What is Depression?
Before we dive into this article, I want you to perform a quick exercise. Let’s begin:
Open your eyes nice and wide, now stand up with your back straight –shoulders pulled back and chest out. You’ll have to keep your eyes wide open and back straight for the entire exercise.
Good so far? Great.
Alright, now start breathing deeply, in your nose and out from your mouth. You’ll immediately start feeling energy, almost like you’re getting ready to charge forward.
Keep breathing deeply, now, extend your hands wide apart e.g. spread your wings. Once they are stretched, I want you to forcefully pull both in like you’re about to clap your hands but stop just before they touch.
Spread your arms out again and repeat this 5 times.
Last step, most importantly, I want you to smile.
How do you feel now? So the point of this exercise is to let you, the reader, know that though depression is complex, there are patterns within it which can be transformed. The simple exercise above may seem silly but the point of it was to break your pattern by use of physical motion (and smiling). Even if you’re not suffering from any form of depression or sadness, the exercise above should help you recognize that any sluggish, lethargic state can be broken simply by controlling your physiology.
Clinically speaking, Major Depressive Disorder (MDD), simply called depression, is a mental disorder of being in a state of low mood for at least two consecutive weeks[R1]. Low mood…hmm, the state of blah. For many, depression can be triggered by feeling overwhelmed by responsibilities, eventually dissuading you from completing any them, subsequently feeling even more depressed. For others it’s caused by life events compounded by [purported] genetic susceptibility. All of which may make you more prone to bouts of sadness for extended periods of time. Well what happens when you don’t fight your way out of this state? What happens if this becomes your new story?
Well like anything if life, if you flex this muscle all too often, you’ll get better at it. This is simplifying, I agree, however it’s the same for any mental state: anxiety, angst, anhedonia, paranoia, stoicism, happiness 🙂 . Practice makes perfect and if you are not taking action to break the cycle it will continue to pull you down further, unless that is your chosen expertise in life, why bother fielding it in your mind?
Depression takes you to some really dark places, it’s essentially putting you in survival mode out of desperation. There is no thriving in this state, thus health, personality, and identity all suffer. What makes you, well YOU, gets erased; you’d wonder why anyone would want to stay in this state for any period of time. Yet it happens and according to the numbers, quite frequently.
Your mind is wired for survival, happiness takes effort and does not come as naturally as say fear or anger. This is on purpose and has kept our species around for millennia. Regardless, non-ideal states, such as depression may be managed by training your mind. What I mean by this is that you have the innate ability built into your mind to both go into a state of depression and bounce out of it, almost immediately. Getting back to the article, let’s start with the symptoms of being in a “low mood”:
- An aversion towards activities normally enjoyed
- Anhedonia (inability to feel pleasure)
- Physical pains without a root cause
- A general loss of energy / motivation
- Memory loss or difficulty recalling thoughts
- Suicidal thoughts
Having bouts of low mood or sadness are absolutely normal, such as the emotions felt after the loss of a loved one or divorce / break up. However, there is still a significant risk here, in that how well and fast you respond will greatly determine your recovery to baseline. We’ll get into more of this later but it’s important to discuss some background on the current state of depression and its diagnosis.
Understanding The History of Major Depressive Disorder (MDD)
Depression was not at the forefront of American mental illness until sometime in the late 1970’s, prior to that “anxiety” was the most common diagnosis[R2]. Though, it was a blanket term for what was considered mental consequence of the industrialized world, family and work. The usual treatment for anxiety included tranquilizers such as meprobamate (Miltown) and later “benzos” such as diazepam (Valium). At the time, these types of meds were the most prescribed in the US, with some 20% of all women and up to 8% of all men being prescribed them[R3].
Subsequently, depression came into the limelight; it is not known quite why it began to overtake the diagnosis of anxiety amongst the American population. Was it a cultural or economic shift causing it? Diet? Something in the water? Again, it was not exactly clear but it was evident that bundling it along with anxiety was no longer working. Without going into the discourse of psychiatry and its credibility within culture at the time, generally speaking, allopathic medicine and patients were not happy. It was primarily the lack of specificity in treating mental illness; the previous diagnosis systems were archaic and needed an overhaul.
The diagnosis “Major Depressive Disorder” emerged during this era, aligned with the third edition of the Diagnostic and Statistical Manual (DSM-III, a classification of mental disorders) release, around 1980[R4]. With this edition, depression and mostly all of its permutations had their own distinct (albeit single) category. This included states such as unipolar depression, melancholia, and short reactive depression. Additionally, MDD diagnosis includes traditional stress symptoms such as sleep disorders, loss of appetite, fatigue, sadness, and focus / concentration difficulty. At this juncture, MDD became the principal nonpsychotic diagnosis, I am sure by now you can see why.
