance and the Neurocircuitry of Personality

In my previous blog, I described “temperament” as one’s constitutionally determined way of responding emotionally to the world and introduced Akiskal’s five affective temperaments:  Depressive, Hyperthymic, Cyclothymic, Irritable, and Anxious (1).  Akiskal’s conceptualization of temperament begins with endophenotypes; that is, the outward expression of a gene or trait.   These descriptive endophenotypes provide the scaffolding from which one learns about the underlying processes involved in their formation and evolution.   This approach to studying personality and temperament can best be described as “top-down” – start with what you observe and go from there, from macro to micro.   Another example of the “top-down” view includes the work of Eysenck, who described three “dimensions” of human personality:  Neuroticism (N), Psychoticism(P), and Extroversion (E) (2).   Still another example is that of Cloninger, who described temperament using the following terms: novelty seeking, harm avoidance, reward dependence, persistence, self-directedness, cooperativeness, and self-transcendence (3).

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Affective Temperaments Part I: What Can Personality Traits Teach Us About Mood States?

Emotional expression, or “affect,” covers a range of temporal domains.  There are “emotions,” moment-to-moment fluctuations which, while intensely experienced, come and go within minutes.  When a given emotional state lasts longer – hours, days, or months – it is described as “mood.”  Finally, there is “temperament,” a lifelong emotional disposition considered to be part of one’s constitutional makeup (1).  When temperament manifests as “affective” – that is to say, appears as a similar but less severe variant of a disordered mood state – things start to get interesting.

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Can Anti-inflammatory Drugs Treat Depression? Some Promising New Evidence But Not Yet Enough

The connection between physical ailments and mood is not a new one. It is well-established that medical illness, ranging from infections to cardiovascular disease, can result in increased symptoms of depression, while depression can predispose people to become physically sick more often.  Now, a growing body of evidence shows that depression and physical illness have something important in common: inflammation.

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