With such an exhaustive scope, MDD functions as a blanket term and we’ve seen this through the numbers; in 2015 alone, 16.1 million Americans (adults over the age of 18) had at least one episode of “MDD” within the previous year. Subsequent to MDD becoming a common diagnosis, increased options to treat the symptoms of MDD have become available. Pharmaceutical companies were quick to shift marketing from tranquilizers to antidepressants, the bad rap garnered from addictive antianxiety meds made this a clear direction. Early antidepressants such as tricyclics and monoamine oxidase inhibitors (MAOIs) were being prescribed more often and by the late 1980’s Selective Serotonin Reuptake Inhibitors (SSRIs) hit the scene. It was a perfect storm for the pharma industry; being that MDD encompassed a nebulous array of symptoms, SSRIs were well positioned to take the market.
Takeaway: Mental illness due to the wear and tear of westernized life was previously linked to anxiety (this term was used for a host of symptoms at the time), however, this paradigm shifted in the late 1970’s. Pressure within the medical field desired specificity, with the DSM-III release, Major Depressive Disorder was born. The term MDD appeared to be a catch-all, many more folks were being diagnosed with this disorder leading to the widespread use of antidepressants.
So, what could be going wrong?
The theories behind depression can be complex; I’ll do my best to keep this simple. Let’s begin with what we have learned thus far:
These are compounds made up of (primarily) a single amino group, hence monoamine. Neurotransmitters such as dopamine, serotonin, norepinephrine, epinephrine, histamine, and melatonin are all monoamines [R5]. These guys are the endogenous chemical messengers of the human body; they are stored in synapses within “synaptic vesicles”, where they are released into a space called the synaptic cleft, from here they bind to receptors on the receiving cell. The receiving end is where the magic happens, the function of the neurotransmitter is executed as it binds to the cell’s receptors. Different neurotransmitters have different functions, in turn, different receptors also have different functions. I’ve always felt images captured this best, see below:
Previously, theories had suggested that inadequate monoamines (typically serotonin, dopamine, or norepinephrine) were the root cause of MDD. Therefore, monoamine oxidase inhibitors were prescribed, these work to inhibit the enzyme responsible for the breakdown of the said neurotransmitters. Another route focused on preventing reuptake of the neurotransmitter serotonin. Selective serotonin reuptake inhibitors (SSRIs) perform this task by preventing the serotonin from being reabsorbed quickly, making it more available. The idea here is to let serotonin do its job longer and depending on the receptor, may lead to an increase in mood.
However, there is a problem. Curing or treating MDD has proven complex, attacking any deficiencies or inefficiencies associated with monoamines does not always work. The monoamine hypothesis has been tested, research has indicated that inducing a depletion of monoamines such as serotonin will NOT lead to consistent (expected) results[R6]. Serotonin has typically been the target for treatment; the theory goes that there may be a deficiency of this neurotransmitter, thus typical treatments aim to prevent reabsorption or reduce the body’s ability to break it down. Recently, SSRI effectiveness was determined to be on par with placebo for those whom are mild to moderately depressed, furthermore adverse effects (such as loss of sex drive) may outweigh the small benefit observed by administration of SSRIs[R7].
The biochemistry of the human brain still remains an enigma, successful treatment for depression is subjective; how do you feel? Is low mood still an issue? If these questions cannot be answered with conviction, then the issue(s) remains, regardless of what biochemical recipe is [thought to be] brewing in one’s mind.
Genetics and Epigenetics:
Consider this, if your physical body was a movie, then your genes are the script and these genes are being directed by your epigenetics.
The genetics of depression are not clearly defined [yet], studies are having difficulty finding consistent correlation of specific genes / polymorphisms within our genome and MDD[R8]. Keeping in mind however, that environment (experiences, exposure, nutrition, nurture etc.) and subsequently epigenetics are significant factors discerning whether or not a specific gene will remain dormant or become active / expressed[R9].
Thus far, many studies have concentrated on genetic susceptibility of individuals towards MDD, based on their threshold for stress.
Think of it this way, if the same exact life events occurred to two different people and one them ended up with MDD while the other thrived, what could have caused such distinct responses? Research indicates that genetics may play a role in these outcomes.
On to a couple notable genes.
One study from 2006 focused on the serotonin transporter, 5-HTTLPR polymorphism (found on the serotonin gene SLC6A45). This study was based on previous work that indicated that 5-HTTLPR may be associated with MDD for individuals whom face social adversity. Their goal was to associate an inclination of MDD and the ability to handle stressors, such as social adversity with the 5-HTTLPR genotype, however the study was unable to replicate the outcome of previous findings[R10]. There goes that hypothesis (yes, I am oversimplifying, a bit), let’s look at one more.
SLC6A15 encodes a sodium-dependent neutral amino acid transporter (mouthful, I know), called B(0)AT2[R11]. A recent study focused on this gene as it was implicated in depression from previous research. It was found to be more common in specific regions of the brain and appeared to be associated with D2 neurons, which responds to dopamine. The study used a mouse model and found something interesting. The mice were susceptible to this disorder and when exposed to chronic social stress, they displayed symptoms of depression (not enjoying their favorite foods, social withdrawal). The researchers found that when exposed to the stress, there was a marked reduction of the SLC6A15 gene within the D2 neurons. Once the SLC6A15 levels were enhanced, the mice were much more resilient to stress[R12].
Inflammation and Depression
Whether inflammation is intensifying depression or the other way around, there appears to be a link. Many of the symptoms of depression are similar to those found when your body is experiencing an increase in inflammatory markers (fatigue, pain, lethargy).
Cytokines are proteins that cells secrete, many types are heavily involved in the inflammatory response (though some are anti-inflammatory). Research has indicated that while SSRIs may reduce symptoms of depression they also reduce inflammatory cytokines such as [interleukins] IL-1β and IL-6[R13]. Additionally, stress, which contributes to depression, has also been shown to also increase the inflammatory response, specifically through an increase in IL-1β[R14].
Exercise is great for the body and mind, however there is an innate inflammatory response that is associated with muscle damage and repair. This is the foundation of resistance training and weight lifting, it’s how we build muscle but it lends itself to inflammation. However, this initial effect is followed by an anti-inflammatory response; the whole point of this cycle may be to dissuade you from proceeding until any physical repercussions are completely repaired.
It’s also important to consider gut biome, the configuration of your gut bacteria greatly affects how your body deals with inflammation. One study, using mice, saw the introduction of Lactobacillus rhamnosus affect GABA (neurotransmitter that modulates excitability) responsible for production in different parts of the brain, this strain had shown a net reduction in anxiety and depression[R15]. Another study, indicated that stressing adult mice without gut bacteria impacted their hypothalamic–pituitary–adrenal (HPA-axis) mediated stress response. Their endocrine systems had produced larger amounts of cortical steroids in response to the stress, additionally they produced less brain derived neurotrophic factor expression (BDNF – a protein that promotes survival and growth of neurons). The inflated stress response was reversed with the introduction of Bifidobacterium infantis[R16].
Dealing with Depression – Bringing it all together
One common denominator in all the aforementioned modalities: your ability to handle, compensate for, and adjust to stress. There are genetic, environmental, and nutritional components defining your threshold, ideally you’d want to keep them in a well-balanced harmony. This is why it’s important to take care of your mind and body; falling on the notion that it’s all genetics, that it runs in the family, or that you just need to go through this phase may inevitability lead to failure.
Depression is a mental state of desperation, the body is shutting down its ability to thrive as this is all you know and the smallest triggers will provide sustenance to it as you lose your ability to thrive / react / surpass etc. Even if you have to force it in the beginning, put a smile on your face and start moving. Get out of the funk faster than you got it in, thrive on.
Get a morning routine as soon as you wake up, I benefit from the following:
Supplement with the following:
- High potency Fish Oil – At least 2g daily
- Vitamin D3[R17] – 5000 IUs daily
- Lithium Orotate – 5mg to 10mg daily (elemental lithium); stacks exceptionally well with caffeine and works great on mood[R18], [R19], [R20]
- SAMe (S-adenosyl- methionine) – 1g to 1.6g daily; methyl donor, helps with inflammation and depression. Assists in the production of neurotransmitters[R21]; anecdotally, this has seen a great response around the web.
- Limit your intake of pro-inflammatory or energy robbing foods. Such as excess simple carbohydrates and most grains (e.g. wheat is known to promote inflammation, not only from the carbohydrates but also from other components like gliadin, amylase-trypsin inhibitors[R22], and lectins)
- Time restricted eating / intermittent fasting – Limit your eating schedule to a 10 hour window, giving your digestion much needed rest (inflammation control)
- Consume some caffeine!
- Moderate weight training and cardio 2 – 3 times a week, important to stay consistent. The “repeated bout effect” can reduce inflammation induced by weight training[R23]. Great for confidence and to get physiology out of a depressive, motionless state.
Daily Cold Therapy
- Cold Showers – Well, start with a hot shower to clean out your pores, scalp, and hair then finish with a very cold 5 minute rinse. The energy reaped from cold showers make them well worth it, additionally it’s helpful for inflammation and promotes both heat and cold-shock proteins[R24].
That’s it for now! Check back for more articles, share our content, and give us your feedback.
- Herzberg D. Happy Pills in America: From Miltown to Prozac. Baltimore: Johns Hopkins University Press; 2009.
- Parry H, Balter MM, Mellinger G, Cisin I, Manheimer D. National Patterns of Psychotherapeutic Drug Use: Archives of General Psychiatry; 1973.
- “Entrez Gene: solute carrier family 6 (neutral amino acid transporter)”
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